Nephrology · KIMS Secunderabad
Renovascular Disease — When Kidney Blood Vessel Disorders Affect Function and Blood Pressure
Renovascular disease encompasses a spectrum of disorders affecting the blood vessels of the kidney — from the large renal arteries that supply blood to the kidney, to the renal veins that drain it, to the small intrarenal vessels (arterioles and glomerular capillaries) that determine filtration at the microscopic level. Each component of the renal vascular system can be affected by different diseases — atherosclerosis, thrombosis, embolism, vasculitis, thrombotic microangiopathy — and each produces a distinct clinical picture. What unites them is the consequence: reduced kidney perfusion, rising blood pressure, and progressive kidney function loss if not identified and treated.
This page serves as a hub for the full spectrum of renovascular disease — providing the clinical framework for understanding how each vascular disorder presents and pointing to the specific KIMS condition pages for the conditions that warrant more detailed discussion. Renal artery stenosis — the most common and most clinically important renovascular condition — is covered in full on its own dedicated KIMS page at /conditions/renal-artery-stenosis/.
The spectrum of renovascular disease
Renovascular disease is best understood by where in the vascular tree the pathology occurs — large artery, vein, or small intrarenal vessels. The cards below cover each condition, its typical presentation, and its specific treatment.
Large vessel — Renal artery stenosis (RAS)
Narrowing of the main renal artery — from atherosclerosis (90% of cases, in patients above 55 with cardiovascular risk factors) or fibromuscular dysplasia (FMD — in young women). Causes renovascular hypertension (RAAS-driven) and ischaemic nephropathy. Full detail at /conditions/renal-artery-stenosis/.
Large vessel — Renal artery occlusion and infarction
Complete or near-complete occlusion of the renal artery — from thromboembolism (atrial fibrillation, cardiac thrombus, aortic dissection, endocarditis), arterial thrombosis in situ (severe atherosclerosis, hypercoagulable state, trauma), or spontaneous renal artery dissection. Causes sudden, severe flank pain (similar to ureteric colic but without haematuria), elevated LDH (from infarcted renal tissue), and rising creatinine if the infarction is extensive or bilateral. CT with contrast shows the perfusion defect. Treatment: anticoagulation for embolic causes, endovascular thromboaspiration or thrombolysis in selected acute cases (within 6 to 12 hours of onset in young patients), management of the underlying cardiac source.
Large vessel — Renal artery aneurysm
Dilation of the renal artery — usually incidental on CT. Risk of rupture is low for aneurysms below 2cm but requires specialist assessment. Surgical repair or endovascular coiling for larger or symptomatic aneurysms.
Venous — Renal vein thrombosis (RVT)
Thrombosis of the renal vein — classified as acute (causing sudden flank pain, haematuria, and acute kidney injury) or chronic (often asymptomatic). The most important predisposing condition is nephrotic syndrome — the loss of natural anticoagulants (protein C, protein S, antithrombin III) in the urine and the elevation of clotting factors (from hepatic upregulation) creates a profoundly prothrombotic state. Membranous nephropathy has the highest risk of RVT among the nephrotic syndrome causes — historically estimated at 25 to 35% (though more recent studies suggest lower rates with modern anti-PLA2R antibody-guided management and prophylactic anticoagulation). Diagnosis of RVT: CT venography or MR venography shows the thrombus within the renal vein. Ultrasound Doppler may show absence of venous flow. Treatment: anticoagulation with LMWH transitioning to warfarin or a DOAC (apixaban is increasingly used in the nephrotic state). Anticoagulation is continued while the nephrotic syndrome is active — the risk of rethrombosis remains as long as the prothrombotic state persists. Thrombolysis for acute RVT in selected cases.
Small vessel — Hypertensive arteriolar nephrosclerosis
Chronic hypertension causes hyaline arteriolosclerosis — thickening and narrowing of the afferent arterioles — progressively reducing blood supply to individual glomeruli. See /conditions/hypertension-kidney-disease/ for full detail.
Small vessel — Malignant hypertension
Severe acute hypertension (blood pressure above 180/120 with end-organ damage) causes fibrinoid necrosis of arterioles and thrombotic microangiopathy in the kidney — rapidly progressive AKI, haematuria, and proteinuria. An emergency requiring immediate blood pressure control with IV antihypertensives in a monitored setting. At KIMS, malignant hypertension with AKI is managed in the nephrology HDU with CRRT support if required.
Small vessel — Thrombotic microangiopathy (TMA)
Small vessel thrombosis from HUS, TTP, preeclampsia, malignant hypertension, or drug causes. See /conditions/hemolytic-uremic-syndrome/ for full detail on the HUS and aHUS subtypes.
Small vessel — Atheroembolic renal disease (cholesterol crystal emboli)
Dislodgement of cholesterol crystals from an aortic atherosclerotic plaque — triggered by arterial catheterisation, vascular surgery, or anticoagulation — causes embolic occlusion of small renal arteries. Presents with acute or subacute kidney injury, livedo reticularis (a lacy purple skin pattern on the legs), digital ischaemia (purple toes), and eosinophilia on blood count. Kidney biopsy shows characteristic cholesterol crystal clefts in small vessels. Treatment is supportive — there is no specific therapy. Statins may help stabilise the responsible plaque.
Key investigations for renovascular disease at KIMS
Renal artery stenosis
Renal Doppler ultrasound · CT angiography · MR angiography · Captopril renogram. The full KIMS RAS pathway is covered on the dedicated /conditions/renal-artery-stenosis/ page.
Renal artery occlusion / infarction
CT with contrast (perfusion defect) · LDH elevation · Urgent anticoagulation assessment. In acute presentations within 6 to 12 hours, endovascular thrombolysis or thromboaspiration may be considered in selected younger patients.
Renal vein thrombosis
CT venography · MR venography · Renal Doppler (absent venous flow) · Coagulation screen + protein C, S, antithrombin. Particularly important in any nephrotic syndrome patient with sudden flank pain or haematuria.
Thrombotic microangiopathy
Blood film (fragmented red cells) · Platelet count · ADAMTS13 activity · Complement studies · Kidney biopsy. ADAMTS13 distinguishes TTP from HUS/aHUS — empirical plasma exchange is started while results are awaited.
Atheroembolic disease
Renal biopsy (cholesterol crystal clefts) · Eosinophilia · Urinary eosinophils · History of recent vascular procedure. A high index of suspicion in any patient with AKI after arterial catheterisation, vascular surgery, or initiation of anticoagulation.
Malignant hypertension
Blood pressure measurement · Fundoscopy (papilloedema, flame haemorrhages) · ECG · Creatinine · Urine dipstick. A nephrology emergency — managed at KIMS in the nephrology HDU with controlled IV blood pressure reduction and CRRT support if required.
Anticoagulation in nephrotic syndrome — when to use it
The decision to anticoagulate a nephrotic syndrome patient prophylactically (before a thromboembolic event) is one of the most clinically nuanced decisions in nephrology. The risk of thromboembolism is highest when serum albumin is below 20 to 25 g/L. Membranous nephropathy with heavy proteinuria and albumin below 20 g/L carries the highest absolute thrombotic risk — prophylactic anticoagulation with LMWH or a DOAC is typically recommended. The decision is balanced against the bleeding risk, particularly in patients with platelet dysfunction or renal failure affecting drug clearance. At KIMS, the nephrologist assesses the thrombotic and bleeding risk for every nephrotic syndrome patient and documents the anticoagulation decision explicitly.
Book a Renovascular Disease Assessment at KIMS
Frequently Asked Questions — Renovascular Disease
Essential hypertension — the most common form, affecting 90 to 95% of hypertensive individuals — has no single identifiable cause. It results from the complex interplay of genetic predisposition, ageing, obesity, dietary sodium, and sympathetic nervous system activity. Renovascular hypertension is secondary hypertension driven by a specific, identifiable cause — typically renal artery stenosis activating the renin-angiotensin system. It should be suspected when hypertension is resistant to three or more antihypertensives, onset is before age 30 (suggesting FMD in young women), there is an acute rise in creatinine when ACE inhibitors or ARBs are started, or there is a history of flash pulmonary edema without cardiac explanation.
Yes — renal vein thrombosis (RVT) is a recognised complication, most commonly occurring in patients with nephrotic syndrome (where loss of natural anticoagulants in the urine creates a prothrombotic state). Acute RVT causes sudden flank pain, haematuria, and acute kidney injury. Chronic RVT may be asymptomatic — discovered incidentally on CT. RVT can also cause pulmonary embolism when the thrombus propagates from the renal vein into the inferior vena cava and breaks off to the lungs. Any nephrotic syndrome patient with sudden flank pain or haematuria requires urgent CT venography to exclude RVT.
Spontaneous renal artery dissection — a tear in the arterial wall — occurs in patients with: fibromuscular dysplasia (the commonest underlying cause), connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome), following blunt trauma to the flank or abdomen, or spontaneously with no identifiable cause. It presents with sudden, severe flank pain (often confused with ureteric colic), haematuria, and hypertension. CT angiography shows the dissection flap. Management: anticoagulation for thrombotic occlusion, endovascular stenting for flow-limiting dissection, blood pressure control.
Malignant hypertension is blood pressure above 180/120 mmHg with evidence of acute end-organ damage — papilloedema (optic nerve swelling visible on fundoscopy), AKI (rising creatinine), cardiac failure, or hypertensive encephalopathy. In the kidneys, the extreme pressure causes fibrinoid necrosis of arterioles — the arterial wall is replaced by fibrin — and thrombotic microangiopathy of the glomerular capillaries. The result: rapidly progressive AKI with haematuria, proteinuria, and rising creatinine. Blood pressure must be reduced in a controlled fashion (not too rapidly — a sudden drop causes cerebral ischaemia) using IV labetalol or nitroprusside in a monitored setting. At KIMS, malignant hypertension with AKI is an emergency managed in the nephrology HDU.
Cholesterol crystal emboli (CCE) occur when atherosclerotic plaques in the aorta or large arteries rupture — releasing cholesterol crystals that embolise to small vessels in the kidneys, skin, intestines, and other organs. Triggers include arterial catheterisation (cardiac catheterisation, aortic procedures), vascular surgery, or spontaneous plaque rupture (sometimes triggered by anticoagulation, which prevents the thrombus that normally covers a ruptured plaque). In the kidneys, the cholesterol crystals lodge in small arteries and arterioles, causing ischaemia and an inflammatory response. Kidney biopsy shows the characteristic needle-shaped cholesterol crystal clefts (the lipid dissolves in processing, leaving empty cleft spaces). There is no specific treatment — management is supportive, with statin therapy to stabilise remaining plaques.
Selected nephrotic syndrome patients should be anticoagulated — specifically those at highest thrombotic risk. The indications for prophylactic anticoagulation at KIMS: serum albumin below 20 g/L, particularly in membranous nephropathy (the highest-risk nephrotic cause), prior thromboembolism, or a hypercoagulable state identified on thrombophilia screen. Low molecular weight heparin (LMWH) or apixaban are the preferred agents. The duration of anticoagulation continues while the nephrotic state is active. The decision is made individually — the nephrologist weighs the thrombotic risk (albumin level, nephrotic cause, prior thrombosis) against the bleeding risk (platelet function, renal impairment affecting drug clearance, falls risk in elderly patients).
Some renovascular conditions are reversible — FMD-related renal artery stenosis responds very well to angioplasty, with blood pressure cure or significant improvement in 50 to 80% of young women. Acute renal vein thrombosis treated promptly with anticoagulation often recanalises with full recovery of kidney function. Acute renal artery occlusion treated within 6 to 12 hours with thrombolysis or thrombectomy may recover kidney function. Atherosclerotic RAS, malignant hypertension-related arteriolar damage, and cholesterol crystal emboli cause more permanent damage — outcomes depend on the extent of pre-existing injury and how quickly the underlying condition is controlled.
KIMS Secunderabad — Dr. V. S. Reddy (Senior Consultant Nephrologist, transplant programme), renal Doppler, CT and MR angiography, CT venography, renal biopsy with NABL pathology, anticoagulation management, coordination with interventional radiology for angioplasty and stenting, 24/7 emergency nephrology for malignant hypertension. NABH and NABL accredited. Call 040-4488-5000.