Renal Pathology Practice Questions

Q: Autosomal recessive Polycystic kidneys - all are true except -

USG shows salt and pepper appearance. ***USG shows salt and pepper appearance*** - The **"salt and pepper" appearance** on imaging is characteristic of **autosomal dominant polycystic kidney disease (ADPKD)** due to multiple renal cysts of varying sizes and associated vascular calcifications, not autosomal recessive polycystic kidney disease (ARPKD). - ARPKD typically presents with **enlarged, hyperechoic kidneys** with loss of corticomedullary differentiation on ultrasound due to numerous small cysts. *Defective gene is PKHD1* - The dysfunctional gene in **autosomal recessive polycystic kidney disease (ARPKD)** is indeed **PKHD1**, located on chromosome 6. - This gene encodes for **fibrocystin/polyductin**, a protein primarily found in renal and biliary epithelial cells, whose mutation leads to cyst formation. *Both kidneys show innumerable cysts* - ARPKD is characterized by **bilateral involvement** with diffuse dilation of the collecting ducts, leading to innumerable small cysts in both kidneys. - These cysts cause significant **renal enlargement** and can lead to severe renal dysfunction. *Seen in adults* - **Autosomal recessive polycystic kidney disease (ARPKD)** typically manifests in **infancy or childhood**, often prenatally or neonatally. - While some milder forms may present later in childhood, it is **not generally seen in adults**; adult-onset polycystic kidney disease is usually autosomal dominant (ADPKD) [1].

Q: The main mechanism of proteinuria in minimal change disease is

Loss of negative charge on membrane. ***Loss of negative charge on membrane*** [1] - The primary defect in **minimal change disease** is a loss of the **negative charge** on the glomerular basement membrane (GBM) and podocytes. - This loss of negative charge allows for the increased filtration of negatively charged proteins, particularly **albumin**, leading to severe proteinuria [1]. *Increase in pore size* - While increased pore size can contribute to proteinuria (e.g., in some forms of glomerulonephritis), it is **not the primary or defining mechanism** in minimal change disease [1]. - The loss of **anionic charge** is the more specific and significant factor for albuminuria in MCD. *Decreased circulation* - **Decreased circulation** (e.g., hypoperfusion) would typically lead to **acute kidney injury** or prerenal azotemia rather than isolated proteinuria and nephrotic syndrome. - This mechanism does not explain the selective albuminuria characteristic of minimal change disease. *Loss of cells* - While some glomerular disorders involve **loss of specific cell types**, such as podocytes in focal segmental glomerulosclerosis (FSGS), minimal change disease is characterized by **foot process effacement** without a significant loss of cells [1]. - The podocytes remain largely intact, but their structural and functional integrity is compromised [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 905-907, 922-923, 927-928.

Q: Edema in nephrotic syndrome is due to ?

Hypoalbuminemia. ***Hypoalbuminemia*** - In **nephrotic syndrome**, damage to the glomerular basement membrane leads to significant **proteinuria**, particularly the loss of **albumin**. [3] - **Hypoalbuminemia** reduces the plasma **oncotic pressure**, causing fluid to shift from the intravascular space into the interstitial space, resulting in **edema**. [1], [3] *Hyperlipidemia* - **Hyperlipidemia** is a common feature of nephrotic syndrome but is not directly responsible for the development of edema. - It results from increased hepatic synthesis of lipoproteins in response to low systemic **oncotic pressure**. *Sodium & water retention* - While **sodium and water retention** do contribute to the exacerbation of edema in nephrotic syndrome, they are secondary events driven by the initial **hypovolemia** resulting from **hypoalbuminemia**. [2] - The reduced effective circulating volume triggers the **renin-angiotensin-aldosterone system** and antidiuretic hormone release, leading to renal sodium and water reabsorption. *Increased venous pressure* - **Increased venous pressure** is not a primary cause of edema in nephrotic syndrome. - It is typically associated with conditions like **congestive heart failure** or local venous obstruction, where it impedes venous return and causes fluid accumulation.

Q: Basic abnormality in a case of nephrotic syndrome is:

Proteinuria. Basic abnormality in a case of nephrotic syndrome is: ***Proteinuria*** - The fundamental abnormality in nephrotic syndrome is **massive proteinuria** (protein excretion > 3.5 g/day in adults), resulting from increased glomerular permeability [1]. - This **proteinuria** leads to hypoalbuminemia, which then triggers many of the other clinical manifestations of the syndrome. *Hyperlipidemia* - **Hyperlipidemia** is a common consequence of nephrotic syndrome, driven by increased hepatic lipoprotein synthesis in response to low plasma oncotic pressure and reduced lipoprotein catabolism. - While characteristic, it is a **secondary abnormality** arising from the primary protein loss rather than the basic underlying cause. *Pedal edema* - **Pedal edema** is a prominent clinical feature of nephrotic syndrome, resulting from the combination of reduced plasma oncotic pressure due to hypoalbuminemia and secondary sodium and water retention [1]. - Although highly visible, it is a **symptom** and a downstream effect, not the primary pathological process. [1] *Hypertension* - **Hypertension** can occur in some cases of nephrotic syndrome, particularly with more severe renal involvement or concurrent fluid overload. - However, it is **not a universal feature** and is generally considered a complication or an associated condition, rather than the core initiating abnormality.

Q: Which component of HBV causes glomerulonephritis?

Hbs Ag. ### HBs Ag - **Hepatitis B surface antigen (HBsAg)** is a viral protein that can form immune complexes with its corresponding antibody within the body [1]. - These **immune complexes** can deposit in the glomeruli of the kidneys, triggering an inflammatory response that leads to **glomerulonephritis**, particularly **membranous nephropathy** or **membranoproliferative glomerulonephritis**. *Anti HBs Ag antibody* - This antibody usually indicates **immunity** to HBV infection, either from vaccination or resolved infection [1]. - While it forms an immune complex with HBsAg, this typically leads to **clearance of the virus** and does not directly cause glomerulonephritis. *HBc Ag* - **Hepatitis B core antigen (HBcAg)** is located within the viral core and is not typically released into the bloodstream as a free antigen [1]. - Therefore, it is **unlikely to directly form immune complexes** in the circulation that could deposit in the kidney. *HBe Ag* - **Hepatitis B e antigen (HBeAg)** indicates active viral replication and high infectivity. - Although it can be detected in the serum, it is **less commonly implicated** in the direct formation of immune complexes leading to glomerulonephritis compared to HBsAg.

Q: Hemolytic uremic syndrome is caused by:

Shiga toxin-producing E. coli and complement dysregulation. Shiga toxin-producing E. coli and complement dysregulation - The most common cause of **hemolytic uremic syndrome (HUS)** is infection with **Shiga toxin-producing E. coli (STEC)**, typically O157:H7, leading to typical HUS [1]. - Atypical HUS (aHUS) is primarily caused by **complement dysregulation**, often due to genetic mutations in complement regulatory proteins [1]. *Streptococcus pneumoniae* - *Streptococcus pneumoniae* can cause HUS, but it is typically associated with **pneumococcal-associated HUS**, a less common form. - The mechanism involves neuraminidase production by the bacteria, which exposes T-antigen on red blood cells, leading to their destruction. *Streptococcus pneumoniae and complement dysregulation* - While both can cause HUS, *Streptococcus pneumoniae* and **complement dysregulation** are typically distinct causes, leading to different forms of the syndrome. - This option incorrectly combines the primary causes of two different subtypes of HUS. *Streptococcus pneumoniae and adenovirus* - *Streptococcus pneumoniae* can cause HUS, but **adenovirus** is not a generally recognized cause of HUS. - HUS is primarily linked to bacterial toxins or genetic complement defects, not typically viral infections like adenovirus. *Enteroinvasive E. coli* - **Enteroinvasive E. coli (EIEC)** causes a dysentery-like illness but does not produce Shiga toxin. - HUS is specifically triggered by toxins that damage endothelial cells, which EIEC does not produce.

Q: Class IV lupus nephritis is:

Diffuse lupus nephritis. ***Diffuse lupus nephritis*** - This is the most **severe** and common form of lupus nephritis, characterized by **widespread inflammation** and proliferation affecting more than 50% of glomeruli [1]. - Patients typically present with **nephrotic-range proteinuria**, **hematuria**, and significant **renal impairment** [1]. *Proliferative lupus nephritis* - This is a general term describing **increased cellularity** within the glomeruli. - While Class IV (diffuse) lupus nephritis is a proliferative form, "proliferative lupus nephritis" alone is not a specific class in the ISN/RPS classification system without further qualification (e.g., focal or diffuse). *Mesangial lupus nephritis* - This refers to Classes I and II, characterized by **mesangial immune deposits** and/or mild mesangial hypercellularity. - It is typically a **milder form** with a better prognosis, unlike the severe presentation of Class IV [1]. *Membranous lupus nephritis* - This corresponds to Class V lupus nephritis, distinguished by **subepithelial immune deposits** and thickening of the glomerular basement membrane. - Patients often present with **nephrotic syndrome** but typically have less severe inflammation or cellular proliferation compared to Class IV. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 230-232.

Q: In Potter syndrome - primary pathology is:

Renal agenesis. ***Renal agenesis*** - **Potter syndrome** is characterized by the absence of kidney development, known as **renal agenesis**, which is the primary underlying pathological event. - This congenital anomaly leads to a cascade of secondary problems due to the kidneys' role in producing amniotic fluid. *Oligohydramnios* - **Oligohydramnios** (low amniotic fluid) is a **consequence** of renal agenesis, not the primary pathology itself. - The fetal kidneys normally produce most of the amniotic fluid after the first trimester, so their absence leads to insufficient fluid. *Dysmorphism* - **Dysmorphic facial features** (such as flattened nose, recessed chin, epicanthic folds) are part of the **Potter sequence**, which refers to a set of features resulting from oligohydramnios. - These features are **secondary effects** caused by the compression of the fetus in the uterus due to reduced amniotic fluid, rather than the primary defect. *Limb defects* - **Limb defects**, such as club feet or contractures, are also **secondary manifestations** of the Potter sequence. - They arise from the **compression** of the fetus in the cramped uterine environment due to severe oligohydramnios, restricting fetal movement and development.

Question 1

Autosomal recessive Polycystic kidneys - all are true except -

Accepted Answer

USG shows salt and pepper appearance

Answer

Defective gene is PKHD1

Answer

Both kidneys show innumerable cysts

Answer

Seen in adults

Question 2

The main mechanism of proteinuria in minimal change disease is

Accepted Answer

Loss of negative charge on membrane

Answer

Increase in pore size

Answer

Decreased circulation

Answer

Loss of cells

Question 3

Edema in nephrotic syndrome is due to ?

Accepted Answer

Hypoalbuminemia

Answer

Hyperlipidemia

Answer

Sodium & water retention

Answer

Increased venous pressure

Question 4

A 10-year-old with history of sore throat 1 week ago presented with sudden onset of hematuria and generalized edema. On examination, hypertension was observed. Lab findings revealed proteinuria, red cell casts in the urine, deranged RFTs, low level of serum complement C3. Which of the following would be the most likely histology if kidney biopsy is performed: -

Accepted Answer

Image A shows histology of PSGN

Answer

Image C shows histology of MGN

Answer

Image B shows histology of MPGN

Answer

Image D shows histology of IgA NEPHROPATHY

Question 5

Basic abnormality in a case of nephrotic syndrome is:

Accepted Answer

Proteinuria

Answer

Hyperlipidemia

Answer

Pedal edema

Answer

Hypertension

Question 6

Which component of HBV causes glomerulonephritis?

Accepted Answer

Hbs Ag

Answer

Anti HBs Ag antibody

Answer

HBc Ag

Answer

Hbe Ag

Question 7

Hemolytic uremic syndrome is caused by:

Accepted Answer

Shiga toxin-producing E. coli and complement dysregulation

Answer

Streptococcus pneumoniae

Answer

Streptococcus pneumoniae and complement dysregulation

Answer

Streptococcus pneumoniae and adenovirus

Answer

Enteroinvasive E. coli

Question 8

Class IV lupus nephritis is:

Accepted Answer

Diffuse lupus nephritis

Answer

Proliferative lupus nephritis

Answer

Mesangial lupus nephritis

Answer

Membranous lupus nephritis

Question 9

Michaelis-Gutmann bodies are seen in

Accepted Answer

Malacoplakia

Answer

Thimble Bladder

Answer

Transitional cell carcinoma of bladder

Answer

Interstitial cystitis

Question 10

In Potter syndrome - primary pathology is:

Accepted Answer

Renal agenesis

Answer

Oligohydramnios

Answer

Dysmorphism

Answer

Limb defects

Renal Pathology — MCQs

Renal Pathology — MCQs

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