Zwężenie tętnicy nerkowej
Patofizjologia i mechanizm

Zwężenie tętnicy nerkowej (ZTN) jest istotną przyczyną wtórnego nadciśnienia tętniczego, występującą u 1-10% pacjentów z nadciśnieniem. Dominującymi etiologiami są miażdżyca (90% przypadków, głównie u osób >45 lat) oraz dysplazja włóknisto-mięśniowa (10%, częściej u kobiet 20-50 lat). Patofizjologia ZTN opiera się na aktywacji układu renina-angiotensyna-aldosteron (RAA), gdzie niedokrwienie nerki stymuluje wydzielanie reniny, prowadząc do wzrostu angiotensyny II i aldosteronu, co skutkuje skurczem naczyń, retencją sodu i wody oraz podwyższeniem ciśnienia tętniczego. Zwężenie powyżej 50-60% powoduje hemodynamicznie istotny gradient ciśnienia (>15-20 mmHg), upośledzenie autoregulacji nerkowej i spadek GFR, co sprzyja rozwojowi nadciśnienia naczyniowo-nerkowego (RVH). Przewlekłe niedokrwienie prowadzi do stresu oksydacyjnego, zapalenia, włóknienia śródmiąższowego i zmian strukturalnych w nerkach, co w 15-20% przypadków skutkuje przewlekłą chorobą nerek.

Patofizjologia zwężenia tętnicy nerkowej

Zwężenie tętnicy nerkowej (ZTN) to schorzenie charakteryzujące się zwężeniem jednej lub obu tętnic nerkowych, które doprowadzają krew do nerek. Jest to istotna przyczyna wtórnego nadciśnienia tętniczego i może stanowić przyczynę nadciśnienia u 1-10% z 50 milionów chorych na nadciśnienie w Stanach Zjednoczonych.12 Patofizjologia tego schorzenia jest złożona i obejmuje wiele współzależnych mechanizmów, które prowadzą do rozwoju nadciśnienia naczyniowo-nerkowego oraz uszkodzenia nerek.

Główne przyczyny zwężenia tętnicy nerkowej

Zwężenie tętnicy nerkowej jest uwarunkowane głównie przez dwa zaburzenia:3

  • Miażdżyca tętnicy nerkowej – stanowi około 90% przypadków, dotyka głównie osoby starsze powyżej 45 roku życia, częściej mężczyzn. Zwężenie miażdżycowe zwykle dotyczy ujścia aortalnego lub proksymalnego odcinka tętnicy nerkowej.45
  • Dysplazja włóknisto-mięśniowa – odpowiada za około 10% przypadków, występuje częściej u młodszych osób, szczególnie u kobiet w wieku 20-50 lat. Dotyczy najczęściej środkowej lub dystalnej części głównej tętnicy nerkowej lub gałęzi wewnątrznerkowych.67

renina-angiotensyna-aldosteron”>Kluczowa rola aldosteron/” title=”układ renina-angiotensyna-aldosteron” class=”to-tag” data-termid=”18104″>układu renina-angiotensyna-aldosteron

Głównym mechanizmem patofizjologicznym w rozwoju zwężenia tętnicy nerkowej jest aktywacja układu renina-angiotensyna-aldosteron (RAA), odgrywającego centralną i kluczową rolę w patogenezie ZTN.38 Zmniejszony przepływ krwi przez nerki wywołuje szereg reakcji fizjologicznych:

  1. Niedokrwienie nerki powoduje stymulację aparatu przykłębuszkowego i zwiększoną sekrecję reniny.9
  2. Renina przekształca angiotensynogen w angiotensynę I, która następnie jest przekształcana przez enzym konwertujący angiotensynę (ACE) w angiotensynę II.10
  3. Angiotensyna II powoduje silny skurcz naczyń oraz stymuluje uwalnianie aldosteronu z kory nadnerczy.5
  4. Aldosteron zwiększa retencję sodu i wody, prowadząc do zwiększenia objętości krwi krążącej i podniesienia ciśnienia tętniczego.11

W przypadku jednostronnego zwężenia tętnicy nerkowej, zdrowa nerka po przeciwnej stronie kompensuje wzrost ciśnienia perfuzji nerkowej poprzez zwiększenie wydalania sodu (natriureza ciśnieniowa), co zapobiega obrzękowi płuc.12 Natomiast w przypadku obustronnego zwężenia tętnic nerkowych, obniżony GFR prowadzi do niezdolności nerek do wydalania sodu i wody, co skutkuje przewodnieniem i może prowadzić do ostrego wzrostu ciśnienia napełniania lewej komory, z następczym zastojem krwi w płucach i obrzękiem płuc.1213

Mechanizmy hemodynamiczne i regulacja GFR

W warunkach prawidłowych, układ autoregulacji utrzymuje stabilny przepływ krwi przez nerki i wskaźnik filtracji kłębuszkowej (GFR) pomimo zmian ciśnienia perfuzji. W przypadku zwężenia tętnicy nerkowej, ten mechanizm jest zaburzony:14

  • GFR jest regulowany przy pomocy angiotensyny II i innych modulatorów. Autoregulacja ulega upośledzeniu, gdy ciśnienie perfuzji nerek spada poniżej 70-85 mmHg.15
  • Istotne upośledzenie funkcji autoregulacji, prowadzące do spadku GFR, zwykle nie jest obserwowane dopóki zwężenie światła tętnicy nie przekroczy 50%.1516
  • Zwężenie powyżej 50-60% powoduje gradient ciśnienia większy niż 15-20 mmHg, co jest hemodynamicznie istotną cechą zwężenia tętnicy nerkowej i możliwym czynnikiem inicjującym rozwój nadciśnienia naczyniowo-nerkowego.17

Badania wykazały, że gdy ciśnienie dystalne do zwężenia tętnicy nerkowej było mniejsze niż 90% ciśnienia aortalnego, uwalnianie reniny z dotkniętej nerki było znacząco podwyższone (renina mierzona w ipsilateralnej żyle nerkowej).18

Fazy rozwoju nadciśnienia naczyniowo-nerkowego

Ewolucja nadciśnienia naczyniowo-nerkowego (renovascular hypertension – RVH) przebiega w trzech fazach:19

  1. Faza zależna od reniny i angiotensyny – bezpośredni wzrost ciśnienia tętniczego jest skutkiem hipereninemii. W przypadku jednostronnego zwężenia, przeciwległa nerka zwiększa wydalanie sodu i wody, utrzymując euwolemię, podczas gdy nerka ze zwężoną tętnicą zatrzymuje sód i produkuje nadmiar reniny w odpowiedzi na niedokrwienie.20
  2. Faza retencji soli – w przypadku zwężenia tętnicy do jedynej czynnej nerki, retencja sodu i wody wraz z działaniem presyjnym angiotensyny II służą utrzymaniu ciśnienia perfuzji nerek. Bodziec do produkcji reniny jest osłabiony, a poziom reniny spada. Nadciśnienie staje się mniej zależne od angiotensyny II, a głównie wynika z przewodnienia.21
  3. Faza niezależna od układu renina-angiotensyna – jeśli niedokrwienie nerek utrzymuje się, przywrócenie prawidłowego przepływu krwi może nie normalizować ciśnienia krwi z powodu wtórnych, nieodwracalnych zmian naczyniowych lub w miąższu nerek.21

W jednostronnym zwężeniu tętnicy nerkowej produkcja reniny jest zwiększona w niedokrwionej nerce, ale obniżona w niezwężonej nerce, która nie podlega temu samemu bodźcowi niedokrwiennemu. W rezultacie, gdy występują dwie nerki z jednostronnym zwężeniem (model „dwie nerki, jedno zwężenie”), hiperreniemia utrzymuje się, a ciśnienie krwi pozostaje podwyższone z powodu działania naczynioskurczowego angiotensyny II.22

Zmiany w strukturze i funkcji nerek

Przewlekłe niedokrwienie nerki prowadzi do istotnych zmian w jej strukturze i funkcji, które można zaobserwować przede wszystkim w tkance cewkowej.515

Procesy zapalno-zwłóknieniowe

Zwężenie tętnicy nerkowej powoduje złożone zmiany patologiczne w nerkach:323

  • Zwiększony stres oksydacyjny i uwalnianie mediatorów prozapalnych przyczyniających się do patologicznej przebudowy tkanki i włóknienia nerek.3
  • Bardziej zaawansowane zwężenie odpowiadające 70-80% okluzji naczyń prowadzi do wymiernego niedotlenienia kory nerki, co wywołuje przerzedzenie mikronaczyń oraz aktywację szlaków zapalnych i oksydacyjnych, powodujących włóknienie śródmiąższowe.24
  • Przewlekłe niedotlenienie i stymulacja aparatu przykłębuszkowego prowadzi do jego hiperplazji.25
  • Angiotensyna II, poza efektem presyjnym, wykazuje silne działanie profibrotyczne, wzmacniane przez wtórne uwalnianie TGF-β.23

W rezultacie, mechanizmy zapalne i profibrotyczne dominujące w zaawansowanym ZTN przyczyniają się do zaawansowanej, patologicznej przebudowy struktury nerki, co świadczy o postępującym przewlekłym uszkodzeniu nerek i ostatecznie stanowi przyczynę 15-20% przypadków przewlekłej choroby nerek.23

Zmiany morfologiczne w zwężeniu tętnicy nerkowej

Patofizjologia zwężenia tętnicy nerkowej prowadzi do zmian w strukturze nerki, które są najbardziej widoczne w tkance cewkowej. Zmiany te obejmują:526

  • Włóknienie – postępujące odkładanie tkanki łącznej włóknistej w miąższu nerki
  • Zmniejszenie rozmiaru komórek cewkowych – wynikające z niedokrwienia i adaptacji
  • Pogrubienie torebki Bowmana – jako reakcja na przewlekłe uszkodzenie
  • Stwardnienie cewkowo-śródmiąższowe (tubuloskleroza) – wynik przewlekłego niedotlenienia
  • Zanik kłębuszków nerkowych – prowadzący do zmniejszenia powierzchni filtracyjnej

W przypadku jednostronnego zwężenia tętnicy nerkowej, można obserwować asymetrię wielkości nerek (różnica 1,5 cm), co wynika z atrofii i włóknienia zajętej nerki.27

Progresja uszkodzenia nerek

Zwężenie tętnicy nerkowej może prowadzić do różnych stopni uszkodzenia nerek:1725

  • Na wczesnym etapie choroby, mimo zmniejszonego przepływu krwi, kora i rdzeń nerki mogą adaptować się bez rozwoju ciężkiego niedotlenienia. Na tym etapie leczenie zachowawcze może zapobiec rozwojowi postępującej utraty funkcji i włóknienia.25
  • W bardziej zaawansowanych przypadkach, gdy zwężenie osiąga 70-80%, rozwija się jawne niedotlenienie kory, które prowadzi do przerzedzenia mikronaczyń i ostatecznie do włóknienia śródmiąższowego.25
  • Ostatecznie, długotrwałe niedotlenienie miąższu nerki staje się procesem nieodwracalnym. Na tym etapie przywrócenie przepływu krwi do nerek nie zapewnia poprawy funkcji nerek ani korzyści klinicznych.24

Badania wskazują, że bez leczenia, 50% przypadków zwężenia tętnicy nerkowej postępuje, czasami do całkowitej niedrożności. Im większe zwężenie przy początkowym rozpoznaniu, tym większe prawdopodobieństwo progresji i całkowitego zamknięcia.28

Mechanizmy molekularne i biochemiczne

Układ kinin-kalikreina i endotelina

Oprócz aktywacji układu renina-angiotensyna-aldosteron, w patogenezie ZTN uczestniczą również inne mechanizmy:329

  • Układ kinin-kalikreina – zaburzenia w tym układzie przyczyniają się do nieprawidłowej regulacji ciśnienia tętniczego i homeostazy sodu
  • Układ endoteliny – endotelina-1 jest silnym wazokonstriktorem, który może nasilać nadciśnienie tętnicze i uszkodzenie nerek
  • Układ współczulny – aktywacja układu współczulnego odgrywa ważną rolę w patogenezie nadciśnienia naczyniowo-nerkowego, głównie poprzez nerwy aferentne nerkowe30

Angiotensyna II, poza bezpośrednim wpływem na naczynia i wydzielanie aldosteronu, wykazuje również działanie prozapalne i profibrotyczne, przyczyniając się do wzrostu zmian strukturalnych w naczyniach krwionośnych i dalszej progresji choroby.31

Stres oksydacyjny i mediatory zapalne

Istotną rolę w patogenezie ZTN odgrywa stres oksydacyjny i reakcje zapalne:332

  • Przewlekłe niedokrwienie nerek powoduje zwiększoną produkcję reaktywnych form tlenu (ROS), które uszkadzają komórki nerkowe
  • Podwyższone poziomy angiotensyny II są związane z cytokinami zapalnymi, które prowadzą do zwiększonej aktywacji szlaków zapalnych i profibrotycznych32
  • Proces zapalny przyczynia się do dysfunkcji śródbłonka naczyniowego, co prowadzi do upośledzonej relaksacji naczyń i następczego włóknienia cewkowo-śródmiąższowego32
  • Zwiększona aktywność adrenergiczna układu współczulnego powoduje uszkodzenie mikronaczyń32

Te mechanizmy molekularne i biochemiczne tworzą błędne koło, które przyspiesza postęp choroby i prowadzi do nieodwracalnych zmian w strukturze i funkcji nerek.

Komplikacje i następstwa zwężenia tętnicy nerkowej

Nadciśnienie naczyniowo-nerkowe

Najpowszechniejszym klinicznym następstwem ZTN jest nadciśnienie naczyniowo-nerkowe (renovascular hypertension – RVH):2917

  • ZTN jest główną przyczyną renovascular hypertension (RVH)26
  • Nadciśnienie naczyniowo-nerkowe charakteryzuje się zazwyczaj ciężkim przebiegiem i opornością na leczenie farmakologiczne17
  • RVH rozwija się w wyniku aktywacji układu renina-angiotensyna-aldosteron wraz z jedno- lub obustronnym niedokrwieniem nerek, co prowadzi do zwiększonej retencji sodu, wtórnego hiperaldosteronizmu i skurczu naczyń33

W jednostronnym zwężeniu tętnicy nerkowej, angiotensyna II indukuje ciśnieniową natriurezę w niezwężonej nerce, powodując hiponatremię w połączeniu z nadciśnieniem.34

Nefropatia niedokrwienna

Długotrwałe zwężenie tętnicy nerkowej prowadzi do nefropatii niedokrwiennej:2335

  • Nefropatia niedokrwienna jest potencjalnie odwracalną przyczyną niewydolności nerek, która może powodować zaburzenia hemodynamiki wewnątrznerkowej i jej następstwa: nadciśnienie tętnicze i przewlekłą chorobę nerek35
  • Szybka progresja ZTN, osiągająca krytyczne zwężenie tętnicy nerkowej, jest możliwym czynnikiem etiologicznym przednerkowej ostrej niewydolności nerek (AKI)23
  • ZTN charakteryzujące się hemodynamicznie istotnym zwężeniem tętnicy nerkowej prowadzi do nadciśnienia naczyniowo-nerkowego, które może współistnieć z dalszymi powikłaniami wynikającymi z rozwoju nefropatii niedokrwiennej23

Zmniejszony przepływ krwi przez nerki z powodu zwężenia powoduje hiperfiltrację kłębuszkową i następową ciśnieniową natriurezę niezwężonej nerki, co objawia się klinicznie hiponatremią.36

Powikłania sercowo-naczyniowe

ZTN może prowadzić do różnych powikłań sercowo-naczyniowych:3713

  • Niestabilna dławica piersiowa – ZTN może nasilać lub powodować epizody niestabilnej dławicy
  • Zastoinowa niewydolność serca – charakteryzująca się obrzękiem płuc z szybkim początkiem (flash pulmonary edema)13
  • Przerost mięśnia sercowego (hipertrofia) – wynikający z przewlekłego nadciśnienia38
  • Nasilenie miażdżycy we wszystkich tętnicach organizmu38

ZTN przyczynia się do tych stanów poprzez trzy ogólne mechanizmy: przeciążenie objętościowe, obwodowy skurcz tętnic i bezpośredni wpływ angiotensyny na mięsień sercowy.37 Ponadto, mechanizm, poprzez który zwężenie tętnicy nerkowej prowadzi do zespołu destabilizacji serca, opiera się na niekontrolowanym nadciśnieniu i retencji płynów, co może prowadzić nie tylko do niewydolności serca, ale także do ostrego zespołu wieńcowego.39

Różnice patofizjologiczne w zależności od etiologii

Zwężenie miażdżycowe

Miażdżyca stanowi najczęstszą przyczynę ZTN, odpowiadając za około 90% przypadków:540

  • Proces miażdżycowy rozpoczyna się od uszkodzenia śródbłonka, chociaż dokładny czynnik inicjujący nie jest dobrze zrozumiany. Może to być dyslipidemia, palenie tytoniu, infekcja wirusowa, uszkodzenie immunologiczne lub podwyższony poziom homocysteiny1
  • W miejscu uszkodzenia zwiększa się przepuszczalność dla lipoprotein o niskiej gęstości (LDL) i migracja makrofagów, z następczą proliferacją komórek śródbłonka i mięśni gładkich, co ostatecznie prowadzi do powstania blaszki miażdżycowej1
  • Blaszki miażdżycowe tworzą się na wewnętrznej ścianie tętnicy nerkowej, powodując jej stwardnienie i zwężenie28
  • Zwężenie miażdżycowe zwykle dotyczy ujścia aortalnego lub proksymalnego odcinka tętnicy nerkowej41

Miażdżycowe zwężenie tętnicy nerkowej jest chorobą postępującą: w 50% przypadków zwężenie postępuje, a u 16% dochodzi do całkowitego zamknięcia. Im większe zwężenie przy początkowym rozpoznaniu, tym większe prawdopodobieństwo progresji i całkowitego zamknięcia.28

Dysplazja włóknisto-mięśniowa

Dysplazja włóknisto-mięśniowa (FMD) odpowiada za około 10% przypadków ZTN i ma odmienną patofizjologię:642

  • FMD charakteryzuje się patologicznym pogrubieniem ściany tętniczej, najczęściej dystalnej części głównej tętnicy nerkowej lub gałęzi wewnątrznerkowych6
  • Pogrubienie może być nieregularne i może obejmować dowolną warstwę (ale najczęściej błonę środkową)6
  • W dysplazji włóknisto-mięśniowej mięśnie w ścianie tętnicy nie rosną prawidłowo, co często zaczyna się w dzieciństwie42
  • Tętnica nerkowa może mieć wąskie odcinki na przemian z szerszymi, dając obraz „sznura pereł” w badaniach obrazowych4243
  • Eksperci nie wiedzą, co powoduje dysplazję włóknisto-mięśniową, ale stan ten jest częstszy u kobiet i może być obecny od urodzenia (wrodzony)42

Pacjenci z dysplazją włóknisto-mięśniową tętnicy nerkowej zwykle mają nadciśnienie naczyniowo-nerkowe bez niewydolności nerek lub towarzyszącej choroby naczyniowej.44

Inne przyczyny zwężenia tętnicy nerkowej

Rzadziej występujące przyczyny ZTN obejmują:2342

  • Zapalenie naczyń (arteritis) – stan zapalny tętnicy45
  • Tętniak tętnicy – miejscowe rozszerzenie tętnicy45
  • Ucisk tętnicy przez masę zewnętrzną, na przykład guz45
  • Rozwarstwienie (tearing) ściany naczynia45
  • Zapalenie Takayasu – może powodować zwężenie tętnicy nerkowej i prowadzić do nagłego początku obrzęku płuc39

W przypadku dzieci z zwężeniem tętnicy nerkowej, zwężona tętnica nerkowa jest często już wąska od urodzenia. Inne przyczyny obejmują zapalenie naczyń i stan genetyczny zwany neurofibromatozą, w którym guzy tworzą się z tkanki nerwowej.46

Implikacje kliniczne patofizjologii ZTN

Znaczenie dla diagnostyki

Zrozumienie patofizjologii ZTN ma kluczowe znaczenie dla właściwej diagnostyki:2347

  • Diagnoza i ocena ZTN opiera się na obrazowych metodach diagnostycznych23
  • Złotym standardem diagnostycznym dla identyfikacji ZTN jest angiografia; jednak technika ta jest inwazyjna i nie powinna być stosowana jako początkowy test diagnostyczny23
  • Nowsze metody, takie jak BOLD MRI, dynamiczne MRI ze wzmocnieniem kontrastowym i renal frame count, w małych badaniach wykazały korelację z obecnością niedokrwienia nerek47

Zwężenie tętnicy nerkowej należy rozważyć u każdego pacjenta z ciężkim lub opornym nadciśnieniem tętniczym, szczególnie u tych, u których stwierdza się pogorszenie funkcji nerek lub znaczącą miażdżycę w innych obszarach naczyniowych.48

Implikacje dla leczenia

Patofizjologia ZTN ma bezpośrednie implikacje dla wyboru strategii leczenia:4449

  • Pacjenci z miażdżycowym ZTN i stabilnym stanem powinni być najpierw leczeni farmakologicznie44
  • Stentowanie tętnicy nerkowej nie jest zalecane dla większości pacjentów z miażdżycowym ZTN, ale może być korzystne dla osób z opornym nadciśnieniem lub szybko postępującą dysfunkcją nerek lub serca44
  • Główne ryzyko obecnej terapii farmakologicznej polega na pogorszeniu funkcji nerek, sytuacji klinicznej często spotykanej podczas wprowadzania inhibitora ACE lub ARB49
  • Większość autorów zaleca angioplastykę z lub bez stentowania, gdy nie można osiągnąć kontroli nadciśnienia, jeśli funkcja nerek się pogarsza i u pacjentów z obrzękiem płuc typu flash49

Zgodnie z wytycznymi przedstawionymi przez American Heart Association/American College of Cardiology Committee dotyczącymi leczenia zwężenia tętnicy nerkowej, leczenie zachowawcze jest leczeniem pierwszego rzutu w przypadku nadciśnienia tętniczego i zachowania funkcji nerek, podczas gdy przezskórna rewaskularyzacja jest leczeniem pierwszej linii w przypadku hemodynamicznie istotnego zwężenia tętnicy nerkowej, nawracającej niewyjaśnionej zastoinowej niewydolności serca i nagłego niewyjaśnionego obrzęku płuc.39

Przewidywanie odpowiedzi na leczenie

Patofizjologia ZTN pomaga również przewidzieć odpowiedź na leczenie:2421

  • Jeśli przepływ krwi zostanie przywrócony podczas pierwszych dwóch faz rozwoju nadciśnienia naczyniowo-nerkowego (faza zależna od reniny i angiotensyny oraz faza retencji soli) i perfuzja nerek zostanie przywrócona, ciśnienie krwi szybko powraca do normalnego poziomu21
  • Jeśli niedokrwienie nerek utrzymuje się i osiągnięta zostanie trzecia faza (niezależna od układu renina-angiotensyna), przywrócenie przepływu krwi do nerek może nie normalizować ciśnienia krwi, prawdopodobnie z powodu wtórnej nieodwracalnej choroby naczyniowej lub miąższowej nerek21
  • Podobnie, jeśli zwężenie tętnicy nerkowej jest długotrwałe i funkcja nerek była upośledzona przez dłuższy czas, przywrócenie przepływu krwi do nerki może nie przywrócić funkcji nerek50

Jasne jest, że większość pacjentów z ZTN może być leczona samym leczeniem zachowawczym. Pytanie brzmi, jak zidentyfikować tych pacjentów, którzy skorzystaliby z rewaskularyzacji. Pacjenci wysokiego ryzyka obejmują osoby z opornym nadciśnieniem, niewyjaśnionym pogorszeniem funkcji nerek, asymetrycznym rozmiarem nerek i nawracającymi epizodami obrzęku płuc typu flash.47

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 12.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Renal Artery Stenosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK430718/
    Renal artery stenosis is narrowing of the one or both of renal arteries. It is the major cause of hypertension and according to some reports is the cause of hypertension in 1% to 10% of the 50 million people in the United States. Atherosclerosis or fibromuscular dysplasia most often cause it. Other associated complications of renal artery stenosis are chronic kidney disease and end-stage renal disease. […] In atherosclerosis, the initiator of endothelial injury although not well understood can be, dyslipidemia, cigarette smoking, viral infection, immune injury, or increased homocysteine levels. At the lesion site, permeability to low-density lipoprotein (LDL) and macrophage migration increases with subsequent proliferation of endothelial and smooth muscle cells and ultimate formation of atherosclerotic plaque. Renal blood flow, which is significantly greater than the perfusion to other organs, along with glomerular capillary hydrostatic pressure is an important determinant of the glomerular filtration rate (GFR). In patients with renal artery stenosis, the chronic ischemia produced by the obstruction of renal blood flow leads to adaptive changes in the kidney which include the formation of collateral blood vessels and secretion of renin by juxtaglomerular apparatus. The renin enzyme has an important role in maintaining homeostasis in that it converts angiotensinogen to angiotensin I. Angiotensin I has then converted to angiotensin II with the help of an angiotensin-converting enzyme (ACE) in the lungs. Angiotensin II is responsible for vasoconstriction and release of aldosterone which causes sodium and water retention, thus resulting in secondary hypertension or renovascular hypertension.
  • #2 The Role of Renal Artery Stenosis
    https://www.uspharmacist.com/article/the-role-of-renal-artery-stenosis
    It has been reported that renal artery stenosis (RAS) is a major cause of renovascular hypertension (RVH). […] Not only does RAS play a role in the pathogenesis of hypertension, it is also increasingly recognized as an important cause of chronic renal insufficiency and end-stage renal disease (ESRD). The most common etiology of RAS is believed to be atherosclerosis, especially in the elderly. RAS progressively decreases blood flow to the kidneys and, eventually, impacts renal function and kidney structure. […] RAS is primarily caused by atherosclerosis, or clogging, narrowing, and hardening of the renal arteries. In these cases, RAS develops when plaque builds up on the inner wall of one or both renal arteries, making them hard and narrow. […] In patients with RAS, the chronic insufficiency produced by the obstruction of renal blood flow leads to kidney changes that are more pronounced in the tubular tissue. These include inflammation, fibrosis, tubulosclerosis, and intrarenal arterial thickening.
  • #3 An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8000991/
    Renal artery stenosis (RAS) is conditioned mainly by two disturbances: fibromuscular dysplasia or atherosclerosis of the renal artery. […] There are multiple pathophysiological mechanisms triggered in response to significant renal artery stenosis, including disturbances within endothelin, kininkallikrein and sympathetic nervous systems, with angiotensin II and the reninangiotensin-aldosterone system (RAAS) playing a central and key role in the pathogenesis of RAS. […] The increased oxidative stress and the release of pro-inflammatory mediators contributing to pathological tissue remodelling and renal fibrosis are also important pathogenetic elements of RAS. […] The activation of RAAS and its haemodynamic consequences is the primary and key element in the pathophysiological cascade triggered in response to renal artery stenosis.
  • #4 Renal Artery Stenosis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/245023-overview
    Renal artery stenosis (RAS) is the major cause of renovascular hypertension and may account for 1-10% of the 50 million cases of hypertension in the United States population. […] Apart from its role in the pathogenesis of hypertension, renal artery stenosis is also increasingly recognized as an important cause of chronic kidney insufficiency and end-stage kidney disease. In older individuals, atherosclerosis is by far the most common etiology of renal artery stenosis. […] As the renal artery lumen progressively narrows, kidney blood flow decreases. Eventually, the decreased perfusion compromises kidney function and structure. […] In patients with atherosclerosis, the initiator of endothelial injury is not clear. However, dyslipidemia, hypertension, cigarette smoking, diabetes mellitus, viral infection, immune injury, and increased homocysteine levels may contribute to endothelial injury.
  • #5 Renal artery stenosis – Wikipedia
    https://en.wikipedia.org/wiki/Renal_artery_stenosis
    Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension a secondary type of high blood pressure. Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease. […] Renal artery stenosis is most often caused by atherosclerosis which causes the renal arteries to harden and narrow due to the build-up of plaque. This is known as atherosclerotic renovascular disease, which accounts for about 90% of cases. This narrowing of renal arteries due to plaque build-up leads to higher blood pressure within the artery and decreased blood flow to the kidney. This decreased blood flow leads to decreased blood pressure in the kidney, which leads to the activation of the Renin-Angiotensin-Aldosterone (RAA) system. Juxtaglomerular cells secrete renin, which converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II then acts on the adrenal cortex to increase secretion of the hormone aldosterone. Aldosterone causes sodium and water retention, leading to an increase in blood volume and blood pressure. Therefore, people with RAS have chronic high blood pressure because their RAA system is hyperactivated. […] The pathophysiology of renal artery stenosis leads to changes in the structure of the kidney that are most noticeable in the tubular tissue. Changes include: Fibrosis, Tubular cell size (decrease), Thickening of Bowman capsule, Tubulosclerosis, Glomerular capillary tuft (atrophy).
  • #6 Renal Artery Stenosis and Occlusion – Genitourinary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/genitourinary-disorders/renovascular-disorders/renal-artery-stenosis-and-occlusion
    Renal artery stenosis is a decrease in blood flow through one or both of the main renal arteries or their branches. Stenosis and occlusion are usually due to thromboemboli, atherosclerosis, or fibromuscular dysplasia. Chronic, progressive stenosis causes refractory hypertension and may lead to chronic kidney disease. […] About 90% of cases are due to atherosclerosis, which is usually bilateral. Almost 10% of cases are due to fibromuscular dysplasia, which is commonly unilateral. Atherosclerosis develops primarily in patients 45 years (more often men) and usually affects the aortic orifice or proximal segment of the renal artery. Chronic progressive stenosis tends to become clinically evident after about 10 years of atherosclerosis, causing renal atrophy and chronic kidney disease. […] Fibromuscular dysplasia is pathologic thickening of the arterial wall, most often of the distal main renal artery or the intrarenal branches. The thickening tends to be irregular and can involve any layer (but most often the media). This disorder develops primarily in younger adults, particularly in women aged 20 to 50 years.
  • #7 The “Silent Enemy” Called Renal Artery Stenosis: A Mini-Review
    https://www.mdpi.com/2813-2475/4/1/10
    Renal artery stenosis (RAS) is a vascular condition characterized by narrowing of one or both renal arteries, leading to reduced blood flow to the kidneys, activation of the renin–angiotensin–aldosterone system (RAAS), and subsequent renovascular hypertension. […] Overactivation of the same cascade potentiates the production of angiotensin II, which induces systemic vasoconstriction, increases sodium and water retention via aldosterone, and activates the sympathetic nervous system. Angiotensin II is also implicated in endothelial dysfunction, oxidative stress, and chronic inflammation, thus impairing vascular remodeling and arterial stiffness, all of which serve to accelerate cardiovascular complications, such as left ventricular hypertrophy, heart failure, and myocardial infarction. […] Etiologically, the causes of RAS are predominantly related to atherosclerosis, responsible for approximately 90% of cases, and fibromuscular dysplasia (FMD), comprising around 10% of diagnoses.
  • #8 An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review
    https://www.mdpi.com/2075-1729/11/3/208
    Renal artery stenosis (RAS) is conditioned mainly by two disturbances: fibromuscular dysplasia or atherosclerosis of the renal artery. […] RAS is an example of renovascular disease, with complex pathophysiology and consequences. There are multiple pathophysiological mechanisms triggered in response to significant renal artery stenosis, including disturbances within endothelin, kinin–kallikrein and sympathetic nervous systems, with angiotensin II and the renin–angiotensin-aldosterone system (RAAS) playing a central and key role in the pathogenesis of RAS. […] The increased oxidative stress and the release of pro-inflammatory mediators contributing to pathological tissue remodelling and renal fibrosis are also important pathogenetic elements of RAS. […] The activation of RAAS and its haemodynamic consequences is the primary and key element in the pathophysiological cascade triggered in response to renal artery stenosis.
  • #9 Renal artery stenosis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Renal_artery_stenosis_pathophysiology
    The reduction in renal blood flow secondary to renal artery stenosis stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system. Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling. […] Renal artery stenosis means the narrowing of both renal arteries leading to the obstruction of blood flow and resulting in the stimulation of RAAS. […] In patients with RAS, the reduced blood flow to the kidneys leads to the formation of collateral blood vessels and increases secretion of renin by juxtaglomerular apparatus and activation of the renin-angiotensin-aldosterone system.
  • #10 Renal artery stenosis | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/renal-artery-stenosis?lang=us
    Renal artery stenosis (RAS) (plural: stenoses) refers to a narrowing of a renal artery. When the process occurs slowly, it leads to secondary hypertension. Acute renal artery stenosis does not lead to hypersecretion of renin. […] When the stenosis occurs slowly, collateral vessels form and supply the kidney. The kidney wrongly senses the reduced flow as low blood pressure (via the juxtaglomerular apparatus) and releases a large amount of renin that converts angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II with the help of angiotensin-converting enzyme (ACE) in the lungs. Angiotensin II is responsible for vasoconstriction and release of aldosterone which causes sodium and water retention, thus resulting in secondary hypertension.
  • #11 The “Silent Enemy” Called Renal Artery Stenosis: A Mini-Review
    https://www.mdpi.com/2813-2475/4/1/10
    The progression of RAS entails a number of structural and functional changes in the arterial walls. In the case of atherosclerosis, apart from the lipid plaque deposition, there is a gain of chronic inflammatory process-induced vascular remodeling. […] The reduction in renal blood flow due to stenosis causes hypoperfusion of the parenchyma, which is detected by juxtaglomerular cells—a set of modified smooth muscle cells located in the afferent glomerular arterioles. In response, there is a compensatory activation of the RAAS, resulting in the release of renin. […] Renin converts angiotensinogen, a hepatic-origin plasma protein, into angiotensin I, which is subsequently converted into angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin II causes systemic vasoconstriction and stimulates the release of aldosterone from the adrenal zona glomerulosa, thus producing sodium and water retention. […] Furthermore, angiotensin II also exerts proinflammatory and profibrotic effects by contributing to an increase in structural alterations of the blood vessels and further progression of the disease.
  • #12 Renal Artery Stenosis | Calgary Guide
    https://calgaryguide.ucalgary.ca/renal-artery-stenosis-pathogenesis-and-clinical-findings/renal-artery-stenosis/
    In unilateral renal artery stenosis, the contralateral (normal) kidney can compensate for the increase in renal perfusion pressure caused by hypertension by increasing sodium excretion (pressure natriuresis), preventing flash pulmonary edema. […] In bilateral renal artery stenosis*, GFR inability for kidney to renal Na+ water excretion volume overload Acute increase in afterload or preload sudden in left ventricular filling pressures blood backup into lungs Pulmonary vasculature hypertension fluid filtration across the pulmonary endothelium into interstitium and alveolar spaces Flash (rapid onset) pulmonary edema.
  • #13
    https://journals.lww.com/md-journal/fulltext/2023/09220/recurrent_flash_pulmonary_edema_in_unilateral.69.aspx
    Flash pulmonary edema can have various causes and can immediately be a life-threatening emergency. However, it can be treated with percutaneous revascularization if it is caused by renal artery stenosis. […] Renal artery stenosis, particularly bilateral renal artery stenosis, is one of the leading causes of flash pulmonary edema. […] Flash pulmonary edema, which can rapidly cause respiratory failure, can occur in patients with renal artery stenosis. […] Patients with a solitary kidney may develop pulmonary edema due to angiotensin-mediated vasoconstriction induced by increased left ventricular afterload. Our patient had a single-functioning kidney with an atrophied and nonfunctioning right kidney. It appears that renal artery stenosis develops in such a single-functioning kidney and induces flash pulmonary edema.
  • #14 Renal artery stenosis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Renal_artery_stenosis_pathophysiology
    This angiotensin II directly causes vasoconstriction and also increases aldosterone which results in the retention of sodium and water thus leads to the development of renovascular hypertension that is also called secondary hypertension. […] Prolonged hypo-perfusion to the kidneys resulting in chronic stimulation and hyperplasia of the juxtaglomerular apparatus. This prolonged ischemia further leads to renal insufficiency and in turn progressive renal atrophy. […] Glomerular filtration rate (GFR) is auto-regulated with the help of angiotensin II and numerous other modulators. The GFR gets affected when the renal perfusion drops below 70 mmHg. The apparent change in GFR is observed once the arterial lumen narrows by more than 50%. Numerous studies reported that GFR is reduced when altogether there is a reduction in renal perfusion pressure by more than 40% and a reduction in mean renal blood flow by 30%. However, even after this, the kidneys cortex and medulla can adapt without the development of severe hypoxia. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and fibrosis. But in cases with more significant stenosis around 70-80%, there is the development of apparent cortical hypoxia and this hypoxia further leads to the rarefaction of microvessels and ultimately leads to the development of interstitial fibrosis. Therefore the loss of renal function and progressive renal disease. Eventually, it becomes irreversible and restoration of blood flow to the kidneys will not help in getting back the kidney functions.
  • #15 Renal Artery Stenosis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/245023-overview
    The formation of atherosclerotic lesions involves increased permeability of endothelium to plasma macromolecules (eg, low-density lipoprotein [LDL]), increased turnover of endothelial cells and smooth muscle cells, and increased numbers of intimal macrophages. […] In patients with renal artery stenosis, the chronic ischemia produced by the obstruction of renal blood flow leads to adaptive changes in the kidney that are more pronounced in the tubular tissue. […] In patients with renal artery stenosis, the GFR is dependent on angiotensin II and other modulators that maintain the autoregulation system between the afferent and efferent arteries and can fail to maintain the GFR when renal perfusion pressure drops below 70-85 mm Hg. […] Significant functional impairment of autoregulation, leading to a decrease in the GFR, is not likely to be observed until arterial luminal narrowing exceeds 50%.
  • #16 The Role of Renal Artery Stenosis
    https://www.uspharmacist.com/article/the-role-of-renal-artery-stenosis
    In patients with RAS, when renal perfusion pressure drops below 70 mmHg to 85 mmHg, the autoregulation system between the afferent and efferent arteries can fail to maintain the glomerular filtration rate (GFR). This will lead to a decrease in the GFR, but will not likely be observed until arterial luminal narrowing exceeds 50%. […] The other main cause of RAS is fibromuscular dysplasia (FMD)the abnormal development or growth of cells on the renal artery wallswhich can cause blood vessels to narrow.
  • #17 An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review
    https://www.mdpi.com/2075-1729/11/3/208
    To sum up, RAS is characterised by different clinical pictures, including asymptomatic disorders diagnosed in kidney imaging, renovascular hypertension, usually characterised by severe course, and chronic ischemic nephropathy, described by pathological remodelling of kidney tissue, ultimately leading to kidney injury and chronic kidney disease. […] The clinical significance of RAS depends on the location of the stenotic changes and the degree of narrowing of the renal artery. […] Stenosis greater than 50–60% causes a pressure gradient greater than 15–20 mmHg, which is a haemodynamically significant feature of renal stenosis and a possible factor initiating renovascular hypertension development. […] The consequences of RAS are manifold, and, as mentioned in the Introduction, RAS may be a solely asymptomatic disorder or it may be accompanied by renovascular hypertension (RVH), eventually developing further consequences.
  • #18 Renal Artery Stenosis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/245023-overview
    The degree of renal artery stenosis that would justify any attempt at either surgical intervention or radiologic intervention is not known. […] One study found that when the pressure distal to renal artery stenosis was less than 90% of aortic pressure, renin release from the affected kidney was significantly elevated (renin being measured in the ipsilateral renal vein).
  • #19 Renovascular Hypertension: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/245140-overview
    A solitary kidney rendered ischemic by RAS is unable to achieve the pressure diuresis required to handle the aldosterone-induced sodium and water retention. The resultant volume expansion contributes to the elevation in blood pressure and also suppresses the production of renin by the stenotic kidney. […] The evolution of RVHT has been described as having the following three stages or phases: Renin-angiotensin-dependent phase, Salt-retention phase, Systemic renin-angiotensin-independent phase. […] In the first phase, the immediate rise in blood pressure is a direct consequence of hyperreninemia. Over days to weeks, blood pressure remains elevated, but the course and presence of hyperreninemia vary with the presence and function of the contralateral kidney. […] When the contralateral kidney is functional, volume expansion is avoided and renin levels remain high. The two kidneys are in opposition; the stenotic kidney avidly retains sodium and produces excess renin in response to renal ischemia, while the nonstenotic kidney excretes sodium and water to maintain euvolemia and renin production decreases. The end result is systemic hypertension that is mediated by both renin and angiotensin.
  • #20 Renovascular Hypertension: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/245140-overview
    A solitary kidney rendered ischemic by RAS is unable to achieve the pressure diuresis required to handle the aldosterone-induced sodium and water retention. The resultant volume expansion contributes to the elevation in blood pressure and also suppresses the production of renin by the stenotic kidney. […] The evolution of RVHT has been described as having the following three stages or phases: Renin-angiotensin-dependent phase, Salt-retention phase, Systemic renin-angiotensin-independent phase. […] In the first phase, the immediate rise in blood pressure is a direct consequence of hyperreninemia. Over days to weeks, blood pressure remains elevated, but the course and presence of hyperreninemia vary with the presence and function of the contralateral kidney. […] When the contralateral kidney is functional, volume expansion is avoided and renin levels remain high. The two kidneys are in opposition; the stenotic kidney avidly retains sodium and produces excess renin in response to renal ischemia, while the nonstenotic kidney excretes sodium and water to maintain euvolemia and renin production decreases. The end result is systemic hypertension that is mediated by both renin and angiotensin.
  • #21 Renovascular Hypertension: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/245140-overview
    In the second phase, in the setting of an ischemic solitary kidney, sodium and water retention, together with the vasopressor effects of angiotensin II, act to maintain renal perfusion pressure. The stimulus to produce renin is stifled, and renin levels fall. Hypertension becomes less dependent on angiotensin II and predominantly results from volume expansion. […] If blood flow is restored during these first two phases and renal perfusion is reinstated, blood pressure soon returns to a normal level. If renal hypoperfusion persists and the third phase is reached, restoration of renal blood flow may not normalize blood pressure, presumably because of secondary irreversible vascular or renal parenchymal disease. […] In the third phase, hypertension often is unremitting, persisting well after the removal of the stenosis. Recalcitrant hypertension in this setting likely represents the presence of ischemic nephropathy in either or both kidneys; patients in whom stenoses were not hemodynamically significant initially also may have persistent hypertension.
  • #22 Renovascular Hypertension: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/245140-overview
    Renovascular hypertension (RVHT) reflects the causal relation between anatomically evident arterial occlusive disease and elevated blood pressure. The coexistence of renal arterial vascular (ie, renovascular) disease and hypertension roughly defines this type of secondary hypertension. […] The chief pathophysiologic mechanism underlying RVHT involves activation of both limbs of the RAAS and depends on the presence or absence of a contralateral kidney. […] Unilateral renal ischemia initiates hypersecretion of renin, which accelerates conversion of angiotensin I to angiotensin II and enhances adrenal release of aldosterone. The result is profound angiotensin-mediated vasoconstriction and aldosterone-induced sodium and water retention. […] In unilateral RAS, renin production is increased in the ischemic kidney but suppressed in the unaffected nonstenotic kidney, which lacks the same ischemic stimulus. Consequently, when two kidneys are present with a unilateral stenosis (two-kidney one-clip model), hyperreninemia persists and blood pressure remains elevated because of an angiotensin II-induced vasoconstrictive effect.
  • #23 An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review
    https://www.mdpi.com/2075-1729/11/3/208
    In sum, renal artery stenosis, characterised by a haemodynamically significant narrowing of the renal artery, produces renovascular hypertension, which may coexist with further complications arising from ischemic nephropathy development. […] The diagnosis and evaluation of RAS is based on the imaging diagnostic modalities. […] The diagnostic gold standard for the identification of RAS is angiography; however, the technique is invasive and should not be used as an initial diagnostic test. […] The other RAS causative factors are uncommon and involve extra- and intrarenal disturbances. […] The rapid progression of RAS, reaching critical renal artery stenosis, is a possible aetiological factor of prerenal acute kidney injury (AKI). […] The more severe and prolonged diminishing of RBF in the stenotic kidney may threaten the oxygen supply to the organ and viability of the tissues, eventually leading to kidney fibrosis, resulting from action of the key compound, AII, which also exerts strong profibrotic effects, augmented by the secondary release of TGF-β. […] The inflammatory and profibrotic mechanisms prevailing in advanced RAS contribute to the advanced, pathological remodelling of the kidney structure, which evidence ongoing chronic kidney injury and ultimately account for up to 15–20% of the cases of chronic kidney disease developing.
  • #24 Renal Artery Stenosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK430718/
    It is reported that more advanced stenosis corresponding to a 70% to 80% of vascular occlusion leads to demonstrable cortical hypoxia, and it is proposed that this hypoxia produce rarefaction of microvessels, as well as activation of inflammatory and oxidative pathways that cause interstitial fibrosis. Therefore loss of renal function in renovascular disease in addition to being a usually reversible consequence of antihypertensive therapy can reflect a progressive narrowing of the renal arteries and/or progressive intrinsic renal disease. Eventually, long-standing parenchymal injury becomes an irreversible process. At this point, restoring renal blood flow provides no recovery of renal function or clinical benefit.
  • #25 Renal artery stenosis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Renal_artery_stenosis_pathophysiology
    This angiotensin II directly causes vasoconstriction and also increases aldosterone which results in the retention of sodium and water thus leads to the development of renovascular hypertension that is also called secondary hypertension. […] Prolonged hypo-perfusion to the kidneys resulting in chronic stimulation and hyperplasia of the juxtaglomerular apparatus. This prolonged ischemia further leads to renal insufficiency and in turn progressive renal atrophy. […] Glomerular filtration rate (GFR) is auto-regulated with the help of angiotensin II and numerous other modulators. The GFR gets affected when the renal perfusion drops below 70 mmHg. The apparent change in GFR is observed once the arterial lumen narrows by more than 50%. Numerous studies reported that GFR is reduced when altogether there is a reduction in renal perfusion pressure by more than 40% and a reduction in mean renal blood flow by 30%. However, even after this, the kidneys cortex and medulla can adapt without the development of severe hypoxia. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and fibrosis. But in cases with more significant stenosis around 70-80%, there is the development of apparent cortical hypoxia and this hypoxia further leads to the rarefaction of microvessels and ultimately leads to the development of interstitial fibrosis. Therefore the loss of renal function and progressive renal disease. Eventually, it becomes irreversible and restoration of blood flow to the kidneys will not help in getting back the kidney functions.
  • #26 The Role of Renal Artery Stenosis
    https://www.uspharmacist.com/article/the-role-of-renal-artery-stenosis
    It has been reported that renal artery stenosis (RAS) is a major cause of renovascular hypertension (RVH). […] Not only does RAS play a role in the pathogenesis of hypertension, it is also increasingly recognized as an important cause of chronic renal insufficiency and end-stage renal disease (ESRD). The most common etiology of RAS is believed to be atherosclerosis, especially in the elderly. RAS progressively decreases blood flow to the kidneys and, eventually, impacts renal function and kidney structure. […] RAS is primarily caused by atherosclerosis, or clogging, narrowing, and hardening of the renal arteries. In these cases, RAS develops when plaque builds up on the inner wall of one or both renal arteries, making them hard and narrow. […] In patients with RAS, the chronic insufficiency produced by the obstruction of renal blood flow leads to kidney changes that are more pronounced in the tubular tissue. These include inflammation, fibrosis, tubulosclerosis, and intrarenal arterial thickening.
  • #27 Renal Artery Stenosis | Calgary Guide
    https://calgaryguide.ucalgary.ca/renal-artery-stenosis-pathogenesis-and-clinical-findings/renal-artery-stenosis/
    Renal Artery Stenosis: Pathogenesis and clinical findings Atherosclerosis: A collection of inflammatory cells, lipids, Fibromuscular Dysplasia: A rare vascular condition characterized by fibrous connective tissue deposits on the renal artery wall abnormal cellular growth in arterial walls, especially renal carotid arteries Narrowing (stenosis) of the renal artery Renal Artery Stenosis can be unilateral or bilateral […] Pressure perfusing the kidney RAAS (renin-angiotensin- aldosterone system) activation pressure gradient in glomerulus Glomerular filtration rate (GFR) Secretion of aldosterone Turbulent blood flow through area of stenosis Abdominal bruit on side of affected kidney(s) Secretion of Angiotensin II Systemic vasoconstriction Hypertension Expression of epithelial sodium channels in cortical collecting duct Blood volume within volume- constrained space of blood vessels Renal blood flow ischemic renal injury Atrophy and fibrosis of affected kidney(s) Unilateral stenosis Kidney size asymmetry (1.5cm difference)
  • #28 Renal Artery Stenosis: Symptoms, Diagnosis and Therapy
    https://www.urology-textbook.com/renal-artery-stenosis.html
    Renal artery stenosis due to arteriosclerosis is a progressive disease: in 50% of cases the obstruction progresses and 16% will suffer from complete closure. The greater the obstruction at initial diagnosis, the more likely the progression and the complete closure. If renal failure requires dialysis due to renal artery stenosis, the prognosis due to vascular complications is poor: median survival of 27 months, and the five-year survival rate is 12%.
  • #28 Renal Artery Stenosis: Symptoms, Diagnosis and Therapy
    https://www.urology-textbook.com/renal-artery-stenosis.html
    Renal artery stenosis is the narrowing of the renal artery, leading to renal arterial hypertension, ischemic nephropathy, and end-stage renal disease (ESRD) (Safian and Textor, 2001) (Textor and Wilcox, 2001). […] Arteriosclerosis is the predominant etiology (90%) of renal artery stenosis, mainly affecting the proximal part of the renal artery. The obstruction is caused by eccentric plaques, which narrow the lumen and may lead to dissection or thrombosis with complete vessel occlusion. […] Renal artery stenosis leads to the activation of the renin-angiotensin-aldosterone system (RAAS), ischemia of the kidney, and renal arterial hypertension. […] Invasive treatment of renal artery stenosis (percutaneous transluminal angioplasty or vascular surgery) is indicated for ischemic nephropathy requiring intervention or inadequate medical control of renal hypertension. An intervention is particularly indicated for a single kidney or bilateral involvement due to the high risk of renal failure.
  • #29 An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8000991/
    However, the pathomechanism of RAS is more complex and also includes other disturbances that ultimately contribute to the development of the diseases mentioned above. […] The consequences of RAS are manifold, and, as mentioned in the Introduction, RAS may be a solely asymptomatic disorder or it may be accompanied by renovascular hypertension (RVH), eventually developing further consequences. […] The rapid progression of RAS, reaching critical renal artery stenosis, is a possible aetiological factor of prerenal acute kidney injury (AKI). […] In sum, renal artery stenosis, characterised by a haemodynamically significant narrowing of the renal artery, produces renovascular hypertension, which may coexist with further complications arising from ischemic nephropathy development. […] There is no doubt that the key player in the pathogenesis of disturbances developing in the course of renal artery stenosis is angiotensin II, which is a common, connecting pathogenetic element of systems functionally linked with RAAS.
  • #30 Pathophysiology of Renal Artery Disease | Thoracic Key
    https://thoracickey.com/pathophysiology-of-renal-artery-disease/
    Even moderate stenosis, especially when superimposed on intrarenal microvascular disease, may contribute to adverse renal outcomes. […] High-grade vascular stenosis eventually leads to a decrease in renal perfusion pressure. […] The immediate increase in blood pressure in RAS results from release of renin from the stenotic kidney. […] Activation of the sympathetic nervous system also plays an important role in the pathogenesis of renovascular hypertension primarily via the renal afferent nerves.
  • #31 The “Silent Enemy” Called Renal Artery Stenosis: A Mini-Review
    https://www.mdpi.com/2813-2475/4/1/10
    The progression of RAS entails a number of structural and functional changes in the arterial walls. In the case of atherosclerosis, apart from the lipid plaque deposition, there is a gain of chronic inflammatory process-induced vascular remodeling. […] The reduction in renal blood flow due to stenosis causes hypoperfusion of the parenchyma, which is detected by juxtaglomerular cells—a set of modified smooth muscle cells located in the afferent glomerular arterioles. In response, there is a compensatory activation of the RAAS, resulting in the release of renin. […] Renin converts angiotensinogen, a hepatic-origin plasma protein, into angiotensin I, which is subsequently converted into angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin II causes systemic vasoconstriction and stimulates the release of aldosterone from the adrenal zona glomerulosa, thus producing sodium and water retention. […] Furthermore, angiotensin II also exerts proinflammatory and profibrotic effects by contributing to an increase in structural alterations of the blood vessels and further progression of the disease.
  • #32
    https://juniperpublishers.com/jojun/JOJUN.MS.ID.555754.php
    In RAS, decreased perfusion pressure to the kidneys is secondary to the stenotic renal artery, leading to RAAS activation. In activating the RAAS, the goal is to increase renal perfusion by increasing systemic blood pressure. In RAS, the vasoconstriction in the efferent arterioles of the glomeruli leads to short-term preservation of the glomerular filtration and protection from hypotension and relative hypoxia. While the RAAS provides short-term protection in RAS, over the long term, it leads to ischemic nephropathy in the affected kidney, hypertensive nephrosclerosis in the unaffected kidney, and glomerulosclerosis and tubule-interstitial fibrosis in both kidneys. […] Glomerulosclerosis and tubule interstitial fibrosis are thought to be caused by elevated levels of angiotensin II, associated with inflammatory cytokines that lead to increased activation of inflammatory and profibrogenic pathways. Additional processes associated with RAS include endothelial dysfunction causing impaired vascular relaxation, leading to tubule-interstitial fibrosis, and increased sympathetic adrenergic activity causing microvascular damage.
  • #33 Renal artery stenosis in a single kidney patient: A case report | Medicina Clínica Práctica
    https://www.elsevier.es/es-revista-medicina-clinica-practica-5-resumen-renal-artery-stenosis-in-single-S2603924922000441
    Renal Artery Stenosis (RAS) is a pathologic state that may lead to resistant hypertension, progressive decline in renal function, cardiac destabilization syndromes, recurrent heart failure, or acute coronary syndromes. […] Renal Artery Stenosis (RAS) is a pathologic state that results in the limitation of renal artery nutritional sources and reduced blood flow to the kidneys. Atherosclerotic renal artery stenosis (ARAS) is defined as a decrease of more than 60% in luminal diameter due to atheroma. ARAS is the most common cause of renovascular hypertension. […] Renal Artery Stenosis (RAS) may cause the following clinical syndromes: Reno-vascular blood pressure: activation of Renin- Angiotensin- Aldosterone (RAAS) along with unilateral and bilateral renal hypoperfusion. This results in sodium retention, secondary hyperaldosteronism, and vascular contraction.
  • #34 Unilateral renal artery stenosis presented with hyponatremic-hypertensive syndrome – case report and literature review | BMC Nephrology | Full Text
    https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-019-1246-9
    Renal artery stenosis is one of the secondary causes of pediatric hypertension. […] The central pathomechanism that underlies hyponatremic hypertension syndrome (HHS) is the stimulation and activation of the renin-angiotensin-aldosterone (RAA) axis which consequently trigger hypertension through vasoconstriction as well as fluid and salt retention. In cases of unilateral renal artery stenosis, angiotensin II induces pressure natriuresis of the non-stenotic kidney and hence produces the unique finding of hyponatremia in conjunction with hypertension. […] The main pathogenesis of HHS is renal ischemia. Hypertension is induced by stimulation of unremitted renin secretion and subsequent angiotensin II-induced vasoconstriction and secondary hyperaldosteronism. Elevated circulating angiotensin II can cause glomerular hyperfiltration and subsequential pressure natriuresis of the non-stenotic kidney, which results in the clinical presentation of hyponatremia.
  • #35 Renal artery stenosis in a single kidney patient: A case report | Medicina Clínica Práctica
    https://www.elsevier.es/es-revista-medicina-clinica-practica-5-resumen-renal-artery-stenosis-in-single-S2603924922000441
    Ischemic nephropathy: is a potentially irreversible cause of renal failure. It may cause intra-renal hemodynamic disturbance and its following consequences: high blood pressure and chronic renal disease. […] The pathophysiology of renal artery stenosis is complex and involves many pathophysiological mechanisms that are interrelated and interdependent. RAS may present as an asymptomatic radiologic abnormality or with renovascular hypertension and ischemic nephropathy contributing to chronic kidney disease, and these conditions may coexist and overlap.
  • #36 Unilateral renal artery stenosis presented with hyponatremic-hypertensive syndrome – case report and literature review | BMC Nephrology | Full Text
    https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-019-1246-9
    Sodium wasting and volume depletion further stimulates the renin excretion. Hyperaldosteronism, secondary to hyperreninemia and volume depletion, lead to hypokalemia which is one of the leading complications of HHS. Glomerular hyperfiltration of contralateral healthy kidney, deriving from hyperreninemia-induced hypertension, could eventually result in tubulointerstitial injury from the effects of hypercalciuria and hyperuricosuria. […] Proteinuria in cases of HHS, sometimes in nephrotic range, can result from the glomerular hyperfiltration, proteinuric effect of angiotensin II, and/or consequence of tubulointerstitial injury caused by prolonging hypercalciuria and hyperuricosuria.
  • #37 Renal artery stenosis: epidemiology and treatment | IJNRD
    https://www.dovepress.com/renal-artery-stenosis-epidemiology-and-treatment-peer-reviewed-fulltext-article-IJNRD
    Renal artery stenosis (RAS) is a common cause of secondary hypertension. […] The mechanism leading to the development of renovascular hypertension is typically classified as either renin-dependent or primarily a result of volume overload. […] When ischemia occurs downstream of a stenotic renal artery, renin is released from juxtaglomerular cells. […] Ischemic nephropathy can be defined as an obstruction causing decreased perfusion leading to renal ischemia and subsequent excretory dysfunction. […] Several interrelated mechanisms have been proposed explaining how a hemodynamically significant lesion ultimately results in interstitial fibrosis. […] RAS may either cause or exacerbate cardiac destabilizing syndromes, including unstable angina (UA) and congestive heart failure characterized by flash pulmonary edema. […] RAS precipitates these conditions through three general mechanisms: volume overload, peripheral arterial vasoconstriction, and direct effects of angiotensin on the myocardium.
  • #38 Renal Vascular Disease | Frankel Cardiovascular Center | Michigan Medicine
    https://www.umcvc.org/conditions-treatments/renal-vascular-disease
    The most common cause of renal artery blockages is arteriosclerosis (the thickening and hardening of artery walls) with cholesterol and plaque build-up. […] Symptoms of renal artery disease include: High blood pressure that is difficult to treat with medicines, especially in women under age 45. […] Worsening of the kidney’s function to clear the body’s waste products, determined by blood samples, especially when high blood pressure medicines are needed, in particular ACE inhibitors like lisinopril. […] If untreated, high blood pressure caused by the kidneys, or renovascular hypertension, may lead to a number of serious cardiovascular and kidney problems, including: Thickening of the heart muscle (hypertrophy) […] Worsening of arteriosclerosis of all the body’s arteries […] Renal failure requiring dialysis.
  • #39
    https://journals.lww.com/md-journal/fulltext/2023/09220/recurrent_flash_pulmonary_edema_in_unilateral.69.aspx
    Takayasu arteritis causes renal artery stenosis and leads to sudden onset of pulmonary edema. […] The mechanism by which renal artery stenosis leads to cardiac destabilization syndrome is believed to be uncontrolled hypertension and volume retention, which can lead not only to heart failure, but also to acute coronary syndrome. […] Management of renal artery stenosis resulting from various causes, including Takayasu arteritis, is largely divided into medical treatment and revascularization. […] According to the guidelines presented by the American Heart Association/American College of Cardiology Committee for the treatment of renal artery stenosis, medical treatment is the first-line treatment for hypertension and preservation of renal function, whereas percutaneous revascularization is the first-line treatment for hemodynamically significant renal artery stenosis, recurrent unexplained congestive heart failure, and sudden unexplained pulmonary edema. […] Flash pulmonary edema can have various causes and can immediately be a life-threatening emergency. However, it can be treated with percutaneous revascularization if it is caused by renal artery stenosis.
  • #40 ACE inhibitors and renal artery stenosis | GPonline
    https://www.gponline.com/ace-inhibitors-renal-artery-stenosis/cardiovascular-system/article/914629
    Renal artery stenosis, defined as narrowing of the renal artery or arteries, can be uni- or bilateral. […] There are two likely pathological processes at work: atherosclerosis and fibromuscular dysplasia. […] Narrowing of the renal artery may be due to atherosclerosis. Atherosclerosis accounts for approximately 70-90 per cent of renal artery stenosis and tends to occur in men over the age of 50. […] The remainder of renal artery stenosis cases are caused by fibromuscular dysplasia, which is seen more frequently in younger females. […] In renal artery stenosis, the afferent pressure is reduced by the narrowed vessel, hence autoregulation is almost exclusively dependent on changes in post-glomerular arteriolar tone. […] Because ACE inhibitors interfere with the production of angiotensin II, autoregulation is impaired, glomerular perfusion falls, renal ischaemic nephropathy develops and renal failure ensues.
  • #41 Renal Artery Stenosis | Concise Medical Knowledge
    https://www.lecturio.com/concepts/renal-artery-stenosis/
    Renal artery stenosis (RAS) is the narrowing of one or both renal arteries, usually caused by atherosclerotic disease or by fibromuscular dysplasia. […] If the stenosis is severe enough, the stenosis causes decreased renal blood flow, which activates the renin-angiotensin-aldosterone system. […] Renovascular hypertension (RVH) is the final result and affects both kidneys and other target organs. […] Pathogenesis of all RAS cases includes a significant decrease of lumen (70% or less than 30% patent) with poststenotic gradient blood pressure being affected. […] Renal hypoperfusion activates the renin-angiotensin-aldosterone system, leading to increased renin, angiotensin, and aldosterone retention and peripheral vascular resistance. […] RAS caused by atherosclerosis usually involves the aortic orifice or the proximal main renal artery.
  • #42 Renal artery stenosis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/renal-artery-stenosis/symptoms-causes/syc-20352777
    Fibromuscular dysplasia. In fibromuscular dysplasia, the muscle in the artery wall doesn’t grow as it should. This often begins in childhood. The renal artery can have narrow sections alternating with wider sections, giving a bead-like appearance in images of the artery. […] The renal artery can narrow so much that the kidney doesn’t get enough blood. This can lead to high blood pressure at a young age. This can happen in one or both kidneys. Experts don’t know what causes fibromuscular dysplasia, but the condition is more common in women and may be something that’s present at birth (congenital). […] Narrowed kidney arteries and fibromuscular dysplasia can affect other arteries in your body as well as your kidney arteries and cause complications. […] Rarely, renal artery stenosis results from other conditions such as inflammation of the blood vessels or a growth that develops in your abdomen and presses on your kidneys’ arteries.
  • #43 Renal Artery Stenosis | Concise Medical Knowledge
    https://www.lecturio.com/concepts/renal-artery-stenosis/
    Without treatment, 50% of cases progress, sometimes to complete obstruction. […] RAS caused by fibromuscular dysplasia typically involves the mid- or distal main renal artery or the intrarenal branches. […] Focal loss of the internal elastic lamina, with intervening fibromuscular hyperplasia, produces the typical string of beads appearance on an angiogram.
  • #44 Diagnosis and treatment of renal artery stenosis | Nature Reviews Nephrology
    https://www.nature.com/articles/nrneph.2009.230
    A reduction in the diameter of the renal arteries can lead to hypertension, renal dysfunction and/or pulmonary edema. […] About 90% of patients with renal artery stenosis have atherosclerosis, and 10% have fibromuscular dysplasia. […] Atherosclerotic renal artery stenosis is a common condition that typically occurs in patients at high risk of cardiovascular disease with coexistent vascular disease at nonrenal sites. […] Renal impairment associated with atherosclerotic RAS is both a marker and a risk factor for cardiovascular disease. […] Patients with atherosclerotic RAS and a stable condition should be treated first with medication. […] Renal artery stenting is not recommended for most patients with atherosclerotic RAS, but it might be beneficial for those with refractory hypertension or rapidly progressing renal or cardiac dysfunction. […] Patients with fibromuscular dysplasia of the renal artery usually have renovascular hypertension without renal failure or associated vascular disease.
  • #45 Renal Artery Stenosis Causes, Symptoms, Treatment, Diagnosis
    https://www.medicinenet.com/renal_artery_stenosis/article.htm
    Renal artery stenosis (narrowing) is a decrease in the diameter of the renal arteries. The resulting restriction of blood flow to the kidneys may lead to impaired kidney function (renal failure) and high blood pressure (hypertension), referred to as renovascular hypertension, or RVHT („reno” for kidney and „vascular” for blood vessels). […] The majority of renal artery stenosis is caused by atherosclerosis (hardening and narrowing of blood vessel wall from the inside) similar to the process that occurs in blood vessels in the heart and other parts of the body. […] Less common causes of renal artery stenosis are rare conditions such as fibromuscular dysplasia of the vessels (narrowing of the vessel due to internal thickening of the blood vessel wall), arteritis (inflammation of the blood vessel), or dissection (tearing and division of the blood vessel wall).
  • #46 Renal Artery Stenosis | Boston Children’s Hospital
    https://www.childrenshospital.org/conditions/renal-artery-stenosis
    The renal arteries are the blood vessels that carry blood to the kidneys. Renal artery stenosis occurs when one or more of these vessels become narrowed. This can lead to decreased blood flow to your childs kidney or kidneys, as well as increased blood pressure, a condition known as renovascular hypertension. […] In most children with renal artery stenosis, the affected renal artery is already narrow at birth. Other causes include vasculitis (inflammation of the blood vessels) and the genetic condition neurofibromatosis, in which tumors form from nerve tissue. Renal artery stenosis is also associated with midaortic syndrome, a rare condition in which part of the aorta (the hearts largest blood vessel) that runs through the chest and abdomen becomes narrow. This can lead to lower blood flow to other parts of the body, including the kidneys.
  • #47 Renal Artery Stenosis: Diagnosis and Management | SpringerLink
    https://link.springer.com/chapter/10.1007/978-3-319-56042-7_40
    Renal artery stenosis (RAS) is commonly atherosclerotic in origin and its incidence increases with age. Decreased renal perfusion causes renal ischemia, which activates the reninangiotensinaldosterone system and increases a variety of inflammatory and pro-fibrotic cytokines. This results in the development of hypertension and a decline in renal function. […] It is clear that the majority of patients with RAS can be treated with medical therapy alone. The question is how to identify those patients who would benefit from revascularization. High-risk patients include those with resistant hypertension, unexplained worsening renal function, asymmetric renal size, and recurrent episodes of flash pulmonary. […] Several newer methodologies including BOLD MRI, dynamic contrast enhanced MRI and renal frame count have, in small studies, been shown to correlate with the presence of renal ischemia.
  • #48 How to manage renovascular hypertension
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-13/How-to-manage-renovascular-hypertension
    Renal artery stenosis must be considered in any patient with a history of severe or resistant hypertension, especially in those associating a decline in renal function or significant atherosclerosis in other vascular territories. […] In theory, renal artery stenosis results in increased blood pressure values and declined renal function; as a consequence, removal of the obstruction (the stenosis) should allow proper hypertension (HTN) control and good restoration of renal function. […] Renal artery stenosis causes clinical syndromes that go from asymptomatic obstruction (incidental renal artery stenosis) to RVH and ischemic nephropathy. […] Atherosclerotic disease of renal arteries may progress to complete arterial occlusion. When the entire renal parenchyma is affected (i.e., in bilateral stenosis or stenosis to a solitary kidney), renal artery stenosis may cause severe deterioration of renal function, often referred to as ischemic nephropathy.
  • #49 How to manage renovascular hypertension
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-13/How-to-manage-renovascular-hypertension
    The major risk of current pharmacologic therapy resides in the decline of renal function, a clinical situation often encountered when introducing an ACE inhibitor or ARB. […] The role of revascularisation in the treatment of atherosclerotic renal-artery stenosis is still controversial. Recently published trials did not prove superiority of interventional therapy, but most authors recommend angioplasty with or without stenting when HTN control cannot be achieved, if renal function is declining and in patients with flash pulmonary oedema.
  • #50 Renal Artery Stenosis: Symptoms, Treatment, Diagnosis & Causes
    https://www.emedicinehealth.com/renal_artery_stenosis/article_em.htm
    If the renal artery stenosis causes less than 50% narrowing of the artery and if kidney function is maintained, medications that block the actions of angiotensin may be used in association with routine monitoring of the renal artery status with ultrasound. […] The most frequently used invasive procedure to open a narrowed renal artery uses the same type of procedure that is used in heart disease. Balloon angioplasty allows a radiologist to insert a catheter, or narrow tube, into the femoral artery in the groin and advance it to the area of narrowing in the renal artery. […] If angioplasty fails or is not technically feasible, formal bypass surgery may be considered. […] Unfortunately, if the renal artery stenosis is longstanding and kidney function has been compromised for a prolonged period of time, return blood flow to the kidney may not return to kidney function. […] Renal artery stenosis is one potentially reversible cause of high blood pressure. […] Diagnosis is made by imaging the artery with ultrasound, computerized tomography, or arteriography. […] Treatment may be medical or surgical.