Renal Pathology Practice Questions

Q: The prognosis of rapidly progressive glomerulonephritis (crescentic GN) depends on

Number of crescents. ***Number of crescents*** - The **number of glomeruli affected by crescents** is the most significant prognostic indicator in rapidly progressive glomerulonephritis. A higher percentage of crescentic glomeruli correlates with worse renal function outcomes. - A **renal biopsy finding of fewer than 25% crescentic glomeruli** often indicates a better prognosis with potential for recovery, while **more than 50% involvement** suggests a poor prognosis with a high likelihood of end-stage renal disease. *Size of crescents* - While crescents vary in size, the **extent of glomerular involvement (percentage of glomeruli with crescents)** is more clinically relevant for prognosis than the individual size of each crescent. - The size of an individual crescent does not independently predict renal outcome as effectively as the overall burden of crescentic disease. *Shape of crescents* - The **shape of crescents (e.g., circumferential vs. segmental)** is a descriptive feature but does not independently determine the prognosis. - The critical factor remains the **presence and number of crescents**, as these signify severe glomerular injury, regardless of their specific morphology. *Cellularity of crescents* - Crescents can be **cellular, fibrocellular, or fibrous**. The composition reflects the stage of injury and healing, with fibrous crescents indicating chronic, irreversible damage [1]. - Although the **cellularity of crescents indicates activity and potential for reversibility**, the *number of affected glomeruli* (i.e., the extent of crescent formation) remains the primary determinant of renal prognosis [1]. **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. 528-529.

Q: Anaplasia in Wilms' tumor is evident by what features?

Pleomorphic nuclei. ***Pleomorphic nuclei*** - Anaplastic cells in Wilm's tumor are characterized by **pleomorphic nuclei**, indicating significant variation in size and shape typical of malignancy [1]. - The presence of pleomorphic nuclei suggests loss of **cellular differentiation**, a hallmark of anaplasia [2]. *Increased mitosis* - While increased mitotic figures can indicate a **growing tumor**, it does not specifically denote **anaplasia** itself. - Mitosis can be observed in both benign and malignant lesions, making it a non-specific indicator. *p53 mutation* - Although p53 mutations are associated with many cancers, they are not specific to **anaplastic features** in Wilm's tumor. - Anaplastic histology is defined by nuclear characteristics rather than specific genetic mutations. *Large nucleus* - While anaplastic cells can have large nuclei, the **pleomorphism** in size and shape is more definitive for anaplasia [1]. - Simply having a large nucleus does not necessarily reflect the **abnormal variability** that characterizes anaplasia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 278. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 276-278.

Q: Membranous glomerulonephritis with reduced complement levels is seen in?

Systemic Lupus Erythematosus (SLE). ***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.

Q: Renal cell carcinoma is characterized by which of the following histopathological features?

Clear cell morphology with abundant cytoplasm. ***Invades Renal Vein*** - **Renal cell carcinoma** is known for **venous invasion**, particularly involving the renal vein, which can lead to **thrombus formation** [1][2]. - This feature is significant for staging and prognosis, often indicating **advanced disease** [2]. *Hematuria usually absent* - **Hematuria** is often present in renal cell carcinoma, contrary to this assertion. - The presence of **blood in urine** is a common symptom that can raise suspicion for malignancy. *Arises from proximal convoluted tubule* - While renal cell carcinoma originates from the **epithelial cells**, it primarily arises from the **proximal tubule**, but this option lacks the specificity related to its histopathology. - More accurately, the clear cell type is the most common variant associated with this tumor [1]. *More common in females* - Renal cell carcinoma is actually more prevalent in **males**, contradicting this statement. - The male-to-female ratio is approximately **2:1**, making it less common in females. **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.

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

Collagen type IV. ***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.

Q: Nephrocalcinosis in a systemic granulomatous disease is due to:

Overproduction of 1,25 dihydroxy vitamin D. ***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.

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

Focal segmental glomerulosclerosis.. ***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.

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

More common in females. ***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.

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

Presence of immune complex deposits. ***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.

Q: A female who presents with a cough and bloody sputum is diagnosed with granulomatosis with polyangiitis. Which of the following is the characteristic renal histological feature of granulomatosis with polyangiitis?

Focal necrotizing glomerulonephritis. ***Focal necrotizing glomerulonephritis*** - Granulomatosis with polyangiitis is characterized by **focal necrotizing glomerulonephritis**, which is a common renal manifestation [1]. - This histological feature reveals **segmental necrosis** of glomeruli with the presence of crescents, indicative of a **vasculitis-associated kidney injury** [1]. *Minimal change disease* - Primarily associated with **nephrotic syndrome**, does not exhibit the **necrotizing features** typical of granulomatosis with polyangiitis. - Characterized by **foot process effacement** on electron microscopy, which is not relevant in this context. *Rapidly progressive glomerulonephritis* - While granulomatosis may cause this, the specific **histological feature** of interest is the **focal necrotizing pattern** rather than generalized rapid progression. - This term refers to a clinical presentation rather than a distinct histological finding. *Nodular glomerulosclerosis* - Typically associated with **diabetic nephropathy**, not with granulomatosis with polyangiitis. - Histologically manifests as **nodules** in glomeruli, which differ from the **necrotizing lesions** observed in this condition. **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. 536-537.

Question 1

The prognosis of rapidly progressive glomerulonephritis (crescentic GN) depends on

Accepted Answer

Number of crescents

Answer

Size of crescents

Answer

Cellularity of crescents

Answer

Shape of crescents

Question 2

Anaplasia in Wilms' tumor is evident by what features?

Accepted Answer

Pleomorphic nuclei

Answer

p53 mutation

Answer

Increased cell division

Answer

Enlarged nucleus

Question 3

Membranous glomerulonephritis with reduced complement levels is seen in?

Accepted Answer

Systemic Lupus Erythematosus (SLE)

Answer

Hepatitis B infection

Answer

Plasmodium malariae infection

Answer

Syphilis infection

Question 4

Renal cell carcinoma is characterized by which of the following histopathological features?

Accepted Answer

Clear cell morphology with abundant cytoplasm

Answer

Nested/alveolar growth pattern

Answer

High nuclear grade with prominent nucleoli

Answer

Rich capillary network

Question 5

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

Accepted Answer

Collagen type IV

Answer

Collagen type I

Answer

Collagen type III

Answer

Collagen type VII

Question 6

Nephrocalcinosis in a systemic granulomatous disease is due to:

Accepted Answer

Overproduction of 1,25 dihydroxy vitamin D

Answer

Dystrophic calcification

Answer

Mutation in calcium sensing receptors

Answer

Increased reabsorption of calcium

Question 7

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

Accepted Answer

Focal segmental glomerulosclerosis.

Answer

Membranous glomerulonephritis.

Answer

Membranoproliferative glomerulonephritis.

Answer

Minimal change disease.

Question 8

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

Accepted Answer

More common in females

Answer

Invades Renal Vein

Answer

Hematuria may occur

Answer

Arises from proximal convoluted tubule

Question 9

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

Accepted Answer

Presence of immune complex deposits

Answer

Effacement of podocytes on electron microscope

Answer

Normal light microscopy findings

Answer

Good response to steroids in nephrotic syndrome

Question 10

A female who presents with a cough and bloody sputum is diagnosed with granulomatosis with polyangiitis. Which of the following is the characteristic renal histological feature of granulomatosis with polyangiitis?

Accepted Answer

Focal necrotizing glomerulonephritis

Answer

Nodular glomerulosclerosis

Answer

Rapidly progressive glomerulonephritis

Answer

Minimal change disease

Renal Pathology — MCQs

Renal Pathology — MCQs

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