Tubulointerstitial and Renovascular Diseases — WACS Viva & Clinical Scenarios (Nephrology)

Exam-style tubulointerstitial and renovascular diseases viva scenarios with examiner probes and model answers for Internal Medicine candidates.

Scenarios covered

• SCENARIO 1: A 54-year-old male presents with a progressive rise in serum creatinine from a baseline of 90 micromol/L to 380 micromol/L over three weeks. He was treated with omeprazole and amoxicillin-clavulanic acid for dyspepsia and sinusitis two weeks prior. Urinalysis reveals low-grade proteinuria (0.6 g/24 hours), sterile pyuria, and white blood cell casts without dysmorphic red blood cells. A renal biopsy demonstrates extensive interstitial oedema with a dense inflammatory infiltrate composed of T-lymphocytes, macrophages, and prominent eosinophils invading the tubular basement membrane (tubulitis),
• SCENARIO 2: A 28-year-old woman is evaluated for treatment-resistant hypertension (blood pressure 178/104 mmHg despite triple therapy with amlodipine, hydrochlorothiazide, and bisoprolol). Physical examination reveals a right epigastric systolic-diastolic bruit. Biochemical assessment shows hypokalaemia (serum potassium 3.1 mmol/L) and elevated plasma renin activity and aldosterone levels. Renal duplex ultrasound reveals elevated peak systolic velocities (>200 cm/s) in the middle and distal portions of the right main renal artery with post-stenotic turbulence. Contrast angiography demonstrates alternating
• SCENARIO 3: A 42-year-old female presents with recurrent nephrolithiasis, severe muscle weakness, and polyuria. Arterial blood gas shows a normal anion gap (hyperchloraemic) metabolic acidosis (pH 7.28, HCO₃⁻ 14 mmol/L, serum chloride 112 mmol/L, serum potassium 2.9 mmol/L). Urinalysis shows a urine pH of 6.2 despite systemic acidosis. Urinary electrolytes are: sodium 48 mmol/L, potassium 32 mmol/L, chloride 42 mmol/L. Outline the systematic calculation of the urine anion gap, the exact subtype of renal tubular acidosis (RTA) present, the underlying molecular defect, and the appropriate initial medical re
• SCENARIO 4: A 68-year-old male with generalized atherosclerosis undergoes percutaneous coronary intervention for acute coronary syndrome. Three weeks later, he develops worsening renal function, livedo reticularis on both lower extremities, digital cyanosis ("blue toe syndrome") with intact peripheral pulses, and transient confusion. Laboratory investigations reveal serum creatinine of 340 micromol/L, peripheral eosinophilia (12%), and hypocomplementaemia (depressed C3 and C4). Describe the precise pathophysiology, renal histopathological findings, key differential diagnoses, and management principles for
• SCENARIO 5: A 36-year-old man presents for a pre-employment medical evaluation. He reports a family history of early stroke and dialysis dependency in his father. His blood pressure is 156/96 mmHg. Abdominal examination reveals bilateral, non-tender, palpable, bosselated flank masses. Renal ultrasonography confirms enlarged kidneys bilaterally with multiple fluid-filled cysts of varying sizes throughout the cortex and medulla. What are the genetic mechanisms, major extrarenal complications requiring active surveillance, and pharmacological strategies for retarding cyst growth in Autosomal Dominant Polycys