Renal Pathology Practice Questions

Q: Michaelis-Gutmann bodies are seen in:

Malakoplakia. ***Malakoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic cytoplasmic inclusions found in histiocytes (von Hansemann cells) in **malakoplakia**. - These bodies represent partially digested bacterial fragments, particularly from *E. coli*, and are rich in iron and calcium. *Xanthogranulomatous pyelonephritis* - This condition is characterized by a destructive inflammatory process in the kidney with **foamy macrophages** (xanthoma cells) and often associated with chronic obstruction and infection [1]. - It does **not** feature Michaelis-Gutmann bodies; rather, it often shows a collection of lipid-laden macrophages. *Renal osteodystrophy* - This refers to a spectrum of **bone abnormalities** that occur in patients with **chronic kidney disease** [2], [3]. - It involves disruptions in bone turnover and mineralization due to metabolic disturbances, not the presence of specific bacterial inclusions [2]. *Nail patella syndrome* - This is a rare **autosomal dominant genetic disorder** affecting bone, joint, and kidney development. - It is characterized by small or absent **patellae**, fingernail and toenail abnormalities, and is associated with mutations in the *LMX1B* gene. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 668-669. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1194-1195.

Q: In minimal change disease following is not seen -

Normal electron microscopic appearance. ***Normal electron microscopic appearance*** - In **minimal change disease**, electron microscopy characteristically shows **effacement of podocyte foot processes**, which is not a normal appearance [1]. - This effacement is the underlying cause for the increased permeability of the glomerular filtration barrier leading to proteinuria. *Light microscopy normal* - **Minimal change disease** is named for the fact that the **glomeruli appear normal** or nearly normal on light microscopy [1]. - No significant inflammatory changes, cellular proliferation, or basement membrane thickening are typically visible [1]. *Good response to steroids* - **Minimal change disease** is known for its **excellent response to corticosteroids**, with remission of proteinuria in most cases [1]. - This distinguishes it from many other causes of nephrotic syndrome, which often have a poorer response to steroids. *Massive proteinuria* - **Massive proteinuria** (typically >3.5 g/24 hours in adults) is a **hallmark characteristic** of nephrotic syndrome, of which minimal change disease is a primary cause [1]. - The loss of large amounts of protein in the urine leads to symptoms like edema and hypoalbuminemia [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 921-923, 927-928.

Q: A diagnosed case of SLE has renal biopsy finding suggestive of mesangial proliferative nephropathy. It belongs to which class of lupus nephritis:

Class II. ***Class II*** - **Mesangial proliferative lupus nephritis (Class II)** is characterized by mesangial hypercellularity and/or mesangial matrix expansion with mesangial immune deposits. - While it can be associated with proteinuria, it generally has a **better prognosis** and less severe clinical manifestations compared to more advanced classes of lupus nephritis. *Class IV* - **Class IV lupus nephritis (diffuse lupus nephritis)** is the most common and severe form, characterized by extensive immune deposits and inflammation in the glomerular capillaries [1]. - This class typically presents with significant proteinuria, hematuria, renal insufficiency, and often requires **aggressive immunosuppressive therapy** [1]. *Class III* - **Class III lupus nephritis (focal lupus nephritis)** involves proliferative lesions affecting less than 50% of glomeruli, with immune deposits primarily in the subendothelial space [1]. - It often manifests with proteinuria and hematuria, and can progress to more severe forms if not adequately treated [1]. *Class I* - **Class I lupus nephritis (minimal mesangial lupus nephritis)** is characterized by normal glomeruli on light microscopy but with mesangial immune deposits on immunohistochemistry or electron microscopy [1]. - It is typically associated with **minimal or no clinical symptoms** and a very good prognosis, rarely leading to significant renal dysfunction. **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: A 5-year-old child suffering from nephrotic syndrome is responding well to steroid therapy. What would be the most likely finding on light microscopy?

No finding. ***No finding*** - The most common cause of nephrotic syndrome in children is **minimal change disease (MCD)**. Histologically, MCD is characterized by **normal-appearing glomeruli** on light microscopy, hence "no finding." [1] - The characteristic changes in MCD, such as **effacement of podocyte foot processes**, are only visible on **electron microscopy**, not light microscopy. [1] *Fusion of foot process* - This change, more accurately described as **effacement (flattening and merging) of podocyte foot processes**, is the **hallmark lesion of minimal change disease**. [1] - However, this finding is detectable only with **electron microscopy**, not with light microscopy. [1] *Basement membrane thickening* - **Thickening of the glomerular basement membrane (GBM)** is characteristic of diseases like **membranous nephropathy** [1] or **diabetic nephropathy**. - These conditions typically present differently and are less common causes of nephrotic syndrome in children, especially those responding well to steroids. [1] *Hypercellular glomeruli* - **Glomerular hypercellularity** suggests proliferative glomerulonephritis, such as post-streptococcal glomerulonephritis or IgA nephropathy. [1] - These conditions usually do not cause nephrotic syndrome as their primary presentation and are not characterized by good response to steroid therapy in children. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-928.

Q: In minimal change disease, which of the following is seen?

No immunodeposits. ***No immunodeposits*** - Minimal change disease (MCD) is characterized by the **absence of immune complex deposition** in the glomeruli [1]. - This lack of immunodeposits is a key diagnostic feature, distinguishing it from other types of glomerulonephritis [1]. *Immunodeposits in blood vessels* - Immunodeposits in blood vessels are typically associated with **vasculitic conditions**, such as ANCA-associated vasculitis or cryoglobulinemic vasculitis. - This finding is not characteristic of minimal change disease, which primarily affects the podocytes of the glomeruli. *Immunodeposits in mesangium* - Mesangial immunodeposits are characteristic of conditions like **IgA nephropathy** or **membranoproliferative glomerulonephritis** [1]. - These conditions involve immune complex deposition within the mesangial matrix, which is absent in minimal change disease [1]. *Immunodeposits in glomerulus* - While "glomerulus" is a broad term, the absence of **immune complex deposition** within the glomerulus (including capillary loops, mesangium, and subepithelial/subendothelial spaces) is precisely what defines minimal change disease [1]. - The primary abnormality in MCD is **podocyte foot process effacement**, not immune complex deposition [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Q: Xanthogranulomatous infection is caused by:

All of the options. ***All of the options*** - **Xanthogranulomatous pyelonephritis (XGP)** is a severe, chronic infectious process of the kidney, often associated with a combination of factors including **urinary tract obstruction**, specific bacterial infections, and the presence of kidney stones (nephrolithiasis) [1]. - **Proteus mirabilis** is a common cause of XGP due to its ability to produce urease, which hydrolyzes urea into ammonia, increasing urinary pH and promoting the formation of struvite stones, thus acting in concert with obstruction and stones [1]. *Nephrolithiasis* - While **kidney stones** are a major predisposing factor for XGP, they do not solely cause the infection; they primarily create an environment conducive to bacterial colonization and obstruction. - The presence of stones, particularly **struvite stones**, can lead to persistent infection and the characteristic inflammatory response seen in XGP. *Proteus Mirabilis* - **Proteus mirabilis** is frequently isolated in cases of XGP, but it typically acts in conjunction with urinary obstruction and/or nephrolithiasis [1]. - This bacterium contributes significantly to the pathophysiology by promoting stone formation and maintaining a chronic infectious state, but it is not the sole cause. *Urinary obstruction* - **Urinary tract obstruction** is a key predisposing factor that prevents proper drainage, leading to stasis and increasing susceptibility to infection [1]. - While essential for the development of XGP, obstruction alone does not directly cause the characteristic xanthogranulomatous inflammation without the presence of bacteria and often stones. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940.

Q: A 14-year-old boy presents to the hospital with severe leg swelling that started 2 weeks ago. He also notes feeling tired and having little energy to play sports with his friends. His past medical history is negative and he is not taking any medications. On examination, his blood pressure is 163/96 mm Hg, and there is pedal edema up to his knees, as well as periorbital edema. His remaining clinical exam is normal. A urinalysis is positive for 3+ proteinuria and on 24-hour urine collection the total protein excretion is 5.4 grams/day. He undergoes a renal biopsy and there are no changes seen on light microscopy, but electron microscopy shows foot process fusion and no deposits on the membranes. Which of the following is the most likely diagnosis?

minimal change disease. ***minimal change disease*** - This diagnosis is strongly supported by the patient's age (child/adolescent), presentation with **nephrotic syndrome** (edema, severe proteinuria), and characteristic renal biopsy findings of **foot process fusion** on electron microscopy with **no changes on light microscopy**. [1] - **Minimal change disease** is the most common cause of nephrotic syndrome in children and typically presents with sudden onset of edema and significant proteinuria without hematuria or other signs of inflammation. [1], [2] *membranous glomerulonephritis* - This condition typically presents with **nephrotic syndrome** but is more common in adults and usually shows **thickening of the glomerular basement membrane** with subepithelial deposits on electron microscopy, which were not seen in this case. - Light microscopy in membranous glomerulonephritis often reveals diffuse capillary wall thickening, which is absent here. *focal glomerulosclerosis* - While **focal segmental glomerulosclerosis (FSGS)** can cause nephrotic syndrome and foot process effacement, light microscopy would show **sclerosis in segments of some glomeruli**, which is not described. [2] - FSGS is often characterized by the presence of **scarring** in the glomeruli, which is absent in this patient's biopsy report. [3] *mesangial proliferative glomerulonephritis* - This would show **proliferation of mesangial cells** on light microscopy, often associated with mesangial immune deposits, which is not consistent with the "no changes seen on light microscopy" finding. - This condition frequently presents with **hematuria** in addition to proteinuria, which is not mentioned in the patient's symptoms.

Q: Most common nephropathy in world is?

IgA nephropathy. ***IgA nephropathy*** - **IgA nephropathy**, also known as **Berger's disease**, is the most common cause of primary glomerulonephritis worldwide [1]. - It is characterized by the deposition of **IgA immune complexes** in the glomeruli [1]. *FSGS* - **Focal segmental glomerulosclerosis (FSGS)** is a significant cause of nephrotic syndrome but is not the most common primary glomerulonephritis overall [1]. - It is more prevalent in certain populations and is a leading cause of **end-stage renal disease**. *Minimal Change ds* - **Minimal change disease** is the most common cause of nephrotic syndrome in children but is less common in adults and overall [1]. - It typically presents with **nephrotic range proteinuria** and a characteristic foot process effacement on electron microscopy. *Adult PSGN* - **Post-streptococcal glomerulonephritis (PSGN)** typically occurs after a streptococcal infection and is acute, not the most common chronic nephropathy [1]. - While it can occur in adults, it is far more common in children and is characterized by a latency period after infection [1].

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].

Question 1

Michaelis-Gutmann bodies are seen in:

Accepted Answer

Malakoplakia

Answer

Xanthogranulomatous pyelonephritis

Answer

Renal osteodystrophy

Answer

Nail patella syndrome

Question 2

In minimal change disease following is not seen -

Accepted Answer

Normal electron microscopic appearance

Answer

Light microscopy normal

Answer

Good response to steroids

Answer

Massive proteinuria

Question 3

A diagnosed case of SLE has renal biopsy finding suggestive of mesangial proliferative nephropathy. It belongs to which class of lupus nephritis:

Accepted Answer

Class II

Answer

Class IV

Answer

Class III

Answer

Class I

Question 4

A 5-year-old child suffering from nephrotic syndrome is responding well to steroid therapy. What would be the most likely finding on light microscopy?

Accepted Answer

No finding

Answer

Fusion of foot process

Answer

Basement membrane thickening

Answer

Hypercellular glomeruli

Question 5

In minimal change disease, which of the following is seen?

Accepted Answer

No immunodeposits

Answer

Immunodeposits in blood vessels

Answer

Immunodeposits in mesangium

Answer

Immunodeposits in glomerulus

Question 6

A 2 year old child is seen on a routine visit in the pediatric clinic. Abdominal examination demonstrates a palpable, non-tender mass on the left side of the abdomen. The mother had no idea the mass was present and the pediatrician did not note the presence of the mass at the child's 18-month's visit for immunisation. Physical examination is otherwise unremarkable. If a CT guided biopsy of the mass were performed, which of the following histological patterns would be most suggestive of the likely diagnosis?

Accepted Answer

Triphasic pattern with tubule formation, spindle cells, and blastemal elements

Answer

Invasive papillary lesions with delicate connective tissue stalk covered with epithelium resembling that lining the bladder.

Answer

Cords of clear cells with rounded or polygonal shape and abundant clear cytoplasm

Answer

Small dark cells embedded in a finely fibrillar matrix with formation of numerous rosettes

Question 7

Xanthogranulomatous infection is caused by:

Accepted Answer

All of the options

Answer

Nephrolithiasis

Answer

Proteus Mirabilis

Answer

Urinary obstruction

Question 8

A 14-year-old boy presents to the hospital with severe leg swelling that started 2 weeks ago. He also notes feeling tired and having little energy to play sports with his friends. His past medical history is negative and he is not taking any medications. On examination, his blood pressure is 163/96 mm Hg, and there is pedal edema up to his knees, as well as periorbital edema. His remaining clinical exam is normal. A urinalysis is positive for 3+ proteinuria and on 24-hour urine collection the total protein excretion is 5.4 grams/day. He undergoes a renal biopsy and there are no changes seen on light microscopy, but electron microscopy shows foot process fusion and no deposits on the membranes. Which of the following is the most likely diagnosis?

Accepted Answer

minimal change disease

Answer

membranous glomerulonephritis

Answer

focal glomerulosclerosis

Answer

mesangial proliferative glomerulonephritis

Question 9

Most common nephropathy in world is?

Accepted Answer

IgA nephropathy

Answer

FSGS

Answer

Minimal Change ds

Answer

Adult PSGN

Question 10

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

Renal Pathology — MCQs

Renal Pathology — MCQs

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