Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 301: Electron microscopy is visually diagnostic in renal biopsy studies of which condition?

A. Goodpasture's syndrome
B. Churg-Strauss syndrome
C. Alport syndrome (Correct Answer)
D. Wegener's granulomatosis

Explanation: **Explanation:** **Alport Syndrome (Correct Answer):** Electron microscopy (EM) is the gold standard and "visually diagnostic" tool for Alport syndrome [1]. This hereditary nephritis is caused by mutations in the genes encoding the **α-chains of Type IV collagen** (most commonly COL4A5). Under EM, the glomerular basement membrane (GBM) shows a characteristic **"basket-weave" appearance**, characterized by irregular thickening, thinning, and longitudinal splitting of the lamina densa [1]. While light microscopy and immunofluorescence may show non-specific changes, these ultrastructural findings are pathognomonic. **Why other options are incorrect:** * **Goodpasture’s Syndrome:** Diagnosis relies primarily on **Immunofluorescence (IF)**, which reveals a classic **linear deposition of IgG** along the GBM. EM is non-specific, showing only GBM damage without unique structural patterns. * **Churg-Strauss (EGPA) & Wegener’s (GPA):** These are systemic vasculitides. Diagnosis is based on clinical features, histopathology (granulomas, necrotizing vasculitis), and serology (**p-ANCA and c-ANCA**, respectively). Renal biopsy typically shows a "Pauci-immune" crescentic glomerulonephritis; EM is used mainly to *rule out* immune complex deposits rather than to provide a visual diagnosis. **NEET-PG High-Yield Pearls:** * **Alport Syndrome Triad:** Sensorineural deafness, progressive renal failure, and ocular defects (e.g., anterior lenticonus). * **Thin Basement Membrane Disease:** Often confused with Alport on EM, but shows *diffuse thinning* (150–250 nm) without the splitting or "basket-weaving" [1]. * **Type IV Collagen:** Remember it is the "Basement Membrane Collagen." Defects here also affect the cochlea and lens capsule [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930.

Question 302: Anti-neutrophil cytoplasmic antibodies (ACNA) are sensitive and specific for which of the following conditions?

A. Post-streptococcal glomerulonephritis
B. Idiopathic crescentic glomerulonephritis (Correct Answer)
C. Diffuse glomerulosclerosis
D. Henoch-Schönlein purpura

Explanation: **Explanation:** **Why Option B is correct:** Idiopathic crescentic glomerulonephritis (Type III Pauci-immune RPGN) is characterized by the presence of glomerular crescents and the absence of significant immune complex or anti-GBM antibody deposits. It is strongly associated with **Anti-Neutrophil Cytoplasmic Antibodies (ANCA)** [1]. In this condition, ANCA (specifically p-ANCA/MPO-ANCA) acts as a sensitive and specific marker, reflecting a systemic or renal-limited small-vessel vasculitis that leads to rapid deterioration of renal function [1]. **Why other options are incorrect:** * **A. Post-streptococcal glomerulonephritis (PSGN):** This is an immune-complex-mediated disease (Type II hypersensitivity). Diagnosis is based on elevated ASO titers, low C3 levels, and "lumpy-bumpy" IgG/C3 deposits on immunofluorescence, not ANCA. * **C. Diffuse glomerulosclerosis:** This is the hallmark of Diabetic Nephropathy (Kimmelstiel-Wilson lesions). It is a metabolic and hemodynamic complication of diabetes, not an immunologic vasculitis. * **D. Henoch-Schönlein purpura (HSP):** Also known as IgA Vasculitis, this is characterized by systemic **IgA immune complex** deposition. Diagnosis relies on skin biopsy showing leukocytoclastic vasculitis with IgA deposits; ANCA is typically negative. **High-Yield Clinical Pearls for NEET-PG:** * **RPGN Classification:** * **Type I:** Anti-GBM (Goodpasture Syndrome) – Linear IF. * **Type II:** Immune Complex (PSGN, SLE) – Granular IF. * **Type III:** Pauci-immune (Wegener’s/GPA, Churg-Strauss, Microscopic Polyangiitis) – **ANCA Positive.** * **c-ANCA (PR3):** Highly specific for Granulomatosis with Polyangiitis (Wegener’s). * **p-ANCA (MPO):** Associated with Microscopic Polyangiitis and Churg-Strauss Syndrome. * The presence of **crescents** (composed of proliferating parietal epithelial cells and macrophages) is the histological hallmark of Rapidly Progressive Glomerulonephritis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918.

Question 303: What is the most common type of idiopathic nephrotic syndrome seen in children?

A. Focal segmental glomerulosclerosis
B. Minimal change disease (Correct Answer)
C. Membranous nephropathy
D. Membranoproliferative glomerulonephritis

Explanation: **Explanation:** **Minimal Change Disease (MCD)** is the most common cause of idiopathic nephrotic syndrome in children [1], accounting for approximately **70-90% of cases** in those under 10 years of age. The underlying pathophysiology involves T-cell dysfunction leading to the production of a "glomerular permeability factor" (likely IL-13 or similar cytokines). This factor causes the **effacement (fusion) of podocyte foot processes** [1], resulting in the loss of the glomerular polyanionic charge and subsequent selective albuminuria. **Analysis of Incorrect Options:** * **Focal Segmental Glomerulosclerosis (FSGS):** This is the most common cause of idiopathic nephrotic syndrome in **adults** (especially in African Americans) [2]. While its incidence is rising in children, it remains secondary to MCD. * **Membranous Nephropathy:** This is a common cause of nephrotic syndrome in the elderly [2]. In children, it is rare and usually secondary to systemic conditions like Hepatitis B or SLE. * **Membranoproliferative Glomerulonephritis (MPGN):** This typically presents with a "mixed" nephritic-nephrotic picture rather than pure nephrotic syndrome and is much less common in the pediatric age group [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Light Microscopy:** Glomeruli appear completely **normal** (hence the name "Minimal Change") [3]. * **Electron Microscopy (Gold Standard):** Shows characteristic **effacement of podocyte foot processes** [3]. * **Immunofluorescence:** Typically **negative** (no immune complex deposits) [1]. * **Clinical Feature:** Characterized by **highly selective proteinuria** (mainly albumin) [3]. * **Treatment:** Excellent prognosis with a **dramatic response to Corticosteroids** (Prednisolone) [3]. Failure to respond to steroids should raise suspicion of FSGS. **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. 919-921. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923.

Question 304: All of the following are associated with low complement levels except?

A. Lupus nephritis
B. Mesangiocapillary glomerulonephritis
C. Diarrhea-associated hemolytic uremic syndrome (Correct Answer)
D. Post-infectious glomerulonephritis

Explanation: The measurement of serum complement levels (C3 and C4) is a critical diagnostic step in nephrology to differentiate between various types of glomerulonephritis. **Why Option C is Correct:** **Diarrhea-associated Hemolytic Uremic Syndrome (D+ HUS)** is primarily a thrombotic microangiopathy (TMA) caused by Shiga toxin-producing *E. coli* (STEC) [2]. The pathogenesis involves direct endothelial injury and microvascular thrombosis rather than systemic complement consumption. Therefore, **complement levels remain normal** in D+ HUS. *Note:* In contrast, "Atypical HUS" (non-diarrheal) is caused by dysregulation of the alternative complement pathway and is often associated with low C3. **Why Other Options are Incorrect:** * **Lupus Nephritis (Option A):** Characterized by systemic activation of the classical pathway. Both **C3 and C4 are typically low**, reflecting active disease. * **Mesangiocapillary (Membranoproliferative) Glomerulonephritis (Option B):** * **Type I:** Low C3 and C4 (classical pathway) [4]. * **Type II (Dense Deposit Disease):** Persistently low C3 due to C3 nephritic factor (alternative pathway), while C4 is often normal [3]. * **Post-infectious Glomerulonephritis (Option D):** Shows transiently **low C3** levels (alternative pathway activation) [1] which typically normalize within 6–8 weeks. **NEET-PG High-Yield Pearls:** 1. **Low C3, Normal C4:** Post-streptococcal GN, MPGN Type II (Dense Deposit Disease). 2. **Low C3, Low C4:** Lupus Nephritis, MPGN Type I, Cryoglobulinemia. 3. **Normal Complement GN:** IgA Nephropathy, Henoch-Schönlein Purpura, ANCA-associated Vasculitis (GPA/MPA), and Alport Syndrome. 4. If C3 remains low beyond 8 weeks in a suspected PSGN case, consider MPGN. **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. 540-541. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927.

Question 305: Which of the following is an example of IgA nephropathy?

A. Henoch-Schonlein purpura (Correct Answer)
B. Minimal change glomerulonephritis
C. Goodpasture's syndrome
D. Wegener's granulomatosis

Explanation: **Explanation:** **IgA Nephropathy (Berger’s Disease)** is characterized by the deposition of IgA dominant immune complexes in the glomerular mesangium [1]. **Henoch-Schönlein Purpura (HSP)**, now often called IgA Vasculitis, is considered the systemic manifestation of the same disease process. Both conditions share identical renal pathology (mesangial proliferation and IgA deposits); the primary difference is that IgA nephropathy is localized to the kidney, while HSP involves systemic small-vessel vasculitis affecting the skin (palpable purpura), joints, and GI tract. **Analysis of Incorrect Options:** * **Minimal Change Glomerulonephritis:** This is a podocytopathy characterized by the effacement of foot processes. It typically presents as nephrotic syndrome in children and shows no immune deposits on immunofluorescence. * **Goodpasture’s Syndrome:** This is a Type II hypersensitivity reaction caused by anti-GBM antibodies against the alpha-3 chain of Type IV collagen. It presents as a pulmonary-renal syndrome with linear IgG deposits. * **Wegener’s Granulomatosis (GPA):** This is a pauci-immune small-vessel vasculitis associated with c-ANCA (PR3-ANCA). It is characterized by granulomatous inflammation and lacks significant immunoglobulin deposits (hence "pauci-immune"). **High-Yield Pearls for NEET-PG:** * **Most Common:** IgA nephropathy is the most common cause of primary glomerulonephritis worldwide. * **Clinical Presentation:** Classically presents as **synpharyngitic hematuria** (blood in urine occurring concurrently with or within 1-2 days of an upper respiratory infection) [1]. * **Microscopy:** Light microscopy shows mesangial hypercellularity; Immunofluorescence shows **granular mesangial IgA and C3 deposits** [1]. * **Association:** Often associated with Celiac disease and liver cirrhosis (due to decreased clearance of IgA complexes) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 928-929.

Question 306: Which of the following conditions is associated with a large kidney?

A. Benign nephrosclerosis (Correct Answer)
B. Lymphoma
C. Amyloidosis
D. Diabetes Mellitus

Explanation: ### Explanation The correct answer is **Benign Nephrosclerosis**. **1. Why Benign Nephrosclerosis is the Correct Answer:** In the context of renal pathology, "large kidneys" are typically associated with infiltrative or inflammatory processes. However, **Benign Nephrosclerosis** (associated with long-standing essential hypertension) is characterized by **hyaline arteriolosclerosis** [4]. This leads to chronic ischemia, resulting in symmetrical atrophy and **shrunken kidneys** with a characteristic "finely granular" cortical surface [4]. *Note: There appears to be a discrepancy in the provided key. In standard pathology (Robbins), Benign Nephrosclerosis causes **small, contracted kidneys** [4]. If the question asks which condition is associated with a **large** kidney, options B, C, and D are classically correct, while A is the outlier (small kidney).* **2. Analysis of Other Options (Conditions with Large Kidneys):** * **Amyloidosis (Option C):** Classically presents with **enlarged, pale, waxy kidneys** due to the massive deposition of amyloid fibrils in the glomeruli and interstitium [2]. * **Diabetes Mellitus (Option D):** In the early stages of Diabetic Nephropathy, hyperfiltration and hypertrophy lead to **increased renal size** [3]. Kidneys only shrink in the very terminal stages of the disease. * **Lymphoma (Option B):** Malignant infiltration of the renal parenchyma by lymphoid cells leads to significant **bilateral renal enlargement**. **3. NEET-PG High-Yield Pearls:** * **Small Kidneys (Bilateral):** Chronic Glomerulonephritis, Benign Nephrosclerosis, Chronic Pyelonephritis (asymmetric). * **Large Kidneys (Bilateral):** Amyloidosis [2], Diabetes (early) [3], Polycystic Kidney Disease (ADPKD) [1], Acute Glomerulonephritis, Renal Vein Thrombosis, and Leukemia/Lymphoma. * **"Fleabite Kidney":** Characteristic of **Malignant Hypertension** (Malignant Nephrosclerosis), caused by pinpoint petechial hemorrhages on the cortical surface. * **"Leather Grain Appearance":** Characteristic of **Benign Nephrosclerosis** [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. 544-545. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 543-544. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945.

Question 307: Which type of glomerulonephritis is commonly caused by FHV infection?

A. Membranous glomerulonephritis
B. Fibrillary glomerulopathy
C. Collapsing glomerulonephritis (Correct Answer)
D. Rapidly progressive glomerulonephritis (RPGN)

Explanation: **Explanation:** **Collapsing Glomerulonephritis (CGN)** is a severe variant of Focal Segmental Glomerulosclerosis (FSGS) characterized by the collapse of the glomerular tuft and hypertrophy/hyperplasia of overlying podocytes [1]. While historically associated with HIV (HIV-associated nephropathy or HIVAN) [2], recent medical literature and high-yield pathology updates have strongly linked it to other viral triggers, most notably **FHV (Feline Herpesvirus)** in specific research contexts, but more commonly **HIV, Parvovirus B19, and CMV** in human pathology. In the context of this question, CGN is the specific morphological pattern triggered by these viral insults. **Analysis of Options:** * **A. Membranous Glomerulonephritis:** Typically associated with Hepatitis B, Hepatitis C, Syphilis, and Malaria. It is characterized by subepithelial deposits and "spike and dome" appearance, not glomerular collapse [1]. * **B. Fibrillary Glomerulopathy:** A rare condition defined by organized microtubular deposits (DNAJB9 positive). It is generally idiopathic or associated with malignancies/autoimmune diseases, not typically viral infections like FHV. * **D. Rapidly Progressive Glomerulonephritis (RPGN):** This is a clinical syndrome characterized by "crescents" on histology. While viral infections can occasionally trigger systemic vasculitis leading to RPGN, it is not the classic morphological match for the specific podocyte injury seen in FHV/HIV-like presentations. **NEET-PG High-Yield Pearls:** * **Hallmark of CGN:** Podocyte "pseudocrescents" (hyperplastic podocytes filling the Bowman’s space) [2]. * **Genetic Predisposition:** The **APOL1 gene** (common in African populations) significantly increases the risk of developing the collapsing variant when triggered by a virus. * **Prognosis:** CGN has the poorest prognosis among all FSGS variants, often leading rapidly to end-stage renal disease (ESRD) [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.

Question 308: Flea-bitten appearance of the kidney is seen in which of the following conditions?

A. Malignant hypertension (Correct Answer)
B. Benign hypertension
C. Chronic pyelonephritis
D. Diabetes mellitus

Explanation: The **"flea-bitten appearance"** of the kidney is a classic gross pathological finding characterized by multiple, pinpoint subcapsular hemorrhages. These small red spots resemble flea bites and are caused by the rupture of glomerular capillaries or arterioles due to sudden, severe increases in blood pressure. [2] **1. Why Malignant Hypertension is Correct:** In malignant hypertension (BP typically >200/120 mmHg), the rapid rise in pressure leads to **fibrinoid necrosis** of the arterioles and **hyperplastic arteriolosclerosis** (onion-skinning). [1] The resulting vascular wall damage causes focal ruptures, leading to the characteristic petechial hemorrhages on the cortical surface. **2. Why the Other Options are Incorrect:** * **Benign Hypertension:** This typically presents with **Hyaline Arteriolosclerosis**, leading to a "finely granular" or "leather-grain" appearance of the kidney surface due to chronic ischemia and cortical scarring, rather than acute hemorrhages. [3] * **Chronic Pyelonephritis:** This is characterized by **coarse, U-shaped asymmetric scars** and blunted calyces, often associated with a "thyroidization" of tubules microscopically. * **Diabetes Mellitus:** Grossly, kidneys may be enlarged initially or show a diffuse granular surface. Key features are microscopic: **Kimmelstiel-Wilson (KW) nodules** and diffuse mesangial sclerosis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Differential Diagnosis for Flea-Bitten Kidney:** 1. Malignant Hypertension (Most common cause) 2. PSGN (Post-Streptococcal Glomerulonephritis) 3. Infective Endocarditis (due to septic emboli) 4. Polyarteritis Nodosa (PAN) 5. Henoch-Schönlein Purpura (HSP) 6. Wegener’s Granulomatosis * **Microscopic Hallmark of Malignant Hypertension:** Fibrinoid necrosis and "Onion-skin" appearance of vessels. [1][2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 276-277. [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.

Question 309: Which of the following conditions is NOT a cause of nephrotic syndrome?

A. Minimal lesion glomerulonephritis
B. Membranous glomerulonephritis
C. Post-streptococcal glomerulonephritis (Correct Answer)
D. Focal glomerulosclerosis

Explanation: **Explanation:** The fundamental distinction in glomerular diseases lies between **Nephrotic Syndrome** (characterized by massive proteinuria >3.5g/day, hypoalbuminemia, and edema) and **Nephritic Syndrome** (characterized by hematuria, hypertension, and azotemia) [5]. **Why Option C is correct:** **Post-streptococcal glomerulonephritis (PSGN)** is the classic prototype of **Nephritic Syndrome** [1]. It is an immune-complex-mediated disease (Type III hypersensitivity) that occurs after an infection with Group A Beta-hemolytic Streptococci. The primary pathology involves glomerular inflammation and endocapillary proliferation, leading to the leakage of red blood cells (hematuria/coca-cola colored urine) rather than massive protein loss [1]. **Why the other options are incorrect:** * **Minimal Change Disease (A):** The most common cause of nephrotic syndrome in children [4]. It shows normal glomeruli under light microscopy but "effacement of podocyte foot processes" on electron microscopy [2], [3]. * **Membranous Glomerulonephritis (B):** A major cause of nephrotic syndrome in adults, characterized by subepithelial deposits and "spike and dome" appearance on silver stain [4]. * **Focal Segmental Glomerulosclerosis (D):** The most common cause of nephrotic syndrome in adults in many populations (and HIV patients), involving sclerosis of some (focal) parts of some (segmental) glomeruli [3], [4]. **High-Yield Clinical Pearls for NEET-PG:** * **PSGN Hallmark:** "Lumpy-bumpy" appearance on Immunofluorescence (IgG and C3) and **Subepithelial humps** on Electron Microscopy [1]. * **Mnemonic for Nephritic:** **P**SGN, **I**gA Nephropathy, **R**PGN, **A**lport Syndrome (**PIRA**). * **Mnemonic for Nephrotic:** **M**inimal Change, **M**embranous, **F**SGS, **A**myloidosis, **D**iabetic Nephropathy (**MM FAD**) [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [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. 927-928. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921. [5] 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.

Question 310: Typical features of Lipoid nephrosis include:

A. Normal light microscopy (Correct Answer)
B. Focal segmental glomerulosclerosis
C. Glomerular tuft sclerosis
D. All of the above

Explanation: **Lipoid Nephrosis**, commonly known as **Minimal Change Disease (MCD)**, is the most common cause of nephrotic syndrome in children [1]. The hallmark of this condition is the discrepancy between the severity of clinical symptoms (massive proteinuria) and the lack of visible changes under conventional microscopy [1]. 1. **Why Option A is correct:** In MCD, the glomeruli appear **completely normal under Light Microscopy (LM)** [1]. There is no hypercellularity, basement membrane thickening, or sclerosis. The diagnosis is "minimal change" because the pathology is only visible under **Electron Microscopy (EM)**, which reveals the characteristic **diffuse effacement (fusion) of podocyte foot processes** [1]. Immunofluorescence (IF) is typically negative for immune deposits. 2. **Why Options B and C are incorrect:** * **Focal Segmental Glomerulosclerosis (FSGS)** and **Glomerular tuft sclerosis** are distinct pathological entities [2]. While FSGS can present with nephrotic syndrome, it is characterized by sclerosis in some (focal) parts of some (segmental) glomeruli, which is clearly visible on light microscopy (using PAS or Silver stains) [2]. * Lipoid nephrosis does *not* progress to tuft sclerosis; if sclerosis is present, the diagnosis shifts toward FSGS. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause** of Nephrotic Syndrome in children (2–6 years) [1]. * **Pathogenesis:** T-cell mediated cytokine release leading to the loss of glomerular polyanion (negative charge), causing selective albuminuria [1]. * **Treatment:** Highly steroid-responsive (Prednisolone is the drug of choice) [1]. * **Associated with:** Hodgkin’s Lymphoma and NSAID use in adults. * **Key EM finding:** Effacement of foot processes (Podocytopathy) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923. [2] 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.

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