Renovascular hypertension (RHT): Renovascular hypertension is a form of secondary hypertension caused by stenotic or occlusive lesions of the renal arteries. Common causes include atherosclerotic renal artery stenosis (most common), fibromuscular dysplasia, trauma with arterial dissection, aortic dissection, embolism, extrinsic fibrous bands, radiation-induced fibrosis, Takayasu’s arteritis, and polyarteritis nodosa.
Occlusive lesions reduce renal perfusion pressure, which activates the renin-angiotensin-aldosterone system. Later, endothelin activation, increased sympathetic nervous system activity, and oxidative stress contribute to persistent hypertension. Endothelial dysfunction (reduced vasodilator responses) and increased sodium retention are also seen. Critical stenosis is typically present when the renal artery lumen is narrowed by >70-75%.
Clinically, RHT can present with hypertension in all age groups, including younger individuals and children. Typical presentations include:
On examination, abdominal bruits may be heard on auscultation.
Initial imaging is renal artery duplex ultrasound. Findings include increased flow velocity (>180 cm/sec) at the stenosis, delayed upstroke in distal vessels, and a high renal resistive index (RRI). Captopril renography assesses functional status. CT angiography and MR angiography are highly sensitive and specific. Catheter angiography is the gold standard for diagnosis. Fibromuscular dysplasia shows a characteristic “string of beads” appearance due to alternating stenotic and dilated segments.
Management includes antihypertensive therapy (ACE inhibitors, ARBs, aliskiren, calcium channel blockers, diuretics, beta blockers, etc.) and treatment of associated risk factors such as dyslipidemia, glucose intolerance, and diabetes. ACE inhibitors and ARBs are contraindicated in bilateral renal artery stenosis because they may precipitate renal failure by reducing GFR. Smoking cessation and maintaining weight in the normal range are recommended.
Renal revascularization is considered when blood pressure and/or clinical status can’t be adequately managed with medical therapy alone. Options include renal artery angioplasty with or without stenting, renal artery bypass, or endarterectomy. Some cases may require nephrectomy, especially with unilateral occlusive lesions. Renal angioplasty is preferred in fibromuscular dysplasia.
Renal vein thrombosis: Renal vein thrombosis occurs in hypercoagulable states such as protein C or S deficiency, factor V Leiden mutation, antiphospholipid syndrome, nephrotic syndrome, pregnancy, severe dehydration, post-renal transplant states, extension of renal cell carcinoma into the renal veins, and trauma. Most patients have involvement of both renal veins.
It may present as an acute or chronic disorder.
Renal ultrasound may show an enlarged, hyperechoic kidney. CT and MR renal venography can be used for confirmation; conventional invasive venography is the gold standard.
Management includes treating the underlying disorder and anticoagulation (heparin, warfarin). In selected cases, percutaneous thrombectomy with local thrombolytic therapy or surgical thrombectomy may be performed.
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