Renal Pathology — MCQs

A 46-year-old woman has had worsening malaise for the past 36 hours. Her urine output is markedly diminished, and it has a cloudy brown appearance. On examination, she has periorbital edema. Laboratory findings include serum creatinine of 2.8 mg/dL and urea nitrogen of 30 mg/dL. A renal biopsy is performed and on microscopic examination shows focal necrosis in glomeruli with glomerular basement membrane breaks and crescent formation. No immune deposits are identified with immunofluorescence. Which of the following autoantibodies is most likely detectable in her serum?

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 331: What is the most common type of renal lesion in children?

A. Lipoid nephrosis (Correct Answer)
B. Membranoproliferative glomerulonephritis
C. Focal glomerulonephritis
D. Diffuse glomerulosclerosis

Explanation: **Explanation:** **Lipoid nephrosis**, also known as **Minimal Change Disease (MCD)**, is the most common cause of nephrotic syndrome in children, accounting for approximately 70–90% of cases under the age of 10 [1]. The term "lipoid nephrosis" refers to the characteristic accumulation of lipids in the proximal convoluted tubules, a secondary change resulting from heavy proteinuria. * **Why Option A is correct:** MCD is defined by "minimal" changes on light microscopy (normal-appearing glomeruli) but shows **diffuse effacement of podocyte foot processes** on electron microscopy [1]. It is highly steroid-responsive and typically presents with sudden onset massive edema and selective proteinuria [1]. **Analysis of Incorrect Options:** * **B. Membranoproliferative glomerulonephritis (MPGN):** This is more common in adolescents and young adults [1]. It presents with a "tram-track" appearance on light microscopy and usually manifests as a mixed nephritic-nephrotic picture. * **C. Focal glomerulonephritis:** This is a descriptive term for lesions involving only some glomeruli (e.g., IgA nephropathy). While IgA nephropathy is the most common primary glomerulonephritis *worldwide* [1], it is not the most common lesion in the pediatric nephrotic age group. * **D. Diffuse glomerulosclerosis:** This is typically a late-stage finding in chronic kidney disease or diabetic nephropathy, not a primary lesion characteristic of childhood renal disease. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Nephrotic Syndrome in adults:** Focal Segmental Glomerulosclerosis (FSGS) (globally) or Membranous Nephropathy [1]. * **Pathognomonic finding for MCD:** Effacement of foot processes (Electron Microscopy) [1]. * **Immunofluorescence in MCD:** Characteristically **negative** (no immune deposits) [1]. * **Treatment of choice:** Corticosteroids (Prednisolone) [1]. It has an excellent prognosis in children. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-928.

Question 332: Birt-Hogg-Dubé syndrome is associated with which of the following conditions?

A. Renal cell carcinoma (Correct Answer)
B. Lung carcinoma
C. Stomach carcinoma
D. Ovarian carcinoma

Explanation: **Explanation:** **Birt-Hogg-Dubé (BHD) syndrome** is an autosomal dominant genodermatosis caused by a germline mutation in the **FLCN gene**, which encodes the protein **folliculin**. This syndrome is characterized by a triad of cutaneous, pulmonary, and renal manifestations. 1. **Why Renal Cell Carcinoma (RCC) is correct:** Patients with BHD have a significantly increased risk (up to sevenfold) of developing bilateral and multifocal renal tumors. The most characteristic histological subtype associated with BHD is **Chromophobe RCC** or **Oncocytic hybrid tumors** (a mix of chromophobe and oncocytoma features), though clear cell and papillary RCC can also occur [1]. 2. **Why other options are incorrect:** * **Lung Carcinoma:** While BHD is associated with pulmonary findings like **basal lung cysts** and **spontaneous pneumothorax**, it does not predispose patients to bronchogenic carcinoma. * **Stomach/Ovarian Carcinoma:** There is no established clinical or genetic association between BHD syndrome and an increased risk of gastric or ovarian malignancies. **High-Yield Clinical Pearls for NEET-PG:** * **Cutaneous Triad:** Fibrofolliculomas (most common), trichodiscomas, and acrochordons (skin tags). * **Pulmonary:** Multiple thin-walled lung cysts (usually basal) leading to recurrent spontaneous pneumothorax. * **Genetics:** Mutation in the **FLCN gene** on chromosome **17p11.2**. * **Differential Diagnosis:** Must be distinguished from **Von Hippel-Lindau (VHL)**, which is associated with Clear Cell RCC, and **Hereditary Papillary RCC (MET mutation)** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959.

Question 333: All of the following decrease in Nephrotic syndrome except-

A. Fibrinogen (Correct Answer)
B. Thyroxin
C. Transferrin
D. Albumin

Explanation: In **Nephrotic Syndrome**, the fundamental pathology is increased glomerular permeability, leading to massive proteinuria (typically >3.5g/day). This results in the loss of various plasma proteins, but the liver’s compensatory response creates a unique biochemical profile [1]. ### Why Fibrinogen is the Correct Answer While the kidney loses proteins, the liver attempts to compensate for the low oncotic pressure by increasing the synthesis of proteins and lipids. **Fibrinogen** is a high-molecular-weight protein that is too large to be easily filtered through the damaged basement membrane. Consequently, its hepatic synthesis increases significantly while its excretion remains low, leading to **increased plasma levels**. This contributes to the hypercoagulable state (thrombotic tendency) characteristic of Nephrotic Syndrome. ### Why Other Options are Incorrect * **Albumin (D):** This is the most abundant protein lost in the urine due to its relatively small size and loss of the glomerular polyanionic charge (especially in Minimal Change Disease) [1]. Hypoalbuminemia is a hallmark of the syndrome. * **Transferrin (C):** This iron-transporting protein is lost in the urine, which can lead to microcytic hypochromic anemia resistant to iron therapy. * **Thyroxin (B):** Thyroid-binding globulin (TBG) is lost in the urine. This leads to a decrease in total T4 levels, though patients usually remain clinically euthyroid because free T4 levels are often maintained. ### NEET-PG High-Yield Pearls * **Hyperlipidemia:** Low oncotic pressure triggers hepatic synthesis of lipoproteins (VLDL, LDL), leading to "fatty casts" and "maltese crosses" in urine. * **Hypercoagulability:** Caused by increased Fibrinogen and loss of **Antithrombin III**, Protein C, and Protein S in urine. Renal vein thrombosis is a classic complication. * **Infections:** Patients are prone to infections (especially *S. pneumoniae*) due to the loss of **IgG** and Complement factors (Factor B). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 905-907.

Question 334: Michaelis-Guttmann bodies are characteristic findings in which of the following conditions?

A. Analgesic nephropathy
B. Hampton's line
C. Malacoplakia (Correct Answer)
D. Erythroplasia

Explanation: **Explanation:** **Malacoplakia** is a chronic inflammatory condition most commonly affecting the urinary bladder, though it can occur in the kidneys. It is characterized by the presence of soft, yellowish, slightly raised mucosal plaques. 1. **Why Malacoplakia is Correct:** The hallmark histological feature of Malacoplakia is the **Michaelis-Guttmann (MG) body**. These are laminated, mineralized (calcified) concretions found within the cytoplasm of large, foamy macrophages known as **von Hansemann cells**. MG bodies form due to the incomplete digestion of bacteria (usually *E. coli*) by lysosomes, leading to the deposition of iron and calcium. They stain positive with **PAS, Von Kossa (for calcium), and Perls' Prussian Blue (for iron).** 2. **Analysis of Incorrect Options:** * **Analgesic Nephropathy:** Characterized by chronic tubulointerstitial nephritis and **renal papillary necrosis** due to long-term intake of NSAIDs or phenacetin. * **Hampton’s Line:** This is a **radiological sign** (not a pathological body) seen on a barium meal study, indicating a benign gastric ulcer. * **Erythroplasia (of Queyrat):** This is a clinical term for **Carcinoma in situ** of the glans penis, appearing as a velvety red plaque. **High-Yield Clinical Pearls for NEET-PG:** * **Organism:** Most commonly associated with ***E. coli*** infection. * **Pathogenesis:** Defect in phagocytic/bactericidal function of macrophages. * **Staining:** Michaelis-Guttmann bodies have a **"targetoid" or "owl's eye"** appearance and are best highlighted by the **Von Kossa stain**. * **Classic Triad:** Chronic UTI + Von Hansemann cells + Michaelis-Guttmann bodies = Malacoplakia.

Question 335: Which of the following is FALSE regarding Hemolytic Uremic Syndrome (HUS)?

A. Thrombocytopenia is present (Correct Answer)
B. Schistocytes are seen in peripheral blood
C. It can be caused by E. coli
D. Renal failure is not seen

Explanation: **Explanation:** The question asks for the **FALSE** statement regarding Hemolytic Uremic Syndrome (HUS). However, there appears to be a discrepancy in the provided key: **Option D is the false statement**, as renal failure is a hallmark of the condition. **1. Why Option D is the correct answer (The False Statement):** Hemolytic Uremic Syndrome is defined by a classic triad: **Microangiopathic Hemolytic Anemia (MAHA), Thrombocytopenia, and Acute Kidney Injury (Renal Failure).** [2] Renal failure is not only "seen" but is the primary cause of morbidity, often presenting with oliguria, hematuria, and elevated creatinine. Therefore, stating that renal failure is not seen is incorrect. **2. Analysis of other options:** * **Option A (Thrombocytopenia):** This is **True**. Platelets are consumed during the formation of microthrombi within small blood vessels (consumptive thrombocytopenia). [3] * **Option B (Schistocytes):** This is **True**. As RBCs pass through fibrin-rich microthrombi in damaged capillaries, they are mechanically shredded, resulting in fragmented cells called schistocytes (helmet cells) on peripheral smear. [2] * **Option C (E. coli):** This is **True**. Typical HUS (D+ HUS) is most commonly caused by **Shiga-like toxin** producing *E. coli* (serotype **O157:H7**), usually following contaminated food intake. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Endothelial injury leads to platelet activation and microvascular thrombosis. [1] * **Atypical HUS:** Caused by dysregulation of the **alternative complement pathway** (e.g., Factor H deficiency). [1] * **Biopsy Findings:** Characterized by **Thrombotic Microangiopathy (TMA)**; glomeruli show thickened capillary walls and "subendothelial fluff." [2] * **Treatment:** Supportive care for typical HUS; **Eculizumab** (C5 inhibitor) for atypical HUS. Avoid antibiotics in Shiga-toxin HUS as they may increase toxin release. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 946-947. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 540-541. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668.

Question 336: All are causes of immune complex associated membranoproliferative glomerulonephritis in the adult population, EXCEPT?

A. Infective endocarditis
B. Systemic lupus erythematosus (SLE)
C. Monoclonal gammopathy of undetermined significance
D. Isoniazid (INH) (Correct Answer)

Explanation: Explanation: Membranoproliferative Glomerulonephritis (MPGN) is a pattern of glomerular injury characterized by basement membrane thickening and mesangial hypercellularity [1]. The current classification divides MPGN into **Immune-complex mediated** (driven by chronic antigenemia) and **Complement-mediated** (driven by alternative pathway dysregulation) [4]. **Why Isoniazid (INH) is the correct answer:** Isoniazid is a common cause of **Drug-induced Lupus Erythematosus (DILE)**. However, unlike idiopathic SLE, DILE rarely involves the kidneys. When drug-induced renal injury does occur (e.g., with Hydralazine), it typically manifests as a **Pauci-immune ANCA-associated vasculitis** or Crescentic GN, not an immune-complex MPGN pattern. Therefore, INH is not a recognized cause of MPGN. **Analysis of Incorrect Options:** * **Infective Endocarditis:** Chronic infections are classic triggers for immune-complex MPGN. Persistent bacteremia leads to the formation of circulating immune complexes that deposit in the subendothelial space [3]. * **Systemic Lupus Erythematosus (SLE):** Lupus Nephritis Class IV (Diffuse Proliferative GN) frequently presents with an MPGN pattern on light microscopy due to extensive subendothelial "wire-loop" deposits [2]. * **Monoclonal Gammopathy (MGUS):** Paraproteinemias (including MGUS and Multiple Myeloma) can lead to "Monoclonal Gammopathy of Renal Significance" (MGRS), which frequently presents as an immune-complex MPGN pattern [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Look for the "Tram-track" appearance (double contour) of the GBM due to mesangial interposition [1]. * **Hepatitis C:** The most common viral cause of immune-complex MPGN (often associated with Cryoglobulinemia) [3]. * **C3 Glomerulopathy:** If the MPGN pattern shows *only* C3 deposition (no immunoglobulins), suspect Dense Deposit Disease or C3 Glomerulonephritis [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 911. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535.

Question 337: Which of the following renal cell carcinomas (RCC) does not exhibit papillary architecture histologically?

A. Xp11 translocation carcinoma
B. Bellini duct carcinoma
C. Succinate dehydrogenase-deficient RCC (Correct Answer)
D. Papillary carcinoma

Explanation: ### Explanation The correct answer is **Succinate dehydrogenase (SDH)-deficient RCC**. **1. Why SDH-deficient RCC is correct:** SDH-deficient RCC is a rare, distinct subtype of renal cell carcinoma characterized by the loss of the SDHB subunit. Histologically, it is defined by a **solid or nested growth pattern** of cells with eosinophilic cytoplasm containing characteristic **intracytoplasmic vacuoles or inclusions**. Unlike the other options, it classically lacks a papillary architecture. **2. Analysis of Incorrect Options:** * **Xp11 translocation carcinoma:** This tumor typically affects younger patients and characteristically shows a **mixed papillary and nested architecture** with clear cells and voluminous cytoplasm [1]. * **Bellini duct carcinoma (Collecting Duct Carcinoma):** This is a highly aggressive tumor arising from the medulla. It characteristically exhibits a **tubulopapillary architecture** associated with a prominent desmoplastic stromal reaction. * **Papillary carcinoma:** As the name implies, this is the prototype of papillary architecture in the kidney [1]. It is divided into Type 1 (basophilic) and Type 2 (eosinophilic) and is often associated with trisomy 7 and 17 [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **SDH-deficient RCC:** Look for the "vacuolated cytoplasm" and "loss of SDHB staining" on IHC. It is associated with germline mutations in SDH genes (Paraganglioma-pheochromocytoma syndrome). * **Xp11 Translocation RCC:** Associated with *TFE3* gene fusions; it is the most common RCC in children [1]. * **Chromophobe RCC:** Often confused with SDH-deficient RCC due to eosinophilic cytoplasm, but it shows "koilocytic" perinuclear halos and "hale’s colloidal iron" positivity [1]. * **Most common RCC overall:** Clear cell RCC (associated with VHL gene mutation on Chromosome 3p) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 957-961.

Question 338: Which of the following can cause nephrocalcinosis?

A. Hyperparathyroidism
B. Tuberculosis of the kidney
C. Hypercalcemia
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Nephrocalcinosis** refers to the generalized deposition of calcium salts within the renal parenchyma (interstitium and tubules), leading to impaired renal function [1], [2]. It is distinct from nephrolithiasis (stones in the collecting system). **Why "All of the Above" is Correct:** The pathogenesis of nephrocalcinosis is broadly divided into two mechanisms: 1. **Metastatic Calcification (Options A & C):** This occurs in normal tissues due to high serum calcium levels (**Hypercalcemia**). **Hyperparathyroidism** is the most common cause of this, as excess PTH increases bone resorption and intestinal calcium absorption [2], [3]. Other causes include Vitamin D toxicity, Sarcoidosis, and Milk-alkali syndrome [2]. 2. **Dystrophic Calcification (Option B):** This occurs in necrotic or damaged tissues despite normal serum calcium levels. **Renal Tuberculosis** causes extensive caseous necrosis; as the tissue heals or remains chronic, calcium deposits in these necrotic areas (often visible on X-ray as "putty kidney"). **Clinical Pearls for NEET-PG:** * **Medullary Nephrocalcinosis:** The most common form. High-yield causes include **Distal Renal Tubular Acidosis (Type 1 RTA)** and **Medullary Sponge Kidney**. * **Cortical Nephrocalcinosis:** Much rarer; typically follows **Acute Tubular Necrosis (ATN)** or **Cortical Necrosis** (e.g., post-abruptio placentae). * **Imaging:** On ultrasound, it appears as hyperechoic renal pyramids. On X-ray, it may present as diffuse fine stippling of the renal parenchyma [1]. * **Consequence:** If untreated, it leads to chronic interstitial nephritis and progressive renal failure [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 76-77. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 539-540. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 667-668.

Question 339: Basket weave appearance on electron microscopy is classically seen in which of the following conditions?

A. Rapidly progressive glomerulonephritis (RPGN)
B. Alport's syndrome (Correct Answer)
C. Henoch-Schonlein purpura (HSP)
D. IgA nephropathy

Explanation: **Explanation:** **Alport’s Syndrome (Correct Answer):** The "basket-weave" appearance is the pathognomonic electron microscopic (EM) finding for Alport’s syndrome. This condition is caused by mutations in the genes encoding the **α-3, α-4, or α-5 chains of Type IV collagen** (most commonly X-linked) [1]. These mutations lead to a defective glomerular basement membrane (GBM). On EM, the GBM shows irregular thickening and thinning with **longitudinal splitting and splintering of the lamina densa**, creating the characteristic "basket-weave" pattern. **Incorrect Options:** * **RPGN:** Characterized by the presence of **crescents** (proliferation of parietal epithelial cells and monocytes) in Bowman’s space on light microscopy. EM findings vary depending on the underlying cause (e.g., subepithelial humps or linear IgG). * **Henoch-Schönlein Purpura (HSP) & IgA Nephropathy:** These are part of the same disease spectrum. The hallmark finding is **mesangial IgA deposits** on immunofluorescence and mesangial electron-dense deposits on EM. They do not involve the structural splitting of the GBM. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad of Alport’s:** 1. Hereditary nephritis (hematuria/ESRD), 2. Sensorineural deafness, 3. Ocular defects (e.g., Anterior Lenticonus) [1]. * **Thin Basement Membrane Disease (Benign Familial Hematuria):** Also involves Type IV collagen mutations but shows only diffuse thinning of the GBM without the splitting/basket-weaving seen in Alport’s [1]. * **Inheritance:** Most common is **X-linked Dominant** (COL4A5 mutation) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930.

Question 340: A 46-year-old woman has had worsening malaise for the past 36 hours. Her urine output is markedly diminished, and it has a cloudy brown appearance. On examination, she has periorbital edema. Laboratory findings include serum creatinine of 2.8 mg/dL and urea nitrogen of 30 mg/dL. A renal biopsy is performed and on microscopic examination shows focal necrosis in glomeruli with glomerular basement membrane breaks and crescent formation. No immune deposits are identified with immunofluorescence. Which of the following autoantibodies is most likely detectable in her serum?

A. Anti-DNA topoisomerase antibody
B. Anti-glomerular basement membrane antibody
C. Anti-neutrophil cytoplasmic autoantibody (Correct Answer)
D. Antinuclear antibody

Explanation: The clinical presentation of malaise, periorbital edema, oliguria, and elevated creatinine (2.8 mg/dL) indicates **Rapidly Progressive Glomerulonephritis (RPGN)**. The hallmark histological finding of **crescents** (composed of parietal epithelial cells and macrophages) and **glomerular basement membrane (GBM) breaks** confirms this diagnosis [3]. **Why Option C is Correct:** RPGN is classified into three types based on Immunofluorescence (IF) patterns: 1. **Type I (Anti-GBM):** Linear IgG deposits. 2. **Type II (Immune Complex):** Granular deposits (e.g., SLE, PSGN). 3. **Type III (Pauci-immune):** **No immune deposits** on IF [1]. The biopsy shows "no immune deposits," identifying this as **Pauci-immune RPGN**. This condition is strongly associated with **Anti-Neutrophil Cytoplasmic Autoantibodies (ANCA)** [1]. It is typically seen in systemic vasculitides like Granulomatosis with Polyangiitis (c-ANCA/PR3) or Microscopic Polyangiitis (p-ANCA/MPO). **Why Incorrect Options are Wrong:** * **Option A (Anti-DNA topoisomerase):** Also known as Anti-Scl-70, it is a marker for Diffuse Cutaneous Systemic Sclerosis, which causes renal crisis via vascular thickening, not crescentic GN. * **Option B (Anti-GBM antibody):** This would show **linear** IF staining (Goodpasture Syndrome). The question explicitly states no immune deposits were found. * **Option D (Antinuclear antibody):** ANA is the screening test for SLE. Lupus nephritis (Type II RPGN) would show a **granular** "full-house" IF pattern [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Crescents** are formed when fibrin and inflammatory cells leak into Bowman’s space through GBM breaks [3]. * **Pauci-immune RPGN** is the most common cause of RPGN in elderly patients. * **Rule of thumb:** If the question says "Crescents" + "Negative IF," the answer is always **ANCA** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 230-232. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 528-529.

Practice by Chapter

Congenital Anomalies of the Kidney

Practice Questions

Glomerular Diseases

Practice Questions

Tubular and Interstitial Diseases

Practice Questions

Vascular Diseases of the Kidney

Practice Questions

Cystic Diseases of the Kidney

Practice Questions

Urinary Tract Obstruction and Stones

Practice Questions

Renal Tumors

Practice Questions

Kidney in Systemic Diseases

Practice Questions

Renal Transplantation Pathology

Practice Questions

Urinary Tract Infections

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free