Renal pathology — MCQs
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A 58-year-old woman with HbA1c of 10 % is referred to an ophthalmologist because of vision loss. An image of her retina is shown below, If this patient were to undergo renal biopsy, what will be the pathologic findings?
All are true about the condition shown except:
Which is not a true statement about this anomaly of kidney?
All are correct about the condition shown in the image except: (NEET Pattern 2018)
Which urine crystals are shown in the figure below?
The kidney biopsy image shows presence of:
Kidney biopsy report shown in the image depicts:
Comment on the diagnosis of light microscopy finding in kidney biopsy. (Recent NEET Pattern 2016-17)
All are true about the presentation in kidney biopsy shown except: (Recent NEET Pattern 2016-17)
All are causes of this glomerular presentation except: (Recent NEET Pattern 2016-17)
Renal pathology US Medical PG Practice Questions and MCQs
Question 1: A 58-year-old woman with HbA1c of 10 % is referred to an ophthalmologist because of vision loss. An image of her retina is shown below, If this patient were to undergo renal biopsy, what will be the pathologic findings?
- A. Nodular glomerulosclerosis, mesangial expansion, and basement membrane thickening (Correct Answer)
- B. Scattered crescentic lesions with fibrin and plasma proteins
- C. Vascular intimal thickening and hyaline deposition
- D. Subepithelial immune complex deposits
- E. Wire-loop lesions and subendothelial deposits
Explanation: ***Nodular glomerulosclerosis, mesangial expansion, and basement membrane thickening*** - The patient's high HbA1c and vision loss (suggesting **diabetic retinopathy**) indicate **diabetes mellitus**. The classic renal pathology findings in **diabetic nephropathy** include **Kimmelstiel-Wilson nodules** (nodular glomerulosclerosis), **mesangial expansion**, and **glomerular basement membrane thickening** [1]. - These changes are due to chronic hyperglycemia leading to advanced glycation end-product (AGE) accumulation and hemodynamic changes, causing **glomerular hypertrophy** and **sclerosis** [1]. *Scattered crescentic lesions with fibrin and plasma proteins* - This describes **crescentic glomerulonephritis**, which is characteristic of rapidly progressive glomerulonephritis (RPGN). - While RPGN can cause kidney failure, it is not the primary renal manifestation of long-standing, uncontrolled diabetes. *Vascular intimal thickening and hyaline deposition* - This describes **hyaline arteriolosclerosis**, which is commonly seen in **hypertension** and **diabetes**, affecting afferent and efferent arterioles. - While present in diabetic nephropathy, it is a vascular change and not the primary glomerular lesion that defines diabetic nephropathy. *Subepithelial immune complex deposits* - This is characteristic of **membranous nephropathy**, a common cause of nephrotic syndrome. - It is an immune-mediated disease and not the typical renal pathology associated with uncontrolled diabetes mellitus. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1121-1122.
Question 2: All are true about the condition shown except:
- A. Cysts at junction of distal tubule and collecting duct
- B. Spider leg deformity
- C. Anemia
- D. Low renin due to pressure atrophy of JG apparatus (Correct Answer)
- E. Berry aneurysms
Explanation: ***Low renin due to pressure atrophy of JG apparatus*** - This statement is incorrect. In conditions like **autosomal dominant polycystic kidney disease (ADPKD)**, the expanding cysts can cause **ischemia** of the surrounding renal parenchyma, leading to activation of the **renin-angiotensin-aldosterone system (RAAS)** and **high renin levels**, contributing to hypertension [1]. - **Pressure atrophy** of the JG apparatus leading to low renin is not a characteristic feature of cystic kidney diseases like ADPKD. *Cysts at junction of distal tubule and collecting duct* - **Autosomal dominant polycystic kidney disease (ADPKD)**, a common cystic kidney condition, is characterized by the formation of cysts primarily from the **distal tubules** and **collecting ducts** [2]. - These cysts progressively enlarge, leading to kidney failure. *Spider leg deformity* - **Spider leg deformity** refers to the characteristic appearance of the renal calyces on imaging (e.g., intravenous pyelogram or CT urogram) in **medullary sponge kidney (MSK)**. - This condition involves dilatation of the **collecting ducts** in the renal medulla, which can appear as a "spider leg" or "brush" pattern. *Anemia* - **Anemia** is a common complication in patients with **chronic kidney disease (CKD)**, including those with polycystic kidney disease, as the kidneys lose their ability to produce sufficient **erythropoietin** [1]. - However, in the early stages of ADPKD, patients may sometimes present with **polycythemia** due to increased erythropoietin production from the cystic kidneys, though anemia eventually develops as kidney function declines. **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. 525-526. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 544-545.
Question 3: Which is not a true statement about this anomaly of kidney?
- A. Fusion of lower poles of the kidneys
- B. Association with Turner syndrome
- C. No risk of Wilms tumor (Correct Answer)
- D. Renal function usually is normal
- E. Associated with increased risk of renal calculi
Explanation: ***No risk of Wilms tumor*** - Horseshoe kidney, the anomaly described, actually has an **increased risk of Wilms tumor**, not no risk. - The risk is about 2-8 times higher than in the general population. *Fusion of lower poles of the kidneys* - This is the **classic anatomical description** of a horseshoe kidney, where the lower poles are fused across the midline [1]. - The fusion typically occurs at the **isthmus**, which can be fibrous or parenchymatous. *Association with Turner syndrome* - Horseshoe kidney is indeed **commonly associated with Turner syndrome** (XO karyotype). - Approximately 15-20% of individuals with Turner syndrome have a horseshoe kidney. *Renal function usually is normal* - In most cases, the **renal function of a horseshoe kidney is normal** [1], provided there are no other associated anomalies or complications. - However, they are more prone to complications like **hydronephrosis**, **calculi**, and infections due to altered anatomy. **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. 545-546.
Question 4: All are correct about the condition shown in the image except: (NEET Pattern 2018)
- A. Most common site is middle esophagus (Correct Answer)
- B. Most common gross presentation is fungating subtype
- C. Stage 3 cancer oesophagus has 25 % survival rate
- D. Vomiting of previous day food items
- E. Loss of ganglion cells in myenteric plexus
Explanation: ***Most common site is middle esophagus*** - The question asks for the incorrect statement, and this statement is actually **correct** for esophageal squamous cell carcinoma (SCC), which is the most common type of esophageal cancer globally. - **Squamous cell carcinoma** of the esophagus most frequently occurs in the **middle third** of the esophagus [1]. *Most common gross presentation is fungating subtype* - This statement is incorrect. The most common gross presentation of esophageal carcinoma is the **ulcerative type**, followed by fungating and infiltrative types [1]. - **Fungating tumors** are exophytic and protrude into the lumen, but they are not the most common gross morphology. *Stage 3 cancer oesophagus has 25 % survival rate* - This statement is incorrect. The 5-year survival rate for **Stage III esophageal cancer** is significantly lower, typically ranging from **10-15%**, not 25% [2][3]. - Survival rates for esophageal cancer are generally poor, especially in advanced stages due to early metastasis and late presentation. *Vomiting of previous day food items* - This statement is incorrect. Vomiting of previous day's food items is characteristic of **pyloric stenosis** or **gastric outlet obstruction**, not typically esophageal cancer. - Esophageal cancer usually presents with **dysphagia** (difficulty swallowing) and **regurgitation** of recently ingested food, not undigested food from the previous day [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 766-767. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 349-350. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 765-766.
Question 5: Which urine crystals are shown in the figure below?
- A. Triple phosphate crystals
- B. Uric acid crystals
- C. Cystine crystals
- D. Calcium oxalate dihydrate crystals (Correct Answer)
- E. Calcium oxalate monohydrate crystals
Explanation: ***Calcium oxalate dihydrate crystals*** - The crystals shown are **octahedral** in shape, resembling small **envelopes**, which is characteristic of calcium oxalate dihydrate crystals. - These crystals typically appear in **acidic urine** and are the most common type of crystals that can lead to **kidney stones**. - Found in conditions like hyperoxaluria, ethylene glycol poisoning, and vitamin C excess. *Incorrect: Triple phosphate crystals* - Also known as **struvite crystals**, these have a characteristic **"coffin lid"** appearance. - Form in **alkaline urine** and are associated with urinary tract infections caused by urease-producing bacteria. *Incorrect: Uric acid crystals* - Appear as **rhomboid** or **rosette-shaped** crystals in **acidic urine**. - Associated with hyperuricemia, gout, and tumor lysis syndrome. *Incorrect: Cystine crystals* - Have a distinctive **hexagonal** shape and appear in acidic urine. - Pathognomonic for **cystinuria**, an inherited disorder of amino acid transport. *Incorrect: Calcium oxalate monohydrate crystals* - Have a **dumbbell** or **oval** shape, distinct from the envelope-shaped dihydrate form. - Also associated with hyperoxaluria and ethylene glycol poisoning.
Question 6: The kidney biopsy image shows presence of:
- A. Benign nephrosclerosis
- B. Malignant nephrosclerosis (Correct Answer)
- C. Minimal change disease
- D. Lupus nephritis
- E. Diabetic nephropathy
Explanation: ***Malignant nephrosclerosis*** - Histologically, **malignant nephrosclerosis** is characterized by **fibrinoid necrosis** of afferent arterioles and small arteries, along with **hyperplastic arteriolosclerosis** (onion-skinning) [1][2]. - These changes are indicative of severe, accelerated hypertension causing acute vascular damage in the kidney [1][3]. *Benign nephrosclerosis* - Characterized by **hyaline arteriolosclerosis** (thickening and narrowing of small arteries and arterioles due to deposition of hyaline material) and **fibroelastic hyperplasia** of larger interlobular arteries [4]. - These changes are associated with chronic, long-standing hypertension and typically do not involve fibrinoid necrosis or onion-skinning [3][4]. *Minimal change disease* - On light microscopy, the glomeruli appear normal, hence the term "minimal change." - The characteristic finding is **effacement of foot processes** of podocytes on electron microscopy, which is not described as fibrinoid necrosis or onion-skinning. *Lupus nephritis* - A spectrum of glomerular diseases caused by systemic lupus erythematosus, with various classes showing different histological patterns. - Common findings include **immune complex deposition** (subendothelial, subepithelial, or mesangial), **mesangial proliferation**, and sometimes **wire loop lesions** or **crescent formation**, but not typically fibrinoid necrosis of arterioles as the primary defining feature. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 541-542. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945.
Question 7: Kidney biopsy report shown in the image depicts:
- A. Focal segmental glomerulosclerosis
- B. Nodular glomerulosclerosis (Correct Answer)
- C. Armanni Ebstein changes
- D. Membranoproliferative glomerulonephritis
- E. Diffuse glomerulosclerosis
Explanation: ***Nodular glomerulosclerosis*** - The image likely depicts **Kimmelstiel-Wilson nodules**, which are characteristic of **diabetic nephropathy** and fall under the umbrella of nodular glomerulosclerosis [1]. - These nodules are **acellular, eosinophilic, PAS-positive** masses found in the mesangium [1]. *Focal segmental glomerulosclerosis* - Characterized by **sclerosis** affecting only some glomeruli (**focal**) and only parts of the affected glomeruli (**segmental**). - It typically presents with **effacement of foot processes** on electron microscopy and is a common cause of nephrotic syndrome. *Armanni Ebstein changes* - These are **glycogen-rich vacuolations** seen in the **tubular epithelial cells** of the kidney, particularly in the proximal tubules, in patients with **uncontrolled diabetes mellitus**. - They are a sign of **osmotic nephrosis** due to severe hyperglycemia, not a primary glomerular lesion. *Membranoproliferative glomerulonephritis* - Characterized by **mesangial and endothelial cell proliferation** and **thickening of the glomerular basement membrane** (GBM). - Often shows a **"tram-track" appearance** on light microscopy due to GBM splitting, which is not the primary feature depicted. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1121-1122.
Question 8: Comment on the diagnosis of light microscopy finding in kidney biopsy. (Recent NEET Pattern 2016-17)
- A. Focal segmental glomerulosclerosis
- B. Diffuse glomerulosclerosis
- C. Nodular glomerulosclerosis (Correct Answer)
- D. Minimal change disease
- E. Membranoproliferative glomerulonephritis
Explanation: ***Nodular glomerulosclerosis*** - This finding is characteristic of **diabetic nephropathy**, specifically the **Kimmelstiel-Wilson lesions** [1]. - It involves the formation of **nodular deposits** in the mesangium, leading to glomerulosclerosis. *Focal segmental glomerulosclerosis* - Characterized by **sclerosis** affecting only **some glomeruli** (focal) and only **parts of the glomerular tuft** (segmental). - It is a common cause of **nephrotic syndrome** and is often associated with HIV, heroin abuse, or genetic mutations. *Diffuse glomerulosclerosis* - Implies widespread sclerosis affecting **most or all glomeruli diffusely**. - This is a general term and can be seen in various end-stage renal diseases, not specific to a single primary diagnosis like nodular glomerulosclerosis. *Minimal change disease* - On light microscopy, the glomeruli appear **normal**, hence the term "minimal change" [2]. - The characteristic finding is **effacement of foot processes** on electron microscopy [2], and it is a common cause of nephrotic syndrome in children. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1121. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923.
Question 9: All are true about the presentation in kidney biopsy shown except: (Recent NEET Pattern 2016-17)
- A. Loss of foot processes
- B. IgG and properdin deposits (Correct Answer)
- C. Hyalinosis
- D. Seen with HIV associated nephropathy
- E. Presents with nephrotic syndrome
Explanation: ***IgG and properdin deposits*** - The question asks for what is *not* true about the presentation in a kidney biopsy. **IgG and properdin deposits** are characteristic of **dense deposit disease (DDD)** or C3 glomerulopathy, not typically seen in the context of **focal segmental glomerulosclerosis (FSGS)**, which is often implied by the other options. - FSGS is primarily a podocyte disorder, and while immune deposits can occur, IgG and properdin are not its defining immunofluorescence features. In FSGS, immunofluorescence is negative other than non-specific trapping of IgM and C3 in the segmental lesions [1]. The diagnosis requires absence of immune deposits on IF [4]. *Loss of foot processes* - **Loss of foot processes** (podocyte effacement) is a hallmark ultrastructural finding in conditions causing **proteinuria**, including **focal segmental glomerulosclerosis (FSGS)** and minimal change disease [1][3]. - This morphological change is directly responsible for increased glomerular permeability to proteins. Podocyte injury is an underlying mechanism of proteinuria in FSGS [3]. *Hyalinosis* - **Hyalinosis** refers to the accumulation of homogeneous, eosinophilic material, often plasma proteins, within the glomerulus. - It is a characteristic feature of **focal segmental glomerulosclerosis (FSGS)**, particularly in the sclerotic segments, with segmental obliteration of glomerular capillary tufts by sclerosis frequently accompanied by hyalinosis [1]. *Seen with HIV associated nephropathy* - **HIV-associated nephropathy (HIVAN)** is a specific form of **collapsing focal segmental glomerulosclerosis (FSGS)** [1][2]. - It is characterized by prominent tubular microcysts and severe interstitial inflammation and fibrosis, in addition to the collapsing glomerular lesions. FSGS may be secondary to infection such as HIV [3], and the collapsing variant has an unfavorable course [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. 531-532. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 924-925. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 530-531.
Question 10: All are causes of this glomerular presentation except: (Recent NEET Pattern 2016-17)
- A. HIV
- B. Reflux nephropathy (Correct Answer)
- C. Hepatitis B
- D. Heroin abuse
- E. Obesity
Explanation: ***Reflux nephropathy*** - This condition primarily causes **tubulointerstitial damage** and **scarring**, leading to chronic kidney disease, but it is not a direct cause of a primary glomerular presentation like **focal segmental glomerulosclerosis (FSGS)**. - While it can lead to proteinuria, it's usually due to secondary glomerular changes from chronic damage rather than a primary glomerular disease. *HIV* - **HIV-associated nephropathy (HIVAN)** is a common cause of **collapsing FSGS**, a specific glomerular presentation [1] [2]. - It is characterized by rapid progression to end-stage renal disease and often presents with heavy proteinuria [1]. *Hepatitis B* - Hepatitis B infection is strongly associated with **membranous nephropathy** and, less commonly, with **membranoproliferative glomerulonephritis (MPGN)**, both of which are distinct glomerular presentations [1]. - These conditions involve immune complex deposition in the glomeruli. *Heroin abuse* - Heroin abuse is a well-known cause of **focal segmental glomerulosclerosis (FSGS)**, often presenting as **heroin-associated nephropathy** [3] [4]. - This condition typically leads to significant proteinuria and progressive renal failure [3] [4]. **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. 531-532. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 924-925. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 530-531.
Practice by Chapter
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