Renal Pathology Practice Questions

Q: Splitting of the glomerular basement membrane is seen in

Membranoproliferative glomerulonephritis. ***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.

Q: What is the primary cause of edema in nephritic syndrome?

Sodium and water retention. ***Sodium and water retention*** - In nephritic syndrome, **sodium and water retention** occurs due to kidney inflammation, leading to fluid overload [1]. - This results in increased **blood volume**, causing edema as a key clinical feature [1]. *Increased in plasma protein concentration* - Nephritic syndrome typically leads to **decreased**, not increased, plasma protein levels due to proteinuria. - Higher plasma protein levels would not contribute to edema; in fact, they would do the opposite by promoting osmotic balance. *Reduced plasma osmotic pressure* - While reduced osmotic pressure contributes to edema, in nephritic syndrome, the main factor is sodium and water retention [1]. - This oes not accurately describe the underlying cause in nephritic syndrome. *Decreased in plasma protein concentration* - Although nephritic syndrome may involve decreased protein concentration, edema is primarily due to **fluid retention** [1]. - Directly stating decreased plasma proteins oversimplifies the dynamic fluid balance that is disrupted in nephritic syndrome.

Q: Subepithelial deposits occur in which type of renal disease?

Membranous glomerulonephritis. ***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.

Q: Which type of nephrotic syndrome is most commonly associated with malaria?

Minimal change disease (MCD). Minimal change disease (MCD) - While various nephropathies can be associated with malaria, minimal change disease is most commonly reported, particularly in children living in endemic areas. [1] - The exact mechanism is unclear but may involve altered T-cell function or cytokine production triggered by malarial infection leading to podocyte dysfunction. [1] Membranoproliferative glomerulonephritis (MPGN) - MPGN is more commonly associated with chronic infections like Hepatitis C and certain autoimmune diseases, rather than acute or chronic malaria as the primary cause of nephrotic syndrome. - While chronic parasitic infections can sometimes be linked to MPGN, it is not the most frequent cause of nephrotic syndrome in the context of malaria. Membranous nephropathy - This condition is often associated with Hepatitis B, syphilis, or certain malignancies, and autoimmune diseases. - It is not the most prevalent form of nephrotic syndrome directly attributed to malarial infection. Focal segmental glomerulosclerosis (FSGS) - FSGS has a wide range of etiologies, including HIV infection, drug-induced causes, and genetic mutations. [1] - Although it can be secondary to various insults, it is not the most common form of nephrotic syndrome seen specifically with malaria.

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

Subendothelial IgG deposits in renal biopsy. ***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.

Q: In Wilms' tumor, what leads to the emergence of resistance to chemotherapy?

Anaplastic features in tumor cells. ***Anaplasia*** - Anaplasia in Wilms' tumor is associated with **poor differentiation**, leading to increased **resistance to chemotherapy** due to altered cell growth and survival pathways. - Tumors exhibiting anaplastic features often have a more aggressive behavior, resulting in **treatment failure** and **recurrence** despite chemotherapy. *Capsular infiltration* - While capsular infiltration indicates **tumor aggressiveness**, it does not directly contribute to **chemotherapy resistance** mechanisms. - It primarily reflects **advanced stage** or local spread rather than alterations in drug response. *Nephrogenic rests* - Nephrogenic rests are **pre-existing lesions** that can predispose to Wilms' tumor [1] but are not directly tied to **chemotherapy resistance**. - They are typically changes related to **developmental anomalies** rather than mechanisms of drug resistance. *Monophasic morphology* - Monophasic morphology refers to the **uniform appearance** of tumor cells, which typically indicates less heterogeneity and does not imply **resistance to chemotherapy**. - This characteristic may affect prognosis but is not a mechanism contributing to **chemotherapy failure**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 486-490.

Q: IgA nephropathy is classified as which type of glomerulonephritis?

Mesangioproliferative glomerulonephritis. ***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.

Q: The most common histological variant of renal cell carcinoma is

Clear cell type. ***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.

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

Autosomal recessive inheritance. **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 1

Splitting of the glomerular basement membrane is seen in

Accepted Answer

Membranoproliferative glomerulonephritis

Answer

Acute glomerulonephritis

Answer

Membranous glomerulonephritis

Answer

Goodpasture's syndrome

Question 2

What is the primary cause of edema in nephritic syndrome?

Accepted Answer

Sodium and water retention

Answer

Decreased plasma protein concentration

Answer

Reduced plasma osmotic pressure

Answer

Increased plasma protein concentration

Question 3

Subepithelial deposits occur in which type of renal disease?

Accepted Answer

Membranous glomerulonephritis

Answer

Minimal change glomerulonephritis

Answer

Lupus Nephritis

Answer

Membranoproliferative glomerulonephritis Type 1

Question 4

What is the least likely cause of renal papillary necrosis?

Accepted Answer

Posterior urethral valves

Answer

Sickle cell disease

Answer

Analgesic nephropathy

Answer

Diabetes with UTI

Question 5

Which type of nephrotic syndrome is most commonly associated with malaria?

Accepted Answer

Minimal change disease (MCD)

Answer

Membranoproliferative glomerulonephritis (MPGN)

Answer

Membranous nephropathy

Answer

Focal segmental glomerulosclerosis (FSGS)

Question 6

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

Accepted Answer

Subendothelial IgG deposits in renal biopsy

Answer

Hemoptysis

Answer

Antibody to alpha-3 chain of type IV collagen (COL4A3)

Answer

Linear IgG deposits on the glomerular basement membrane

Question 7

In Wilms' tumor, what leads to the emergence of resistance to chemotherapy?

Accepted Answer

Anaplastic features in tumor cells

Answer

Nephrogenic rests associated with Wilms' tumor

Answer

Tumor capsular infiltration

Answer

Monophasic tumor morphology

Question 8

IgA nephropathy is classified as which type of glomerulonephritis?

Accepted Answer

Mesangioproliferative glomerulonephritis

Answer

Membranous glomerulonephritis

Answer

Focal glomerulonephritis

Answer

Crescentic glomerulonephritis

Question 9

The most common histological variant of renal cell carcinoma is

Accepted Answer

Clear cell type

Answer

Chromophobe carcinoma

Answer

Papillary carcinoma

Answer

Collecting duct carcinoma

Question 10

Which of the following statements about fibronectin glomerulopathy is false?

Accepted Answer

Autosomal recessive inheritance

Answer

Ultrastructural feature is presence of large electron-dense mesangial or subendothelial deposits

Answer

Glomerular enlargement and PAS+ trichrome mesangial deposit

Answer

Glomeruli do not consistently stain for Ig and complement

Renal Pathology — MCQs

Renal Pathology — MCQs

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