Kidney II for NEET PG Pathology: ATN, Interstitial Nephritis, Pyelonephritis, Polycystic Kidney, Stones, HUS, Renal Cell Carcinoma, Wilms, Bladder Cancer

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🎯 Exam priority: High. Expect: ATN casts and causes, drug-induced interstitial nephritis, myeloma cast nephropathy, papillary necrosis settings, ADPKD genes and extrarenal features, stone types (struvite and staghorn), HUS vs TTP, RCC risk factors and paraneoplastic syndromes, Wilms associations, and bladder cancer risk factors.

CBME mapping: PA 27.8–27.16. Glomerular disease, AKI and CKD are in article 21; urine examination in article 16; haemolytic anaemias and TTP from the blood side in article 14.

Tubules, infection, cysts, stones, vessels and tumours of the kidney and bladder. Drawn by TrackNation.

Tubules and Interstitium

• Acute tubular necrosis: from hypotension or sepsis (renal hypoperfusion) and nephrotoxic drugs; also myoglobin (rhabdomyolysis), haemoglobin (massive haemolysis), burns, tumour lysis and myeloma. Sediment: muddy brown granular casts and epithelial cells; urine sodium high, FENa above 1–2%.

• Acute interstitial nephritis: mostly allergic drug reactions or infections. Fever and urticarial rash come early, but the full triad of fever, rash and eosinophilia is seen in fewer than 10%. Latency ranges from 1 day (rifampicin) to 18 months (NSAIDs).

• Myeloma kidney: filtered light chains (Bence Jones protein) overwhelm the proximal tubule and bind Tamm-Horsfall protein distally to form obstructive casts — cast nephropathy.

• Analgesic nephropathy: chronic interstitial disease; papillary necrosis late; higher risk of urothelial (transitional cell) carcinoma. Contrast nephropathy: creatinine rises 24–48 hours after IV contrast, usually temporary.

• Renal tubular acidosis: type 1 (distal) — poor hydrogen ion excretion; type 2 (proximal) — poor bicarbonate reabsorption; type 4 — aldosterone deficiency or resistance.

Pyelonephritis and Vessels

• Acute pyelonephritis: in a normal urinary tract, E. coli strains with adhesins for urothelium cause 80%; others are Klebsiella, Proteus, occasionally Pseudomonas. White cell casts show inflammation. Papillary necrosis complicates pyelonephritis with diabetes, obstruction, sickle cell disease, transplants, candidiasis or analgesic nephropathy.

• Chronic pyelonephritis (reflux nephropathy): scarring and atrophy from repeated inflammation, mostly with major anatomic abnormalities and strongly linked to vesicoureteral reflux in childhood.

• Renal artery stenosis: about 90% atherosclerotic (often bilateral); about 10% fibromuscular dysplasia (often unilateral, women 20–50). Renal infarcts are wedge-shaped. Hypertensive arteriolar nephrosclerosis is a leading diagnosis in kidney failure.

• Thrombotic microangiopathy: HUS = microangiopathic haemolytic anaemia, thrombocytopenia and AKI, usually in children after Shiga toxin–producing E. coli O157:H7 haemorrhagic colitis. TTP: low ADAMTS13, Coombs-negative haemolysis; neurological signs commoner and renal failure less common than in HUS.

Cysts, Stones and Obstruction

• ADPKD: PKD1 (chromosome 16, polycystin 1) in most, PKD2 (chromosome 4) in the rest. Kidney failure in 35–45% by age 60. Extrarenal: liver cysts in most, cerebral (berry) aneurysms in 4–10%, mitral valve prolapse, aortic regurgitation, diverticula, hernias.

• ARPKD: rare (1 in 10,000), kidney failure in childhood. Nephronophthisis (autosomal recessive) and ADTKD (autosomal dominant): cysts confined to the medulla or corticomedullary junction; end-stage disease in childhood vs at 30–50.

• Stones: see the table. A staghorn calculus fills the whole calyceal system and is typically struvite. Struvite stones are infected foreign bodies and must be removed completely.

• Obstructive uropathy → hydronephrosis. Commonest cause by age: children — anatomic (posterior urethral valves in boys, junction stenosis); young adults — stones; older adults — prostatic enlargement or cancer.

Renal and Urothelial Tumours

• Renal cell carcinoma: the commonest renal cancer (men 2:1, diagnosed 65–74). Risks: smoking (doubles risk), obesity, hypertension, acquired cystic disease on dialysis, von Hippel-Lindau and tuberous sclerosis. Haematuria, flank pain, mass, fever of unknown origin — often found incidentally. Tumour thrombus grows into the renal vein and sometimes the IVC. Paraneoplastic syndromes in 20%: polycythaemia (erythropoietin), hypercalcaemia, anaemia. Spread: nodes, lung, adrenal, liver, brain, bone.

• Wilms tumour (nephroblastoma): embryonal tumour with blastemal, stromal and epithelial elements; children under 5; painless abdominal mass; bilateral in 5–10%. WT1 deletion; WAGR = Wilms, aniridia, genitourinary malformations and intellectual disability; also hemihypertrophy.

• Bladder cancer: urothelial (transitional cell) carcinoma > 90%, mostly papillary; presents with haematuria. Risks: smoking (≥ 50% of cases), long-term cyclophosphamide, dye-industry aromatic amines, chronic irritation. Squamous carcinoma goes with schistosomiasis and chronic irritation.

Traps the Examiner Sets

• Muddy brown casts = ATN; white cell casts = pyelonephritis or interstitial inflammation; red cell casts = glomerulonephritis.

• Staghorn = struvite = Proteus (urea splitting).

• ADPKD gene on chromosome 16; berry aneurysm is the feared extrarenal killer.

• HUS: child + bloody diarrhoea + kidney; TTP: low ADAMTS13, brain more than kidney.

• Bladder squamous carcinoma = schistosomiasis; urothelial = smoking.

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Muddy brown = Many dead tubules (ATN) — casts

• 🧠 Staghorn = Struvite = Splitting urea (Proteus) — stones

• 🧠 PKD1 = 16 letters? — Polycystic Kidney Disease 1 sits on chromosome 16 — ADPKD gene

• 🧠 HUS = Hamburger, Uraemia, Small child — HUS

• 🧠 TTP = Thinking (neuro) more than peeing (renal) — TTP vs HUS

• 🧠 WAGR = Wilms, Aniridia, Genitourinary, and the R for intellectual disability — Wilms

• 🧠 Schisto makes Squamous — bladder cancer

Rapid-Revision Cards

• ATN

  Hypotension, sepsis, nephrotoxins, myoglobin; muddy brown casts.

• Acute interstitial nephritis

  Drug allergy; fever, rash; triad < 10%.

• Myeloma kidney

  Light chains + Tamm-Horsfall → casts.

• Analgesic nephropathy

  Papillary necrosis late; urothelial cancer.

• Contrast nephropathy

  Creatinine ↑ at 24–48 h.

• UTI organism

  E. coli 80% (normal tract).

• Papillary necrosis

  Diabetes, obstruction, sickle, analgesics.

• Chronic pyelonephritis

  Reflux nephropathy; scars; VUR.

• Renal artery stenosis

  90% atherosclerosis; 10% FMD (women 20–50).

• HUS

  Child, O157:H7, MAHA + low platelets + AKI.

• TTP

  Low ADAMTS13; neuro > renal.

• ADPKD genes

  PKD1 chr 16 (most); PKD2 chr 4.

• ADPKD extrarenal

  Liver cysts, berry aneurysm, MVP.

• ARPKD

  1 in 10,000; childhood failure.

• Nephronophthisis

  AR; medullary cysts; child ESKD.

• Stones

  Ca 85%, struvite 5–15%, urate 5–10%, cystine 1–2%.

• Staghorn

  Struvite; Proteus, Klebsiella.

• Obstruction by age

  Child valves; young stones; old prostate.

• RCC risks

  Smoking, obesity, HTN, dialysis cysts, VHL.

• RCC paraneoplastic

  20%: polycythaemia, hypercalcaemia.

• Wilms

  < 5 yr; painless mass; WT1; WAGR; bilateral 5–10%.

• Bladder cancer

  Urothelial > 90%; smoking ≥ 50%.

• Squamous bladder

  Schistosomiasis.

Sources

Facts in this article were checked against these documents.

• MSD Manual Professional: Acute Tubular Necrosis; Tubulointerstitial Nephritis; Myeloma-Related Kidney Disease; Analgesic Nephropathy; Contrast Nephropathy; Renal Tubular Acidosis — Merck & Co. (MSD Manuals), reviewed 2024–26 (link)

• MSD Manual Professional: Bacterial Urinary Tract Infections; Reflux Nephropathy — Merck & Co. (MSD Manuals), reviewed 2026 (link)

• MSD Manual Professional: Renal Artery Stenosis; Hypertensive Arteriolar Nephrosclerosis; ADPKD; Nephronophthisis and ADTKD — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• MSD Manual Professional: Hemolytic-Uremic Syndrome; Thrombotic Thrombocytopenic Purpura — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• MSD Manual Professional: Urinary Calculi; Obstructive Uropathy; Renal Cell Carcinoma; Bladder Cancer; Wilms Tumor — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• Competency Based Undergraduate Curriculum, Pathology (PA 27) — National Medical Commission, 2024

Test Yourself: Practice Questions

Thirty-two questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. After a prolonged hypotensive episode during sepsis, a patient becomes oliguric; urine shows muddy brown granular casts and epithelial cells. The lesion is

• (a) prerenal azotaemia

• (b) minimal change disease

• (c) acute glomerulonephritis

• (d) acute tubular necrosis

Q2. After a crush injury, a patient passes tea-coloured urine and develops acute kidney injury. The pigment damaging the tubules is

• (a) myoglobin

• (b) bilirubin

• (c) haemosiderin

• (d) melanin

Q3. Days after starting a new antibiotic, a patient develops fever, an urticarial rash and rising creatinine. The likely renal lesion is

• (a) acute (allergic) interstitial nephritis

• (b) ADPKD

• (c) post-streptococcal GN

• (d) renal artery stenosis

Q4. In drug-induced acute interstitial nephritis, the classic triad of fever, rash and eosinophilia is present in

• (a) nearly all patients

• (b) fewer than 10% of patients

• (c) only children

• (d) about half

Q5. In a patient with multiple myeloma, distal tubules are blocked by casts. The casts form when light chains combine with

• (a) Tamm-Horsfall protein

• (b) IgA

• (c) fibrin

• (d) albumin only

Q6. A long-term analgesic user with chronic kidney disease is at increased risk of which cancer?

• (a) transitional cell carcinoma of the urinary tract

• (b) renal cell carcinoma only

• (c) Wilms tumour

• (d) prostate cancer

Q7. Contrast nephropathy typically appears as a creatinine rise

• (a) after 3 months

• (b) 24–48 hours after IV contrast, usually temporary

• (c) only with oral contrast

• (d) within 10 minutes

Q8. In patients with a structurally normal urinary tract, the organism causing about 80% of urinary infections is

• (a) Escherichia coli

• (b) Proteus mirabilis

• (c) Staphylococcus saprophyticus

• (d) Pseudomonas aeruginosa

Q9. A diabetic with acute pyelonephritis is found to have necrosis of the renal papillae. This complication is called

• (a) renal vein thrombosis

• (b) nephrocalcinosis

• (c) papillary necrosis

• (d) renal cell carcinoma

Q10. Coarse cortical scars with atrophy in a young adult who had vesicoureteral reflux in childhood indicate

• (a) ADPKD

• (b) reflux nephropathy (chronic pyelonephritis)

• (c) renal infarcts from emboli

• (d) diabetic nephropathy

Q11. A 30-year-old woman has hypertension from a unilateral renal artery stenosis caused by irregular, mainly medial wall thickening. The cause is most likely

• (a) renal vein thrombosis

• (b) atherosclerosis

• (c) Takayasu arteritis

• (d) fibromuscular dysplasia

Q12. Most renal artery stenosis is due to

• (a) fibromuscular dysplasia (90%)

• (b) trauma

• (c) atherosclerosis (about 90%, often bilateral)

• (d) vasculitis

Q13. After bloody diarrhoea, a 4-year-old develops haemolytic anaemia with red cell fragments, thrombocytopenia and acute kidney injury. The likely organism is

• (a) Vibrio cholerae

• (b) Salmonella typhi

• (c) rotavirus

• (d) Shiga toxin–producing E. coli O157:H7

Q14. Thrombotic thrombocytopenic purpura is distinguished from HUS by

• (a) positive direct Coombs test

• (b) high platelet count

• (c) absence of schistocytes

• (d) severely reduced ADAMTS13 activity

Q15. An adult with bilateral enlarged cystic kidneys has a family history of kidney failure on dialysis in his father. The commonest mutated gene and its chromosome are

• (a) WT1 on chromosome 11

• (b) PKD1 on chromosome 16

• (c) PKD2 on chromosome 4 in most cases

• (d) PKHD1 on chromosome 6

Q16. The intracranial lesion that makes ADPKD dangerous, present in about 4–10% of patients, is

• (a) arachnoid cyst only

• (b) brain metastasis

• (c) cerebral (berry) aneurysm

• (d) meningioma

Q17. The commonest extrarenal finding in ADPKD is

• (a) lung cysts

• (b) splenic cysts

• (c) hepatic cysts

• (d) pancreatic cancer

Q18. A cardiac lesion associated with ADPKD is

• (a) Ebstein anomaly

• (b) tetralogy of Fallot

• (c) coarctation

• (d) mitral valve prolapse

Q19. A child with polyuria, polydipsia and progressive kidney failure has normal-sized or small kidneys with cysts at the corticomedullary junction; the inheritance is autosomal recessive. This is

• (a) ADTKD

• (b) nephronophthisis

• (c) ADPKD

• (d) simple cysts

Q20. The commonest composition of urinary stones is

• (a) uric acid

• (b) calcium (mainly calcium oxalate)

• (c) cystine

• (d) struvite

Q21. A woman with recurrent Proteus urinary infections has a large stone filling the entire calyceal system. Its composition is most likely

• (a) uric acid

• (b) calcium oxalate

• (c) magnesium ammonium phosphate (struvite)

• (d) cystine

Q22. Stones that form only in the presence of an inherited amino acid transport defect are

• (a) uric acid stones

• (b) cystine stones

• (c) calcium oxalate stones

• (d) struvite stones

Q23. The commonest cause of urinary obstruction in a newborn boy is

• (a) bladder cancer

• (b) benign prostatic hyperplasia

• (c) posterior urethral valves

• (d) renal stones

Q24. A 65-year-old smoker has haematuria, flank pain and a renal mass; haemoglobin is raised. The tumour and the cause of polycythaemia are

• (a) Wilms tumour — androgens

• (b) renal cell carcinoma — erythropoietin

• (c) angiomyolipoma — EPO always

• (d) urothelial carcinoma — PTHrP

Q25. A familial syndrome strongly predisposing to renal cell carcinoma is

• (a) Peutz-Jeghers syndrome

• (b) von Hippel-Lindau disease

• (c) Lynch syndrome

• (d) Li-Fraumeni syndrome

Q26. Renal cell carcinoma characteristically spreads by

• (a) spreading along nerves

• (b) growing into the renal vein and sometimes the inferior vena cava

• (c) seeding the peritoneum

• (d) direct invasion of the colon only

Q27. A long-term dialysis patient develops a solid renal mass. A recognised predisposing condition is

• (a) minimal change disease

• (b) renal artery stenosis

• (c) nephronophthisis

• (d) acquired cystic kidney disease

Q28. A 3-year-old has a painless abdominal mass, absent irises (aniridia) and genital anomalies. The tumour and deleted gene are

• (a) Wilms tumour — WT1

• (b) retinoblastoma — RB1

• (c) hepatoblastoma — APC

• (d) neuroblastoma — MYCN

Q29. Microscopy of a childhood renal tumour shows blastemal, stromal and epithelial elements. The tumour is

• (a) oncocytoma

• (b) angiomyolipoma

• (c) renal cell carcinoma

• (d) Wilms tumour

Q30. The single most common risk factor for bladder cancer is

• (a) cigarette smoking

• (b) schistosomiasis

• (c) bladder stones

• (d) cyclophosphamide

Q31. A man with long-standing urinary schistosomiasis develops bladder cancer. The likely histological type is

• (a) adenocarcinoma always

• (b) urothelial carcinoma in situ only

• (c) small cell carcinoma

• (d) squamous cell carcinoma

Q32. The commonest histological type of bladder cancer is

• (a) adenocarcinoma

• (b) urothelial (transitional cell) carcinoma

• (c) squamous cell carcinoma

• (d) sarcoma

Active Recall

From memory: list causes and casts of ATN; describe drug-induced interstitial nephritis and myeloma kidney; give the organism and complications of pyelonephritis and define reflux nephropathy; contrast atherosclerotic and fibromuscular renal artery stenosis and HUS with TTP; describe ADPKD genetics and extrarenal features; rank stone types; and summarise RCC, Wilms tumour and bladder cancer risks and features.