Renal Vascular Disease PDF

Renal vascular disease Lecture Number 8.2 Status Done Type Lecture 8.2 Renal Vascular Disease Overview Renal vascular disease includes a range of disorders characterized by the reduction or loss of renal arterial or venous blood flow. These conditions lead to...

Renal vascular disease Lecture Number 8.2 Status Done Type Lecture 8.2 Renal Vascular Disease Overview Renal vascular disease includes a range of disorders characterized by the reduction or loss of renal arterial or venous blood flow. These conditions lead to clinical syndromes such as renovascular hypertension (RVH), ischemic renal disease, unstable cardiac syndromes, renal infarction, atheroembolic renal disease, and renal vein thrombosis. This lecture focuses on classifying these disorders, elucidating the pathophysiology of RVH, describing clinical features, and outlining diagnostic and management strategies for renal artery disease. Learning Objectives Objective 1: Classify renovascular disorders. Objective 2: Describe the pathophysiology of renovascular hypertension. Objective 3: Outline the clinical features of renovascular hypertension. Objective 4: Illustrate diagnostic and management strategies for renal artery disease. Key Concepts and Definitions Renovascular Hypertension (RVH): A syndrome of elevated blood pressure caused by reduced renal perfusion, which activates the renin-angiotensin- aldosterone system (RAAS). Most frequent form of secondary hypertension. Renal Artery Stenosis (RAS): The most common cause of RVH. Major etiologies: Atherosclerosis (90%): Predominantly affects individuals over 50 years with systemic atherosclerosis, diabetes, and a smoking history. Fibromuscular Dysplasia: Affects younger women (15–50 years), characterized by smooth muscle cell proliferation and fibrosis. Ischemic Renal Disease (IRD): Caused by severe vascular occlusion exceeding adaptive limits, leading to tissue injury, progressive fibrosis, and irreversible kidney damage. Renal Infarction : Abrupt loss of blood flow to the kidney, leading to ischemia. Symptoms include flank pain, microhematuria, and proteinuria. Renal Vein Thrombosis (RVT): Obstruction of renal venous drainage, commonly seen in neonates, patients with nephrotic syndrome, or hypercoagulable states. Clinical Applications Case Study: A 65-year-old male with uncontrolled hypertension and prior atherosclerosis presents with refractory hypertension and suspected RVH. Initial Doppler ultrasound reveals significant stenosis, confirmed by angiography. Management includes antihypertensives and consideration of angioplasty.  Diagnostic Approach: Physical Exam : Abdominal bruits, evidence of atherosclerosis, or renal dysfunction. Imaging: Doppler ultrasound (initial), CTA/MRA (further characterization), angiography (gold standard). Treatment Options: RVH: Pharmacological: ACE inhibitors, ARBs, diuretics (contraindicated in bilateral RAS or single functioning kidney). Revascularization: Indicated in fibromuscular dysplasia or severe atherosclerosis with flash pulmonary edema or acute kidney injury. Renal Infarction : Pain control, anticoagulation for thrombosis or embolism. RVT: Anticoagulation or surgical intervention as needed. Complications: RVH can progress to ischemic nephropathy, flash pulmonary edema, or CKD. Pathophysiology 1. Unilateral Renal Artery Stenosis: RAAS activation in the affected kidney drives angiotensin II-mediated hypertension. The contralateral kidney compensates via natriuresis, leading to volume balance and sustained hypoperfusion of the stenotic kidney. 2. Bilateral Renal Artery Stenosis: Both kidneys experience reduced perfusion, leading to sodium retention and volume expansion. Resulting hypertension is primarily volume-mediated, with normal to low levels of angiotensin II. 3. Ischemic Progression : Critical stenosis (>60%) reduces perfusion, exceeding the kidney’s autoregulatory capacity. Leads to macrophage activation, fibrosis, and tubular cell loss. Pharmacology ACE Inhibitors and ARBs: First-line agents in unilateral RAS; contraindicated in bilateral RAS or single functioning kidney due to risk of renal dysfunction. Diuretics: Manage volume overload and hypertension. Calcium Channel Blockers: Provide additional blood pressure control. Anticoagulants: Essential in managing RVT and thromboembolic events. Differential Diagnosis Primary Hypertension : Gradual onset, responsive to standard therapy. Pheochromocytoma: Episodic hypertension with catecholamine surges. Systemic Vasculitis: Associated with systemic inflammatory markers and other organ involvement. Investigations Doppler Ultrasound: Non-invasive, initial test; operator-dependent. CTA/MRA: High sensitivity and specificity for RAS; CTA visualizes stents better, while MRA avoids nephrotoxicity. Angiography: Gold standard, allows pressure gradient measurement and therapeutic angioplasty. Key Diagrams and Visuals Summary and Key Takeaways RVH is the most common secondary hypertension and often arises from RAS due to atherosclerosis or fibromuscular dysplasia. Unilateral RAS induces angiotensin II-mediated hypertension; bilateral RAS results in volume expansion-driven hypertension. Diagnosis relies on imaging, with angiography as the definitive test. Management includes targeted antihypertensive therapy, lifestyle modifications, and selective revascularization. Further Reading/References Brenner’s and Rector's "The Kidney" (comprehensive coverage of renal vascular diseases). Vesna D. Garovic, "Circulation" (detailed pathophysiology and management strategies for RVH and ischemic nephropathy). Comprehensive Medical Nephrology (diagnostic and therapeutic approaches). Questions/Clarifications Question 1: What factors determine the reversibility of ischemic damage in renal artery disease? Question 2: How do imaging modalities compare in detecting fibromuscular dysplasia versus atherosclerotic RAS? Question 3: What criteria should prompt consideration of revascularization in atherosclerotic RAS?