Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 581: IgA nephropathy is not associated with which of the following?

A. Focal mesangial proliferation
B. Gross hematuria concurrent with upper respiratory infection
C. Immunofluorescence deposits contain IgA and IgG
D. Decreased complement level (Correct Answer)

Explanation: ***Decreased complement level*** - IgA nephropathy is typically associated with **normal serum complement levels** (C3 and C4), which is an important distinguishing feature. - Unlike post-streptococcal glomerulonephritis or lupus nephritis where complement levels are **low/decreased**, IgA nephropathy does not cause systemic complement consumption. - While complement activation does occur locally in the glomerulus (via lectin and alternative pathways), it does not lead to a decrease in serum complement levels. *Focal mesangial proliferation* - This is a **common histological finding** in IgA nephropathy, reflecting the proliferative response to IgA deposition in the mesangium. - The mesangial cells proliferate in an attempt to clear the immune deposits. *Gross hematuria concurrent with upper respiratory infection* - This is a **classic clinical presentation** of IgA nephropathy, often referred to as **synpharyngitic hematuria**. - The episode of gross hematuria typically occurs **within 1-2 days** of the onset of an upper respiratory tract infection, distinguishing it from post-streptococcal glomerulonephritis where hematuria appears 1-3 weeks later. *Immunofluorescence deposits contain IgA and IgG* - The defining feature of IgA nephropathy on immunofluorescence is the **predominant deposition of IgA**, often accompanied by C3. - While IgA is the primary immunoglobulin, **IgG and IgM can also be present** in variable amounts, but IgA must be the dominant or co-dominant immunoglobulin for the diagnosis.

Question 582: Renal stones which are laminated and irregular in outline are

A. Uric acid
B. Calcium oxalate (Correct Answer)
C. Struvite
D. Cystine

Explanation: ***Calcium oxalate*** - **Calcium oxalate stones** are the most common type of kidney stones and characteristically present with a **laminated** (layered) and **irregular, spiculated outline** due to their crystalline structure - They are typically **radio-opaque** on X-rays due to their calcium content - The irregular outline distinguishes them from other stone types *Uric acid* - **Uric acid stones** are often **smooth**, hard, and **yellowish-brown** in appearance - They are **radio-lucent** on standard X-rays and are associated with conditions like gout or acidic urine - Their smooth surface contrasts with the irregular calcium oxalate stones *Struvite* - **Struvite stones** (magnesium ammonium phosphate) are strongly associated with **urinary tract infections** (UTIs) and can form **staghorn calculi**, filling the renal pelvis - They tend to be **friable** and have a **smooth or glistening** surface, often growing quite large - Associated with urease-producing bacteria *Cystine* - **Cystine stones** are caused by a genetic disorder affecting amino acid transport and generally appear **smooth, waxy, and hexagonal crystal-shaped** - They are typically **moderately radio-opaque** but less dense than calcium stones - The smooth, waxy appearance differs from the irregular calcium oxalate stones

Question 583: According to WHO/ISN classification, which class of lupus nephritis shows a membranous pattern in SLE?

A. Diffuse proliferative pattern
B. Membranous pattern (Correct Answer)
C. Mesangial pattern involvement
D. Focal proliferative pattern

Explanation: ***Membranous pattern*** - This corresponds to **Class V lupus nephritis** in the WHO/ISN classification, characterized by widespread immune complex deposition along the **glomerular basement membrane (GBM)**. - The subepithelial immune deposits lead to GBM thickening, creating the characteristic membranous pattern on light microscopy. - This pattern resembles idiopathic membranous nephropathy but occurs in the context of SLE. *Mesangial pattern involvement* - This refers to **Class I (minimal mesangial LN)** or **Class II (mesangial proliferative LN)**, where immune deposits are primarily confined to the mesangium. - There is minimal or no involvement of the glomerular capillary walls, distinguishing it from the membranous pattern. *Diffuse proliferative pattern* - This is **Class IV lupus nephritis**, the most severe form characterized by widespread **endocapillary and/or extracapillary proliferation** involving ≥50% of glomeruli. - The primary feature is cellular proliferation (mesangial, endocapillary, epithelial crescents), not the subepithelial immune deposits typical of membranous pattern. *Focal proliferative pattern* - This corresponds to **Class III lupus nephritis**, involving **endocapillary or extracapillary proliferation** in <50% of glomeruli. - Distinguished by focal (not diffuse) involvement and active proliferation rather than the membranous pattern seen in Class V.

Question 584: What is the primary mechanism involved in the pathogenesis of acute proliferative glomerulonephritis?

A. Immune complex mediated (Correct Answer)
B. T-cell mediated cytotoxicity
C. Direct antibody-mediated injury
D. Type IV hypersensitivity reaction

Explanation: ***Immune complex mediated*** - The pathogenesis of **acute proliferative glomerulonephritis** is primarily caused by **immune complexes** that deposit in the glomeruli, leading to inflammation [1]. - This is typically associated with **post-streptococcal infections**, where the body's immune response generates complexes that affect kidney function [1]. *Cytotoxic T-cell mediated* - This mechanism involves T-cells directly damaging cells, which is not the primary cause of **acute proliferative glomerulonephritis**. - It is more relevant in conditions like **viral infections** or **transplant rejection**, rather than immune complex diseases. *Antibody mediated* - While antibodies play a role in various diseases, acute proliferative glomerulonephritis is primarily mediated by **immune complexes**, not just antibodies alone [1]. - This oes not account for the presence of **complexes formed from antigens**, which is crucial in the pathogenesis [1]. *Cell-mediated (Type IV)* - Type IV hypersensitivity involves delayed-type hypersensitivity, typically seen in **tuberculosis** or **contact dermatitis**, not in acute glomerulonephritis. - The inflammation in this case is due to **immune complexes**, rather than a purely cell-mediated response [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-916.

Question 585: Which of the following statements is true regarding light microscopy findings in minimal change disease?

A. Foot process effacement is observed under electron microscopy, not light microscopy.
B. Anti-GBM antibodies are associated with Goodpasture syndrome, not minimal change disease.
C. No significant changes are seen under light microscopy. (Correct Answer)
D. IgA deposits are characteristic of IgA nephropathy, not minimal change disease.

Explanation: ***No change seen*** - In minimal change disease, **light microscopy** typically shows no significant changes, which is a key characteristic of the condition [1]. - The disease primarily affects the **podocytes** leading to **nephrotic syndrome**, while light microscopy does not reveal any abnormalities [1]. *Loss of foot process seen* - Loss of foot processes is actually observed under **electron microscopy**, not light microscopy. - Light microscopy remains normal, differentiating minimal change disease from other glomerular diseases. *IgA deposits seen* - IgA deposits are associated with **IgA nephropathy**, which is a different condition characterized by mesangial deposition. - Minimal change disease does not have **immunofluorescence** findings, and thus shows no such deposits on light microscopy [1]. *Anti GBM Abs seen* - Anti-GBM antibodies are characteristic of **Goodpasture syndrome**, which presents with significant changes in glomerular structure. - In minimal change disease, there are no **anti-GBM antibodies** or major changes visible under light microscopy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Question 586: In glomerulus subendothelial deposits are seen in?

A. Goodpasture syndrome (linear IgG deposits in the basement membrane)
B. MPGN type I (subendothelial deposits) (Correct Answer)
C. MPGN type II (intramembranous deposits)
D. IgA nephropathy (mesangial IgA deposits)

Explanation: ***MPGN type I*** - **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1]. - This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1]. *Good pasture syndrome* - Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits. - Typically, it presents with **crescent formation** in the glomeruli rather than deposits. *MPGN type II* - Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1]. - It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology. *IgA nephropathy* - Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially. - It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.

Question 587: Oncocytic carcinoma arises from -

A. Perivascular region
B. Renal glomerulus
C. Loop of Henle
D. Collecting duct (intercalated cells) (Correct Answer)

Explanation: ***Collecting duct*** - Oncocytic carcinoma primarily originates from the **collecting ducts** of the kidney, where oncocytes are characteristically found [1]. - It is associated with specific **morphological features**, including abundant eosinophilic cytoplasm. *Loop of henle* - This part of the nephron primarily functions in **concentration of urine** and is not a common site for oncocytic tumors. - Tumors arising here typically do not exhibit **oncocytic features** and are more often linked to different renal cell types. *Glomerulus* - The glomerulus is involved in **filtration of blood** and lacks oncocytic differentiation. - Oncocytic carcinoma does not arise from glomerular structures, as it features distinct cellular characteristics. *Perivascular* - This term refers to the tissue surrounding blood vessels and is not a site for oncocytic carcinoma development. - Such tumors would not align with the histological features or origins typically seen in oncocytic carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 959.

Question 588: What is the most common cause of nephritic syndrome in adults, excluding IgA nephropathy?

A. FSGS
B. Membranous glomerulonephritis
C. Membranoproliferative glomerulonephritis (Correct Answer)
D. Post-infectious glomerulonephritis

Explanation: ***None*** - Nephritic syndrome in adults is often caused by various conditions, but there is **no single most common cause** that universally applies. - The true prevalence can vary by population, but conditions like **IgA nephropathy** or **post-infectious glomerulonephritis** [1] are frequently encountered rather than one specific disease. *Membranoproliferative glomerulonephritis* - This condition can cause a **nephritic syndrome** [1], but it is not the most common cause in adults, often seen in association with **hepatitis C** or other infections. - In practice, **IgA nephropathy** or **post-streptococcal glomerulonephritis** [1] are more frequently recognized causes of nephritic syndrome in adults. *Membranous glomerulonephritis* - Primarily presents with **nephrotic syndrome** rather than nephritic features [1], making it less likely to be cited as a common cause of nephritic syndrome. - It is associated with **anti-phospholipase A2 receptor antibodies** but lacks the inflammatory features of nephritis [1]. *FSGN* - **Focal Segmental Glomerulosclerosis** is associated with nephrotic syndrome and doesn't typically lead to classic nephritic features, such as hematuria and hypertension [1]. - Its primary presentation is with **proteinuria** and possible renal failure but not with the typical characteristics of nephritic syndrome [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 915-919.

Question 589: Which of the following is the MOST COMMON cause of acute hypocomplementemia in children following an infection?

A. PSGN (Correct Answer)
B. Membranous GN
C. Focal Segmental Glomerulosclerosis (FSGS)
D. Membranoproliferative GN (MPGN)

Explanation: ***PSGN*** - **Post-streptococcal glomerulonephritis (PSGN)** is the **most common cause of acute hypocomplementemia** in children following a streptococcal infection [1]. - Characterized by **immune complex deposition** in the glomeruli with activation of the complement system [2]. - Results in **transient hypocomplementemia** (both C3 and C4 decreased) that typically normalizes within 6-8 weeks. - Classic presentation: acute nephritic syndrome 1-3 weeks after pharyngitis or 3-6 weeks after skin infection [1]. *Membranous GN* - **Membranous glomerulonephritis** presents with **nephrotic syndrome** and immune complex deposition [2]. - Associated with **normal complement levels** in most cases. - Complement activation is not severe enough to cause significant consumption. *Focal Segmental Glomerulosclerosis (FSGS)* - **FSGS** causes nephrotic syndrome with **scarring of selected glomeruli** [3]. - **Not an immune complex-mediated disease**, hence no complement consumption [3]. - Complement levels remain **normal**. *Membranoproliferative GN (MPGN)* - **MPGN** can also cause hypocomplementemia, particularly Type II (dense deposit disease) with persistent C3 consumption due to C3 nephritic factor. - However, **MPGN is much less common** than PSGN in the pediatric population. - Type I MPGN may show low C3 with normal or low C4. - PSGN remains the **classic and most frequent** acute post-infectious cause [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Question 590: Mitochondrial abnormalities are associated with which of the following conditions?

A. Krabbe's disease
B. Fabry disease
C. Leigh syndrome (Correct Answer)
D. Fanconi syndrome

Explanation: ***Fanconi syndrome*** - Fanconi syndrome is associated with **renal tubular dysfunction**, leading to **metabolic acidosis** and hypophosphatemia, often showing mitochondrial abnormalities [1]. - It can be linked to certain **toxins and genetic disorders**, affecting mitochondrial function, particularly in the context of renal cells. *Fanconi syndrome* - This option is a repeat and should not be considered separately; the proper acknowledgment of Fanconi syndrome is included in the correct answer. - The condition itself is not missed but stated correctly under the correct answer. *Krabbe's disease* - Krabbe's disease primarily involves **galactocerebrosidase deficiency** and affects the central nervous system, not primarily linked to mitochondrial dysfunction [2]. - It presents with **neuropathy**, **global developmental delay**, and **progressive weakness**, which are distinct from mitochondrial disorders. *Fabry disease* - Fabry disease is caused by **alpha-galactosidase A deficiency**, leading to lysosomal accumulation, primarily affecting **vascular and renal systems**. - Mitochondrial dysfunction is not a primary feature, making it distinguishable from mitochondrial abnormalities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1246-1247. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1304-1305.

Practice by Chapter

Congenital Anomalies of the Kidney

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Glomerular Diseases

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Tubular and Interstitial Diseases

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Vascular Diseases of the Kidney

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Cystic Diseases of the Kidney

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Urinary Tract Obstruction and Stones

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Renal Tumors

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Kidney in Systemic Diseases

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Renal Transplantation Pathology

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Urinary Tract Infections

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