Renovascular hypertension (RHT): It is secondary hypertension as a result of stenotic or occlusive lesions of the renal arteries. Common causes include atherosclerotic renal artery stenosis (most common cause), fibromuscular dysplasia, trauma with arterial dissection, aortic dissection, embolism, extrinsic fibrous bands, radiation induced fibrosis, Takayasu’s arteritis and polyarteritis nodosa. Occlusive lesions decrease the renal perfusion pressure leading to activation of the renin-angiotensin-aldosterone system. This is followed later on by activation of endothelin, sympathetic nervous system and oxidative stress that perpetuates the hypertension. Endothelial dysfunction with decrease in vasodilator responses and increased sodium retention are seen. Narrowing of the renal artery lumen of >70-75% is seen in critical stenosis. Clinically it presents with hypertension in all age groups including in younger individuals and children, in young women (fibromuscular dysplasia), new-onset HT after the age of 55 years, accelerated hypertension with cardiac failure and acute pulmonary edema and treatment resistant hypertension. Abdominal bruits may be heard on auscultation.
Initial imaging study is renal artery duplex ultrasound which shows increased velocity of flow (>180 cm/sec) at the site of stenosis, delayed upstroke in the distal vessels and a high renal resistive index or RRI. Captopril renography gives an assessment of functional status. CT angiography or MR angiography are highly sensitive and specific. Catheter angiography is the gold standard for diagnosis. Fibromuscular dysplasia gives a characteristic “string of beads” appearance due to alternate stenotic and dilated areas.
Management is with antihypertensive agents like ACE inhibitors, ARBs, Aliskerin, calcium channel blockers, diuretics, beta blockers, etc and managing dyslipidemia, glucose intolerance and diabetes. ACE inhibitors and ARBs are contraindicated in bilateral renal artery stenosis as they may precipitate renal failure by reducing GFR. Smoking should be stopped and weight should be maintained in normal range. Renal revascularization is needed if patients cannot be managed well on medical therapy alone. Techniques include renal artery angioplasty with/without stenting, renal artery bypass or endarterectomy. Some cases may need nephrectomy especially those with unilateral occlusive lesions. Renal angioplasty is preferred in fibromuscular dysplasia.
Renal vein thrombosis: It is seen in hypercoagulable conditions like protein C or S deficiency, factor V leiden mutation, antiphospholipid syndrome, nephrotic syndrome, pregnancy, severe dehydration, post renal transplant, extension of renal cell carcinoma into the renal veins, trauma etc. Most patients have involvement of both renal veins. It presents as an acute or chronic disorder. Acute type presents with flank pain, AKI, gross hematuria, proteinuria, vomiting, fever etc. Left renal vein thrombosis can present as a varicocele. Chronic type may be asymptomatic. Renal ultrasound will show an enlarged and hyper-echoic kidney. CT and MR renal venography or conventional invasive venography (gold standard) can be done for confirmation. Management is by treating the underlying disorder, anticoagulants, heparin, warfarin and rarely, percutaneous thrombectomy with local thrombolytic therapy or surgical thrombectomy can be done.
Sign up for free to take 1 quiz question on this topic