Renal Pathology — MCQs
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A 45-year-old man presents with hematuria. Renal biopsy demonstrates a focal necrotizing glomerulitis with crescent formation. The patient has a history of intermittent hemoptysis and intermittent chest pain of moderate intensity. A previous chest x-ray had demonstrated multiple opacities, some of which were cavitated. The patient also has chronic cold-like nasal symptoms. Which of the following is the most likely diagnosis?
Which of the following statements about Xanthogranulomatous pyelonephritis is not true?
Which of the following is a characteristic histological finding in Alport syndrome?
The important light microscopical features in Alport syndrome are all, EXCEPT:
A 45-year-old male with a history of recurrent ureteric calculi presented with fever. Following right-sided nephrectomy, gross and histological views were obtained. What is your diagnosis?
Which condition is characterized by effacement of the foot processes of the podocytes?
Post-streptococcal glomerulonephritis (PSGN) is associated with which of the following?
Post-infective glomerulonephritis typically presents as:
SUPAR is a blood marker for which of the following conditions?
Which protein defect causes Finnish nephrotic syndrome?
Renal Pathology Indian Medical PG Practice Questions and MCQs
Question 471: A 45-year-old man presents with hematuria. Renal biopsy demonstrates a focal necrotizing glomerulitis with crescent formation. The patient has a history of intermittent hemoptysis and intermittent chest pain of moderate intensity. A previous chest x-ray had demonstrated multiple opacities, some of which were cavitated. The patient also has chronic cold-like nasal symptoms. Which of the following is the most likely diagnosis?
- A. Aspergillosis
- B. Polyarteritis nodosa
- C. Renal carcinoma metastatic to the lung
- D. Wegener's granulomatosis (Correct Answer)
Explanation: ### Explanation The clinical presentation describes a classic triad of upper respiratory tract, lower respiratory tract, and renal involvement, which is the hallmark of **Granulomatosis with Polyangiitis (GPA)**, formerly known as **Wegener’s Granulomatosis** [1]. **1. Why Wegener’s Granulomatosis is Correct:** * **Upper Respiratory Tract:** Chronic "cold-like" nasal symptoms (often manifesting as sinusitis or saddle-nose deformity) [1]. * **Lower Respiratory Tract:** Hemoptysis and chest pain with imaging showing **cavitary nodules/opacities** [5]. * **Renal Involvement:** Focal necrotizing glomerulitis with **crescents** (Rapidly Progressive Glomerulonephritis - RPGN) [2], [4]. * **Pathology:** It is a small-vessel vasculitis characterized by necrotizing granulomas and is strongly associated with **c-ANCA (PR3-ANCA)** [1], [3]. **2. Why the Other Options are Incorrect:** * **A. Aspergillosis:** While it can cause cavitary lung lesions (fungal ball), it does not typically cause necrotizing glomerulitis or chronic upper airway symptoms in an immunocompetent host. * **B. Polyarteritis Nodosa (PAN):** PAN is a medium-vessel vasculitis. While it involves the kidney (causing microaneurysms and hypertension), it characteristically **spares the lungs** [1], [5]. * **C. Renal Cell Carcinoma (RCC):** While RCC can cause hematuria and lung metastases ("cannonball" lesions), it would not explain the necrotizing glomerulitis or the chronic upper respiratory symptoms. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Triad:** Upper RT + Lower RT + Kidneys = GPA [4]. * **Serology:** c-ANCA (anti-proteinase 3) is highly specific (>90%) [1], [3]. * **Biopsy:** Look for "geographic necrosis" and palisading granulomas. * **Treatment:** Cyclophosphamide and Corticosteroids (Rituximab is an alternative). * **Differential:** Goodpasture Syndrome also presents with lung-renal symptoms but **lacks upper airway involvement** and shows linear IgG deposits on immunofluorescence [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 931-933. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [4] 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. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519.
Question 472: Which of the following statements about Xanthogranulomatous pyelonephritis is not true?
- A. Foam cells are seen
- B. Associated with tuberculosis (Correct Answer)
- C. Yellow nodules are seen
- D. Giant cells may be seen
Explanation: **Xanthogranulomatous Pyelonephritis (XGP)** is a chronic, destructive form of pyelonephritis characterized by the replacement of renal parenchyma with granulomatous tissue. ### **Explanation of the Correct Answer** **Option B (Associated with tuberculosis) is NOT true.** XGP is primarily associated with **chronic urinary tract infections (UTIs)** caused by urea-splitting organisms, most commonly ***Proteus mirabilis*** and ***Escherichia coli*** [1]. It is not caused by *Mycobacterium tuberculosis*. While both conditions involve granulomatous inflammation, XGP is a response to chronic bacterial infection and urinary obstruction (often by staghorn calculi), whereas renal TB presents with caseating necrosis and different histopathological markers. ### **Analysis of Other Options** * **Option A (Foam cells are seen):** This is a hallmark feature. XGP is characterized by an accumulation of **lipid-laden macrophages (xanthoma cells)**, which give the tissue its characteristic "foamy" appearance [1]. * **Option C (Yellow nodules are seen):** Macroscopically, XGP presents as large, orange-yellow nodules that can mimic Renal Cell Carcinoma (RCC) [1]. This yellow color is due to the high lipid content within the foam cells. * **Option D (Giant cells may be seen):** Histology typically shows a mixture of plasma cells, lymphocytes, neutrophils, and **multinucleated giant cells** as part of the chronic inflammatory infiltrate [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **The "Great Mimicker":** XGP is often mistaken for Renal Cell Carcinoma (RCC) on imaging due to its mass-like appearance [1]. * **The "Bear Paw" Sign:** On CT scan, the cross-sectional appearance of dilated calyces and thinned cortex resembles a bear's paw. * **Association:** Strongly linked with **Staghorn calculi** (struvite stones) and chronic obstruction [1]. * **Michaelis-Gutmann bodies:** These are NOT seen in XGP; they are the hallmark of **Malakoplakia**, another chronic inflammatory renal condition. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940.
Question 473: Which of the following is a characteristic histological finding in Alport syndrome?
- A. Foamy cells in the interstitium
- B. Foamy cells in tubular epithelial cells
- C. Thickening of the glomerular basement membrane (GBM) (Correct Answer)
- D. Thinning of the glomerular basement membrane (GBM)
Explanation: **Explanation:** **Alport Syndrome** is a hereditary nephritis caused by mutations in the genes encoding the **α-chains of Type IV collagen** (most commonly *COL4A5*). Type IV collagen is a structural cornerstone of the Glomerular Basement Membrane (GBM) [1]. 1. **Why Option C is Correct:** The hallmark of Alport syndrome under electron microscopy (EM) is the **irregular thickening and thinning** of the GBM with **lamination** (splitting) of the lamina densa. This creates a classic **"basket-weave" appearance**. While both thinning and thickening occur, the progressive, irregular thickening and splitting are the diagnostic pathological features that distinguish it from Thin Basement Membrane Disease [1]. 2. **Why Other Options are Incorrect:** * **Option A & B:** While "foam cells" (lipid-laden macrophages) can be seen in the interstitium in Alport syndrome, they are a **non-specific** reactive finding to proteinuria and are not the primary diagnostic histological characteristic of the disease. They are not typically found in the tubular epithelial cells. * **Option D:** Although thinning of the GBM is seen in the *early* stages of Alport syndrome, it is the defining feature of **Thin Basement Membrane Disease (Benign Familial Hematuria)** [1]. In Alport syndrome, the pathology progresses to the characteristic thickened, split membrane. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most commonly **X-linked Dominant** [1]. * **Clinical Triad:** Hereditary nephritis (hematuria/ESRD), **Sensorineural deafness**, and Ocular defects (**Anterior Lenticonus**) [1]. * **Diagnosis:** EM is the gold standard ("Basket-weave" appearance). Immunofluorescence shows a lack of staining for Type IV collagen α-chains [1]. * **Differential:** Always distinguish from Thin Basement Membrane Lesion, which presents with isolated hematuria but lacks deafness and the "basket-weave" GBM [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930.
Question 474: The important light microscopical features in Alport syndrome are all, EXCEPT:
- A. Interstitial fibrosis
- B. Tubular hypertrophy (Correct Answer)
- C. Segmental proliferative
- D. Glomerular changes
Explanation: Alport Syndrome is a hereditary nephritis caused by mutations in the **COL4A3, COL4A4, or COL4A5** genes, leading to defective Type IV collagen synthesis. This primarily affects the basement membranes of the kidney, eye, and cochlea [1]. **Why "Tubular Hypertrophy" is the correct answer:** In Alport syndrome, the chronic progression of the disease leads to **tubular atrophy**, not hypertrophy [1]. As the glomeruli become sclerosed and interstitial fibrosis sets in, the associated tubules undergo degenerative changes, leading to wasting and atrophy [1]. **Analysis of Incorrect Options:** * **Glomerular changes:** Early light microscopy may be normal, but as the disease progresses, it typically shows focal segmental glomerulosclerosis (FSGS) or global sclerosis [1]. * **Segmental proliferative:** Some cases exhibit focal or diffuse mesangial proliferation or segmental proliferative glomerulonephritis before progressing to sclerosis. * **Interstitial fibrosis:** This is a hallmark of chronic renal involvement in Alport syndrome [1]. A classic light microscopic finding is the presence of **interstitial foam cells** (lipid-laden macrophages), which result from the malabsorption of tubular lipids. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (85%). * **Electron Microscopy (Gold Standard):** Shows characteristic **"Basket-weave appearance"** due to irregular thickening, thinning, and splitting of the Glomerular Basement Membrane (GBM). * **Clinical Triad:** 1. Hereditary Nephritis (Hematuria/ESRD), 2. Sensorineural hearing loss, 3. Ocular defects (Anterior Lenticonus is pathognomonic). * **Diagnosis:** Skin biopsy can sometimes be used for diagnosis (staining for the alpha-5 chain of Type IV collagen) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930.
Question 475: A 45-year-old male with a history of recurrent ureteric calculi presented with fever. Following right-sided nephrectomy, gross and histological views were obtained. What is your diagnosis?
- A. Chronic pyelonephritis with hydronephrosis (Correct Answer)
- B. Renal cell carcinoma
- C. Autosomal dominant polycystic kidney disease
- D. Cystic dysplastic kidney
Explanation: ***Chronic pyelonephritis with hydronephrosis*** - History of **recurrent ureteric calculi** leads to chronic **obstruction** causing **hydronephrosis** and subsequent chronic pyelonephritis with characteristic **thyroidization** pattern. - Gross findings show **dilated renal pelvis and calyces** with **cortical thinning**, while histology reveals **colloid-like tubular casts**, **periglomerular fibrosis**, and **chronic lymphocytic infiltrate**. *Renal cell carcinoma* - Typically presents as a **solid mass** with **clear cell** or **papillary architecture**, not as dilated collecting system with inflammatory changes. - Usually shows **hemorrhage** and **necrosis** on gross examination, lacking the **hydronephrotic** changes seen with obstruction. *Autosomal dominant polycystic kidney disease* - Characterized by **multiple large cysts** throughout both kidneys with **enlarged kidney size**, not unilateral involvement with calculi history. - Family history is usually positive and presents with **bilateral** involvement and **hypertension**, without the inflammatory thyroidization pattern. *Cystic dysplastic kidney* - A **developmental anomaly** presenting in **neonates/infants** with **primitive ducts** and **cartilage formation** on histology. - Not associated with **calculi** or **infection**, and shows **dysplastic tissue** rather than inflammatory changes and thyroidization.
Question 476: Which condition is characterized by effacement of the foot processes of the podocytes?
- A. Minimal change disease (Correct Answer)
- B. Focal segmental glomerulosclerosis
- C. Acute glomerulonephritis
- D. Membranous nephropathy
Explanation: **Explanation:** **Minimal Change Disease (MCD)** is the most common cause of nephrotic syndrome in children [1]. The hallmark of this condition is the **diffuse effacement (flattening/fusion) of the foot processes of podocytes**, which is visible only under **Electron Microscopy (EM)** [2]. Under Light Microscopy, the glomeruli appear normal (hence "minimal change"), and Immunofluorescence is typically negative [1]. The underlying pathophysiology involves T-cell-mediated cytokine production that damages the glomerular polyanion charge, leading to selective proteinuria (mainly albumin) [2]. **Analysis of Incorrect Options:** * **B. Focal Segmental Glomerulosclerosis (FSGS):** While FSGS also shows podocyte effacement, its defining feature is segmental scarring (sclerosis) of some glomeruli visible on Light Microscopy [4]. In the context of "characteristic" findings for exams, MCD is the classic answer for isolated foot process effacement [1]. * **C. Acute Glomerulonephritis (PSGN):** This is a nephritic syndrome characterized by hypercellularity of the glomeruli and subepithelial "humps" (immune complexes) on EM, rather than primary podocyte effacement. * **D. Membranous Nephropathy:** This is characterized by diffuse thickening of the glomerular basement membrane (GBM) due to subepithelial deposits, creating a "spike and dome" appearance on silver stains [3]. **High-Yield Pearls for NEET-PG:** * **MCD Treatment:** Highly responsive to **Corticosteroids** (Steroid-sensitive) [2]. * **Associated Condition:** Hodgkin Lymphoma (in adults). * **Proteinuria Type:** Highly selective (Albuminuria) [2]. * **EM is the Gold Standard:** Necessary for diagnosis because Light Microscopy and Immunofluorescence are unremarkable [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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921. [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 477: Post-streptococcal glomerulonephritis (PSGN) is associated with which of the following?
- A. Subepithelial immune deposits
- B. Nephritis along with acute renal failure
- C. Low complement levels
- D. All of the above (Correct Answer)
Explanation: Post-streptococcal glomerulonephritis (PSGN) is a classic example of a **Type III hypersensitivity reaction** occurring 1–4 weeks after a Group A Beta-hemolytic Streptococcal infection (pharyngitis or impetigo) [1]. * **Subepithelial immune deposits (Option A):** On electron microscopy, PSGN is characterized by large, electron-dense **"subepithelial humps"** [1]. These represent the deposition of immune complexes (IgG, IgM, and C3) between the epithelial cells (podocytes) and the glomerular basement membrane. * **Nephritis and Acute Renal Failure (Option B):** PSGN typically presents as an **Acute Nephritic Syndrome** [1]. Clinical features include hematuria (cola-colored urine), hypertension, and periorbital edema. In severe cases, the inflammatory process significantly reduces the Glomerular Filtration Rate (GFR), leading to oliguria and acute renal failure. * **Low Complement Levels (Option C):** The pathogenesis involves the activation of the **alternative complement pathway**. This leads to the consumption of serum complement proteins, resulting in **low C3 levels**. Notably, C4 levels usually remain normal. Since all individual statements are hallmark features of the disease, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Light Microscopy:** Shows "Starry sky" or "Lumpy-bumpy" appearance on Immunofluorescence (C3 and IgG) [1]. * **Serology:** Elevated ASO titers (common after pharyngitis) or Anti-DNase B (more sensitive after skin infections/impetigo). * **Prognosis:** Excellent in children (95% recover completely); however, adults have a higher risk of progressing to Chronic Kidney Disease (CKD) or RPGN [1]. * **Complement Recovery:** C3 levels typically return to normal within 6–8 weeks. If they remain low, consider Membranoproliferative Glomerulonephritis (MPGN). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-917.
Question 478: Post-infective glomerulonephritis typically presents as:
- A. Acute renal failure
- B. Nephrotic syndrome
- C. Nephritic syndrome (Correct Answer)
- D. Asymptomatic hematuria
Explanation: **Explanation:** **Post-Infectious Glomerulonephritis (PSGN)** is the classic prototype of **Nephritic Syndrome** [1]. It typically occurs 1–3 weeks after a Group A Beta-hemolytic Streptococcal infection (pharyngitis or impetigo). The underlying mechanism is a **Type III Hypersensitivity reaction**, where immune complexes (containing the SpeB antigen) deposit in the subepithelial space, leading to the characteristic "lumpy-bumpy" appearance on immunofluorescence and "subepithelial humps" on electron microscopy [1], [4]. **Why Nephritic Syndrome is correct:** Nephritic syndrome is characterized by an inflammatory rupture of the glomerular capillaries [3]. This leads to the classic clinical triad: 1. **Hematuria:** Often described as "cola-colored" or "smoky" urine due to RBC casts [3]. 2. **Hypertension and Edema:** Resulting from salt and water retention [3]. 3. **Azotemia:** Decreased GFR leading to oliguria and rising creatinine [3]. **Why other options are incorrect:** * **Acute Renal Failure (ARF):** While PSGN can cause a transient decline in renal function, it rarely progresses to full-blown ARF or Rapidly Progressive Glomerulonephritis (RPGN) in children. * **Nephrotic Syndrome:** This is characterized by massive proteinuria (>3.5g/day), hypoalbuminemia, and hyperlipidemia (e.g., Minimal Change Disease) [2]. PSGN involves "sub-nephrotic" range proteinuria. * **Asymptomatic Hematuria:** This is more characteristic of IgA Nephropathy (Berger’s disease) or Alport Syndrome, where there is persistent or recurrent hematuria without the full systemic inflammatory features of PSGN. **High-Yield Pearls for NEET-PG:** * **Serology:** Low C3 levels are hallmark; C4 is usually normal. ASO titers are elevated in post-pharyngeal cases, while Anti-DNase B is more sensitive for post-skin infections. * **Morphology:** Light microscopy shows a "starry sky" or "garland" pattern of granular deposits [4]. * **Prognosis:** Excellent in children (>95% recover); more likely to progress to chronic renal failure in adults. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 527-528. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 918-919. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 915-916.
Question 479: SUPAR is a blood marker for which of the following conditions?
- A. Minimal change disease
- B. Membranous nephropathy
- C. Focal segmental glomerulosclerosis (Correct Answer)
- D. All the above
Explanation: **suPAR (Soluble Urokinase Plasminogen Activator Receptor)** is a circulating protein that has emerged as a key biomarker and potential pathogenic factor for **Focal Segmental Glomerulosclerosis (FSGS)**, particularly the primary (idiopathic) form. 1. **Why FSGS is correct:** Research indicates that high levels of suPAR in the blood bind to and activate **$\beta$3 integrins** on the surface of podocytes. This activation leads to podocyte foot process effacement, detachment, and subsequent proteinuria. It is especially useful in clinical practice to differentiate primary FSGS from other causes [1] and to predict the risk of recurrence after kidney transplantation. 2. **Why other options are incorrect:** * **Minimal Change Disease (MCD):** While MCD also involves podocyte injury, it is primarily considered a T-cell mediated cytokine disorder [2]. suPAR levels are typically not elevated in MCD, making it a useful marker to distinguish FSGS from MCD. * **Membranous Nephropathy (MN):** The hallmark biomarker for primary MN is the **PLA2R (Phospholipase A2 Receptor) antibody** [3]. suPAR does not play a role in the pathogenesis of the subepithelial deposits seen in MN. **High-Yield Pearls for NEET-PG:** * **FSGS Hallmark:** Light microscopy shows segmental sclerosis in some (focal) glomeruli [1]. * **Electron Microscopy:** Shows global effacement of podocyte foot processes (similar to MCD, but with structural scarring) [2]. * **Genetic Association:** Mutations in the **APOL1 gene** (common in African lineage) are strongly associated with increased susceptibility to FSGS [2]. * **Other Markers:** While suPAR is a circulating factor, **CD80 (B7-1)** is another molecule studied in podocyte injury pathways. **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. 530-531. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-928. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 921-922.
Question 480: Which protein defect causes Finnish nephrotic syndrome?
- A. Nephrin (Correct Answer)
- B. Podocin
- C. Alpha actinin
- D. CD2 activated protein
Explanation: **Explanation:** **Congenital Nephrotic Syndrome of the Finnish type (CNF)** is an autosomal recessive disorder characterized by massive proteinuria starting in utero or shortly after birth. 1. **Why Nephrin is correct:** The primary defect in Finnish nephrotic syndrome is a mutation in the **NPHS1 gene**, which encodes the protein **Nephrin**. Nephrin is a key transmembrane glycoprotein located in the **slit diaphragm** between podocyte foot processes [1]. It acts as a structural scaffold and signaling molecule; its absence leads to the collapse of the filtration barrier, resulting in profound albuminuria and a characteristic "microcystic" dilation of the proximal tubules. 2. **Why the other options are incorrect:** * **Podocin (Option B):** Mutations in the **NPHS2 gene** encoding Podocin cause **Steroid-Resistant Nephrotic Syndrome (SRNS)**, typically presenting as focal segmental glomerulosclerosis (FSGS) in childhood [1]. * **Alpha-actinin-4 (Option C):** Mutations in the **ACTN4 gene** are associated with autosomal dominant forms of **FSGS** [1]. It is an actin-binding protein that maintains the podocyte cytoskeleton. * **CD2-associated protein (Option D):** CD2AP interacts with nephrin and podocin; mutations are rare but can lead to inherited forms of FSGS. **High-Yield Clinical Pearls for NEET-PG:** * **Gene Mnemonic:** **N**ephrin = **N**PHS**1** (Finnish); **P**odocin = **N**PHS**2** (SRNS/FSGS). * **Clinical Marker:** Elevated **Alpha-fetoprotein (AFP)** in maternal serum or amniotic fluid is a diagnostic clue for Finnish nephrotic syndrome. * **Morphology:** Light microscopy shows **microcystic dilation** of proximal convoluted tubules. * **Treatment:** These patients do not respond to steroids; the definitive treatment is bilateral nephrectomy followed by renal transplantation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 905-907, 923-924.
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Congenital Anomalies of the Kidney
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Glomerular Diseases
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Tubular and Interstitial Diseases
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Vascular Diseases of the Kidney
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Cystic Diseases of the Kidney
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Urinary Tract Obstruction and Stones
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Renal Tumors
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Kidney in Systemic Diseases
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Renal Transplantation Pathology
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Urinary Tract Infections
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