08.2 Renal vascular disease

Renal Vascular Disease Overview

• Renal vascular disease involves conditions reducing or blocking renal artery or vein blood flow
• Conditions include renovascular hypertension (RVH), ischemic renal disease, renal infarction, atheroembolic renal disease, and renal vein thrombosis
• This study focuses on classifying these disorders, explaining the pathophysiology of RVH, describing clinical features, and outlining diagnostic and treatment strategies for renal artery disease

Learning Objectives

• Classify renovascular disorders
• Explain the pathophysiology of renovascular hypertension
• Outline the clinical features of renovascular hypertension
• Illustrate diagnostic and management strategies for renal artery disease

Key Concepts and Definitions

• Renovacular Hypertension (RVH): Elevated blood pressure from reduced kidney perfusion, activating the renin-angiotensin-aldosterone system (RAAS)
• Most frequent form of secondary hypertension
• Renal Artery Stenosis (RAS): Common cause of RVH, most often caused by atherosclerosis (90%) or fibromuscular dysplasia.
• Atherosclerosis: Primarily affects individuals over 50 and with systemic components such as diabetes and smoking history
• Fibromuscular dysplasia: Affects women aged 15-50, characterized by smooth muscle cell proliferation and fibrosis
• Ischemic Renal Disease (IRD): Severe vascular occlusion causing tissue damage, progressing to irreversible kidney damage.
• Renal Infarction: Sudden loss of blood flow to the kidney, characterized by ischemia, flank pain, microhematuria, and proteinuria
• Renal Vein Thrombosis (RVT): Blocked renal vein drainage. Common in neonates, patients with nephrotic syndrome or hypercoagulable states

Clinical Applications

• A 65-year-old male with uncontrolled hypertension and prior atherosclerosis possibly has renovascular hypertension, diagnosed by Doppler ultrasound and angiography
• Management often involves antihypertensives and potential angioplasty considerations

Diagnostic Approach

• Physical exam may reveal abdominal bruits, atherosclerosis, or signs of renal dysfunction
• Imaging includes Doppler ultrasound, CTA/MRA, and angiography for further characterization

Pathophysiology

• Unilateral Renal Artery Stenosis: Angiotensin II-mediated hypertension in the affected kidney, with compensatory natriuresis in the unaffected kidney, resulting in sustained hypoperfusion
• Bilateral Renal Artery Stenosis: Both kidneys have reduced perfusion, leading to sodium retention and volume expansion, the primary driver of hypertension is volume, with normal or low angiotensin II
• Ischemic Progression: Critical stenosis (>60%) reduces perfusion, exceeding the kidney's autoregulatory capacity, leading to macrophage activation, fibrosis, and tubular cell loss

Pharmacology

• ACE inhibitors and ARBs are first-line treatments for unilateral RAS. Contraindicated in bilateral RAS
• Diuretics manage volume overload
• Calcium channel blockers provide additional blood pressure control

Differential Diagnosis

• Primary hypertension
• Pheochromocytoma (episodic hypertension with catecholamine surges)
• Systemic vasculitis (associated with systemic inflammatory markers and other organ involvement)

Investigations

• Doppler ultrasound is a non-invasive initial test
• CTA/MRA has high sensitivity and specificity for identifying RAS, with CTA potentially imaging stents better than MRA, which avoids nephrotoxicity
• Angiography is the gold standard for confirming RAS, allowing pressure gradient measurement and facilitating therapeutic angioplasty

Summary and Key Takeaways

• Renovascular hypertension (RVH) is the most frequent secondary hypertension often caused by renal artery stenosis (RAS), either from atherosclerosis or fibromuscular dysplasia
• Unilateral RAS causes angiotensin II-mediated hypertension, bilateral RAS leads to volume expansion-driven hypertension.
• Diagnosis usually relies on imaging, and management includes targeted therapy, lifestyle modifications, and possible revascularization.