100+ Free Cert Nephrology(SA) Phys Practice Questions

Explanation: KDIGO Stage 1 AKI is defined as an absolute increase in serum creatinine by ≥26.5 µmol/L within 48 hours, or a relative increase in serum creatinine to 1.5 to 1.9 times baseline within 7 days, or urine output <0.5 mL/kg/h for 6–12 hours.

Explanation: In patients actively receiving loop diuretics, sodium reabsorption in the thick ascending limb is inhibited, rendering FENa and urine sodium falsely elevated (>1% and >20 mmol/L) even in true prerenal states. Fractional excretion of urea (FEUrea) is independent of loop diuretic action because urea reabsorption occurs primarily in the proximal tubule and inner medullary collecting duct. An FEUrea <35% strongly indicates prerenal azotemia.

Explanation: Aminoglycosides are freely filtered at the glomerulus and endocytosed by megalin-cubilin receptor complexes on the brush border of proximal convoluted tubule (S1/S2) epithelial cells. They accumulate within lysosomes, causing lysosomal rupture, mitochondrial toxicity, phospholipidosis, and cell necrosis leading to non-oliguric ATN.

Explanation: Intravenous volume expansion with isotonic crystalloids (0.9% sodium chloride or sodium bicarbonate) at 1–1.5 mL/kg/h for 12 hours before and after the procedure is the single proven evidence-based measure to prevent CA-AKI in high-risk patients. Large randomized trials (PRESERVE trial) demonstrated no benefit for N-acetylcysteine, dopamine, or fenoldopam.

Explanation: Renal biopsy is the definitive diagnostic gold standard for drug-induced acute interstitial nephritis (AIN). Biopsy demonstrates patchy interstitial edema, inflammatory infiltrate (T-lymphocytes, macrophages, eosinophils, and plasma cells), and tubulitis. Urinary eosinophil testing lacks both sensitivity and specificity for drug-induced AIN.

Explanation: Rhabdomyolysis causes AKI (pigment nephropathy) via three synergistic mechanisms: 1) filtered free myoglobin precipitates with Tamm-Horsfall protein in acidic tubular fluid causing distal cast obstruction; 2) ferrihemate generation exerts direct toxic oxidative cytotoxicity on proximal tubular cells; and 3) severe fluid sequestration into damaged muscle triggers volume depletion and renal vasoconstriction.

Explanation: The revised ICA criteria for HRS-AKI require: diagnosis of cirrhosis with ascites; diagnosis of AKI according to KDIGO criteria; no response after at least 48 hours of diuretic withdrawal and volume expansion with albumin (1 g/kg/day up to a max of 100 g/day); absence of shock; no current or recent exposure to nephrotoxic drugs; and absence of organic kidney disease (proteinuria <500 mg/day, microhematuria <50 RBC/hpf, normal renal ultrasound).

Explanation: Abdominal Perfusion Pressure (APP) / Renal Perfusion Pressure (RPP) in the presence of intra-abdominal hypertension is calculated as: RPP = Mean Arterial Pressure (MAP) - Intra-Abdominal Pressure (IAP). Here, RPP = 70 mmHg - 24 mmHg = 46 mmHg. An RPP < 60 mmHg severely compromises renal blood flow and glomerular filtration.

Explanation: This patient presents with classic Minimal Change Disease (MCD). Light microscopy appears normal (hence 'minimal change') and immunofluorescence is negative. Electron microscopy (EM) characteristically reveals diffuse effacement (flattening/fusion) of visceral epithelial cell (podocyte) foot processes.

Explanation: Transmembrane glycoprotein M-type phospholipase A2 receptor (PLA2R), expressed on human podocytes, is the major target autoantigen in 70–80% of primary membranous nephropathy cases. Circulating anti-PLA2R antibodies correlate with disease activity, histologic severity, and therapeutic response.