Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 601: Membranous glomerulonephritis with reduced complement levels is seen in?

A. Hepatitis B infection
B. Plasmodium malariae infection
C. Syphilis infection
D. Systemic Lupus Erythematosus (SLE) (Correct Answer)

Explanation: ***Systemic Lupus Erythematosus (SLE)*** - SLE is the classic cause of **membranous glomerulonephritis with reduced complement levels** (low C3 and C4) [1] - **Class V lupus nephritis** (membranous pattern) is characterized by widespread immune complex deposition leading to **complement consumption** [1] - The combination of membranous GN + hypocomplementemia is highly suggestive of **secondary membranous nephropathy** due to SLE [1] *Hepatitis B infection* - Hepatitis B is a well-recognized cause of **membranous glomerulonephritis** [2] - However, it typically presents with **NORMAL complement levels**, not reduced complements - This is a key differentiating feature from lupus-associated membranous nephropathy *Plasmodium malariae infection* - Malaria-associated nephropathy classically causes **membranoproliferative GN** (quartan malarial nephropathy), not membranous GN - While complement activation occurs, **membranous pattern with reduced complements** is not characteristic - Complement levels are usually normal or elevated rather than consistently reduced *Syphilis infection* - Syphilis can rarely cause **membranous glomerulonephritis** in secondary or congenital syphilis - Unlike SLE, syphilitic nephropathy does NOT characteristically cause **significant reduction in complement levels** - The absence of hypocomplementemia helps distinguish it from lupus nephritis **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 230. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-911.

Question 602: Alport syndrome is noted because of a defect in what type of collagen?

A. Collagen type I
B. Collagen type III
C. Collagen type VII
D. Collagen type IV (Correct Answer)

Explanation: ***Collagen type IV*** - Alport syndrome is primarily caused by mutations in genes encoding the **alpha chains of type IV collagen**, specifically COL4A3, COL4A4, and COL4A5 genes [1]. - This **type IV collagen** is a major component of the **glomerular basement membrane (GBM)** in the kidneys, leading to its characteristic pathology [1]. *Collagen type I* - Defects in **collagen type I** are primarily associated with **osteogenesis imperfecta**, a condition characterized by brittle bones. - It is the most abundant collagen in the body, found in **skin, tendons, and bone**, but not the primary collagen affected in Alport syndrome. *Collagen type III* - Mutations in **collagen type III** are linked to **Ehlers-Danlos syndrome type IV**, also known as the vascular type, which causes fragile blood vessels and organs [2]. - This type of collagen is prevalent in **hollow organs** and **blood vessels**, and its defect does not explain Alport syndrome's renal, ocular, and auditory features. *Collagen type VII* - Defects in **collagen type VII** are responsible for **dystrophic epidermolysis bullosa**, a severe blistering skin disorder. - This collagen forms **anchoring fibrils** that connect the epidermis to the dermis, and its involvement is distinct from Alport syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 154-155.

Question 603: Nephrocalcinosis in a systemic granulomatous disease is due to:

A. Dystrophic calcification
B. Mutation in calcium sensing receptors
C. Increased reabsorption of calcium
D. Overproduction of 1,25 dihydroxy vitamin D (Correct Answer)

Explanation: ***Overproduction of 1,25 dihydroxy vitamin D*** - In systemic granulomatous diseases, such as **sarcoidosis**, granulomas can produce excess 1,25 dihydroxy vitamin D, leading to **hypercalcemia** and renal deposition of calcium [1]. - This overproduction results in **nephrocalcinosis** due to elevated serum calcium levels, fostering calcium deposition in renal tissues. *Mutation in calcium sensing receptors* - Mutations in calcium-sensing receptors lead to **primary hyperparathyroidism**, not directly linked to systemic granulomatous diseases. - These mutations typically cause **elevated parathyroid hormone (PTH)** rather than affecting vitamin D metabolism. *Increased reabsorption of calcium* - Increased calcium reabsorption typically occurs in renal tubular disorders, rather than as a direct result of granulomatous diseases. - It fails to explain the mechanism of **nephrocalcinosis** related to vitamin D levels in systemic conditions. *Dystrophic calcification* - Dystrophic calcification occurs in damaged tissues regardless of serum calcium levels and is **not specific** to granulomatous diseases. - This process does not account for the systemic effects of **increased 1,25 dihydroxy vitamin D** in causing nephrocalcinosis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 667-668.

Question 604: In reflux nephropathy, which type of glomerular lesion is typically observed?

A. Focal segmental glomerulosclerosis. (Correct Answer)
B. Membranous glomerulonephritis.
C. Membranoproliferative glomerulonephritis.
D. Minimal change disease.

Explanation: ***Focal segmental glomerulosclerosis*** - **Focal segmental glomerulosclerosis (FSGS)** is the most common glomerular lesion found in patients with **reflux nephropathy** progressing to end-stage renal disease. - This lesion is thought to develop as a result of **glomerular hyperfiltration** and hypertrophy in remaining healthy nephrons, leading to adaptive changes that ultimately cause podocyte injury and sclerosis. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is characterized by subepithelial immune complex deposits and is most commonly associated with **autoimmune diseases** or certain infections, not reflux nephropathy. - It typically presents with **nephrotic syndrome** but does not have a direct causal link to chronic vesicoureteral reflux. *Membranoproliferative glomerulonephritis* - **Membranoproliferative glomerulonephritis (MPGN)** is characterized by mesangial and endothelial cell proliferation and thickening of the glomerular basement membrane. - It is often associated with **chronic infections** (e.g., hepatitis C), autoimmune disorders, or complement abnormalities, rather than anatomical urinary tract abnormalities. *Minimal change disease* - **Minimal change disease** is characterized by diffuse effacement of podocyte foot processes on electron microscopy, with minimal changes visible on light microscopy. - It is the most common cause of **nephrotic syndrome in children** and is typically idiopathic, unrelated to structural kidney defects like reflux nephropathy.

Question 605: All are true about renal cell carcinoma, except which of the following?

A. Invades Renal Vein
B. Hematuria may occur
C. More common in females (Correct Answer)
D. Arises from proximal convoluted tubule

Explanation: ***More common in females*** - Renal cell carcinoma is actually **more prevalent in males**, with a ratio of approximately **2:1**. - Its association with risk factors such as **tobacco use** and obesity is also more significant in men. *Invades Renal Vein* - Renal cell carcinoma is known for its **capability to invade** the renal vein and other vascular structures [1] [2]. - This invasion can lead to **complications** such as tumor thrombosis and spreads to distant organs [1]. *Arises from proximal convoluted tubule* - This type of carcinoma arises from the **epithelium of the proximal convoluted tubule**, influencing the tumor's characteristics [1]. - This origin is key for understanding its **pathology** and associated conditions. *Hematuria may occur* - Hematuria, or blood in urine, is a common symptom associated with renal cell carcinoma, reflecting **tumor growth** or obstruction. - It can be an early indicator of the disease and necessitates further **diagnostic evaluation** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 959-961. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 492-493.

Question 606: Which of the following is NOT a characteristic feature of minimal change disease?

A. Effacement of podocytes on electron microscope
B. Normal light microscopy findings
C. Presence of immune complex deposits (Correct Answer)
D. Good response to steroids in nephrotic syndrome

Explanation: ***NSAIDS is the primary cause*** - Minimal change disease is primarily associated with **atopy**, **viruses**, or **lymphoproliferative disorders**, not NSAIDs. - There is insufficient evidence to classify NSAIDs as a significant causative factor in minimal change disease. *Good response to steroids* - Patients with minimal change disease typically exhibit a **good response** to corticosteroids, which is characteristic of this condition [1]. - This response is used to distinguish minimal change disease from other types of nephrotic syndrome [1]. *Effacement of podocytes on electron microscope, normal on light microscope* - Minimal change disease is known for **podocyte effacement**, which can only be detected under an **electron microscope**, while light microscopy appears normal [1]. - This feature is critical for diagnosis and is a hallmark of the disease [1]. *Nil deposit disease* - Minimal change disease is often referred to as a **nil deposit disease** because no significant deposits are observed on light microscopy [1]. - This term reflects the absence of visible immune complex deposits, a unique feature of this condition [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 921-928.

Question 607: Splitting of the glomerular basement membrane is seen in

A. Acute glomerulonephritis
B. Membranous glomerulonephritis
C. Membranoproliferative glomerulonephritis (Correct Answer)
D. Goodpasture's syndrome

Explanation: ***Membranoproliferative glomerulonephritis*** - Characterized by **splitting of the glomerular basement membrane**, often due to the deposition of immune complexes [1]. - It shows a **tram-track appearance** on silver stain, which is a hallmark feature of this condition [1]. *Good pasture's syndrome* - Primarily involves **glomerular and alveolar** basement membranes, leading to **hematuria** and **pulmonary hemorrhage**. - It does not exhibit **splitting of the glomerular basement membrane**; rather, it shows linear **IgG deposits** on immunofluorescence. *Membranous glomerulonephritis* - Characterized by **thickening of the glomerular basement membrane** due to the deposition of immune complexes. - It typically shows **subepithelial immune complex deposits** and does not cause splitting of the basement membrane. *Acute glomerulonephritis* - Usually involves **inflammation of the glomeruli**, leading to **hematuria** and **edema** but does not result in splitting of the basement membrane. - Often secondary to **post-infectious processes**, like post-streptococcal infection. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926.

Question 608: Subepithelial deposits occur in which type of renal disease?

A. Minimal change glomerulonephritis
B. Lupus Nephritis
C. Membranous glomerulonephritis (Correct Answer)
D. Membranoproliferative glomerulonephritis Type 1

Explanation: ***Membranous glomerulonephritis*** - Characterized by **subepithelial immune complex deposits** along the glomerular capillary walls, leading to nephrotic syndrome [1][2]. - These deposits are a hallmark of the disease and can be visualized on electron microscopy as **densely stained areas** beneath the epithelium [2]. *Membranoproliferative glomerulonephritis Type 1* - Features **intrabascular deposits** often associated with complement **activation**, rather than subepithelial deposits [1]. - Typically presents with **proliferative changes** in glomeruli and can have a mixed nephritic-nephrotic picture. *Lupus Nephritis* - Involves **subendothelial deposits** and mesangial immune complex deposition instead of subepithelial [1][3]. - Diverse presentations depend on the class of lupus nephritis, often accompanied by **systemic symptoms** of lupus [3]. *Minimal change glomerulonephritis* - Primarily characterized by **normal appearing glomeruli** on light microscopy, with foot process effacement on electron microscopy. - Does not feature appreciable deposits, and the mechanism typically involves **T-cell dysfunction**, leading to a nephrotic syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 911. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 532-533.

Question 609: What is the least likely cause of renal papillary necrosis?

A. Sickle cell disease
B. Analgesic nephropathy
C. Diabetes with UTI
D. Posterior urethral valves (Correct Answer)

Explanation: ***Posterior urethral valves*** - This is a congenital condition causing **urinary tract obstruction** in male infants, leading to hydronephrosis and renal damage [4]. - While **obstruction** is a recognized cause of papillary necrosis, posterior urethral valves represent the **least likely cause** among these options because it is primarily a **pediatric condition** with a different clinical context than the more common adult causes. - The mechanism is less direct compared to the ischemic and toxic insults from the other causes listed. *Sickle cell disease* - **Sickle cell trait or disease** causes episodes of **vaso-occlusion** in the renal medulla, leading to ischemia and subsequent papillary necrosis [1]. - The abnormal hemoglobin in sickle cells can aggregate and obstruct blood flow, particularly in the hypoxic environment of the renal medulla [1]. - This is a **classic cause** of renal papillary necrosis [1]. *Analgesic nephropathy* - Chronic abuse of certain **analgesics (e.g., NSAIDs, phenacetin)** leads to direct toxic injury and vasoconstriction in the renal medulla, causing **ischemia and necrosis of the renal papillae** [2]. - This is a **well-established and common cause** of renal papillary necrosis. *Diabetes with UTI* - **Diabetes mellitus** increases susceptibility to **pyelonephritis**, and severe or recurrent infections, especially in the setting of diabetes, can lead to **ischemia and necrosis of the renal papillae** [3]. - The combination of microvascular disease from diabetes and inflammation from infection significantly raises the risk [3]. - This is a **classic cause** remembered in the POSTCARD mnemonic. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 948-949. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 934-935. [3] 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. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 542-543.

Question 610: All of the following are features of Goodpasture syndrome, except for which of the following?

A. Hemoptysis
B. Antibody to alpha-3 chain of type IV collagen (COL4A3)
C. Subendothelial IgG deposits in renal biopsy (Correct Answer)
D. Linear IgG deposits on the glomerular basement membrane

Explanation: ***Subendothelial IgG deposits in renal biopsy*** - Goodpasture syndrome is characterized by the presence of **anti-glomerular basement membrane antibodies** [1], not subendothelial IgG deposits. - Renal biopsy typically shows a **linear pattern** of IgG deposition along the glomerular basement membrane [2], rather than subendothelial deposits. *Pulmonary haemorrhage* - A hallmark of Goodpasture syndrome [1], resulting from the antibodies targeting the lungs, leading to **alveolar damage**. - Patients often present with **hemoptysis** and signs of respiratory failure due to pulmonary complications [1]. *Glomerular basement membrane is involved* - This syndrome specifically targets the **glomerular basement membrane**, causing **rapidly progressive glomerulonephritis (RPGN)** [1]. - The involvement of the glomerular basement membrane is a significant feature of Goodpasture syndrome. *Antibody to alpha-3 chain of type IV collagen (COL4A3)* - Goodpasture syndrome is associated with antibodies against the **alpha-3 chain of type IV collagen**, crucial for the pathogenesis. - These antibodies lead to damage in both the **renal and pulmonary** systems due to the shared type IV collagen in the basement membranes. Recovery of renal function may follow early intensive plasmapheresis combined with steroids and cytotoxic agents [3]. **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. 537-538. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 526-527. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 918-919.

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