Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 221: Sickle cell disease is associated with which type of renal cell carcinoma?

A. Medullary (Correct Answer)
B. Papillary
C. Chromophobe
D. Colloid

Explanation: **Explanation:** **Renal Medullary Carcinoma (RMC)** is a highly aggressive, rare malignancy that occurs almost exclusively in young patients (mean age ~20 years) who carry the **Sickle Cell Trait (HbAS)** or, less commonly, Sickle Cell Disease (HbSS). **Why Medullary is correct:** The pathogenesis is linked to the hypoxic and hypertonic environment of the renal medulla [1]. These conditions promote the sickling of red blood cells in the vasa recta, leading to chronic ischemia and micro-infarctions [1]. This chronic injury, combined with the loss of the **SMARCB1 (INI1)** tumor suppressor gene expression (a hallmark of RMC), triggers malignant transformation. It typically presents as a central, infiltrative mass involving the renal pelvis and medulla. **Why other options are incorrect:** * **Papillary RCC:** Associated with trisomy 7 and 17 or MET gene mutations; it is the second most common RCC but has no specific link to hemoglobinopathies. * **Chromophobe RCC:** Originates from intercalated cells of collecting ducts; characterized by "halos" around nuclei and associated with Birt-Hogg-Dubé syndrome. * **Colloid (Mucinous) Carcinoma:** Extremely rare in the kidney; usually refers to a variant of adenocarcinoma often seen in the GI tract or breast, not associated with sickle cell. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Marker:** Loss of **INI1 (SMARCB1)** protein expression on immunohistochemistry. * **Demographics:** Most common in young African-American males with sickle cell trait [1]. * **Prognosis:** Extremely poor; most patients present with metastatic disease at the time of diagnosis. * **Location:** Predominantly involves the **right kidney**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 948-949.

Question 222: Which of the following are renal lesions seen in Multiple Myeloma?

A. Cast nephropathy
B. Amyloid deposition
C. Plasma cell infiltration
D. All of the above (Correct Answer)

Explanation: Multiple Myeloma (MM) is a plasma cell dyscrasia [5] that frequently involves the kidneys, a condition often referred to as **"Myeloma Kidney."** [2] Renal failure is the second most common cause of death in these patients. [2] **Explanation of Options:** * **Cast Nephropathy (Myeloma Kidney):** This is the most common renal lesion. [2] Excess monoclonal light chains (Bence-Jones proteins) are filtered by the glomerulus and precipitate with **Tamm-Horsfall protein** in the distal tubules. [1] This forms hard, waxy, eosinophilic casts that cause tubular obstruction and a characteristic giant cell reaction. [1], [2] * **Amyloid Deposition:** In approximately 10% of MM patients, light chains (specifically the V-region of the λ light chain) are processed into amyloid fibrils, leading to **AL (Primary) Amyloidosis**. [1], [3] These deposits occur in the glomeruli and blood vessels, often resulting in nephrotic syndrome. [4] * **Plasma Cell Infiltration:** Though less common than the above, direct interstitial infiltration by malignant plasma cells can occur in advanced stages of the disease, leading to an interstitial inflammatory response. **Why "All of the above" is correct:** Multiple Myeloma affects the kidney through multiple mechanisms: obstructive (casts), infiltrative (plasma cells), and protein-deposition (amyloid and Light Chain Deposition Disease). [1] **High-Yield Clinical Pearls for NEET-PG:** * **Bence-Jones Proteins:** These are not detected by standard urine dipsticks (which detect albumin) but are found via **sulfosalicylic acid test** or urine electrophoresis. * **Hypercalcemia:** A hallmark of MM (due to bone resorption), it contributes to renal injury by causing nephrocalcinosis and impaired concentrating ability. [1] * **Morphology:** Casts in MM are typically **fractured/cracked** in appearance and surrounded by multinucleated giant cells. [1], [2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617.

Question 223: What is the most common renal tumour?

A. Renal cell carcinoma (Correct Answer)
B. Wilm's tumour
C. Squamous cell carcinoma of the renal pelvis
D. Transitional cell carcinoma of the renal pelvis

Explanation: **Explanation:** **Renal Cell Carcinoma (RCC)** is the most common primary malignancy of the kidney, accounting for approximately **80-85%** of all malignant renal tumors in adults [1]. It originates from the renal tubular epithelium, most commonly the proximal convoluted tubule (in the case of the Clear Cell subtype). **Analysis of Options:** * **A. Renal Cell Carcinoma (Correct):** It is the most frequent renal tumor in adults, typically occurring in the 6th to 7th decades of life. Risk factors include smoking, obesity, hypertension, and acquired cystic kidney disease (ACKD) in dialysis patients [1]. * **B. Wilm’s Tumour (Nephroblastoma):** While it is the most common renal tumor in **children** (typically aged 2–5 years), it is rare in adults. * **C & D. Squamous and Transitional Cell Carcinoma:** These arise from the **urothelium** of the renal pelvis, not the renal parenchyma. Transitional Cell Carcinoma (TCC) is the most common tumor of the renal pelvis, but it is significantly less common than RCC overall [1]. Squamous cell carcinoma is rare and usually associated with chronic irritation (e.g., staghorn calculi). **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Hematuria (most common), flank pain, and a palpable mass (seen in only 10% of cases). * **Most Common Subtype:** Clear Cell RCC (associated with **VHL gene** deletion on Chromosome 3p) [1]. * **Paraneoplastic Syndromes:** RCC is known as the "Internist's Tumor" because it can secrete hormones leading to Polycythemia (EPO), Hypercalcemia (PTHrP), and Hypertension (Renin). * **Staging:** The most important prognostic factor is the pathologic stage (TNM), specifically invasion of the renal vein or perinephric fat [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-961.

Question 224: Bilateral renal cell carcinoma is seen in which of the following conditions?

A. Eagle-Barrett syndrome
B. Beckwith-Wiedemann syndrome
C. Von Hippel-Lindau disease (Correct Answer)
D. Bilateral angiomyolipoma

Explanation: ### **Explanation** **Correct Option: C. Von Hippel-Lindau (VHL) disease** Von Hippel-Lindau disease is an autosomal dominant hereditary cancer syndrome caused by a mutation in the **VHL gene on chromosome 3p25**. The VHL protein normally degrades hypoxia-inducible factor (HIF); its loss leads to increased angiogenesis and cell proliferation. Approximately **25–45%** of patients with VHL develop **Clear Cell Renal Cell Carcinoma (RCC)**. A hallmark of hereditary RCC (like VHL) is that the tumors are frequently **bilateral and multicentric**, occurring at a younger age compared to sporadic cases [1]. **Analysis of Incorrect Options:** * **A. Eagle-Barrett Syndrome (Prune Belly Syndrome):** Characterized by a triad of abdominal muscle deficiency, undescended testes, and urinary tract abnormalities (e.g., megaureter). It is not associated with a predisposition to RCC. * **B. Beckwith-Wiedemann Syndrome:** A pediatric overgrowth disorder (WT2 mutation on Ch 11p15) associated with macroglossia, omphalocele, and hemihypertrophy. It significantly increases the risk of **Wilms tumor (Nephroblastoma)**, not RCC. * **D. Bilateral Angiomyolipoma:** While these are benign mesenchymal tumors frequently seen in **Tuberous Sclerosis** [1], they are not carcinomas. Although they can be bilateral, they do not represent Renal Cell Carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **VHL Syndrome Triad:** Hemangioblastomas (cerebellum/retina), Pheochromocytoma, and Clear Cell RCC. * **Most common type of RCC in VHL:** Clear Cell variant [1]. * **Other syndromes with RCC:** Hereditary Papillary Renal Carcinoma (MET gene) and Birt-Hogg-Dubé syndrome (FLCN gene - associated with chromophobe RCC) [1]. * **Staining:** RCC is typically positive for **Vimentin and CD10**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 957-961.

Question 225: What is the most common infectious agent associated with chronic pyelonephritis?

A. Proteus vulgaris
B. Klebsiella pneumoniae
C. Staphylococcus aureus
D. Escherichia coli (Correct Answer)

Explanation: **Explanation:** **Escherichia coli (E. coli)** is the most common causative agent for both acute and chronic pyelonephritis [1]. Chronic pyelonephritis is a clinicopathologic entity characterized by interstitial inflammation and uneven scarring of the renal parenchyma, typically resulting from recurrent or persistent infections associated with **vesicoureteral reflux (VUR)** or **chronic urinary tract obstruction** [1]. E. coli, a normal inhabitant of the intestinal tract, possesses virulence factors like P-pili that allow it to adhere to the urothelium, facilitating its ascent into the renal pelvis [1]. **Analysis of Incorrect Options:** * **Proteus vulgaris:** While *Proteus* species are common causes of UTIs and are uniquely associated with **struvite (staghorn) calculi** due to their urease-producing ability, they are less frequent than E. coli. Xanthogranulomatous pyelonephritis is a variant often associated with Proteus [2]. * **Klebsiella pneumoniae:** This is a common Gram-negative pathogen in hospital-acquired (nosocomial) UTIs and in patients with diabetes, but it ranks behind E. coli in overall prevalence. * **Staphylococcus aureus:** This organism typically reaches the kidney via the **hematogenous route** (e.g., during bacteremia or endocarditis), leading to renal abscesses, rather than the ascending route typical of chronic pyelonephritis [1]. **High-Yield NEET-PG Pearls:** * **Pathognomonic Histology:** The presence of **"Thyroidization"** of tubules (colloid-like casts in dilated tubules) is a classic microscopic hallmark of chronic pyelonephritis [2]. * **Gross Appearance:** Characterized by **asymmetric, coarse, U-shaped scars** overlying blunted or deformed calyces (unlike glomerulonephritis, which is symmetric) [1][2]. * **Xanthogranulomatous Pyelonephritis:** A rare variant of chronic pyelonephritis often associated with *Proteus* infections, characterized by "foamy" lipid-laden macrophages [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 935-937. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940.

Question 226: Squamous cell carcinoma of the urinary bladder is predisposed to by which of the following?

A. Urolithiasis (Correct Answer)
B. Persistent Urachus
C. Schistosomiasis
D. Smoking

Explanation: The development of **Squamous Cell Carcinoma (SCC)** of the bladder is primarily driven by **chronic irritation and inflammation**, which leads to **squamous metaplasia** of the normal urothelium [1]. Over time, this metaplastic epithelium undergoes dysplastic changes, progressing to malignancy. * **Urolithiasis (Correct):** Chronic irritation from bladder stones is a classic risk factor for SCC. The constant mechanical friction induces protective squamous metaplasia, which serves as the precursor lesion for SCC [1]. Foreign bodies and calculi are recognized causes of chronic bladder pathology [2]. * **Persistent Urachus (Incorrect):** A patent or persistent urachus is specifically associated with **Adenocarcinoma** of the bladder, typically occurring at the dome [3]. * **Schistosomiasis (Incorrect):** While *Schistosoma haematobium* is a major global cause of SCC, it is not the answer here because the question asks for a predisposing factor among the provided options. * **Smoking (Incorrect):** Smoking is the most significant risk factor for **Urothelial (Transitional Cell) Carcinoma**, not SCC. **Clinical Pearls for NEET-PG:** 1. **Most common bladder cancer:** Urothelial (Transitional Cell) Carcinoma (>90%). 2. **SCC Association:** Chronic cystitis, long-term indwelling catheters, and bladder stones [2]. 3. **Schistosomiasis:** The most common cause of SCC in endemic areas (e.g., Egypt). 4. **Exstrophy of Bladder:** Strongly predisposes to **Adenocarcinoma** [4]. 5. **Key Pathology:** Look for "Keratin pearls" and "Intercellular bridges" on histology to confirm SCC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 967-968. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 972-973. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 494-495. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, p. 966.

Question 227: Flea bitten kidney is seen in all of the following conditions except?

A. Malignant hypertension
B. Henoch-Schonlein purpura
C. Diabetes Mellitus (Correct Answer)
D. Polyarteritis nodosa

Explanation: ### Explanation The term **"Flea-bitten kidney"** refers to a gross morphological appearance characterized by multiple, tiny, pinpoint subcapsular hemorrhages (petechiae) on the surface of the kidney. This occurs due to the rupture of glomerular capillaries or arterioles, typically seen in conditions involving acute vascular injury or necrotizing vasculitis. #### Why Diabetes Mellitus is the Correct Answer: **Diabetes Mellitus** is characterized by **diabetic nephropathy**, where the hallmark findings are diffuse or nodular glomerulosclerosis (Kimmelstiel-Wilson lesions) and basement membrane thickening [1]. It is a chronic, progressive fibrotic process rather than an acute necrotizing one. Therefore, it does not produce the pinpoint hemorrhages associated with a flea-bitten appearance. One of the most consistent morphologic features of diabetes is diffuse thickening of basement membranes [1]. #### Analysis of Other Options: * **Malignant Hypertension:** Causes fibrinoid necrosis of arterioles and small arteries (hyperplastic arteriolosclerosis), leading to vessel rupture and classic flea-bitten petechiae [2]. * **Henoch-Schonlein Purpura (HSP):** A systemic IgA vasculitis that involves small vessels. The acute inflammation of glomerular capillaries leads to focal hemorrhages. * **Polyarteritis Nodosa (PAN):** A systemic necrotizing vasculitis of medium and small-sized arteries. When it involves the renal vasculature, it results in focal areas of infarction and hemorrhage. #### High-Yield Clinical Pearls for NEET-PG: * **Differential Diagnosis for Flea-bitten Kidney:** 1. Malignant Hypertension (Most common cause) 2. Subacute Bacterial Endocarditis (SBE) 3. Polyarteritis Nodosa (PAN) 4. Henoch-Schonlein Purpura 5. Wegener’s Granulomatosis (GPA) 6. Post-Streptococcal Glomerulonephritis (PSGN) * **Key Distinction:** Flea-bitten kidney signifies **acute vascular/glomerular damage**, whereas Diabetes signifies **chronic sclerotic damage** [1]. * **Microscopic correlate:** In malignant hypertension, look for "onion-skinning" of vessels [2]; in DM, look for "Kimmelstiel-Wilson nodules" [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1121-1122. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945.

Question 228: All of the following are causes of granular contracted kidney except?

A. Benign nephrosclerosis
B. Chronic pyelonephritis
C. Diabetes mellitus (Correct Answer)
D. Chronic glomerulonephritis

Explanation: **Explanation:** The hallmark of end-stage renal disease is typically the **granular contracted kidney**, where the kidneys are small, shrunken, and have a pitted/granular surface due to scarring and nephron loss. **Why Diabetes Mellitus is the Correct Answer:** In **Diabetic Nephropathy**, the kidneys are characteristically **enlarged or normal-sized**, even in the presence of advanced renal failure [3]. This is due to compensatory hypertrophy, increased basement membrane material, and mesangial expansion (Kimmelstiel-Wilson nodules). While the surface may eventually show some irregularity, they do **not** undergo the significant contraction seen in other chronic renal diseases. **Analysis of Incorrect Options:** * **Benign Nephrosclerosis:** Caused by long-standing hypertension [2]. It leads to hyaline arteriolosclerosis, resulting in ischemia, tubular atrophy, and fine, "leather-grain" granularity with symmetric contraction. * **Chronic Pyelonephritis:** Characterized by asymmetric contraction with **coarse, U-shaped scars** overlying blunted calyces [1]. It is a classic cause of a scarred, shrunken kidney. * **Chronic Glomerulonephritis:** The end-stage of various glomerulonephritides. It results in symmetrically small, contracted kidneys with a diffusely granular surface due to diffuse interstitial fibrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Large Kidneys in Renal Failure:** Think of Diabetes Mellitus, Amyloidosis, Polycystic Kidney Disease (ADPKD), and early-stage HIV-associated nephropathy. * **Granularity Type:** Fine granularity is typical of Benign Nephrosclerosis; coarse granularity/scarring is typical of Chronic Pyelonephritis [1]. * **Flea-bitten Kidney:** Seen in Malignant Hypertension and Infective Endocarditis (due to petechial hemorrhages). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 939. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 541-542. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1121.

Question 229: All of the following are true about thin basement membrane defect, except:

A. Also known as benign familial hematuria
B. Autosomal dominant inheritance
C. Persistent or recurrent microscopic hematuria
D. Impaired renal function (Correct Answer)

Explanation: **Explanation:** **Thin Basement Membrane Disease (TBMD)**, also known as **Benign Familial Hematuria**, is a common hereditary glomerular disease. The correct answer is **D** because TBMD is characterized by an excellent prognosis with **preserved renal function**; progression to chronic kidney disease or renal failure is extremely rare. * **Why Option D is correct:** Unlike Alport Syndrome, TBMD does not typically lead to hypertension, significant proteinuria, or impaired renal function. The glomerular filtration rate (GFR) remains normal throughout life. * **Why Option A is wrong:** TBMD is synonymous with "Benign Familial Hematuria" because of its non-progressive nature and strong familial tendency. * **Why Option B is wrong:** The inheritance pattern is typically **Autosomal Dominant**. It most commonly results from heterozygous mutations in the *COL4A3* or *COL4A4* genes (the same genes involved in Alport Syndrome). * **Why Option C is wrong:** The hallmark clinical presentation is persistent or recurrent **microscopic hematuria**, often discovered incidentally during routine urinalysis in childhood or young adulthood. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy (EM):** This is the gold standard for diagnosis. It shows diffuse thinning of the Glomerular Basement Membrane (GBM), often measuring **150–250 nm** (Normal is ~300–400 nm). * **Light Microscopy & Immunofluorescence:** Usually appear completely **normal**. * **Differential Diagnosis:** It must be distinguished from **Alport Syndrome**, which presents with a "basket-weave" appearance on EM, sensorineural deafness, ocular defects, and progressive renal failure. * **Key Distinction:** TBMD = Heterozygous mutation; Alport Syndrome = X-linked (most common) or Autosomal Recessive (homozygous/compound heterozygous).

Question 230: Subepithelial deposits are characteristic findings in which of the following conditions?

A. Minimal change disease
B. Membranoproliferative glomerulonephritis (MPGN)
C. Membranous glomerulonephritis (MGN) (Correct Answer)
D. Post-streptococcal glomerulonephritis (PSGN)

Explanation: ### Explanation **Correct Answer: C. Membranous glomerulonephritis (MGN)** In **Membranous Glomerulonephritis (MGN)**, the hallmark finding on electron microscopy (EM) is the presence of **subepithelial deposits** [1] (located between the glomerular basement membrane and podocytes). These immune complexes trigger the formation of new basement membrane material around them, leading to the characteristic **"Spikes and Dome"** appearance on Silver stain [1]. This process causes diffuse thickening of the capillary wall without significant cellular proliferation [1]. **Analysis of Incorrect Options:** * **A. Minimal Change Disease:** Characterized by the **absence** of immune deposits. The primary finding is the **effacement (fusion) of podocyte foot processes** on EM. * **B. Membranoproliferative Glomerulonephritis (MPGN):** * **Type I** features **subendothelial** deposits [1]. * **Type II** (Dense Deposit Disease) features **intramembranous** deposits [1]. Both show a "tram-track" appearance due to mesangial interposition. * **D. Post-streptococcal Glomerulonephritis (PSGN):** While PSGN does feature subepithelial deposits, they are specifically described as large, discrete **"subepithelial humps"** [1]. However, MGN is the classic prototype for continuous subepithelial deposition leading to membrane thickening. **High-Yield NEET-PG Pearls:** * **MGN:** Most common cause of Nephrotic syndrome in adults; associated with PLA2R antibodies (primary) and HBV, NSAIDs, or solid tumors (secondary). * **Rule of "Sub-":** * **Subepithelial:** MGN, PSGN (Humps). * **Subendothelial:** MPGN Type I, SLE (Wire loops - Class IV). * **Intramembranous:** MPGN Type II. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 911-927.

Practice by Chapter

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