Renal Artery Stenosis



Renal Artery Stenosis


A. Brad Farris, III, MD





Key Facts


Etiology/Pathogenesis



  • Renal artery stenosis from variety of potential causes results in ischemic atrophy


  • Atherosclerosis with atheromatous plaques is one of the most important etiologies


Clinical Issues



  • Hypertension


  • Proteinuria


  • Renal dysfunction


Macroscopic Features



  • Kidneys small from ischemic atrophy


Microscopic Pathology



  • Focal segmental and global glomerulosclerosis (FSGS) can occur


  • Glomerular basement membrane (GBM) wrinkling


  • Interstitial fibrosis and tubular atrophy (IFTA) and interstitial inflammation



    • Tubular atrophy is of conventional type or may show “endocrine change” or thyroidization


  • Atherosclerosis, arteriosclerosis, arteriolar hyalinosis, and sometimes cholesterol emboli


  • Electron microscopy may show GBM wrinkling and collapse, foot process effacement, and renin granules in hypertrophic juxtaglomerular apparatus


Top Differential Diagnoses



  • Renal artery aneurysms and dissection of aorta or renal artery


  • Neurofibromatosis


  • Takayasu arteritis and other arteritides


  • Fibromuscular dysplasia







Shown here are a shrunken kidney image affected by renal artery stenosis and a granular kidney image affected by hypertension, likely stimulated by renin production by the shrunken kidney.






There are numerous sclerotic, closely approximated glomeruli image and tubular atrophy in a thyroidization pattern image in this kidney affected by renal artery stenosis.


TERMINOLOGY


Abbreviations



  • Renal artery stenosis (RAS)


Synonyms



  • Atherosclerotic renovascular disease: Certain cases of RAS


  • Fibromuscular dysplasia: Selected cases of RAS


  • Renovascular disease


Definitions



  • Narrowing of renal artery lumen sufficient to cause ischemic changes in kidney and hypertension


ETIOLOGY/PATHOGENESIS


Causes of RAS



  • Atherosclerosis



    • Most common cause of occlusion/stenosis of large renal arteries (70-90% of RAS cases)


    • Autopsy studies show RAS in 5-42% of patients


    • Up to 50% of patients with extensive peripheral vascular disease have RAS


    • RAS is bilateral in 33-39%



      • Bilateral RAS has higher incidence of renal failure


    • Patients often have multifocal occlusive vascular disease, including coronary artery disease or peripheral arterial disease



      • Injury is conceptually semiepisodic, leading to “layers” of injury with vessels that are not able to autoregulate, eventually leading to “critical stenosis”


    • Atheromatous plaques



      • More common with age and in those with risk factors (cigarette smoking, HTN, diabetes, hyperlipidemia)


    • Atheroemboli (cholesterol emboli)



      • May occur immediately after or within months of angiographic or surgical procedures involving vessels


      • 0.1-0.8% frequency of symptomatic cholesterol emboli after angiography


      • Incidence of 0.1-3.3% in renal vessels


      • Emboli present in ˜ 31% of patients with aortic aneurysms and ˜ 77% of patients dying shortly after abdominal aortic surgery


  • Thromboembolic


  • Fibromuscular dysplasia


  • Neurofibromatosis


  • Moyamoya disease


  • Takayasu arteritis and other arteritides


  • Dissecting aneurysms of either aorta or renal artery


  • Umbilical artery catheterization in neonates


  • Coarctation of the aorta


  • Irradiation


  • Retroperitoneal fibrosis


  • Compression by tumor


  • Arteriovenous fistula


  • Trauma


Ischemic Renal Disease/Ischemic Nephropathy



  • Fundamental mechanism of injury in RAS


  • Occurs when renal artery has 70-80% or greater stenosis


Goldblatt Kidney



  • Unilateral RAS experimental model developed by Goldblatt has revealed pathophysiology


  • Causes hypertension (HTN) by activation of renal-angiotensin-aldosterone system



    • Ischemic kidney produces renin


    • Increased angiotensin II



      • Increased aldosterone production is stimulated


      • Leads to volume retention, hypervolemia, and increased cardiac output


    • Systemic HTN results




      • Ischemic kidney is protected from effects of HTN


      • Contralateral kidney suffers from effects of HTN (arterial and arteriolar nephrosclerosis)


CLINICAL ISSUES


Epidemiology



  • Age



    • Atherosclerotic RAS primarily affects older patients


  • Gender



    • 2:1 male to female ratio in atherosclerotic RAS


Presentation



  • Renal dysfunction



    • Chronic renal insufficiency



      • Increased serum creatinine and blood urea nitrogen


  • Hypertension


  • Proteinuria



    • Usually of low or moderate degree


    • Particularly occurs in patients with focal segmental glomerulosclerosis (FSGS)


  • Retinopathy


  • Abdominal or flank bruits


  • Hypokalemia may sometimes be seen


  • Family history of HTN may be absent


  • Hyperlipidemia, particularly in patients with atherosclerotic RAS


  • Diabetes


  • Congestive heart failure


  • If atheroemboli are associated with RAS



    • Livedo reticularis


    • Acute renal failure


    • HTN


    • Leg pain


    • Gastrointestinal symptoms


    • Vision loss


    • Peripheral eosinophilia


    • Decreased serum complement


Treatment



  • Surgical approaches



    • Percutaneous transluminal angioplasty



      • Used more often than stent placement


    • Angioplasty



      • Can be coupled with stent placement


      • Particularly useful when stenosis is at renal artery ostium, where angioplasty has higher failure rate


    • Bypass grafts


  • Drugs



    • Antihypertensive agents



      • ACE inhibitors


      • Beta blockers


      • Calcium channel blockers


    • Lipid lowering agents


    • Antidiabetic agents and glucose control


Prognosis



  • With 70-80% narrowing of renal artery lumen, ischemic renal disease may occur and may rapidly progress to failure of affected kidney



    • Around 1/2 progress within 2 years


IMAGE FINDINGS


Radiographic Findings



  • Intraarterial digital subtraction is “gold standard” to demonstrate RAS


  • Other radiographic imaging modalities are useful



    • Magnetic resonance angiography


    • Computed tomographic angiography


    • Color-aided duplex ultrasonography


    • Abdominal aortography



      • If renal artery narrowing, there may be poststenotic dilatation


  • Radiography coupled with renal functional measurements are useful in determining contribution of each kidney to overall renal functioning


MACROSCOPIC FEATURES


General Features



  • Grossly, narrowing of renal artery may be appreciated




    • Origin from aorta involved in approximately 50% of cases



      • Aorta may override renal artery ostium


    • Bilateral disease in up to 60% of cases


    • Can occur from a yellow-white fibroatheromatous plaque (atheroma) in atherosclerotic RAS cases


  • Kidneys may be small in ischemic nephropathy from RAS



    • Most RAS kidneys are < 50% of normal weight


  • Large cortical scars and small cortical cysts may be present


  • Granular capsular surface is often evident because of concurrent arteriolosclerosis


  • Renal cortex is thinned


  • Interlobar and arcuate arteries may appear prominent


MICROSCOPIC PATHOLOGY


Histologic Features



  • Glomeruli



    • Glomeruli may have basement membrane wrinkling



      • Sometimes referred to as an accordion-like wrinkling


      • Particularly appreciable on periodic acid-Schiff (PAS) and silver stains


    • Glomerular capillary tuft may contract toward vascular pole (a process referred to as glomerulus becoming “simplified”), leading to relative increase in Bowman space


    • Intracapsular fibrosis



      • Collagen deposition in Bowman space


      • Occurs 1st near vascular pole, eventually extending toward urinary pole


    • “Atubular glomeruli” may be present



      • Typically are present as residual glomeruli in fibrotic scars


      • Open capillary loops are not attached to tubules on serial sectioning, and mean glomerular volume tends to be larger than in controls


    • FSGS with resultant global sclerosis can occur



      • FSGS occurs as secondary form


      • Proteinuria may be prominent


    • Juxtaglomerular apparatus may be hypertrophic


  • Tubulointerstitium



    • Interstitial fibrosis and tubular atrophy (IFTA), and interstitial inflammation



      • Fibrosis may be diffuse and fine, demonstrable with connective tissue stains (e.g., trichrome)


      • Interstitial fibrosis and inflammation may be more severe in hypertensive nephrosclerosis than in RAS


    • Dilated tubules (“super tubules”)


    • “Classic” atrophic proximal tubules



      • Thickened tubular basement membranes, possibly due to regeneration from repeated tubular injury


      • Numerous mitochondria with decrease in other cellular organelles


    • “Endocrine change” form of atrophic tubules



      • Decreased tubular diameter with narrowed or inconspicuous lumens


      • Cuboidal epithelial cell lining, often with clear cytoplasm


      • Often occur in clusters


      • Terminology derived from resemblance of these renal tubules to endocrine glands such as parathyroid


    • Thyroidization may also be seen, consisting of atrophic tubules filled with proteinaceous cast material


    • Tubular atrophy can be potentially reversible



      • Reversal of atrophy can be accomplished with reestablishment of blood flow in rat model of RAS


      • Atubular glomeruli may be useful prognostic sign (irreversible)


  • Vessels

Tags:
Jul 7, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Renal Artery Stenosis

Full access? Get Clinical Tree
Get Clinical Tree app for offline access