Renal Pathology — MCQs

A 28-year-old woman has noticed increasing lower limb swelling and shortness of breath, with a 2-year history of facial rash, hair loss, arthralgias, and thrombocytopenia. On examination, her blood pressure is 150/90 mmHg, pulse 80/min, with a maculopapular rash on her face, JVP of 4 cm, normal heart sounds, clear lungs, and pedal and periorbital edema. Her creatinine is very high, and a urinalysis reveals many RBCs and RBC casts. For this patient with glomerulonephritis, select the most likely diagnosis on renal biopsy.

Q619

Which of these is the characteristic feature of membranoproliferative glomerulonephritis?

Q620

All of the following are true about xanthogranulomatous pyelonephritis except which of the following?

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 611: IgA nephropathy is classified as which type of glomerulonephritis?

A. Membranous glomerulonephritis
B. Mesangioproliferative glomerulonephritis (Correct Answer)
C. Focal glomerulonephritis
D. Crescentic glomerulonephritis

Explanation: ***Mesangioproliferative glomerulonephritis*** - **IgA nephropathy** classically presents with **mesangial proliferation** and **IgA deposits** in the mesangium, characteristic of this type [1][2]. - The immune complexes primarily accumulate in the mesangium, triggering the proliferation of mesangial cells [1]. *Membranous glomerulonephritis* - Characterized by **thickening of the glomerular basement membrane** due to subepithelial immune complex deposition. - It does not primarily involve mesangial proliferation and is usually associated with **IgG deposits**, not IgA. *Focal glomerulonephritis* - This term describes involvement of **some glomeruli** but not all, or only **parts of individual glomeruli** [2]. - While IgA nephropathy can be focal in presentation, it specifically refers to the **pattern of injury** (mesangial proliferation) rather than the distribution [2]. *Crescentic glomerulonephritis* - Identified by the presence of **crescents** (extracapillary cellular proliferation) in over 50% of glomeruli, indicating severe glomerular injury. - Although IgA nephropathy can rarely progress to crescentic forms, it is not the typical or primary classification [1][2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 535-536. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 928-929.

Question 612: The most common histological variant of renal cell carcinoma is

A. Clear cell type (Correct Answer)
B. Chromophobe carcinoma
C. Papillary carcinoma
D. Collecting duct carcinoma

Explanation: ***Clear cell type*** - The **clear cell variant** is characterized by the presence of large cells with abundant clear cytoplasm and is the most common form of renal cell carcinoma (RCC), accounting for about 70-80% of cases [3]. - It is associated with **Von Hippel-Lindau disease** and often presents in advanced stages with symptoms like hematuria, flank pain, and a palpable mass. *Chromophobe type* - This type accounts for only about **5-10%** of renal cell carcinomas [1] and is characterized by cells with **eosinophilic cytoplasm** and prominent cell membranes [1]. - Typically has a better prognosis compared to the clear cell type, and the distinct histological features differentiate it from the most common variant [1]. *Tubular type* - The tubular type is not a well-defined subtype of renal cell carcinoma and is generally considered under the umbrella of **non-clear cell RCC** variants. - This variant does not commonly appear in most classifications of renal cell carcinoma and is not prominent in studies, unlike the clear cell type. *Papillary type* - The papillary variant represents about **10-15%** of renal cell carcinomas [2] and is characterized by finger-like projections or papillae. - It has distinct genetic alterations (like trisomy 7 and 17) and presents differently from clear cell RCC, making it less common overall [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 959. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 959-961.

Question 613: Which of the following statements about fibronectin glomerulopathy is false?

A. Autosomal recessive inheritance (Correct Answer)
B. Ultrastructural feature is presence of large electron-dense mesangial or subendothelial deposits
C. Glomerular enlargement and PAS+ trichrome mesangial deposit
D. Glomeruli do not consistently stain for Ig and complement

Explanation: **Autosomal recessive inheritance** - **Fibronectin glomerulopathy** is predominantly inherited in an **autosomal dominant** pattern, not autosomal recessive. - This condition is caused by mutations in the **FN1 gene**, which codes for fibronectin, a large glycoprotein involved in tissue organization. *Glomerulus do not consistently stain for Ig and complement* - This statement is **true** for fibronectin glomerulopathy; immunofluorescence typically shows a lack of consistent staining for immunoglobulins and complements. - This absence of immune complex deposition helps differentiate it from immune-mediated glomerular diseases. *Ultrastructural feature is presence of large electron mesangial or subendothelial deposit* - This statement accurately describes a key ultrastructural finding in fibronectin glomerulopathy. - Electron microscopy reveals characteristic **electron-dense deposits** predominantly in the mesangium and subendothelial space. *Glomerular enlargement and PAS+ trichrome mesangial deposit* - This statement also correctly describes features of fibronectin glomerulopathy. - Light microscopy often shows **glomerular enlargement** and the presence of **Periodic Acid-Schiff (PAS)-positive and trichrome-positive mesangial deposits**.

Question 614: Renal papillary necrosis is almost always associated with one of the following conditions:

A. Diabetes-mellitus
B. Analgesic-nephropathy (Correct Answer)
C. Chronic pyelonephritis
D. Post streptococcal GN

Explanation: ***Analgesic-nephropathy*** - Chronic use of certain analgesics (especially **phenacetin**, aspirin, and NSAIDs) can lead to **ischemia** and damage to the renal papillae, causing **papillary necrosis**. - This condition is considered the **classic** cause of renal papillary necrosis and is the most frequently emphasized in medical education. - Analgesic nephropathy shows a very **strong and direct association** with papillary necrosis as a hallmark feature. *Diabetes-mellitus* - **Diabetes mellitus** is actually one of the **most common causes** of renal papillary necrosis in clinical practice, particularly when complicated by **infection** or **ischemia** [1]. - While clinically very common, it causes papillary necrosis through multiple mechanisms and is often associated with coexisting factors like **pyelonephritis** [1], [2] or NSAID use. - In the context of "almost always associated," analgesic nephropathy has a more direct and consistent association. *Chronic pyelonephritis* - **Chronic pyelonephritis** involves recurrent bacterial infections of the kidney parenchyma and can lead to scarring and kidney damage. - While it is indeed a recognized cause of **papillary necrosis** (part of the POSTCARDS mnemonic), it is not as consistently associated as analgesic nephropathy [2]. *Post streptococcal GN* - **Post-streptococcal glomerulonephritis (PSGN)** is an immune-mediated inflammatory kidney disease that typically follows a **streptococcal infection**. - It primarily affects the **glomeruli** and does **not** cause necrosis of the renal papillae, making this option incorrect. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 543-544. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-940.

Question 615: Crescents in glomerular diseases are derived from which of the following components?

A. Epithelial cells + fibrin + macrophages (Correct Answer)
B. Mesangium + fibrin + macrophages
C. Tubule + mesangium + fibrin
D. Mesangium + fibrin

Explanation: ***Epithelial cells + fibrin + macrophage*** - Crescents are formed due to the accumulation of **epithelial cells**, **fibrin**, and **macrophages** in the urinary space [1], commonly seen in rapid progressive glomerulonephritis. - This composition leads to crescent formation, which is associated with **severe glomerular injury** and can indicate a poor prognosis. *Mesangium + fibrin* - Mesangial cells primarily contribute to the structural integrity of the glomeruli but are not involved in crescent formation, which requires epithelial cells. - The absence of **macrophages** in this composition makes it **incomplete** for defining crescents. *Mesangium + fibrin + macrophage* - While macrophages are involved in the inflammatory process, crescents specifically arise from **epithelial cells**, not mesangial cells. - This option fails to highlight the critical role of **epithelial cells** needed for crescent formation in glomeruli. *Tubule + mesangium + fibrin* - Crescents are not formed from tubules or mesangial components but rather from the **proliferation of epithelial cells**. - This oes not accurately represent the **cellular components** necessary for crescent formation, leading to an incorrect conclusion. **References:** [1] 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.

Question 616: HIV-specific renal nephropathy is characterized by which type of glomerular disease?

A. FSGS (Correct Answer)
B. Membranous glomerulonephritis
C. Membranoproliferative glomerulonephritis
D. Mesangioproliferative GN

Explanation: ***FSGS*** - **Focal segmental glomerulosclerosis (FSGS)** is the most common and classic renal pathology associated with **HIV-associated nephropathy (HIVAN)** [2]. - HIVAN is characterized by **collapsing variant FSGS**, which involves **podocyte proliferation** and **tubulointerstitial disease** [1], [3]. - This is the **pathognomonic finding** in HIV-specific nephropathy [3]. *Mesangioproliferative GN* - While mesangial proliferation can be seen in some HIV-infected patients, it is not the **defining or most common feature** of **HIV-specific nephropathy** [1]. - This pattern is more broadly associated with various immune-complex mediated glomerulonephritides. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is characterized by **subepithelial immune complex deposition** and **thickening of the glomerular basement membrane** [1]. - It is not specifically associated with HIV infection but rather with conditions like hepatitis B, systemic lupus erythematosus, and certain medications [1]. *Membranoproliferative glomerulonephritis* - **Membranoproliferative glomerulonephritis (MPGN)** is characterized by **mesangial and endocapillary proliferation** and **glomerular basement membrane thickening** with a "tram-track" appearance [2]. - While sometimes seen in HIV patients, especially those co-infected with **hepatitis C**, it is not the primary or defining lesion of **HIV-associated nephropathy** [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 531-532. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 924-925.

Question 617: Which receptor do antibodies target in primary membranous nephropathy?

A. Phospholipase A2 receptor (Correct Answer)
B. Phospholipase A3 receptor
C. Phospholipase A4 receptor
D. Phospholipase A1 receptor

Explanation: ***Phospholipase A2 receptor*** - Primary membranous nephropathy is characterized by the presence of antibodies against **Phospholipase A2 receptor**, which plays a crucial role in glomerular injury [1]. - These antibodies can be detected in the serum of many patients and are associated with **nephrotic syndrome** in this condition. *Phospholipase A1 receptor* - This receptor is not associated with primary membranous nephropathy and does not play a significant role in renal pathology. - There is a lack of evidence linking antibodies against **Phospholipase A1 receptor** to nephrotic syndrome or kidney damage. *Phospholipase A4 receptor* - There are no known associations between antibodies against **Phospholipase A4 receptor** and primary membranous nephropathy. - This receptor does not typically contribute to the pathogenic mechanisms seen in **membranous nephropathy**. *Phospholipase A3 receptor* - This receptor is not implicated in primary membranous nephropathy and lacks relevant clinical significance regarding antibody production. - Research has not demonstrated involvement of **Phospholipase A3 receptor** in nephrotic syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 911-913.

Question 618: A 28-year-old woman has noticed increasing lower limb swelling and shortness of breath, with a 2-year history of facial rash, hair loss, arthralgias, and thrombocytopenia. On examination, her blood pressure is 150/90 mmHg, pulse 80/min, with a maculopapular rash on her face, JVP of 4 cm, normal heart sounds, clear lungs, and pedal and periorbital edema. Her creatinine is very high, and a urinalysis reveals many RBCs and RBC casts. For this patient with glomerulonephritis, select the most likely diagnosis on renal biopsy.

A. diffuse proliferative GN (Correct Answer)
B. crescentic glomerulonephritis
C. focal segmental glomerulosclerosis
D. membranoproliferative glomerulonephritis

Explanation: ***diffuse proliferative GN*** - This patient's constellation of symptoms, including **facial rash, hair loss, arthralgias, thrombocytopenia**, and **renal involvement** (elevated creatinine, RBCs, and RBC casts), strongly points to **systemic lupus erythematosus (SLE)** [2], [4]. - **Diffuse proliferative glomerulonephritis (DPGN)** is the **most common and severe form of lupus nephritis** (WHO Class IV), characterized by widespread involvement of glomeruli with significant proliferation and inflammation [1]. - On renal biopsy, DPGN shows **subendothelial immune complex deposits** ("wire loop" lesions) and **proliferation of mesangial and endothelial cells** [1]. *crescentic glomerulonephritis* - While crescentic glomerulonephritis can cause a rapid decline in renal function and is associated with some autoimmune conditions, it is a **histological pattern** seen in various rapidly progressive glomerular diseases, not a specific underlying disease entity itself [3]. - The clinical picture here strongly suggests SLE, and while crescent formation can occur in severe lupus nephritis, **DPGN is the more specific and prevalent form** of nephritis for this presentation [1]. *focal segmental glomerulosclerosis* - **Focal segmental glomerulosclerosis (FSGS)** is a common cause of **nephrotic syndrome** and can lead to renal failure, but it is **not typically associated with the systemic symptoms** (rash, arthralgias, hair loss, thrombocytopenia) seen in this patient, which are characteristic of SLE. - While FSGS can rarely occur in lupus nephritis, it is less common than DPGN and lacks the widespread immune-mediated systemic features. *membranoproliferative glomerulonephritis* - **Membranoproliferative glomerulonephritis (MPGN)** can present with nephritic or nephrotic syndrome and may be associated with some autoimmune conditions like **cryoglobulinemia** or chronic infections (Hepatitis C). - However, the overall clinical context of **systemic inflammation, multi-organ involvement** (rash, arthralgias, thrombocytopenia), and the characteristic findings strongly favor **lupus nephritis**, for which **DPGN is the most characteristic finding** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 232. [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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 230.

Question 619: Which of these is the characteristic feature of membranoproliferative glomerulonephritis?

A. Foamy cells
B. Splitting of glomerular basement membrane (Correct Answer)
C. All of the options
D. Subepithelial deposits

Explanation: ***Splitting of glomerular basement membrane*** - Membranoproliferative glomerulonephritis is characterized by the **splitting of the glomerular basement membrane**, visible on electron microscopy [1]. - This finding is associated with **immune complex deposition** and is a hallmark of the disease process [1]. *Sub epithelial deposits* - Sub epithelial deposits are more characteristic of conditions like **post-streptococcal glomerulonephritis** or **membranous nephropathy** rather than membranoproliferative glomerulonephritis. - In membranoproliferative glomerulonephritis, deposits are typically **subendothelial or intramembranous** [1]. *Foamy cells* - Foamy cells are typically seen in conditions like **lipid nephrosis** or **hyperlipidemia**, not specifically in membranoproliferative glomerulonephritis. - They are a result of **lipid accumulation** within macrophages, rather than reflecting a characteristic feature of this condition. *All* - While some features may be present in varying glomerular conditions, **not all options are characteristic of membranoproliferative glomerulonephritis**. - The key feature of splitting of the glomerular basement membrane is solely associated with this specific condition [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 907-908, 911, 925-926.

Question 620: All of the following are true about xanthogranulomatous pyelonephritis except which of the following?

A. It is a form of chronic pyelonephritis
B. Focal form is common in children
C. Seen only in infancy (Correct Answer)
D. Proteus mirabilis is the most common organism

Explanation: ***Seen only in infancy*** - Xanthogranulomatous pyelonephritis can occur in **adults** as well, not just in infancy, making this statement false [1]. - It is often associated with obstructive uropathy and chronic infection across various age groups. *Proteus is most common organism* - While **Proteus** species are commonly associated [1], the most frequent organism in xanthogranulomatous pyelonephritis can also include **E. coli**. - It reflects a polymicrobial infection rather than being limited to a single organism. *It is a form of chronic pyelonephritis* - Xanthogranulomatous pyelonephritis is indeed a variant of **chronic pyelonephritis**, characterized by extensive **granulomatous inflammation** [1]. - This chronic condition arises typically due to obstructive pathology leading to chronic infection. *Focal form is common in children* - The **focal form** is less common in children and is more frequently observed in **adults** with underlying conditions. - Children tend to present with a more diffuse form of **xanthogranulomatous pyelonephritis** when it occurs. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940.

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