Materiały źródłowe

• #1 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  More than 500,000 people in the United States live with end-stage renal disease (ESRD). The development of chronic kidney disease (CKD) and its progression to this terminal disease remains a significant cause of reduced quality of life and premature mortality. […] Many chronic diseases can cause end-stage renal disease. In many developed and developing countries, diabetes mellitus is the leading cause. […] End-stage renal disease is defined as a GFR of less than 15 mL/min. […] Many chronic diseases can cause end-stage renal disease. In many developed and developing countries, diabetes mellitus is the leading cause. […] The decline of kidney function is gradual and may initially present asymptomatically. The natural history of renal failure depends on the etiology of the disease but ultimately involves early homeostatic mechanisms involving hyperfiltration of the nephrons.

• #2 End-Stage Renal Disease | Nutrition Guide for Clinicians

  https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342059/all/End_Stage_Renal_Disease

  Chronic kidney disease (CKD) is a progressive syndrome in which the kidneys lose their ability to filter blood, concentrate urine, excrete waste products, and maintain electrolyte balance. End-stage renal disease (ESRD) is the end result of many forms of CKD. It is characterized by severely limited kidney function that is insufficient to maintain life. Thus, most patients with ESRD require renal replacement therapy via hemodialysis, peritoneal dialysis, or kidney transplantation. […] ESRD is defined by a GFR that is less than 15 mL/min/1.73 m2. […] Due to the kidneys importance in regulating electrolyte and acid-base balance, ESRD leads to hyperkalemia, hyperphosphatemia, often hypocalcemia, and anion gap metabolic acidosis. Vitamin D deficiency is also common. […] In general, once CKD has degenerated to ESRD, it is irreversible. Treatment is aimed at treating complications and replacing renal function via dialysis or transplantation.

• #3 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. […] The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progression to ESRD, (2) inflammation of the classical type characteristic of primary and secondary autoimmune glomerulonephritis and infectious recurrent pyelonephritis, as well as immune reactions in kidney allograft rejection, and (3) chronic systemic inflammation (ChSI), pathogenetically characterized by latent microcirculatory disorders and manifestations of paracoagulation. […] The development of CKD and its progression to ESRD remain significant factors in the decline in quality of life and premature death.

• #4 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  The development of CKD and its progression to ESRD remain significant factors in the decline in quality of life and premature death. […] The importance of local manifestations of ChLGI in the formation of both autosomal dominant and autosomal recessive polycystic kidney disease has also been proven. […] It is important to remember that DKD creates a vicious pathogenetic cycle since chronic kidney disease (CKD) contributes to the development of systemic ChLGI, insulin resistance, and the formation of metabolic syndrome in people who do not have it initially. […] Thus, against the backdrop of systemic ChLGI, the progression of CKD to ESRD is the result of a complex interplay of local and systemic genetic, ontogenetic, and environmental variables, as well as metabolic and immunological components.

• #5 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. […] The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progression to ESRD, (2) inflammation of the classical type characteristic of primary and secondary autoimmune glomerulonephritis and infectious recurrent pyelonephritis, as well as immune reactions in kidney allograft rejection, and (3) chronic systemic inflammation (ChSI), pathogenetically characterized by latent microcirculatory disorders and manifestations of paracoagulation. […] The development of CKD and its progression to ESRD remain significant factors in the decline in quality of life and premature death.

• #6 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation. | EBSCOhost

  https://search.ebscohost.com/login.aspx?direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=16616596&AN=153600278&h=ECK21gPArDKqjMiVZIxYMMRC2iT0cv5jokdAoW279rC%2Bh2xTM7OVL47Z2ePIAg6JD4Gp%2B9nY35CTbmdnY3XlZw%3D%3D&crl=c

  Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. […] In ESRD, irreversible changes in the kidneys are associated with systemic changes of proinflammatory nature and dysfunctions of internal organs, skeletal muscles, and integumentary tissues. […] The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progression to ESRD, (2) inflammation of the classical type characteristic of primary and secondary autoimmune glomerulonephritis and infectious recurrent pyelonephritis, as well as immune reactions in kidney allograft rejection, and (3) chronic systemic inflammation (ChSI), pathogenetically characterized by latent microcirculatory disorders and manifestations of paracoagulation.

• #7 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. […] The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progression to ESRD, (2) inflammation of the classical type characteristic of primary and secondary autoimmune glomerulonephritis and infectious recurrent pyelonephritis, as well as immune reactions in kidney allograft rejection, and (3) chronic systemic inflammation (ChSI), pathogenetically characterized by latent microcirculatory disorders and manifestations of paracoagulation. […] The development of ChSI is closely associated with programmed hemodialysis in ESRD, as well as with the systemic autoimmune process.

• #8 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation. | EBSCOhost

  https://search.ebscohost.com/login.aspx?direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=16616596&AN=153600278&h=ECK21gPArDKqjMiVZIxYMMRC2iT0cv5jokdAoW279rC%2Bh2xTM7OVL47Z2ePIAg6JD4Gp%2B9nY35CTbmdnY3XlZw%3D%3D&crl=c

  The development of ChSI is closely associated with programmed hemodialysis in ESRD, as well as with the systemic autoimmune process. […] Consideration of ESRD pathogenesis from the standpoint of the theory of general pathological processes opens up the scope not only for particular but also for universal approaches to conducting pathogenetic therapies and diagnosing and predicting systemic complications in severe nephropathies.

• #9 Chronic Kidney Disease (CKD): Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/238798-overview

  A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased 50%. […] The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive kidney dysfunction. The increased glomerular capillary pressure may damage the capillaries, leading initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical to those observed in humans with CKD.

• #10 Chronic Kidney Disease (CKD): Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/238798-overview

  A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased 50%. […] The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive kidney dysfunction. The increased glomerular capillary pressure may damage the capillaries, leading initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical to those observed in humans with CKD.

• #11 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Although hyperfiltration and hypertrophy of residual nephrons are beneficial for maintaining GFR, it is found to be a major cause of progressive renal dysfunction. […] The increased glomerular capillary pressure may damage the capillaries, leading to focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. […] Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L.

• #12 Chronic Kidney Disease (CKD): Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/238798-overview

  A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased 50%. […] The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive kidney dysfunction. The increased glomerular capillary pressure may damage the capillaries, leading initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical to those observed in humans with CKD.

• #13 Chronic Kidney Disease (CKD): Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/238798-overview

  Factors other than the underlying disease process and glomerular hypertension that may cause progressive kidney injury include the following: systemic hypertension, nephrotoxins (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], intravenous contrast media), decreased perfusion (eg, from severe dehydration or episodes of shock), proteinuria (in addition to being a marker of CKD), hyperlipidemia, hyperphosphatemia with calcium phosphate deposition, smoking, uncontrolled diabetes. […] Thaker et al found a strong association between episodes of acute kidney injury (AKI) and cumulative risk for the development of advanced CKD in patients with diabetes mellitus who experienced AKI in multiple hospitalizations. […] Findings from the Atherosclerosis Risk in Communities (ARIC) Study, a prospective observational cohort, suggest that inflammation and hemostasis are antecedent pathways for CKD.

• #14 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Although hyperfiltration and hypertrophy of residual nephrons are beneficial for maintaining GFR, it is found to be a major cause of progressive renal dysfunction. […] The increased glomerular capillary pressure may damage the capillaries, leading to focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. […] Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L.

• #15 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  Renal fibrosis is a typical final stage of inflammation that occurs in nearly all nephropathies. […] Local and systemic disruptions of oxygen transport with the formation of hypoxia are common causes of renal sclerosis. […] Many systemic factors of progressive renal failure aggravate it via the mechanisms of vicious pathogenetic cycles and include the following: poisoning of the body with nephrotoxins, excess in the blood of potentially toxic water-soluble drugs, hypoproteinemia, hyperlipidemia, hyperphosphatemia, hyperkalemia, hyponatremia, hyperuricemia, and metabolic acidosis. […] The mutual negative influence of impaired renal function and cardiovascular disease can lead to cardiorenal syndrome. […] There is no doubt that pattern recognition receptors (PRRs) play a key pathogenetic role in ESRD-associated local and systemic disturbances.

• #16 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L. In CKD, the kidneys cannot produce enough ammonia in the proximal tubules to excrete endogenous acid into the urine in the form of ammonium. […] Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. Acidosis also interferes with vitamin D metabolism.

• #17 Chronic Kidney Disease (CKD): Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/238798-overview

  Factors other than the underlying disease process and glomerular hypertension that may cause progressive kidney injury include the following: systemic hypertension, nephrotoxins (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], intravenous contrast media), decreased perfusion (eg, from severe dehydration or episodes of shock), proteinuria (in addition to being a marker of CKD), hyperlipidemia, hyperphosphatemia with calcium phosphate deposition, smoking, uncontrolled diabetes. […] Thaker et al found a strong association between episodes of acute kidney injury (AKI) and cumulative risk for the development of advanced CKD in patients with diabetes mellitus who experienced AKI in multiple hospitalizations. […] Findings from the Atherosclerosis Risk in Communities (ARIC) Study, a prospective observational cohort, suggest that inflammation and hemostasis are antecedent pathways for CKD.

• #18 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  The most common morphological forms of glomerulonephritis leading to ESRD, as well as glomerulonephritis leading to death in ESRD, are usually associated with (a) focal segmental glomerulosclerosis, (b) membranous glomerulonephritis, (c) mesangial proliferative glomerulonephritis, (d) immunoglobulin A (IgA) nephropathy (mesangial and endocapillary hypercellularity 50% glomeruli, glomerulosclerosis, tubular atrophy, and interstitial fibrosis), (e) lupus nephritis, and (f) kidney damage in ShenleinHenoch purpura (focal segmental proliferative glomerulonephritis and rapidly progressive crescentic glomerulonephritis). […] Renal fibrosis is a typical final stage of inflammation that occurs in nearly all nephropathies. […] Many systemic factors of progressive renal failure aggravate it via the mechanisms of vicious pathogenetic cycles and include the following: poisoning of the body with nephrotoxins, excess in the blood of potentially toxic water-soluble drugs, hypoproteinemia, hyperlipidemia, hyperphosphatemia, hyperkalemia, hyponatremia, hyperuricemia, and metabolic acidosis, hypertension, accelerated development of atherosclerosis and heart failure, and rapid progression of diabetes mellitus (with diabetic kidney disease DKD).

• #19 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  Renal fibrosis is a typical final stage of inflammation that occurs in nearly all nephropathies. […] Local and systemic disruptions of oxygen transport with the formation of hypoxia are common causes of renal sclerosis. […] Many systemic factors of progressive renal failure aggravate it via the mechanisms of vicious pathogenetic cycles and include the following: poisoning of the body with nephrotoxins, excess in the blood of potentially toxic water-soluble drugs, hypoproteinemia, hyperlipidemia, hyperphosphatemia, hyperkalemia, hyponatremia, hyperuricemia, and metabolic acidosis. […] The mutual negative influence of impaired renal function and cardiovascular disease can lead to cardiorenal syndrome. […] There is no doubt that pattern recognition receptors (PRRs) play a key pathogenetic role in ESRD-associated local and systemic disturbances.

• #20 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  The emergence of a proinflammatory phenotype in a large number of cells at once determines the effect of their network interaction with the development of tissue stress, for example, through the formation of a cytokine network. […] The characteristic typical signs of renal fibrosis are the development of cellular and tissue proinflammatory stress in the kidneys, including oxidative stress, the formation of inflammasomes, and factors of the proinflammatory secretory phenotype. […] Thus, regardless of the precise causal mechanism or localization of the process, the universal effect of cytokines and other mediators of various renal cells on the development of renal fibrosis has been demonstrated in people and animals. […] The importance of local manifestations of ChLGI in the formation of both autosomal dominant and autosomal recessive polycystic kidney disease has also been proven.

• #21 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  Currently, there are three “large” general pathological processes associated with inflammation: (1) systemic/local chronic low-grade inflammation (ChLGI); (2) local and systemic manifestations of inflammation of the classical (canonical) type; (3) systemic inflammation, which is critical for the life of patients. […] The characteristic typical signs of renal fibrosis are the development of cellular and tissue proinflammatory stress in the kidneys, including oxidative stress, the formation of inflammasomes, and factors of the proinflammatory secretory phenotype. […] Thus, regardless of the precise causal mechanism or localization of the process, the universal effect of cytokines and other mediators of various renal cells on the development of renal fibrosis has been demonstrated in people and animals.

• #22 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  The emergence of a proinflammatory phenotype in a large number of cells at once determines the effect of their network interaction with the development of tissue stress, for example, through the formation of a cytokine network. […] The characteristic typical signs of renal fibrosis are the development of cellular and tissue proinflammatory stress in the kidneys, including oxidative stress, the formation of inflammasomes, and factors of the proinflammatory secretory phenotype. […] Thus, regardless of the precise causal mechanism or localization of the process, the universal effect of cytokines and other mediators of various renal cells on the development of renal fibrosis has been demonstrated in people and animals. […] The importance of local manifestations of ChLGI in the formation of both autosomal dominant and autosomal recessive polycystic kidney disease has also been proven.

• #23 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  Currently, there are three “large” general pathological processes associated with inflammation: (1) systemic/local chronic low-grade inflammation (ChLGI); (2) local and systemic manifestations of inflammation of the classical (canonical) type; (3) systemic inflammation, which is critical for the life of patients. […] The characteristic typical signs of renal fibrosis are the development of cellular and tissue proinflammatory stress in the kidneys, including oxidative stress, the formation of inflammasomes, and factors of the proinflammatory secretory phenotype. […] Thus, regardless of the precise causal mechanism or localization of the process, the universal effect of cytokines and other mediators of various renal cells on the development of renal fibrosis has been demonstrated in people and animals.

• #24 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Although hyperfiltration and hypertrophy of residual nephrons are beneficial for maintaining GFR, it is found to be a major cause of progressive renal dysfunction. […] The increased glomerular capillary pressure may damage the capillaries, leading to focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. […] Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L.

• #25 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L. In CKD, the kidneys cannot produce enough ammonia in the proximal tubules to excrete endogenous acid into the urine in the form of ammonium. […] Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. Acidosis also interferes with vitamin D metabolism.

• #26 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Although hyperfiltration and hypertrophy of residual nephrons are beneficial for maintaining GFR, it is found to be a major cause of progressive renal dysfunction. […] The increased glomerular capillary pressure may damage the capillaries, leading to focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. […] Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L.

• #27 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L. In CKD, the kidneys cannot produce enough ammonia in the proximal tubules to excrete endogenous acid into the urine in the form of ammonium. […] Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. Acidosis also interferes with vitamin D metabolism.

• #28 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. […] Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands. […] Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. […] The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months.

• #29 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Factors that may worsen renal injury include nephrotoxins (NSAIDs), systemic hypertension, proteinuria, dehydration, smoking, hyperlipidemia, uncontrolled diabetes, and hyperphosphatemia. […] Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m; at this point, the kidneys have decreased ability to excrete potassium. […] Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L. In CKD, the kidneys cannot produce enough ammonia in the proximal tubules to excrete endogenous acid into the urine in the form of ammonium. […] Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. Acidosis also interferes with vitamin D metabolism.

• #30 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. […] Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands. […] Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. […] The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months.

• #31 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. Different types of bone disease occur with CKD, as follows: high-turnover bone disease from high parathyroid hormone (PTH) levels, low-turnover bone disease (adynamic bone disease), defective mineralization (osteomalacia), mixed disease, and beta-2-microglobulin associated bone disease. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands.

• #32 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. […] Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands. […] Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. […] The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months.

• #33 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. Different types of bone disease occur with CKD, as follows: high-turnover bone disease from high parathyroid hormone (PTH) levels, low-turnover bone disease (adynamic bone disease), defective mineralization (osteomalacia), mixed disease, and beta-2-microglobulin associated bone disease. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands.

• #34 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. […] Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands. […] Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. […] The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months.

• #35 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. Different types of bone disease occur with CKD, as follows: high-turnover bone disease from high parathyroid hormone (PTH) levels, low-turnover bone disease (adynamic bone disease), defective mineralization (osteomalacia), mixed disease, and beta-2-microglobulin associated bone disease. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands.

• #36 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. […] Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands. […] Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. […] The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months.

• #37 End-Stage Renal Disease | Nutrition Guide for Clinicians

  https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342059/all/End_Stage_Renal_Disease

  It is essential to treat ESRD complications that may arise. When remaining kidney function is markedly reduced, the following complications are often seen in conjunction with dialysis therapy: […] Elevated blood phosphorus concentrations are associated with increased mortality in ESRD patients and increase the risk for cardiovascular events, at least in part by contributing to vascular calcification. […] Management of hyperphosphatemia and renal osteodystrophy has improved with phosphate binders, particularly sevelamer hydrochloride (Renagel), which also helps prevent hypercalcemia-related vascular calcification.

• #38 End-Stage Renal Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499861/

  Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. […] Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands. […] Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. […] The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months.

• #39 End-Stage Renal Disease | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/21081

  Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m. […] Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. […] Renal bone disease is a common complication of CKD. Different types of bone disease occur with CKD, as follows: high-turnover bone disease from high parathyroid hormone (PTH) levels, low-turnover bone disease (adynamic bone disease), defective mineralization (osteomalacia), mixed disease, and beta-2-microglobulin associated bone disease. […] Secondary hyperparathyroidism develops in CKD because of hyperphosphatemia, hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol, and intrinsic alteration in the parathyroid glands.

• #40 Chronic Kidney Disease – Genitourinary Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/genitourinary-disorders/chronic-kidney-disease/chronic-kidney-disease

  Abnormalities of calcium, phosphate, parathyroid hormone (PTH), and vitamin D metabolism can occur, as can renal osteodystrophy. […] Moderate metabolic acidosis (plasma bicarbonate content 15 to 20 mmol/L) is characteristic. […] Anemia is characteristic of moderate to advanced CKD (stage 3). […] The anemia of CKD is normochromic-normocytic, with a hematocrit of 20 to 30% (35 to 40% in patients with polycystic kidney disease). […] The etiology of acute kidney injury (AKI) and CKD is determined based on clinical context, personal and family history, social and environmental factors, medications (including over-the-counter) and supplements, physical examination, and possibly genetic testing. […] The definitive diagnostic tool is renal biopsy, but it is not recommended when ultrasound indicates small, fibrotic kidneys; high procedural risk outweighs low diagnostic yield.

• #41 Inflammatory Syndrome in Chronic Kidney Disease: Pathogenesis and Influence on Outcomes

  https://eurekaselect.com/public/article/30395

  Morbidity and mortality are markedly elevated in chronic kidney disease (CKD) patients as consequence of cardiovascular risk factors clustering. […] CKD results in a chronic, low-grade inflammatory process that becomes evident even in the early stages of the disease. […] In end-stage renal disease (ESRD), elevated CRP levels are a strong predictor of all-cause and cardiovascular mortality. […] Recent studies showed IL-6 to predict more reliably CVD and mortality in ESRD patients. […] Several factors are involved in triggering the inflammatory process including patient-related factors, such as underlying disease, comorbidity, oxidative stress, infectious, genetic or immunologic factors and uremia per se, as well as those arising from dialysis treatment itself, mainly membrane and dialysate biocompatibility.

• #42 Inflammatory Syndrome in Chronic Kidney Disease: Pathogenesis and Influence on Outcomes

  https://eurekaselect.com/public/article/30395

  Morbidity and mortality are markedly elevated in chronic kidney disease (CKD) patients as consequence of cardiovascular risk factors clustering. […] CKD results in a chronic, low-grade inflammatory process that becomes evident even in the early stages of the disease. […] In end-stage renal disease (ESRD), elevated CRP levels are a strong predictor of all-cause and cardiovascular mortality. […] Recent studies showed IL-6 to predict more reliably CVD and mortality in ESRD patients. […] Several factors are involved in triggering the inflammatory process including patient-related factors, such as underlying disease, comorbidity, oxidative stress, infectious, genetic or immunologic factors and uremia per se, as well as those arising from dialysis treatment itself, mainly membrane and dialysate biocompatibility.

• #43 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  To begin with, the development of systemic proinflammatory tissue stress is promoted by the presence of ESRD and PH due to multiple sources of inflammatory stimuli, such as oxidative stress, acidosis, and fluid overload, increased comorbidity, including infections, dialysis procedure, production, and inadequate removal (insufficient clearance) of proinflammatory cytokines. […] Thus, against the backdrop of systemic ChLGI, the progression of CKD to ESRD is the result of a complex interplay of local and systemic genetic, ontogenetic, and environmental variables, as well as metabolic and immunological components.

• #44

  https://link.springer.com/article/10.1007/s10620-014-3287-z

  Moreover, colonic bacterial DNA has been detected in the mesenteric lymph nodes, blood, liver and spleen of animals with experimental CKD. […] Since in healthy humans and animals, the epithelial barrier prevents translocation of bacteria and their harmful by-products and components, the presence of endotoxemia and the detection of the gut microbial DNA in the blood of ESRD patients and in the blood and multiple tissues of CKD animals point to impairment of intestinal barrier structure and function. […] There is mounting evidence that advanced CKD impairs intestinal epithelial barrier structure and function, thereby enabling the entry of endotoxin and other bacterial components in the intestinal wall and systemic circulation. […] In fact, massive depletion of the gastrointestinal epithelial tight junction proteins was reported in CKD animals.

• #45

  https://link.springer.com/article/10.1007/s10620-014-3287-z

  Moreover, colonic bacterial DNA has been detected in the mesenteric lymph nodes, blood, liver and spleen of animals with experimental CKD. […] Since in healthy humans and animals, the epithelial barrier prevents translocation of bacteria and their harmful by-products and components, the presence of endotoxemia and the detection of the gut microbial DNA in the blood of ESRD patients and in the blood and multiple tissues of CKD animals point to impairment of intestinal barrier structure and function. […] There is mounting evidence that advanced CKD impairs intestinal epithelial barrier structure and function, thereby enabling the entry of endotoxin and other bacterial components in the intestinal wall and systemic circulation. […] In fact, massive depletion of the gastrointestinal epithelial tight junction proteins was reported in CKD animals.

• #46

  https://link.springer.com/article/10.1007/s10620-014-3287-z

  Moreover, in vitro studies revealed significant depletion of the tight junction proteins and reduction of trans-epithelial electrical resistance in cultured human colonocytes incubated in media containing human uremic plasma. […] Subsequent experiments have lead to the identification of ammonia, a product of microbial urease, as the principal mediator of uremia-induced intestinal barrier disruption. […] In addition to disrupting the epithelial barrier, advanced CKD alters the composition and function of the intestinal microbiome. […] This phenomenon is driven by the luminal influx of urea, dietary restrictions and pharmacologic interventions that alter the guts biochemical milieu leading to dysbiosis marked by the dominance of urease expressing and indole and p-cresol forming bacteria and the suppression of the short-chain fatty acid-forming bacteria.

• #47

  https://link.springer.com/article/10.1007/s10620-014-3287-z

  Moreover, in vitro studies revealed significant depletion of the tight junction proteins and reduction of trans-epithelial electrical resistance in cultured human colonocytes incubated in media containing human uremic plasma. […] Subsequent experiments have lead to the identification of ammonia, a product of microbial urease, as the principal mediator of uremia-induced intestinal barrier disruption. […] In addition to disrupting the epithelial barrier, advanced CKD alters the composition and function of the intestinal microbiome. […] This phenomenon is driven by the luminal influx of urea, dietary restrictions and pharmacologic interventions that alter the guts biochemical milieu leading to dysbiosis marked by the dominance of urease expressing and indole and p-cresol forming bacteria and the suppression of the short-chain fatty acid-forming bacteria.

• #48

  https://link.springer.com/article/10.1007/s10620-014-3287-z

  Moreover, in vitro studies revealed significant depletion of the tight junction proteins and reduction of trans-epithelial electrical resistance in cultured human colonocytes incubated in media containing human uremic plasma. […] Subsequent experiments have lead to the identification of ammonia, a product of microbial urease, as the principal mediator of uremia-induced intestinal barrier disruption. […] In addition to disrupting the epithelial barrier, advanced CKD alters the composition and function of the intestinal microbiome. […] This phenomenon is driven by the luminal influx of urea, dietary restrictions and pharmacologic interventions that alter the guts biochemical milieu leading to dysbiosis marked by the dominance of urease expressing and indole and p-cresol forming bacteria and the suppression of the short-chain fatty acid-forming bacteria.

• #49

  https://link.springer.com/article/10.1007/s10620-014-3287-z

  Moreover, in vitro studies revealed significant depletion of the tight junction proteins and reduction of trans-epithelial electrical resistance in cultured human colonocytes incubated in media containing human uremic plasma. […] Subsequent experiments have lead to the identification of ammonia, a product of microbial urease, as the principal mediator of uremia-induced intestinal barrier disruption. […] In addition to disrupting the epithelial barrier, advanced CKD alters the composition and function of the intestinal microbiome. […] This phenomenon is driven by the luminal influx of urea, dietary restrictions and pharmacologic interventions that alter the guts biochemical milieu leading to dysbiosis marked by the dominance of urease expressing and indole and p-cresol forming bacteria and the suppression of the short-chain fatty acid-forming bacteria.

• #50 Arterial stiffness in end-stage renal disease—pathogenesis, clinical epidemiology, and therapeutic potentials | Hypertension Research

  https://www.nature.com/articles/s41440-018-0025-5

  Arterial stiffness is an important risk factor for cardiovascular morbidity and mortality in patients with end-stage renal disease (ESRD). […] Pathogenesis of the arteriosclerotic process in ESRD is complex and not yet fully understood. […] Several factors unique to ESRD, such as mineral metabolism disturbances, vascular calcifications, formation of advanced glycation end-products, and acute and chronic volume overload, are proposed to play a particular role in the progression of arteriosclerosis in ESRD. […] Although the mechanistic background of arterial stiffening is not yet fully clear, it seems likely that pathways closely related to ESRD, such as volume overload, mineral metabolism disturbances, vascular calcifications, formation of advanced glycation end-products (AGEs), inflammation and oxidative stress, are prominent mediators of arteriosclerosis.

• #51 Arterial stiffness in end-stage renal disease—pathogenesis, clinical epidemiology, and therapeutic potentials | Hypertension Research

  https://www.nature.com/articles/s41440-018-0025-5

  Arterial stiffness is an important risk factor for cardiovascular morbidity and mortality in patients with end-stage renal disease (ESRD). […] Pathogenesis of the arteriosclerotic process in ESRD is complex and not yet fully understood. […] Several factors unique to ESRD, such as mineral metabolism disturbances, vascular calcifications, formation of advanced glycation end-products, and acute and chronic volume overload, are proposed to play a particular role in the progression of arteriosclerosis in ESRD. […] Although the mechanistic background of arterial stiffening is not yet fully clear, it seems likely that pathways closely related to ESRD, such as volume overload, mineral metabolism disturbances, vascular calcifications, formation of advanced glycation end-products (AGEs), inflammation and oxidative stress, are prominent mediators of arteriosclerosis.

• #52 Arterial stiffness in end-stage renal disease—pathogenesis, clinical epidemiology, and therapeutic potentials | Hypertension Research

  https://www.nature.com/articles/s41440-018-0025-5

  Mechanistic pathways closely related to ESRD are suggested to play a particular role in the progression of arteriosclerosis among these patients. […] The severely impaired capacity of patients with advanced CKD to maintain the homeostasis of sodium and water as well as the inability of hemodialysis patients to reach dry weight are common problems that result in chronic volume overload. […] The severity of vascular calcifications is strongly associated with the progression of arteriosclerosis in ESRD and represents an independent predictor of mortality. […] In advanced CKD, accumulation of AGEs may be either due to reduced renal excretion or due to elevated formation mediated through cumulative carbonyl and oxidative stress. […] Angiopoietin-2 is a Tie-2 receptor that not only plays an important role in angiogenesis but also plays important regulatory roles in several pathophysiological processes, including vascular fibrosis and inflammation.

• #53 Arterial stiffness in end-stage renal disease—pathogenesis, clinical epidemiology, and therapeutic potentials | Hypertension Research

  https://www.nature.com/articles/s41440-018-0025-5

  Mechanistic pathways closely related to ESRD are suggested to play a particular role in the progression of arteriosclerosis among these patients. […] The severely impaired capacity of patients with advanced CKD to maintain the homeostasis of sodium and water as well as the inability of hemodialysis patients to reach dry weight are common problems that result in chronic volume overload. […] The severity of vascular calcifications is strongly associated with the progression of arteriosclerosis in ESRD and represents an independent predictor of mortality. […] In advanced CKD, accumulation of AGEs may be either due to reduced renal excretion or due to elevated formation mediated through cumulative carbonyl and oxidative stress. […] Angiopoietin-2 is a Tie-2 receptor that not only plays an important role in angiogenesis but also plays important regulatory roles in several pathophysiological processes, including vascular fibrosis and inflammation.

• #54 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. […] The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. […] Muscle wasting in ESRD patients is attributed to a variety of factors that collectively contribute to the progressive loss of muscle mass in this population. Metabolic acidosis and impaired insulin/IGF-1 signaling pathways disrupt the regulation of muscle protein synthesis and degradation, leading to muscle atrophy. […] Chronic inflammation, dysregulated appetite regulation, and altered microRNA expression patterns also contribute to muscle wasting in ESRD.

• #55 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. […] The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. […] Muscle wasting in ESRD patients is attributed to a variety of factors that collectively contribute to the progressive loss of muscle mass in this population. Metabolic acidosis and impaired insulin/IGF-1 signaling pathways disrupt the regulation of muscle protein synthesis and degradation, leading to muscle atrophy. […] Chronic inflammation, dysregulated appetite regulation, and altered microRNA expression patterns also contribute to muscle wasting in ESRD.

• #56 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. […] The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. […] Muscle wasting in ESRD patients is attributed to a variety of factors that collectively contribute to the progressive loss of muscle mass in this population. Metabolic acidosis and impaired insulin/IGF-1 signaling pathways disrupt the regulation of muscle protein synthesis and degradation, leading to muscle atrophy. […] Chronic inflammation, dysregulated appetite regulation, and altered microRNA expression patterns also contribute to muscle wasting in ESRD.

• #57 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. […] The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. […] Muscle wasting in ESRD patients is attributed to a variety of factors that collectively contribute to the progressive loss of muscle mass in this population. Metabolic acidosis and impaired insulin/IGF-1 signaling pathways disrupt the regulation of muscle protein synthesis and degradation, leading to muscle atrophy. […] Chronic inflammation, dysregulated appetite regulation, and altered microRNA expression patterns also contribute to muscle wasting in ESRD.

• #58 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. […] The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. […] Muscle wasting in ESRD patients is attributed to a variety of factors that collectively contribute to the progressive loss of muscle mass in this population. Metabolic acidosis and impaired insulin/IGF-1 signaling pathways disrupt the regulation of muscle protein synthesis and degradation, leading to muscle atrophy. […] Chronic inflammation, dysregulated appetite regulation, and altered microRNA expression patterns also contribute to muscle wasting in ESRD.

• #59 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. […] The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. […] Muscle wasting in ESRD patients is attributed to a variety of factors that collectively contribute to the progressive loss of muscle mass in this population. Metabolic acidosis and impaired insulin/IGF-1 signaling pathways disrupt the regulation of muscle protein synthesis and degradation, leading to muscle atrophy. […] Chronic inflammation, dysregulated appetite regulation, and altered microRNA expression patterns also contribute to muscle wasting in ESRD.

• #60 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #61 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #62 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #63 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #64 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #65 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #66 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #67 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #68 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #69 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Muscle wasting by the multiple factors described above has significant impact on physical function. […] Moreover, sarcopenia was associated with higher cardiovascular events (OR = 3.80). […] Both muscle wasting and the deterioration of physical function in ESRD patients receiving HD are associated with increased mortality. […] Understanding the molecular mechanisms underlying muscle wasting in ESRD is crucial for developing targeted therapeutic strategies. […] The ubiquitin-proteasome system (UPS) plays a critical role in the breakdown of muscle proteins. […] In ESRD patients, the UPS is activated, leading to accelerated protein degradation. […] Insulin resistance, a common feature in ESRD, disrupts the IGF-1/Akt signaling cascade, leading to decreased protein synthesis. […] Chronic inflammation, oxidative stress, and mitochondrial dysfunction are interconnected factors that contribute to muscle wasting in ESRD.

• #70 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #71 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. Enhanced protein degradation through the activation of proteolytic pathways, including the UPS, ALP, and caspase-dependent pathways, along with impaired protein synthesis due to insulin resistance, are key contributors to muscle atrophy. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #72 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #73 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. Enhanced protein degradation through the activation of proteolytic pathways, including the UPS, ALP, and caspase-dependent pathways, along with impaired protein synthesis due to insulin resistance, are key contributors to muscle atrophy. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #74 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #75 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. Enhanced protein degradation through the activation of proteolytic pathways, including the UPS, ALP, and caspase-dependent pathways, along with impaired protein synthesis due to insulin resistance, are key contributors to muscle atrophy. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #76 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #77 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. Enhanced protein degradation through the activation of proteolytic pathways, including the UPS, ALP, and caspase-dependent pathways, along with impaired protein synthesis due to insulin resistance, are key contributors to muscle atrophy. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #78 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/view.html?uid=1846&vmd=Full

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #79 Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  https://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2023-0097

  Acidosis stimulates protein degradation and inhibits protein synthesis, exacerbating muscle atrophy. […] Hormonal imbalances are commonly observed in ESRD patients, and contribute to muscle wasting. […] The dialysis process itself results in protein loss. […] Uremic toxins, which accumulate in ESRD, have been implicated in the molecular mechanisms of muscle wasting. […] Collectively, muscle wasting in ESRD is a multifactorial process that involves various molecular mechanisms. Enhanced protein degradation through the activation of proteolytic pathways, including the UPS, ALP, and caspase-dependent pathways, along with impaired protein synthesis due to insulin resistance, are key contributors to muscle atrophy. […] Further research is needed to elucidate the precise interplay and relative contributions of these molecular mechanisms, paving the way for the development of targeted therapeutic strategies to mitigate muscle wasting and improve outcomes for individuals with ESRD.

• #80 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Due to the incapacitating nature of end-stage renal disease, people on dialysis frequently acquire undetected psychopathological disorders. […] There is a high rate of morbidity and mortality in individuals with renal failure due to neurological complications. […] Patients with end-stage renal disease accumulate blood urea and experience nitrogen and electrolyte imbalances due to decreased renal excretion, leading to neurological complications. […] The notion that one or more of these retained toxins influence neurological dysfunction in CKD has been the subject of several studies examining the pathophysiology of neurological disease in CKD. […] There is a complicated relationship between the kidneys and the brain, known as the kidney-brain axis, which contributes to the high incidence of brain abnormalities in patients with ESRD.

• #81 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Due to the incapacitating nature of end-stage renal disease, people on dialysis frequently acquire undetected psychopathological disorders. […] There is a high rate of morbidity and mortality in individuals with renal failure due to neurological complications. […] Patients with end-stage renal disease accumulate blood urea and experience nitrogen and electrolyte imbalances due to decreased renal excretion, leading to neurological complications. […] The notion that one or more of these retained toxins influence neurological dysfunction in CKD has been the subject of several studies examining the pathophysiology of neurological disease in CKD. […] There is a complicated relationship between the kidneys and the brain, known as the kidney-brain axis, which contributes to the high incidence of brain abnormalities in patients with ESRD.

• #82 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Due to the incapacitating nature of end-stage renal disease, people on dialysis frequently acquire undetected psychopathological disorders. […] There is a high rate of morbidity and mortality in individuals with renal failure due to neurological complications. […] Patients with end-stage renal disease accumulate blood urea and experience nitrogen and electrolyte imbalances due to decreased renal excretion, leading to neurological complications. […] The notion that one or more of these retained toxins influence neurological dysfunction in CKD has been the subject of several studies examining the pathophysiology of neurological disease in CKD. […] There is a complicated relationship between the kidneys and the brain, known as the kidney-brain axis, which contributes to the high incidence of brain abnormalities in patients with ESRD.

• #83 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Brain MRI studies have demonstrated structural abnormalities in patients with ESRD. […] Compared to healthy adults of the same age, patients with ESRD had a higher prevalence of white matter lesions, silent infarcts, brain atrophy, and axonal demyelination. […] In order to better understand the functional impairments of brain networks in patients with ESRD, rs-fMRI has recently emerged as a promising approach. […] DMN connectivity impairment in the posterior cingulate cortex, precuneus, and medial prefrontal cortex, or decreased activity in a diffuse pattern across bilateral frontal, parietal, and temporal lobes were found in rs-fMRI studies of patients with ESRD before dialysis was mentioned. […] The rapidity with which these changes take place suggests that toxin-mediated inhibition of neuronal transmission plays a substantial role in the neurological dysfunction seen in CKD.

• #84 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Brain MRI studies have demonstrated structural abnormalities in patients with ESRD. […] Compared to healthy adults of the same age, patients with ESRD had a higher prevalence of white matter lesions, silent infarcts, brain atrophy, and axonal demyelination. […] In order to better understand the functional impairments of brain networks in patients with ESRD, rs-fMRI has recently emerged as a promising approach. […] DMN connectivity impairment in the posterior cingulate cortex, precuneus, and medial prefrontal cortex, or decreased activity in a diffuse pattern across bilateral frontal, parietal, and temporal lobes were found in rs-fMRI studies of patients with ESRD before dialysis was mentioned. […] The rapidity with which these changes take place suggests that toxin-mediated inhibition of neuronal transmission plays a substantial role in the neurological dysfunction seen in CKD.

• #85 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Brain MRI studies have demonstrated structural abnormalities in patients with ESRD. […] Compared to healthy adults of the same age, patients with ESRD had a higher prevalence of white matter lesions, silent infarcts, brain atrophy, and axonal demyelination. […] In order to better understand the functional impairments of brain networks in patients with ESRD, rs-fMRI has recently emerged as a promising approach. […] DMN connectivity impairment in the posterior cingulate cortex, precuneus, and medial prefrontal cortex, or decreased activity in a diffuse pattern across bilateral frontal, parietal, and temporal lobes were found in rs-fMRI studies of patients with ESRD before dialysis was mentioned. […] The rapidity with which these changes take place suggests that toxin-mediated inhibition of neuronal transmission plays a substantial role in the neurological dysfunction seen in CKD.

• #86 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Brain MRI studies have demonstrated structural abnormalities in patients with ESRD. […] Compared to healthy adults of the same age, patients with ESRD had a higher prevalence of white matter lesions, silent infarcts, brain atrophy, and axonal demyelination. […] In order to better understand the functional impairments of brain networks in patients with ESRD, rs-fMRI has recently emerged as a promising approach. […] DMN connectivity impairment in the posterior cingulate cortex, precuneus, and medial prefrontal cortex, or decreased activity in a diffuse pattern across bilateral frontal, parietal, and temporal lobes were found in rs-fMRI studies of patients with ESRD before dialysis was mentioned. […] The rapidity with which these changes take place suggests that toxin-mediated inhibition of neuronal transmission plays a substantial role in the neurological dysfunction seen in CKD.

• #87 End-Stage Renal Disease and Neurological Connection – European Medical Journal

  https://www.emjreviews.com/nephrology/article/end-stage-renal-disease-and-neurological-connection-j120123/

  Brain MRI studies have demonstrated structural abnormalities in patients with ESRD. […] Compared to healthy adults of the same age, patients with ESRD had a higher prevalence of white matter lesions, silent infarcts, brain atrophy, and axonal demyelination. […] In order to better understand the functional impairments of brain networks in patients with ESRD, rs-fMRI has recently emerged as a promising approach. […] DMN connectivity impairment in the posterior cingulate cortex, precuneus, and medial prefrontal cortex, or decreased activity in a diffuse pattern across bilateral frontal, parietal, and temporal lobes were found in rs-fMRI studies of patients with ESRD before dialysis was mentioned. […] The rapidity with which these changes take place suggests that toxin-mediated inhibition of neuronal transmission plays a substantial role in the neurological dysfunction seen in CKD.

• #88 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/en-frailty-in-end-stage-renal-articulo-resumen-S2013251423000226

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. […] Reduced intake contributes to sarcopenia and later physical frailty. […] The increased levels of pro-inflammatory cytokines like interleukin (IL-6) and tumour necrosis factor alpha (TNF-a) leads to impaired signalling of the anabolic hormones insulin and insulin-like growth factor-1 (IGF)-1. […] Metabolic acidosis also activates caspase-3 and inhibits intracellular signalling of insulin and IGF-1. […] Cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. […] These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #89 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/es-frailty-in-end-stage-renal-articulo-resumen-S0211699521002071

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. Its prevalence increases as chronic kidney disease (CKD) progresses. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. Additionally, standard management of ESRD, including kidney replacement therapies, may have a lower benefit or may be even potentially harmful in the presence of frailty. […] The pathogenesis of frailty in ESRD is multifactorial. Reduced intake contributes to sarcopenia and later physical frailty. The contributing factors for loss of appetite include the uraemic milieu, inflammation, comorbid illnesses, medications and associated low mood and cognitive impairment.

• #90 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/en-frailty-in-end-stage-renal-articulo-resumen-S2013251423000226

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. […] Reduced intake contributes to sarcopenia and later physical frailty. […] The increased levels of pro-inflammatory cytokines like interleukin (IL-6) and tumour necrosis factor alpha (TNF-a) leads to impaired signalling of the anabolic hormones insulin and insulin-like growth factor-1 (IGF)-1. […] Metabolic acidosis also activates caspase-3 and inhibits intracellular signalling of insulin and IGF-1. […] Cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. […] These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #91 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/es-frailty-in-end-stage-renal-articulo-resumen-S0211699521002071

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. Its prevalence increases as chronic kidney disease (CKD) progresses. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. Additionally, standard management of ESRD, including kidney replacement therapies, may have a lower benefit or may be even potentially harmful in the presence of frailty. […] The pathogenesis of frailty in ESRD is multifactorial. Reduced intake contributes to sarcopenia and later physical frailty. The contributing factors for loss of appetite include the uraemic milieu, inflammation, comorbid illnesses, medications and associated low mood and cognitive impairment.

• #92 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/es-frailty-in-end-stage-renal-articulo-resumen-S0211699521002071

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. Its prevalence increases as chronic kidney disease (CKD) progresses. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. Additionally, standard management of ESRD, including kidney replacement therapies, may have a lower benefit or may be even potentially harmful in the presence of frailty. […] The pathogenesis of frailty in ESRD is multifactorial. Reduced intake contributes to sarcopenia and later physical frailty. The contributing factors for loss of appetite include the uraemic milieu, inflammation, comorbid illnesses, medications and associated low mood and cognitive impairment.

• #93 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/en-frailty-in-end-stage-renal-articulo-resumen-S2013251423000226

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. […] Reduced intake contributes to sarcopenia and later physical frailty. […] The increased levels of pro-inflammatory cytokines like interleukin (IL-6) and tumour necrosis factor alpha (TNF-a) leads to impaired signalling of the anabolic hormones insulin and insulin-like growth factor-1 (IGF)-1. […] Metabolic acidosis also activates caspase-3 and inhibits intracellular signalling of insulin and IGF-1. […] Cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. […] These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #94 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/en-frailty-in-end-stage-renal-articulo-resumen-S2013251423000226

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. […] Reduced intake contributes to sarcopenia and later physical frailty. […] The increased levels of pro-inflammatory cytokines like interleukin (IL-6) and tumour necrosis factor alpha (TNF-a) leads to impaired signalling of the anabolic hormones insulin and insulin-like growth factor-1 (IGF)-1. […] Metabolic acidosis also activates caspase-3 and inhibits intracellular signalling of insulin and IGF-1. […] Cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. […] These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #95 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/en-frailty-in-end-stage-renal-articulo-resumen-S2013251423000226

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. […] Reduced intake contributes to sarcopenia and later physical frailty. […] The increased levels of pro-inflammatory cytokines like interleukin (IL-6) and tumour necrosis factor alpha (TNF-a) leads to impaired signalling of the anabolic hormones insulin and insulin-like growth factor-1 (IGF)-1. […] Metabolic acidosis also activates caspase-3 and inhibits intracellular signalling of insulin and IGF-1. […] Cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. […] These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #96 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/en-frailty-in-end-stage-renal-articulo-resumen-S2013251423000226

  Frailty is common in end stage renal disease (ESRD) and is a marker of poor outcomes. […] The pathogenesis of frailty in ESRD is multifactorial including uraemia and dialysis related factors. […] The pathogenesis of frailty in ESRD is multifactorial and is different from the general population since uraemia and dialysis are significant contributors. […] Reduced intake contributes to sarcopenia and later physical frailty. […] The increased levels of pro-inflammatory cytokines like interleukin (IL-6) and tumour necrosis factor alpha (TNF-a) leads to impaired signalling of the anabolic hormones insulin and insulin-like growth factor-1 (IGF)-1. […] Metabolic acidosis also activates caspase-3 and inhibits intracellular signalling of insulin and IGF-1. […] Cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. […] These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #97 Frailty in end stage renal disease: Current perspectives | Nefrología

  https://www.revistanefrologia.com/es-frailty-in-end-stage-renal-articulo-resumen-S0211699521002071

  It has been shown that 1, 25(OH)2 D is a determinant of physical function and muscle size in those with CKD. So deficiency of Vitamin D also may be a factor in the development of frailty in CKD. […] Finally, cellular senescence, loss of telomeric structures, mitochondrial dysfunction, increased free radical production and poor DNA repair capability are important in the ageing process and the development of frailty. These processes occur prematurely in CKD population ultimately leading to sarcopenia, vascular dysfunction and progressive organ damage.

• #98 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8584056/

  To begin with, the development of systemic proinflammatory tissue stress is promoted by the presence of ESRD and PH due to multiple sources of inflammatory stimuli, such as oxidative stress, acidosis, and fluid overload, increased comorbidity, including infections, dialysis procedure, production, and inadequate removal (insufficient clearance) of proinflammatory cytokines. […] Thus, against the backdrop of systemic ChLGI, the progression of CKD to ESRD is the result of a complex interplay of local and systemic genetic, ontogenetic, and environmental variables, as well as metabolic and immunological components.

• #99 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

  https://www.mdpi.com/1422-0067/22/21/11453

  The development of CKD and its progression to ESRD remain significant factors in the decline in quality of life and premature death. […] The importance of local manifestations of ChLGI in the formation of both autosomal dominant and autosomal recessive polycystic kidney disease has also been proven. […] It is important to remember that DKD creates a vicious pathogenetic cycle since chronic kidney disease (CKD) contributes to the development of systemic ChLGI, insulin resistance, and the formation of metabolic syndrome in people who do not have it initially. […] Thus, against the backdrop of systemic ChLGI, the progression of CKD to ESRD is the result of a complex interplay of local and systemic genetic, ontogenetic, and environmental variables, as well as metabolic and immunological components.

• #100 The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation. | EBSCOhost

  https://search.ebscohost.com/login.aspx?direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=16616596&AN=153600278&h=ECK21gPArDKqjMiVZIxYMMRC2iT0cv5jokdAoW279rC%2Bh2xTM7OVL47Z2ePIAg6JD4Gp%2B9nY35CTbmdnY3XlZw%3D%3D&crl=c

  The development of ChSI is closely associated with programmed hemodialysis in ESRD, as well as with the systemic autoimmune process. […] Consideration of ESRD pathogenesis from the standpoint of the theory of general pathological processes opens up the scope not only for particular but also for universal approaches to conducting pathogenetic therapies and diagnosing and predicting systemic complications in severe nephropathies.

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