Renal Pathology Practice Questions

Q: In a survey, many children are examined and were found to have urogenital abnormalities. Which congenital anomaly is associated with increased risk of bladder carcinoma?

Bladder exstrophy. ***Bladder exstrophy*** - **Bladder exstrophy** involves the bladder being open and exposed on the abdominal surface, leading to chronic inflammation and irritation of the urothelium [1]. - This chronic irritation significantly increases the risk of developing **adenocarcinoma** of the bladder (approximately 4-5% lifetime risk), and less commonly, squamous cell carcinoma [1]. - The persistent exposure and metaplastic changes in the bladder epithelium are the primary mechanisms for malignant transformation [1]. *Double ureter* - A **double ureter** is a duplication of the ureter draining a single kidney, which usually has two separate renal pelves. - While it can be associated with issues like **vesicoureteral reflux** or obstruction, it generally does not increase the risk of bladder carcinoma. *Medullary sponge kidney* - **Medullary sponge kidney** is a congenital malformation characterized by dilation of the collecting ducts in the renal pyramids. - It is primarily associated with **recurrent kidney stones** and urinary tract infections, but not with an increased risk of bladder carcinoma. *Unilateral renal agenesis* - **Unilateral renal agenesis** is a condition where one kidney fails to develop. The other kidney is typically hypertrophied to compensate. - While it can be associated with other urogenital anomalies, it does not directly increase the risk of developing bladder carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, p. 966.

Q: ANCA is most specific and sensitive marker for

Idiopathic crescentic glomerulonephritis. ***Idiopathic crescentic glomerulonephritis*** - **ANCA** (Anti-neutrophil cytoplasmic antibodies) are highly specific and sensitive for certain **pauci-immune necrotizing glomerulonephritides**, which often present as **idiopathic crescentic glomerulonephritis** [1]. - **Crescentic glomerulonephritis** without immune complex deposition (pauci-immune) is frequently associated with **ANCA-associated vasculitis**, making ANCA a crucial diagnostic marker [1]. *Membranoproliferative glomerulonephritis* - This condition is primarily characterized by alterations in glomerular basement membrane and mesangial cell proliferation, often associated with **immune complex deposition** or **complement dysregulation**, not typically ANCA. - While various types exist, **ANCA is not a primary diagnostic marker** for membranoproliferative glomerulonephritis. *Post streptococcal Glomerulonephritis* - This form of glomerulonephritis is triggered by a preceding **streptococcal infection** and is characterized by **immune complex deposition** in the glomeruli [1]. - It is diagnosed by evidence of infection (e.g., elevated ASO titers) and specific **complement activation profiles**, not ANCA [1]. *Focal segmental Glomerulosclerosis* - This primary glomerular disease is characterized by **segmental scarring of the glomeruli**, leading to proteinuria, and is often **idiopathic** or secondary to various causes like genetic mutations or viral infections [1]. - It is not an autoimmune vasculitis and is **not associated with ANCA**.

Q: 2-year-old child is seen for a well-child visit in a pediatric clinic. Abdominal examination demonstrates a palpable, non-tender mass on the left side of the abdomen. The mother had no idea where the mass was present and the pediatrician did not note the presence of the mass at the child's 18-month well-child visit. Physical examination is otherwise unremarkable. Abnormalities of which of the following chromosomes have been linked to this disease?

11. ***Correct: Option 11*** - The presentation of a **palpable, non-tender abdominal mass** in a 2-year-old child, especially one that has grown since the last visit, is highly suggestive of **Wilms tumor (nephroblastoma)**. - **Wilms tumor** is associated with genetic abnormalities, particularly on **chromosome 11**, involving genes such as **WT1** (11p13) and **WT2** (11p15.5). - These genetic mutations are found in approximately **10-15% of Wilms tumors**, and chromosome 11 abnormalities are the most well-established genetic link to this disease. *Incorrect: Option 15* - While other chromosomal abnormalities can be associated with childhood cancers, **chromosome 15** is not typically implicated in the primary genetic etiology of Wilms tumor. - Specific genetic syndromes linked to chromosome 15 (e.g., Prader-Willi, Angelman syndrome) have distinct phenotypic presentations unrelated to a solitary renal mass. *Incorrect: Option 5* - Abnormalities on **chromosome 5** are not primarily linked to the development of Wilms tumor. - **Cri-du-chat syndrome** (deletion on chromosome 5p) is a known genetic condition associated with chromosome 5 abnormalities, but it presents with distinct craniofacial features and developmental delays, not an abdominal mass. *Incorrect: Option 3* - **Chromosome 3** abnormalities are more commonly associated with certain adult cancers, such as renal cell carcinoma, or other developmental anomalies. - It does not have a direct, well-established link to the pathogenesis of **Wilms tumor** in children.

Q: Investigation of choice for confirming Henoch Schönlein Purpura is

Renal Biopsy. ***Renal Biopsy*** - **Biopsy (renal or skin)** showing **IgA deposition** is the **confirmatory investigation** for Henoch-Schönlein Purpura (HSP) when histological confirmation is needed [1]. - **Renal biopsy** demonstrates characteristic **IgA-dominant immune deposits** in the mesangium and glomerular capillaries, along with **mesangial proliferation** [1]. - While HSP is primarily a **clinical diagnosis** based on palpable purpura, age < 20 years, abdominal pain, and renal involvement, biopsy provides **definitive confirmation** in atypical presentations or when diagnosis is uncertain. - Immunofluorescence showing **IgA deposition** is the pathognomonic finding [1]. *Serum IgA levels* - Serum IgA levels may be elevated in approximately **50% of HSP cases**, but this is **neither sensitive nor specific**. - **Normal serum IgA does NOT exclude HSP**, making it unreliable as a confirmatory test. - Elevated IgA can occur in many other conditions (IgA nephropathy without vasculitis, liver disease, infections). - Provides only supportive evidence, not confirmation. *CRP levels* - **C-reactive protein (CRP)** is a **non-specific inflammatory marker** that may be elevated in HSP. - Cannot distinguish HSP from other inflammatory or infectious conditions. - Has no role in confirming the diagnosis. *DTPA* - **DTPA scan** assesses **renal perfusion and function** but does not provide diagnostic information about the underlying pathology. - Cannot detect the characteristic **IgA-mediated vasculitis** of HSP. - Not useful for confirming the diagnosis. **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. 526-527.

Q: Characteristic of acute Glomerulonephritis is?

RBC cast. ***RBC cast*** - The presence of **red blood cell casts** in urine is the **hallmark** of glomerulonephritis, indicating glomerular inflammation and hemorrhage [1]. - These casts are formed when red blood cells enter the renal tubules and are molded within the **protein matrix** of the tubule. *Hemoglobinuria* - **Hemoglobinuria** refers to free hemoglobin in the urine, often seen in conditions involving **intravascular hemolysis**, not directly indicative of glomerular damage [2]. - While red blood cells may be present in glomerulonephritis resulting in gross or microscopic hematuria, free hemoglobin in urine is distinct from the presence of red blood cells or RBC casts [2]. *Hyaline cast* - **Hyaline casts** are composed primarily of Tamm-Horsfall protein and can be seen in **healthy individuals**, especially after exercise, or in conditions like dehydration. - Their presence is **non-specific** and does not point directly to acute glomerulonephritis. *Broad cast* - **Broad casts** (or "waxy casts") are larger than typical casts and are associated with **end-stage renal disease** and chronic kidney failure, indicating severely dilated and hypertrophied tubules. - They are not characteristic of the acute inflammation seen in acute glomerulonephritis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 915-916. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640.

Q: A 7-year-old boy presented with generalized edema. Urine examination revealed marked albuminuria. Serum biochemical examinations showed hypoalbuminemia with hyperlipidemia. Kidney biopsy was undertaken. On light microscopic examination, the kidney appeared normal. Electron microscopic examination is most likely to reveal:

Fusion of foot processes of the glomerular epithelial cells. ***Fusion of foot processes of the glomerular epithelial cells*** - This finding, also known as **effacement of podocyte foot processes**, is the characteristic electron microscopic feature of **minimal change disease (MCD)** [1]. - MCD is the most common cause of **nephrotic syndrome** in children, presenting with generalized edema, marked albuminuria, hypoalbuminemia, and hyperlipidemia, with a normal appearance on light microscopy [1]. *Deposition of electron dense material in the basement membrane* - This suggests diseases like **membranous nephropathy** or **post-infectious glomerulonephritis**, which typically involve immune complex deposition. - These conditions usually show abnormalities on **light microscopy** (e.g., thickened capillary loops in membranous nephropathy) and differ clinically [1]. *Rarefaction of glomerular basement membrane* - **Rarefaction** or thinning of the glomerular basement membrane is associated with conditions like **Alport syndrome** or **thin basement membrane disease**. - These are typically associated with **hematuria**, which is not mentioned as a primary symptom in this case, and often have a genetic component. *Thin basement membrane* - A **thin basement membrane** is the hallmark of **thin basement membrane disease** (also known as benign familial hematuria). - This condition primarily presents with **microscopic hematuria** and does not typically cause the complete nephrotic syndrome found in this child [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-923.

Q: Wilms tumor occurs in:

Kidney. ***Kidney*** - **Wilms tumor** (also known as nephroblastoma) is a **malignant tumor** that originates in the **kidney** and affects primarily children [1]. - It arises from **embryonic renal blastema** and is the most common kidney cancer in children [2]. *Bronchus* - The bronchus is part of the respiratory system, and while tumors can occur here (e.g., **bronchogenic carcinoma**), Wilms tumor does not originate in the bronchus. - Tumors in the bronchus are primarily seen in adults and are often associated with smoking. *Liver* - The liver is a common site for childhood tumors, such as **hepatoblastoma**, but it is not the origin of Wilms tumor [1]. - Hepatic tumors have different cellular origins and clinical presentations compared to renal tumors. *Stomach* - Tumors of the stomach in children are rare and typically involve conditions like **lymphoma** or **sarcoma**, not Wilms tumor. - The stomach is an organ of the digestive system with distinct developmental origins from the kidney. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 211-212. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 487-490.

Q: Post streptococcal glomerulonephritis causes -

Nephritic syndrome. ***Nephritic syndrome*** - **Post-streptococcal glomerulonephritis (PSGN)** is a classic cause of **nephritic syndrome** [2], characterized by **glomerular inflammation** [1]. - Key features of nephritic syndrome include **hematuria**, **oliguria**, **hypertension**, and mild proteinuria with edema [2]. *Primary Nephrotic syndrome* - **Nephrotic syndrome** is defined by massive **proteinuria** (>3.5g/day), **hypoalbuminemia**, **edema**, and **hyperlipidemia** [2]. - PSGN typically presents with **microscopic or gross hematuria** and only moderate proteinuria, not the heavy proteinuria characteristic of nephrotic syndrome [2]. *Chronic renal failure* - While severe or recurrent cases of PSGN can eventually lead to **chronic kidney disease (CKD)** [3], it is not the immediate or primary presentation. - PSGN typically presents as an **acute** glomerulonephritis [1]. *Secondary Nephrotic syndrome* - **Secondary nephrotic syndrome** refers to nephrotic syndrome caused by systemic diseases (e.g., diabetes, lupus). - PSGN is an inflammatory condition primarily affecting the glomeruli, leading to nephritic features rather than dominant nephrotic range proteinuria [2]. **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. 916-917.

Q: All are true about minimal change disease (Minimal Change GN) except –

IgG deposition in mesangium. ***IgG deposition in mesangium*** - **Minimal Change Disease (MCD)** is characterized by the absence of significant immune complex deposition in the glomeruli [1]. - The hallmark of MCD on immunofluorescence is typically **negative or minimal staining for immunoglobulins (like IgG)** and complement components [1]. *Common in age group 2–9 years* - **Minimal Change Disease** is the most common cause of **nephrotic syndrome** in children, particularly in the 2-9 year age range [1]. - It accounts for approximately 80% of nephrotic syndrome cases in this pediatric population. *Selective proteinuria* - MCD causes damage to the **glomerular basement membrane's charge barrier**, leading to the loss of only smaller proteins like **albumin** [2]. - This results in **selective proteinuria**, where larger proteins like globulins are retained [2]. *Responds to steroids* - MCD is well-known for its excellent response to **corticosteroid therapy**, with the majority of patients achieving complete remission [1],[2]. - This characteristic responsiveness is a key diagnostic and therapeutic feature of the disease [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923.

Question 1

In a survey, many children are examined and were found to have urogenital abnormalities. Which congenital anomaly is associated with increased risk of bladder carcinoma?

Accepted Answer

Bladder exstrophy

Answer

Double ureter

Answer

Medullary sponge kidney

Answer

Unilateral renal agenesis

Question 2

ANCA is most specific and sensitive marker for

Accepted Answer

Idiopathic crescentic glomerulonephritis

Answer

Membranoproliferative glomerulonephritis

Answer

Post streptococcal Glomerulonephritis

Answer

Focal segmental Glomerulosclerosis

Question 3

2-year-old child is seen for a well-child visit in a pediatric clinic. Abdominal examination demonstrates a palpable, non-tender mass on the left side of the abdomen. The mother had no idea where the mass was present and the pediatrician did not note the presence of the mass at the child's 18-month well-child visit. Physical examination is otherwise unremarkable. Abnormalities of which of the following chromosomes have been linked to this disease?

Accepted Answer

11

Answer

15

Answer

5

Answer

3

Question 4

Investigation of choice for confirming Henoch Schönlein Purpura is

Accepted Answer

Renal Biopsy

Answer

Serum IgA levels

Answer

CRP levels

Answer

DTPA

Question 5

Characteristic of acute Glomerulonephritis is?

Accepted Answer

RBC cast

Answer

Hemoglobinuria

Answer

Hyaline cast

Answer

Broad cast

Question 6

Triphasic Cells seen in Wilm's tumour are

Accepted Answer

Stromal Cells, Blastemal Cells, Epithelial Cells

Answer

Stromal Cells, Epithelial Cells, Embryonal Cells

Answer

Mesenchymal Cells, Stromal Cells, Embryonal Cells

Answer

Epithelial Cells

Question 7

A 7-year-old boy presented with generalized edema. Urine examination revealed marked albuminuria. Serum biochemical examinations showed hypoalbuminemia with hyperlipidemia. Kidney biopsy was undertaken. On light microscopic examination, the kidney appeared normal. Electron microscopic examination is most likely to reveal:

Accepted Answer

Fusion of foot processes of the glomerular epithelial cells

Answer

Deposition of electron dense material in the basement membrane

Answer

Rarefaction of glomerular basement membrane

Answer

Thin basement membrane

Question 8

Wilms tumor occurs in:

Accepted Answer

Kidney

Answer

Bronchus

Answer

Liver

Answer

Stomach

Question 9

Post streptococcal glomerulonephritis causes -

Accepted Answer

Nephritic syndrome

Answer

Primary Nephrotic syndrome

Answer

Chronic renal failure

Answer

Secondary Nephrotic syndrome

Question 10

All are true about minimal change disease (Minimal Change GN) except –

Accepted Answer

IgG deposition in mesangium

Answer

Common in age group 2–9 years

Answer

Selective proteinuria

Answer

Responds to steroids

Renal Pathology — MCQs

Renal Pathology — MCQs

On this page

Practice by Chapter

Want unlimited practice?