{"id":36442,"date":"2026-04-03T14:43:37","date_gmt":"2026-04-03T09:13:37","guid":{"rendered":"https:\/\/atsixty.com\/?p=36442"},"modified":"2026-04-03T15:10:54","modified_gmt":"2026-04-03T09:40:54","slug":"renal-pathology-mcq-set-2","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/04\/03\/renal-pathology-mcq-set-2\/","title":{"rendered":"Renal Pathology MCQ Set-2"},"content":{"rendered":"\n<div id=\"atsixty-rp-quiz\">\n<style>\n#atsixty-rp-quiz {\n  --terra: #C0603A;\n  --terra-light: #d4795a;\n  --terra-pale: #fdf3ef;\n  --teal: #2A7A6F;\n  --teal-light: #3a9688;\n  --teal-pale: #eef6f5;\n  --ink: #1e1e1e;\n  --muted: #6b6b6b;\n  --rule: #e2d8d4;\n  --correct-bg: #e8f5e9;\n  --correct-border: #43a047;\n  --wrong-bg: #fdecea;\n  --wrong-border: #e53935;\n  --white: #fff;\n  --shadow: 0 2px 16px rgba(192,96,58,0.08);\n  font-family: Georgia, 'Times New Roman', serif;\n  color: var(--ink);\n  margin: 1rem 0 2rem;\n}\n#atsixty-rp-quiz * { box-sizing: border-box; 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Renal biopsy light microscopy shows segmental sclerosis and hyalinosis predominantly at the glomerular tip lesion. Electron microscopy shows foot process effacement with tubuloreticular inclusions in endothelial cells. The most likely diagnosis is:\",\n      correctAnswer: \"HIV-associated nephropathy (HIVAN) \u2014 collapsing variant of FSGS\",\n      opts: [\n        \"HIV-associated nephropathy (HIVAN) \u2014 collapsing variant of FSGS\",\n        \"Minimal change disease \u2014 secondary to antiretroviral drug toxicity\",\n        \"Membranous nephropathy \u2014 anti-PLA2R-positive, immune-complex type\",\n        \"Amyloid A nephropathy \u2014 secondary to chronic HIV-related infection\"\n      ],\n      exp: \"<strong>HIVAN<\/strong>: most common cause of ESRD in HIV patients of African descent. Collapsing FSGS \u2014 glomerular capillary tuft collapses + overlying podocyte proliferation. Tubuloreticular inclusions in endothelial cells (interferon-induced). Rapid progression to ESRD without ART. <strong>Treatment: ART<\/strong> is the cornerstone \u2014 halts progression. ACEI\/ARB for proteinuria. Non-collapsing FSGS also occurs. <em>Tip lesion<\/em> FSGS has better prognosis than collapsing. <em>MCD<\/em>: no sclerosis, no TRI. <em>Membranous<\/em>: subepithelial spikes.\",\n      difficulty: \"hard\",\n      concept: \"HIVAN \/ FSGS\"\n    },\n    {\n      q: \"A 19-year-old man with a known family history of haematuria and progressive renal failure has bilateral sensorineural deafness and ocular abnormalities (anterior lenticonus). Renal biopsy electron microscopy shows irregular thickening and thinning of the GBM with a distinctive 'basket-weave' or 'lamellation' pattern. The most likely mutation and inheritance pattern are:\",\n      correctAnswer: \"COL4A5 mutation \u2014 X-linked dominant (most common form)\",\n      opts: [\n        \"NPHS1 mutation (nephrin) \u2014 autosomal recessive, Finnish-type congenital nephrotic syndrome\",\n        \"COL4A5 mutation \u2014 X-linked dominant (most common form)\",\n        \"TRPC6 mutation \u2014 autosomal dominant FSGS with late onset\",\n        \"PKD1 mutation \u2014 autosomal dominant, bilateral cystic kidney disease\"\n      ],\n      exp: \"<strong>Alport syndrome<\/strong>: hereditary nephritis due to mutations in type IV collagen genes. Most common: <strong>COL4A5<\/strong> (X-linked, 85%) \u2014 affects \u03b15 chain of type IV collagen. Also: COL4A3\/COL4A4 (autosomal recessive). EM hallmark: <strong>basket-weave lamellation<\/strong> of GBM \u2014 alternating thick and thin segments with splitting of the lamina densa. Clinical triad: haematuria \u2192 ESRD + sensorineural deafness + <em>anterior lenticonus<\/em>. Males (hemizygous) reach ESRD by 20\u201330s. Females (carriers): haematuria, slower progression.\",\n      difficulty: \"medium\",\n      concept: \"Alport Syndrome\"\n    },\n    {\n      q: \"A 52-year-old woman presents with nephrotic syndrome: proteinuria 6.2 g\/day, serum albumin 2.0 g\/dL, non-pitting pedal oedema. Hepatitis B surface antigen is positive. Renal biopsy light microscopy shows diffuse thickening of the GBM with a 'spike and dome' pattern on silver stain. Immunofluorescence shows granular IgG and C3 along the GBM. Electron microscopy confirms subepithelial electron-dense deposits. The most common autoantibody in the idiopathic form of this disease is directed against:\",\n      correctAnswer: \"Phospholipase A2 receptor (PLA2R) on podocytes\",\n      opts: [\n        \"Double-stranded DNA (dsDNA) \u2014 systemic lupus erythematosus\",\n        \"\u03b13 chain of type IV collagen \u2014 Goodpasture anti-GBM disease\",\n        \"Phospholipase A2 receptor (PLA2R) on podocytes\",\n        \"Thrombospondin type-1 domain-containing 7A (THSD7A) \u2014 secondary membranous\"\n      ],\n      exp: \"<strong>Membranous nephropathy (MN)<\/strong>: most common cause of nephrotic syndrome in adults >40 years. Subepithelial immune deposits \u2192 GBM spikes (silver stain). Idiopathic (primary) MN: <strong>anti-PLA2R antibodies<\/strong> (70\u201380%) \u2014 target the M-type phospholipase A2 receptor on podocytes. Positive PLA2R serology avoids need for biopsy in typical cases. Secondary causes: HBV, malignancy, SLE, drugs (gold, penicillamine). Complications: renal vein thrombosis (nephrotic state). <em>THSD7A<\/em>: 5% of primary MN. Treatment: RAAS blockade; rituximab for refractory cases.\",\n      difficulty: \"medium\",\n      concept: \"Membranous Nephropathy\"\n    },\n    {\n      q: \"A 30-year-old woman with systemic lupus erythematosus has proteinuria 4.8 g\/day, haematuria, RBC casts, and serum creatinine 2.1 mg\/dL. C3 and C4 are both low; anti-dsDNA titre is markedly elevated. Renal biopsy shows diffuse endocapillary proliferation involving >50% of glomeruli, subendothelial and mesangial deposits, and 'wire-loop' lesions on light microscopy. According to the ISN\/RPS classification, this is:\",\n      correctAnswer: \"Class IV (diffuse proliferative lupus nephritis) \u2014 worst prognosis without treatment\",\n      opts: [\n        \"Class II (mesangial proliferative lupus nephritis) \u2014 mild, often asymptomatic\",\n        \"Class III (focal proliferative lupus nephritis) \u2014 <50% glomeruli involved\",\n        \"Class V (membranous lupus nephritis) \u2014 subepithelial deposits, nephrotic syndrome\",\n        \"Class IV (diffuse proliferative lupus nephritis) \u2014 worst prognosis without treatment\"\n      ],\n      exp: \"<strong>Lupus nephritis (LN)<\/strong> ISN\/RPS classes: I (minimal mesangial), II (mesangial proliferative), III (focal \u2014 <50% glomeruli), <strong>IV (diffuse \u2014 >50% glomeruli, worst prognosis)<\/strong>, V (membranous), VI (advanced sclerosing). Class IV features: endocapillary proliferation, <strong>wire-loop lesions<\/strong> (massive subendothelial deposits), 'full house' IF (IgG, IgA, IgM, C3, C1q). Low C3+C4 = classical pathway activation. Treatment: induction with mycophenolate mofetil + steroids; maintenance with MMF or azathioprine. Hydroxychloroquine reduces flares.\",\n      difficulty: \"medium\",\n      concept: \"Lupus Nephritis\"\n    },\n    {\n      q: \"A 14-year-old boy develops haematuria, proteinuria, and hypertension 10 days after a skin infection. Renal biopsy shows mesangial and endocapillary proliferation with a 'lobular' glomerular pattern. Immunofluorescence reveals C3 dominant deposits with scanty immunoglobulin. Electron microscopy shows mesangial, subendothelial, and subepithelial (intramembranous) deposits. Serum C3 is persistently low; C3 nephritic factor is detected. The most likely diagnosis is:\",\n      correctAnswer: \"Membranoproliferative glomerulonephritis type II (Dense Deposit Disease \u2014 C3 glomerulopathy)\",\n      opts: [\n        \"Post-streptococcal glomerulonephritis \u2014 transient hypocomplementaemia, subepithelial humps only\",\n        \"IgA nephropathy \u2014 dominant mesangial IgA, normal complement, synpharyngitic\",\n        \"Membranoproliferative glomerulonephritis type II (Dense Deposit Disease \u2014 C3 glomerulopathy)\",\n        \"Lupus nephritis Class IV \u2014 full-house immunofluorescence, positive ANA\/anti-dsDNA\"\n      ],\n      exp: \"<strong>Dense Deposit Disease (DDD) \/ MPGN type II<\/strong>: now classified under C3 glomerulopathies. Pathogenesis: <strong>C3 nephritic factor<\/strong> (IgG autoantibody stabilising C3 convertase) \u2192 uncontrolled alternative complement pathway activation \u2192 persistently low C3, near-normal C4. EM: dense, ribbon-like osmiophilic deposits within the GBM lamina densa (pathognomonic). LM: lobular mesangial pattern, double-contour 'tram-track' GBM (also seen in MPGN type I). IF: C3 dominant, scant or absent Ig. May be associated with partial lipodystrophy. Treatment: eculizumab in refractory cases.\",\n      difficulty: \"hard\",\n      concept: \"C3 Glomerulopathy \/ DDD\"\n    },\n    {\n      q: \"A 45-year-old man with multiple myeloma develops progressive renal failure. Urinalysis shows proteinuria that tests negative on dipstick but positive on sulphosalicylic acid test (SSA). Urine immunofixation reveals free monoclonal lambda light chains. Renal biopsy shows 'fractured' casts with surrounding giant cell reaction in distal tubules and collecting ducts. Tubular atrophy is prominent. The most likely diagnosis is:\",\n      correctAnswer: \"Myeloma cast nephropathy (myeloma kidney)\",\n      opts: [\n        \"Myeloma cast nephropathy (myeloma kidney)\",\n        \"AL amyloidosis \u2014 apple-green birefringence on Congo red, glomerular involvement\",\n        \"Light chain deposition disease \u2014 non-fibrillary deposits, nodular glomerulosclerosis\",\n        \"Hypercalcaemic nephropathy \u2014 nephrocalcinosis, interstitial deposits of calcium\"\n      ],\n      exp: \"<strong>Myeloma cast nephropathy<\/strong>: most common cause of renal failure in myeloma. Free light chains (especially lambda) precipitate with Tamm-Horsfall protein in distal tubules \u2192 obstructive casts with <strong>giant cell (macrophage) reaction<\/strong>. Dipstick: negative (detects albumin); SSA\/heat test: positive (detects all proteins including Bence Jones). Treatment: chemotherapy (bortezomib-based) + hydration; high-dose dexamethasone; consider plasma exchange. Contrast with: <em>AL amyloidosis<\/em> (Congo red +, glomerular, waxy deposits) and <em>LCDD<\/em> (nodular sclerosis, PAS+ deposits, non-fibrillary on EM).\",\n      difficulty: \"medium\",\n      concept: \"Myeloma Kidney\"\n    },\n    {\n      q: \"A 68-year-old woman with longstanding rheumatoid arthritis develops nephrotic syndrome with proteinuria 5.5 g\/day. Renal biopsy Congo red stain shows apple-green birefringence under polarised light. Electron microscopy shows randomly arranged non-branching fibrils of 8\u201312 nm diameter in the mesangium and subendothelium. Serum amyloid A (SAA) protein is elevated. The most likely type of renal amyloidosis and its protein precursor are:\",\n      correctAnswer: \"AA amyloidosis \u2014 serum amyloid A protein (acute-phase reactant)\",\n      opts: [\n        \"AL amyloidosis \u2014 monoclonal immunoglobulin light chains (plasma cell dyscrasia)\",\n        \"AA amyloidosis \u2014 serum amyloid A protein (acute-phase reactant)\",\n        \"A\u03b22M amyloidosis \u2014 \u03b22-microglobulin in long-term dialysis patients\",\n        \"ATTR amyloidosis \u2014 transthyretin, associated with cardiac involvement predominantly\"\n      ],\n      exp: \"<strong>AA amyloidosis<\/strong>: secondary amyloidosis; complicates chronic inflammatory conditions \u2014 <strong>rheumatoid arthritis<\/strong>, ankylosing spondylitis, bronchiectasis, familial Mediterranean fever, chronic osteomyelitis. Precursor: SAA (acute-phase protein from liver) \u2192 AA fibrils. Renal involvement common \u2192 nephrotic syndrome \u2192 ESRD. Congo red stain: apple-green birefringence (polarised). EM: randomly arranged, non-branching fibrils 8\u201312 nm. <em>AL amyloidosis<\/em>: light chains (plasma cell dyscrasia, myeloma). Distinction: immunohistochemistry with anti-AA vs anti-kappa\/lambda antibodies. Treatment: control underlying disease.\",\n      difficulty: \"medium\",\n      concept: \"Renal Amyloidosis\"\n    },\n    {\n      q: \"A 35-year-old woman develops fever, maculopapular rash, arthralgia, and oliguria 10 days after starting ampicillin for a UTI. Urinalysis shows sterile pyuria, haematuria, mild proteinuria, and eosinophiluria (Hansel stain positive). Serum creatinine has risen sharply. The most likely diagnosis, biopsy finding, and mechanism are:\",\n      correctAnswer: \"Acute interstitial nephritis (AIN) \u2014 interstitial oedema + lymphocytic infiltrate + eosinophils; type IV hypersensitivity\",\n      opts: [\n        \"Acute tubular necrosis \u2014 muddy brown casts, tubular epithelial cell necrosis; ischaemic injury\",\n        \"Granulomatous interstitial nephritis \u2014 non-caseating granulomas; sarcoidosis or TB\",\n        \"Acute pyelonephritis \u2014 neutrophilic infiltrate, WBC casts, bacterial infection\",\n        \"Acute interstitial nephritis (AIN) \u2014 interstitial oedema + lymphocytic infiltrate + eosinophils; type IV hypersensitivity\"\n      ],\n      exp: \"<strong>Acute interstitial nephritis (AIN)<\/strong>: most common cause \u2014 <strong>drugs<\/strong> (beta-lactam antibiotics, NSAIDs, PPIs, sulfonamides, rifampicin). Triad: fever + rash + eosinophilia (only 10\u201315% have all three \u2014 do not wait for full triad). Urinalysis: sterile pyuria, haematuria, eosinophiluria (Hansel stain). Biopsy: <strong>interstitial oedema, lymphocytic and eosinophilic infiltrate<\/strong>, no glomerular involvement. Mechanism: hapten-induced <strong>type IV (T-cell mediated)<\/strong> hypersensitivity. Treatment: stop offending drug; steroids if no recovery in 5\u20137 days. NSAID-induced AIN may coexist with MCD.\",\n      difficulty: \"medium\",\n      concept: \"Acute Interstitial Nephritis\"\n    },\n    {\n      q: \"A 72-year-old hypertensive man with a 20-year history of taking a combination analgesic (phenacetin + aspirin + caffeine) develops slowly progressive renal failure, sterile pyuria, and microscopic haematuria. Urine cytology shows atypical transitional cells. CT urogram reveals a filling defect in the right renal pelvis with calcified ring-like shadows in the papillae. The most likely complication uniquely associated with prolonged analgesic nephropathy is:\",\n      correctAnswer: \"Transitional cell carcinoma (urothelial carcinoma) of the renal pelvis and ureter\",\n      opts: [\n        \"Transitional cell carcinoma (urothelial carcinoma) of the renal pelvis and ureter\",\n        \"Clear cell renal cell carcinoma arising from proximal tubular epithelium\",\n        \"Squamous cell carcinoma of the bladder secondary to schistosomiasis\",\n        \"Wilms tumour (nephroblastoma) \u2014 late-onset, radiation-induced, post-analgesic\"\n      ],\n      exp: \"<strong>Analgesic nephropathy<\/strong>: chronic interstitial nephritis from prolonged mixed analgesic use (phenacetin is the key culprit \u2014 now withdrawn). Lesions: papillary necrosis \u2192 calcified ghost papillae ('ring sign') \u2192 cortical scarring. Sterile pyuria is characteristic. Critical complication: <strong>urothelial (transitional cell) carcinoma of the renal pelvis<\/strong> \u2014 8\u201310\u00d7 increased risk, bilateral, multifocal. Phenacetin metabolite (paracetamol) is the carcinogen. Contrast: schistosomiasis \u2192 <em>squamous<\/em> cell carcinoma of bladder (calcified bladder wall, Egypt). Regular urine cytology surveillance is mandatory.\",\n      difficulty: \"hard\",\n      concept: \"Analgesic Nephropathy\"\n    },\n    {\n      q: \"A 55-year-old man with longstanding hypertension and bilateral renal bruits undergoes investigations. Renal angiography shows a beaded appearance of the right renal artery mid-segment. Plasma renin activity is markedly elevated. Which mechanism best explains the contralateral (left) kidney's behaviour in this condition?\",\n      correctAnswer: \"Contralateral kidney suppresses renin and retains sodium due to higher perfusion pressure\",\n      opts: [\n        \"Contralateral kidney also develops ischaemia and secretes renin equally\",\n        \"Contralateral kidney undergoes compensatory hypertrophy but renin secretion is unchanged\",\n        \"Contralateral kidney suppresses renin and retains sodium due to higher perfusion pressure\",\n        \"Contralateral kidney develops juxtaglomerular hyperplasia identical to the ischaemic side\"\n      ],\n      exp: \"<strong>Renovascular hypertension \u2014 fibromuscular dysplasia (FMD)<\/strong>: beaded appearance of renal artery (mid and distal segments), predominantly in young women. Goldblatt model: ischaemic kidney \u2192 high renin \u2192 angiotensin II \u2192 systemic hypertension. Contralateral kidney: exposed to <em>high pressure<\/em> \u2192 pressure natriuresis \u2192 <strong>suppressed renin secretion + sodium loss<\/strong>. This asymmetry is the basis of the Captopril renogram and selective renal vein renin sampling (ischaemic side:contralateral ratio >1.5 is diagnostic). Treatment: percutaneous transluminal angioplasty (PTA) \u2014 curative for FMD.\",\n      difficulty: \"hard\",\n      concept: \"Renovascular Hypertension\"\n    },\n    {\n      q: \"A newborn boy is delivered at 34 weeks gestation with oligohydramnios, bilateral palpable flank masses, and respiratory distress from pulmonary hypoplasia. Ultrasound shows bilateral enlarged, echogenic kidneys with innumerable tiny cysts arranged radially. Potter sequence features are present. The most likely diagnosis and its associated hepatic lesion are:\",\n      correctAnswer: \"Autosomal recessive polycystic kidney disease (ARPKD) \u2014 congenital hepatic fibrosis\",\n      opts: [\n        \"Autosomal recessive polycystic kidney disease (ARPKD) \u2014 congenital hepatic fibrosis\",\n        \"Autosomal dominant PKD (ADPKD) \u2014 hepatic cysts, berry aneurysms, presents in adults\",\n        \"Multicystic dysplastic kidney \u2014 unilateral, non-hereditary, no viable nephrons\",\n        \"Medullary cystic kidney disease \u2014 salt-wasting nephropathy in older children\"\n      ],\n      exp: \"<strong>ARPKD<\/strong>: gene <strong>PKHD1<\/strong> (chromosome 6p21, encodes fibrocystin\/polyductin). Presents at birth or in utero. Bilateral diffuse collecting duct ectasia \u2192 radially arranged microcysts (< 1 cm). Potter sequence: oligohydramnios \u2192 pulmonary hypoplasia \u2192 facial deformity + limb deformity. Invariably associated with <strong>congenital hepatic fibrosis<\/strong> (CHF) \u2014 periportal fibrosis \u2192 portal hypertension, biliary dilatation (Caroli's). Survivors face ESRD + portal hypertension. Contrast: ADPKD neonatal (rare, severe) vs typical adult form; ADPKD hepatic lesion = discrete cysts (not fibrosis).\",\n      difficulty: \"medium\",\n      concept: \"ARPKD\"\n    },\n    {\n      q: \"A 5-year-old girl is found to have a large abdominal mass crossing the midline on physical examination. CT shows a suprarenal mass with calcification (stippled, eggshell pattern), elevated urinary VMA and HVA, and elevated serum NSE. Bone marrow biopsy shows tumour cells. The feature that <em>most reliably<\/em> distinguishes this tumour from Wilms tumour is:\",\n      correctAnswer: \"Suprarenal (adrenal) location, catecholamine metabolites in urine, and calcification\",\n      opts: [\n        \"Bilateral renal involvement with intrarenal cysts and haemorrhage\",\n        \"WT1 deletion at chromosome 11p13 with associated aniridia\",\n        \"Suprarenal (adrenal) location, catecholamine metabolites in urine, and calcification\",\n        \"Triphasic histology with blastemal, stromal, and epithelial components\"\n      ],\n      exp: \"<strong>Neuroblastoma<\/strong>: most common extracranial solid tumour of childhood; arises from neural crest cells (adrenal medulla most common, 50%). Key features: <strong>suprarenal\/paraspinal<\/strong> location (not intrarenal), catecholamine excess \u2192 elevated urinary <strong>VMA + HVA<\/strong>, elevated NSE; calcification in 90%; bone marrow metastases; <em>N-MYC<\/em> amplification (poor prognosis). Wilms tumour: intrarenal, triphasic histology, WT1\/WT2 mutations, no catecholamines, no calcification. Crossing the midline is more typical of neuroblastoma (Wilms: usually does not cross midline unless bilateral). Opsoclonus-myoclonus-ataxia: paraneoplastic neuroblastoma.\",\n      difficulty: \"medium\",\n      concept: \"Neuroblastoma vs Wilms\"\n    },\n    {\n      q: \"During routine imaging for unrelated back pain, a 38-year-old man is found to have a horseshoe kidney. The kidneys are fused at their lower poles across the midline. Which embryological error and the most common complication of this anomaly are correct?\",\n      correctAnswer: \"Failure of separation of metanephric blastema \u2014 ureteropelvic junction obstruction and recurrent UTI\/calculi\",\n      opts: [\n        \"Failure of ureteric bud induction of metanephric blastema \u2014 bilateral renal agenesis (Potter)\",\n        \"Failure of separation of metanephric blastema \u2014 ureteropelvic junction obstruction and recurrent UTI\/calculi\",\n        \"Abnormal rotation of the pronephros during ascent \u2014 ectopic ureter draining below the sphincter\",\n        \"Incomplete division of the ureteric bud \u2014 duplex collecting system with vesicoureteric reflux\"\n      ],\n      exp: \"<strong>Horseshoe kidney<\/strong>: most common renal fusion anomaly (1:400). Lower poles fuse across midline, held by the <strong>inferior mesenteric artery<\/strong> which prevents further ascent. Embryological basis: fusion of metanephric blastema before complete cephalad migration (week 4\u20138). Complications: <strong>UPJ obstruction<\/strong> (impaired drainage due to abnormal ureteric angulation) \u2192 hydronephrosis, calculi, recurrent UTI; also associated with <em>Wilms tumour<\/em>, <em>Turner syndrome<\/em> (45X), and cardiovascular anomalies. Usually asymptomatic; discovered incidentally. Surgical intervention only if symptomatic obstruction.\",\n      difficulty: \"easy\",\n      concept: \"Horseshoe Kidney\"\n    },\n    {\n      q: \"A 40-year-old woman with nephrotic syndrome (membranous nephropathy, proteinuria 7 g\/day) develops acute severe flank pain, macroscopic haematuria, and worsening oedema. CT with contrast shows a filling defect in the left renal vein extending into the IVC. Doppler confirms absent flow. Which pathophysiological mechanism best explains the predisposition to this complication in nephrotic syndrome?\",\n      correctAnswer: \"Urinary loss of antithrombin III and protein C\/S creates a prothrombotic state\",\n      opts: [\n        \"Hyperviscosity from elevated fibrinogen alone causes venous occlusion\",\n        \"Urinary loss of antithrombin III and protein C\/S creates a prothrombotic state\",\n        \"Thrombocytosis from bone marrow stimulation by hypoalbuminaemia causes venous thrombosis\",\n        \"Reduced renal prostaglandin synthesis from GBM damage causes renal vein spasm\"\n      ],\n      exp: \"<strong>Renal vein thrombosis (RVT)<\/strong>: classic complication of nephrotic syndrome, especially <strong>membranous nephropathy<\/strong> (highest risk, up to 30%). Mechanism: <strong>urinary loss of natural anticoagulants<\/strong> \u2014 antithrombin III, protein C, protein S (all low MW) \u2014 combined with elevated procoagulants (fibrinogen, factor VIII, von Willebrand factor) retained due to high MW \u2192 hypercoagulable state. Presents: acute flank pain, haematuria, worsening proteinuria. Chronic RVT: may be silent. Treatment: anticoagulation (warfarin or LMWH); treat underlying nephropathy. Pulmonary embolism risk is high.\",\n      difficulty: \"hard\",\n      concept: \"Renal Vein Thrombosis\"\n    },\n    {\n      q: \"A 65-year-old man with a longstanding history of cigarette smoking, recurrent painless haematuria, and obstructive uropathy is found to have a mass in the renal pelvis. CT urogram shows a filling defect with proximal hydronephrosis. Cystoscopy reveals no bladder lesion. Histology of the resected specimen shows nests and cords of malignant epithelial cells with abundant pink cytoplasm and central comedonecrosis. Which tumour marker and its utility are most relevant here?\",\n      correctAnswer: \"FGFR3 mutation \u2014 commonly mutated in low-grade urothelial carcinoma of the renal pelvis; useful for non-invasive detection in urine\",\n      opts: [\n        \"Alpha-fetoprotein (AFP) \u2014 elevated in yolk sac tumour, useful for monitoring testicular germ cell tumours\",\n        \"CA 19-9 \u2014 elevated in pancreatic adenocarcinoma, not relevant to urothelial malignancy\",\n        \"PSA (prostate-specific antigen) \u2014 elevated in prostate carcinoma, not specific to upper tract urothelial carcinoma\",\n        \"FGFR3 mutation \u2014 commonly mutated in low-grade urothelial carcinoma of the renal pelvis; useful for non-invasive detection in urine\"\n      ],\n      exp: \"<strong>Urothelial (transitional cell) carcinoma of the renal pelvis<\/strong>: 5\u201310% of renal tumours. Risk factors: <strong>smoking<\/strong> (most important), analgesic nephropathy (phenacetin), aristolochic acid (Balkan endemic nephropathy), Lynch syndrome. Histology: urothelial\/TCC architecture. Molecular: <strong>FGFR3 mutations<\/strong> (fibroblast growth factor receptor 3) \u2014 common in low-grade papillary urothelial carcinoma; used in urine-based molecular tests (e.g. UroVysion FISH, Urothelial CarcinoMA FGFR PCR). Management: nephroureterectomy. Synchronous bladder lesions in 30\u201350%; surveillance cystoscopy required.\",\n      difficulty: \"hard\",\n      concept: \"Urothelial Carcinoma \u2014 Renal Pelvis\"\n    }\n  ];\n\n  function shuffle(arr) {\n    const a = [...arr];\n    for (let i = a.length - 1; i > 0; i--) {\n      const j = Math.floor(Math.random() * (i + 1));\n      [a[i], a[j]] = [a[j], a[i]];\n    }\n    return a;\n  }\n\n  let session = [], answered = [], total = 0;\n\n  function prepareSession() {\n    session = shuffle(BANK).map(q => {\n      const opts = shuffle(q.opts);\n      return { ...q, opts, ansIdx: opts.indexOf(q.correctAnswer) };\n    });\n    answered = new Array(session.length).fill(null);\n    total = 0;\n    Q.sn.textContent = '0';\n    Q.sm.textContent = session.length * 4;\n  }\n\n  function diffBadge(d) {\n    return d ? `<span class=\"diff diff-${d}\">${d}<\/span>` : '';\n  }\n\n  function conceptBadge(c) {\n    return c ? `<span class=\"tag-concept\">${c}<\/span>` : '';\n  }\n\n  function buildQuiz() {\n    Q.container.innerHTML = '';\n    Q.sr.textContent = session.length;\n\n    session.forEach((q, i) => {\n      const card = document.createElement('div');\n      card.className = 'q-card';\n\n      const letters = ['A','B','C','D'];\n      const optsHTML = q.opts.map((opt, j) => `\n        <div class=\"opt\" id=\"rp-o-${i}-${j}\">\n          <span class=\"opt-letter\">${letters[j]}<\/span>\n          <span>${opt}<\/span>\n        <\/div>`).join('');\n\n      card.innerHTML = `\n        <div class=\"q-head\">\n          <div class=\"q-num\" id=\"rp-n-${i}\">${i + 1}<\/div>\n          <div class=\"q-text\">${q.q}<\/div>\n        <\/div>\n        <div class=\"options\">${optsHTML}<\/div>\n        <div class=\"explanation\" id=\"rp-e-${i}\">\n          <div class=\"exp-label\">Explanation ${diffBadge(q.difficulty)}${conceptBadge(q.concept)}<\/div>\n          ${q.exp}\n        <\/div>`;\n\n      Q.container.appendChild(card);\n      q.opts.forEach((_, j) => {\n        document.getElementById(`rp-o-${i}-${j}`)\n          .addEventListener('click', () => answer(i, j));\n      });\n    });\n\n    Q.submit.classList.remove('visible');\n  }\n\n  function answer(qi, oi) {\n    if (answered[qi] !== null) return;\n    const q = session[qi];\n    const ok = oi === q.ansIdx;\n    answered[qi] = ok ? 'correct' : 'wrong';\n    total++;\n\n    q.opts.forEach((_, j) => {\n      const el = document.getElementById(`rp-o-${qi}-${j}`);\n      if (j === q.ansIdx)       el.classList.add('correct');\n      else if (j === oi && !ok) el.classList.add('wrong');\n      else                      el.classList.add('dimmed');\n    });\n\n    document.getElementById(`rp-e-${qi}`).classList.add('show');\n    document.getElementById(`rp-n-${qi}`).classList.add(ok ? 'answered-c' : 'answered-w');\n\n    updateStats();\n    updateProgress();\n    if (total === session.length) Q.submit.classList.add('visible');\n  }\n\n  function updateStats() {\n    const c = answered.filter(a => a === 'correct').length;\n    const w = answered.filter(a => a === 'wrong').length;\n    const r = answered.filter(a => a === null).length;\n    const n = (c * 4) - w;\n    Q.sc.textContent = c;\n    Q.sw.textContent = w;\n    Q.sr.textContent = r;\n    Q.sn.textContent = n >= 0 ? '+' + n : n;\n    Q.sm.textContent = session.length * 4;\n  }\n\n  function updateProgress() {\n    Q.progress.style.width = (total \/ session.length * 100) + '%';\n  }\n\n  function showScore() {\n    const c  = answered.filter(a => a === 'correct').length;\n    const w  = answered.filter(a => a === 'wrong').length;\n    const sk = answered.filter(a => a === null).length;\n    const mx = session.length * 4;\n    const ns = (c * 4) - w;\n    const pc = Math.round((ns \/ mx) * 100);\n    const bw = Math.max(0, Math.min(100, pc));\n    const msg = pc >= 85 ? 'Outstanding! Excellent command of renal pathology.' :\n                pc >= 65 ? 'Good foundation \u2014 revisit the explanations for gaps.' :\n                pc >= 50 ? 'Passing, but targeted revision is recommended.' :\n                pc >= 0  ? 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