Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 341: Onion skin lesions, in the muscular layer of arteriole, are seen in which of the following conditions?

A. Systemic Lupus Erythematosus (SLE)
B. Benign nephrosclerosis
C. Malignant nephrosclerosis (Correct Answer)
D. Rapidly Progressive Glomerulonephritis (RPGN)

Explanation: **Explanation:** The "onion skin" lesion is a hallmark histopathological feature of **Malignant Nephrosclerosis**, which occurs in the setting of malignant hypertension (typically BP >200/120 mmHg) [1][2]. **1. Why Malignant Nephrosclerosis is Correct:** The underlying mechanism is **Hyperplastic Arteriolosclerosis** [2]. Severe hypertension causes endothelial injury and platelet proliferation, leading to the release of growth factors [1]. This stimulates the concentric proliferation of smooth muscle cells and the deposition of collagen in the tunica media. On light microscopy, this appears as laminated, concentric layers of cells and basement membrane, resembling the layers of an onion [1]. This process results in critical narrowing of the arteriolar lumen [1]. **2. Why Other Options are Incorrect:** * **Systemic Lupus Erythematosus (SLE):** While SLE affects the kidneys (Lupus Nephritis), its classic vascular finding is "wire-loop" lesions (subendothelial deposits) in the glomeruli, not onion-skinning of arterioles. * **Benign Nephrosclerosis:** This is characterized by **Hyaline Arteriolosclerosis**, where chronic, mild hypertension causes plasma protein leakage across the endothelium, appearing as a pink, homogeneous, structureless thickening of the vessel wall [2]. * **RPGN:** This is a clinical syndrome characterized by "crescents" in Bowman’s space (composed of parietal epithelial cells and macrophages) [1], not specific arteriolar wall changes. **3. NEET-PG High-Yield Pearls:** * **Malignant Nephrosclerosis:** Associated with **Fibrinoid Necrosis** (necrotizing arteriolitis) and a "flea-bitten kidney" appearance (pinpoint petechial hemorrhages) [1]. * **Benign Nephrosclerosis:** Associated with a "finely granular" cortical surface and hyaline changes. * **Onion-skinning elsewhere:** Also seen in the spleen in SLE (around penicilliary arteries) and in Primary Sclerosing Cholangitis (periductal fibrosis). **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.

Question 342: Hypocomplementemia is seen in which of the following conditions?

A. Lupus nephritis (Correct Answer)
B. Focal glomerulonephritis
C. Minimal change disease
D. All of the above

Explanation: Hypocomplementemia in renal pathology occurs when the complement system is excessively consumed via the classical or alternative pathways due to immune complex deposition. **1. Why Lupus Nephritis is Correct:** Systemic Lupus Erythematosus (SLE) is the prototype of immune-complex-mediated diseases (Type III Hypersensitivity) [1]. In Lupus Nephritis, DNA-anti-DNA complexes deposit in the glomeruli, leading to robust activation of the **classical complement pathway** [2]. This results in the consumption of C3 and C4 [1], leading to low serum complement levels. **2. Why Other Options are Incorrect:** * **Minimal Change Disease (MCD):** This is a podocytopathy characterized by T-cell dysfunction and loss of glomerular polyanion. It is **not** an immune-complex-mediated disease; therefore, complement levels remain normal. * **Focal Glomerulonephritis:** While this is a morphological description (seen in conditions like IgA Nephropathy), most primary focal GN types (except those associated with SLE or Endocarditis) do not typically present with systemic hypocomplementemia [1]. Specifically, IgA nephropathy (the most common focal GN) usually has normal serum C3/C4. **Clinical Pearls for NEET-PG:** To master "Hypocomplementemic Glomerulonephritis," remember the **"MP-SLE-P"** mnemonic: 1. **M**embranoproliferative GN (MPGN) - Type I (Classical) and Type II (Alternative/C3 Nephropathy). 2. **P**ost-Streptococcal GN (PSGN) - Characterized by low C3 but often **normal C4** [1]. 3. **S**ystemic Lupus Erythematosus (SLE). 4. **L**ebman-Sacks/Endocarditis-associated GN. 5. **E**ssential Mixed Cryoglobulinemia. * **High-Yield Fact:** If a question mentions low C3 but **normal C4**, think PSGN or MPGN Type II. If **both C3 and C4** are low, think 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. 910-915.

Question 343: Renal angiomyolipoma is associated with which of the following conditions?

A. Tuberous sclerosis (Correct Answer)
B. Neurofibromatosis 1
C. Neurofibromatosis 2
D. None of the above

Explanation: **Explanation:** **Renal Angiomyolipoma (AML)** is a benign mesenchymal tumor composed of three distinct elements: thick-walled blood vessels (**Angio**), smooth muscle (**Myo**), and mature adipose tissue (**Lipoma**). 1. **Why Tuberous Sclerosis is correct:** While most AMLs are sporadic, approximately **25–50% of patients with Tuberous Sclerosis Complex (TSC)** develop these tumors [1]. Conversely, when an AML is bilateral or multicentric, it is almost pathognomonic for TSC. The association is linked to mutations in the **TSC1 (hamartin)** or **TSC2 (tuberin)** genes, which lead to overactivation of the mTOR pathway, resulting in abnormal cell growth and hamartoma formation. 2. **Why the other options are incorrect:** * **Neurofibromatosis 1 (NF1):** Characterized by Lisch nodules, café-au-lait spots, and neurofibromas. While NF1 is associated with renal artery stenosis and pheochromocytomas, it is not linked to AML. * **Neurofibromatosis 2 (NF2):** Primarily associated with bilateral acoustic neuromas (schwannomas), meningiomas, and ependymomas. It has no association with renal hamartomas. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of TSC (Vogt’s Triad):** Seizures, mental retardation, and adenoma sebaceum (facial angiofibromas) [1]. * **Imaging:** On CT, the presence of **fat density** within a renal mass is highly suggestive of AML. * **Complication:** Large AMLs (>4 cm) are prone to spontaneous hemorrhage, known as **Wunderlich syndrome**. * **Immunohistochemistry:** AMLs are positive for **HMB-45** (a melanocytic marker), which is a classic "catchy" fact for pathology exams. * **Treatment:** Everolimus (an mTOR inhibitor) is used specifically for TSC-associated AML. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1318-1319.

Question 344: HIV infection is most commonly associated with which type of glomerulonephritis?

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

Explanation: **Explanation:** **Correct Answer: C. Collapsing glomerulonephritis** Collapsing glomerulonephritis is the hallmark histological pattern of **HIV-Associated Nephropathy (HIVAN)** [1]. It is considered a severe variant of Focal Segmental Glomerulosclerosis (FSGS) [2]. The pathogenesis involves direct infection of visceral epithelial cells (podocytes) by the HIV virus, leading to their proliferation and subsequent collapse of the glomerular tuft [2]. **Key Histological Features:** * Global collapse of the glomerular capillaries [2]. * Hypertrophy and hyperplasia of podocytes [1]. * **Tubuloreticular inclusions** within endothelial cells (seen on Electron Microscopy), which are induced by high levels of interferon-alpha. --- **Analysis of Incorrect Options:** * **A. Membranous glomerulonephritis:** While it can be associated with Hepatitis B, Hepatitis C, and Syphilis, it is not the classic presentation of HIVAN [1]. * **B. Fibrillary glomerulopathy:** This is a rare condition characterized by extracellular deposits of non-amyloid fibrils. It is not specifically linked to HIV. * **D. Rapidly progressive glomerulonephritis (RPGN):** This is a clinical syndrome characterized by a rapid decline in renal function and "crescents" on biopsy. While HIV patients can develop various renal issues, RPGN is not the primary or most common association. --- **High-Yield Clinical Pearls for NEET-PG:** * **HIVAN** typically presents in patients with low CD4 counts and high viral loads, often as **nephrotic syndrome** with rapidly progressing renal failure. * It is significantly more common in patients of **African descent** due to the presence of **APOL1 gene** risk variants. * On ultrasound, kidneys in HIVAN are often **enlarged and echogenic**, unlike the shrunken kidneys usually seen in chronic kidney disease. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) is the mainstay of management and can slow progression. **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 345: Nephrocalcinosis is seen in which of the following conditions?

A. Medullary sponge disease (Correct Answer)
B. Acute pyelonephritis
C. Acute glomerulonephritis
D. Chronic pyelonephritis

Explanation: **Explanation:** **Nephrocalcinosis** refers to the generalized deposition of calcium salts (calcium oxalate or calcium phosphate) within the renal parenchyma, most commonly involving the renal medulla [1]. **1. Why Medullary Sponge Kidney (MSK) is correct:** In Medullary Sponge Kidney, there is congenital ectasia (dilation) of the collecting ducts. This leads to **urinary stasis** within the dilated ducts, which promotes the precipitation of calcium salts. Approximately 40–80% of patients with MSK develop nephrocalcinosis or nephrolithiasis. On imaging, this typically presents as a "bouquet of flowers" or "paintbrush" appearance due to the calcified dilated ducts. **2. Why the other options are incorrect:** * **Acute Pyelonephritis:** This is an acute bacterial infection of the renal pelvis and parenchyma characterized by neutrophilic infiltration and abscess formation, not calcium deposition [2]. * **Acute Glomerulonephritis:** This involves immune-mediated inflammation of the glomeruli (e.g., PSGN). It presents with hematuria and hypertension, but does not cause parenchymal calcification. * **Chronic Pyelonephritis:** While this leads to renal scarring and "thyroidization" of tubules, it is not a primary cause of nephrocalcinosis [2]. Calcification, if present, is usually dystrophic and localized, rather than the diffuse parenchymal deposition seen in nephrocalcinosis. **NEET-PG High-Yield Pearls:** * **Most common cause of Medullary Nephrocalcinosis:** Hyperparathyroidism (due to hypercalcemia) [1]. * **Most common cause of Cortical Nephrocalcinosis:** Acute Tubular Necrosis (ATN) or Cortical Necrosis (often post-partum). * **Distinction:** Nephrolithiasis refers to stones in the *pelvicalyceal system*, whereas Nephrocalcinosis refers to calcium in the *renal parenchyma* [3]. * **Other causes of Medullary Nephrocalcinosis:** Distal Renal Tubular Acidosis (Type 1 RTA), Sarcoidosis, and Vitamin D intoxication [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. 539-540. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 934-935. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 76-77.

Question 346: A patient with clinical features of Glomerulonephritis presents with granular staining on immunofluorescence. All of the following causes are associated with normal C3 levels except?

A. IgA Nephropathy
B. Henoch-Schönlein purpura
C. Fibrillary GN
D. Cryoglobulinemia (Correct Answer)

Explanation: ### Explanation The core concept tested here is the differentiation of glomerular diseases based on **serum complement (C3) levels**. Granular staining on immunofluorescence (IF) indicates immune-complex deposition [1]. These diseases are categorized into those with **hypocomplementemia** (low C3) and those with **normal complement levels**. **Why Cryoglobulinemia is the correct answer:** Cryoglobulinemia (specifically Type II and III) is a classic cause of **hypocomplementemia**. It involves the formation of immune complexes (often associated with Hepatitis C) that aggressively activate the classical complement pathway. This leads to significantly **low levels of C3 and characteristically very low C4**. **Analysis of Incorrect Options (Normal C3 levels):** * **IgA Nephropathy (Berger’s Disease):** This is the most common GN worldwide [2]. While it involves IgA deposition in the mesangium, it does not typically activate the systemic complement cascade enough to lower serum C3 levels [2]. * **Henoch-Schönlein Purpura (HSP):** Considered the systemic version of IgA nephropathy, it presents with the same renal pathology and similarly maintains **normal serum C3 and C4 levels**. * **Fibrillary GN:** A rare condition characterized by organized microtubular deposits. Although it shows granular IF (usually IgG and C3), serum complement levels remain **normal**. **NEET-PG High-Yield Pearls:** * **Low C3 + Low C4:** Cryoglobulinemia, SLE (Lupus Nephritis) [3]. * **Low C3 + Normal C4:** Post-Streptococcal Glomerulonephritis (PSGN) [1], Membranoproliferative GN (MPGN) Type II (Dense Deposit Disease) [4]. * **Normal C3 + Normal C4:** IgA Nephropathy, HSP, ANCA-associated vasculitis (Pauci-immune), Alport Syndrome. * **Mnemonic for Low Complement:** "Many Patients Stay Calm" → **M**PGN, **P**SGN, **S**LE, **C**ryoglobulinemia. **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. 535-536. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 532-533. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.

Question 347: Characteristic renal biopsy immunofluorescence findings that lead to the diagnosis of Berger's disease are:

A. Predominantly IgA deposition in the subepithelial region
B. Predominantly IgG deposition in the subendothelial region
C. Predominantly IgG deposition in the glomerular basement membrane
D. Predominantly IgA deposition in the mesangium (Correct Answer)

Explanation: **Explanation:** **Berger’s Disease (IgA Nephropathy)** is the most common cause of primary glomerulonephritis worldwide. The hallmark of this condition is the deposition of **galactose-deficient IgA1** immune complexes within the kidney [2]. 1. **Why Option D is Correct:** The definitive diagnosis of Berger’s disease requires Immunofluorescence (IF) microscopy. The characteristic finding is **predominant, granular IgA deposition** localized specifically in the **mesangium** [1]. This occurs because the mesangial cells have receptors (like CD71) that bind these abnormal IgA complexes, leading to mesangial proliferation and matrix expansion. 2. **Why Other Options are Incorrect:** * **Option A:** Subepithelial deposits are characteristic of **Membranous Nephropathy** (IgG and C3) or **Post-Streptococcal Glomerulonephritis** (humps) [1]. * **Option B:** Subendothelial deposits are typical of **Membranoproliferative Glomerulonephritis (MPGN) Type I** or **Lupus Nephritis** [1]. * **Option C:** Linear IgG deposition along the Glomerular Basement Membrane (GBM) is the classic finding in **Goodpasture Syndrome** (Anti-GBM disease) [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Classically presents as **synpharyngitic hematuria** (gross hematuria occurring concurrently or within 1-2 days of an upper respiratory tract infection) [3]. * **Light Microscopy:** Shows mesangial hypercellularity. * **Electron Microscopy:** Confirms **dense deposits** in the mesangium [1]. * **Association:** Often associated with **Henoch-Schönlein Purpura (HSP)**, which is considered the systemic version of the same pathology. * **Prognosis:** The presence of hypertension and persistent proteinuria are poor prognostic indicators. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 911. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 535-536. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 928-929. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915.

Question 348: Which gene is commonly involved in mutations leading to renal cell carcinoma?

A. VHL (Correct Answer)
B. TP53
C. NF1
D. BRCA-1

Explanation: **Explanation:** **1. Why VHL is the correct answer:** The **VHL (Von Hippel-Lindau) gene**, located on **chromosome 3p25**, is a tumor suppressor gene. It is the most common genetic driver in Renal Cell Carcinoma (RCC), specifically the **Clear Cell subtype** (which accounts for ~70-80% of cases). * **Mechanism:** Under normal conditions, the VHL protein targets **Hypoxia-Inducible Factor (HIF-1α)** for degradation. When VHL is mutated or lost (via the "two-hit" hypothesis), HIF-1α accumulates, leading to the overexpression of angiogenic factors like **VEGF** and **PDGF**, which drive tumor growth and hypervascularity. This occurs in both sporadic cases (90%) and hereditary VHL syndrome. **2. Why the other options are incorrect:** * **TP53:** Known as the "guardian of the genome," it is the most commonly mutated gene in human cancers overall (e.g., Li-Fraumeni syndrome), but it is not the primary or specific driver for RCC. * **NF1:** Mutations in the Neurofibromin 1 gene on chromosome 17 lead to **Neurofibromatosis Type 1**, characterized by neurofibromas, Lisch nodules, and café-au-lait spots, not typically RCC. * **BRCA-1:** This gene is primarily associated with hereditary **breast and ovarian cancer** syndromes. **3. High-Yield Clinical Pearls for NEET-PG:** * **Clear Cell RCC:** Associated with **3p deletion** (VHL gene) [1]. * **Papillary RCC:** Associated with **MET proto-oncogene** mutations (Trisomy 7 and 17) [1]. * **Chromophobe RCC:** Characterized by multiple chromosome losses and a better prognosis [1]. * **Classic Triad of RCC:** Hematuria, palpable mass, and flank pain (seen in only 10% of patients). * **Paraneoplastic Syndromes:** RCC is the "great mimicker," often secreting EPO (polycythemia), Renin (hypertension), or PTHrP (hypercalcemia) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-961. [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.

Question 349: What is the most common predisposing factor for chronic pyelonephritis?

A. Diabetes mellitus
B. Renal stone
C. Posterior urethral valve
D. Vesicoureteric reflux (Correct Answer)

Explanation: **Explanation:** Chronic pyelonephritis (CPN) is a chronic tubulointerstitial renal disorder characterized by renal scarring and deformity of the pelvicalyceal system. [1] **Why Vesicoureteric Reflux (VUR) is the correct answer:** VUR is the most common predisposing factor for chronic pyelonephritis, particularly in children. [1] It involves the retrograde flow of urine from the bladder into the ureters and renal pelvis due to an incompetent vesicoureteric junction. This "reflux nephropathy" allows infected urine to reach the renal parenchyma, leading to recurrent bouts of inflammation, parenchymal scarring, and eventually chronic renal failure. [1] **Analysis of Incorrect Options:** * **Diabetes Mellitus:** While DM is a major risk factor for acute pyelonephritis and papillary necrosis, it is not the primary cause of the structural scarring seen in CPN. [2] * **Renal Stones:** Nephrolithiasis causes "Obstructive Pyelonephritis." While chronic obstruction can lead to CPN, it is statistically less common as a primary driver compared to VUR. [1] * **Posterior Urethral Valve:** This is a common cause of urinary tract obstruction in male infants, but it leads to CPN indirectly by causing secondary VUR or stasis. VUR remains the more direct and frequent mechanism for the pathology. **High-Yield NEET-PG Pearls:** * **Morphology:** The hallmark of CPN is **irregular, asymmetric coarse scars** overlying a dilated, blunted, or deformed calyx (U-shaped scars). [1] * **Microscopy:** Look for **"Thyroidization" of tubules** (tubules dilated and filled with eosinophilic hyaline casts resembling thyroid follicles). [3] * **Classification:** CPN is divided into two types: **Reflux Nephropathy** (most common) and **Chronic Obstructive Pyelonephritis**. [1] * **Xanthogranulomatous Pyelonephritis:** A rare variant of CPN associated with *Proteus* infections and "Staghorn" calculi, characterized by foamy macrophages (xanthoma cells). [3] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-939. [2] 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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940.

Question 350: Which of the following statements is FALSE regarding Goodpasture's disease?

A. Antibodies are directed against the non-collagenous (NC-1) domain of the alpha-3 chain of type IV collagen.
B. Complement levels are typically normal.
C. The prognosis is generally poor if untreated.
D. Linear deposition of IgG along the glomerular basement membrane is characteristic. (Correct Answer)

Explanation: **Explanation:** The question asks for the **FALSE** statement regarding Goodpasture’s disease. While linear deposition of IgG is a hallmark of the disease, the provided answer key marks it as the "correct" choice for being false, which suggests a technical error in the question's framing or a specific nuance regarding the distinction between **Goodpasture Syndrome** (pulmonary-renal) and **Goodpasture Disease** (isolated renal) [3]. However, in the context of NEET-PG, all four options are technically **TRUE** statements. Let’s analyze the facts: 1. **Pathogenesis (Option A):** This is **TRUE**. The disease is caused by autoantibodies against the **NC1 domain of the α3 chain of Type IV collagen**, found in the glomerular and alveolar basement membranes [2]. 2. **Complement Levels (Option B):** This is **TRUE**. Unlike post-streptococcal glomerulonephritis or SLE, Goodpasture’s is a Type II hypersensitivity reaction. Complement is consumed locally at the basement membrane, but **serum complement levels (C3, C4) remain normal**. 3. **Prognosis (Option C):** This is **TRUE**. Without aggressive treatment (plasmapheresis and immunosuppression), it rapidly progresses to end-stage renal disease or fatal pulmonary hemorrhage [3]. 4. **Immunofluorescence (Option D):** This is **TRUE**. The classic finding is **linear deposition of IgG** (and sometimes C3) along the GBM [1], [2]. **Clinical Pearls for NEET-PG:** * **Triad:** Glomerulonephritis, pulmonary hemorrhage, and anti-GBM antibodies. * **Morphology:** On light microscopy, it presents as **Crescentic Glomerulonephritis** (RPGN Type I). * **HLA Association:** Strongly associated with **HLA-DRB1** [3]. * **Treatment:** Plasmapheresis is the gold standard to remove circulating antibodies [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 526-527. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 537-538.

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