Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 401: In Leprosy, what is the most common renal lesion observed?

A. Membranous glomerulonephritis (MGN) (Correct Answer)
B. Membranoproliferative glomerulonephritis (MPGN)
C. Focal glomerulosclerosis
D. Diffuse glomerulosclerosis

Explanation: **Explanation:** Renal involvement in Leprosy (Hansen’s disease) is a significant cause of morbidity, occurring primarily due to immune complex deposition or secondary complications of chronic inflammation. **1. Why Membranous Glomerulonephritis (MGN) is correct:** MGN is considered the most common specific histopathological renal lesion in leprosy patients [1], [2]. The pathogenesis involves the deposition of circulating immune complexes (containing *Mycobacterium leprae* antigens) in the subepithelial space of the glomerular basement membrane [1], [3]. This is particularly prevalent in the lepromatous spectrum and during Type 2 Lepra reactions (Erythema Nodosum Leprosum/ENL), where high bacterial loads and intense humoral responses trigger immune complex-mediated injury. **2. Analysis of Incorrect Options:** * **Membranoproliferative glomerulonephritis (MPGN):** While MPGN can occur due to chronic infections [4], it is less frequently reported in leprosy compared to MGN. * **Focal and Diffuse Glomerulosclerosis:** These are generally end-stage patterns of glomerular injury or associated with conditions like hypertension and diabetes. They are not the primary or characteristic immunopathological lesions associated with leprosy. **3. High-Yield Clinical Pearls for NEET-PG:** * **Secondary Amyloidosis (AA type):** While MGN is the most common *glomerulonephritis*, many textbooks and studies cite **Secondary Amyloidosis** as a very frequent cause of renal failure and nephrotic syndrome in chronic, long-standing lepromatous leprosy due to persistent inflammation [1]. * **Type 2 Lepra Reaction (ENL):** This is a classic example of a **Type III Hypersensitivity reaction**, which often manifests clinically as acute glomerulonephritis or interstitial nephritis. * **Other lesions:** Other reported findings include proliferative glomerulonephritis and chronic interstitial nephritis. Always prioritize MGN or Amyloidosis based on the specific phrasing of the question (lesion vs. cause of renal failure). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921. [2] 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. [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. 925-926.

Question 402: What is the most specific histological lesion in diabetic nephropathy?

A. Widening of glomerular basement membrane
B. Generalized mesangial thickening
C. Occlusion of glomeruli with fibrin caps
D. Hyalinization of afferent arterioles and Kimmelstiel-Wilson bodies (Correct Answer)

Explanation: **Explanation:** Diabetic nephropathy is a leading cause of end-stage renal disease. The correct answer highlights the two most characteristic findings: **Kimmelstiel-Wilson (KW) nodules** [1] and **hyaline arteriolosclerosis** [3]. 1. **Kimmelstiel-Wilson Bodies:** These are ovoid, laminated, PAS-positive hyaline nodules located in the periphery of the glomerulus within the mesangial matrix [1]. While diffuse mesangial sclerosis is more common, KW nodules are considered **pathognomonic (highly specific)** for diabetes. 2. **Arteriolar Hyalinosis:** Diabetes uniquely affects both **afferent and efferent arterioles**. The presence of hyaline deposits in the efferent arteriole is highly suggestive of diabetes, though the question combines it with the specific KW nodules [3]. **Analysis of Incorrect Options:** * **Option A (GBM Widening):** This is the **earliest** morphological change detectable by electron microscopy, but it is not specific as it occurs in various other glomerular diseases. * **Option B (Generalized Mesangial Thickening):** Also known as diffuse glomerulosclerosis, this is the **most common** histological change in diabetes [1]. However, it lacks the specificity of KW nodules. * **Option C (Fibrin Caps):** These are eosinophilic accumulations over the glomerular capillaries. While seen in diabetes, they are also found in other conditions like hypertensive nephrosclerosis and are not specific [2]. **NEET-PG High-Yield Pearls:** * **Earliest change:** Microalbuminuria (30–300 mg/day). * **Earliest structural change:** Thickening of the Glomerular Basement Membrane (GBM). * **Most common lesion:** Diffuse mesangial sclerosis [1]. * **Most specific lesion:** Kimmelstiel-Wilson nodules (Nodular glomerulosclerosis) [1]. * **Vascular hallmark:** Hyaline arteriolosclerosis affecting both afferent and efferent arterioles [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1121-1122. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 907-908. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945.

Question 403: Which chromosomal abnormality is associated with Chromophilic Renal Cell Carcinoma?

A. 3p
B. Trisomy 7 and 17 (Correct Answer)
C. 6q
D. t(3, 11)

Explanation: **Explanation:** **Chromophilic Renal Cell Carcinoma (RCC)**, also known as **Papillary RCC**, is the second most common subtype of renal cell carcinoma. Its pathogenesis is distinct from the more common Clear Cell RCC [1]. **1. Why Trisomy 7 and 17 is correct:** Papillary (Chromophilic) RCC is characterized by specific cytogenetic gains rather than losses. The most characteristic genetic signature involves **trisomy of chromosomes 7 and 17**, along with the loss of the Y chromosome in males [1]. * **Trisomy 7** is particularly significant as it houses the **MET proto-oncogene** [1]. Overexpression or mutation of the MET gene (a receptor tyrosine kinase for hepatocyte growth factor) leads to uncontrolled cell proliferation, which is the hallmark of the hereditary form of Papillary RCC [1]. **2. Why other options are incorrect:** * **Option A (3p):** Deletion of the short arm of chromosome 3 (3p-) is the classic hallmark of **Clear Cell RCC**. This region contains the **VHL (von Hippel-Lindau) gene** [1]. * **Option C (6q):** Deletions in 6q are occasionally seen in various tumors but are not a defining diagnostic feature for any major RCC subtype. * **Option D (t(3, 11)):** Translocations involving chromosome 3 are associated with familial Clear Cell RCC, while translocations involving Xp11.2 define **Translocation RCC** (MiT family). **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Papillary RCC presents with a papillary growth pattern and contains **Psammoma bodies** and **foamy macrophages** within the fibrovascular cores [1]. * **Staining:** These tumors are typically **CK7 positive** (especially Type 1). * **Subtypes:** Type 1 (better prognosis, MET mutations) vs. Type 2 (more aggressive, associated with Fumarate Hydratase deficiency). * **Chromophobe RCC:** Associated with **monosomy** (loss) of multiple chromosomes (1, 2, 6, 10, 13, 17, 21) and shows "halos" around nuclei. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959.

Question 404: Epimembranous deposition is seen in which condition?

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

Explanation: **Explanation:** **Membranous Glomerulonephritis (MGN)** is characterized by the accumulation of immune complexes in the **subepithelial space** (between the glomerular basement membrane and the podocytes) [1]. In renal pathology, the term **"Epimembranous"** is synonymous with subepithelial [1]. These deposits trigger the formation of new basement membrane material that protrudes between the deposits, creating the classic **"Spike and Dome" appearance** seen on Silver stain [2]. On Immunofluorescence, these deposits appear as a diffuse granular pattern of IgG and C3 [2]. **Why the other options are incorrect:** * **Focal Segmental Glomerulosclerosis (FSGS):** This involves sclerosis (collagen deposition) and hyalinosis within segments of some glomeruli. It is not characterized by immune complex deposition; rather, it involves podocyte injury and effacement. * **Minimal Change Disease (MCD):** This is characterized by the "null" finding on light microscopy and the absence of immune deposits. The primary pathology is the diffuse effacement of podocyte foot processes visible only on electron microscopy. * **Membranoproliferative Glomerulonephritis (MPGN):** This condition features **subendothelial** (Type I) or **intramembranous** (Type II/Dense Deposit Disease) deposits [3]. It is distinguished by the "tram-track" appearance due to mesangial cell interposition [4]. **High-Yield NEET-PG Pearls:** * **Most common cause** of Nephrotic syndrome in adults (though FSGS is rising in prevalence). * **Primary MGN:** Associated with antibodies against **Phospholipase A2 Receptor (PLA2R)**. * **Secondary MGN:** Associated with HBV, SLE (Class V), gold/penicillamine, and occult malignancies (lung/colon). * **Morphology:** Thickened capillary loops on LM; "Spike and Dome" on Silver stain; Granular IF [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 911. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 921. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926.

Question 405: Which of the following is NOT a feature of familial hemolytic uremic syndromes?

A. Characterized by microangiopathic hemolytic anemia
B. Hemolysis results from an inherited intrinsic red cell abnormality (Correct Answer)
C. Atypical HUS is a severe disease with up to 15% mortality in the acute phase
D. 50% of cases progress to end-stage renal disease

Explanation: ### Explanation **1. Why Option B is the correct answer (The "False" statement):** Hemolytic Uremic Syndrome (HUS) is a **Microangiopathic Hemolytic Anemia (MAHA)** [2]. In HUS, the hemolysis is **extrinsic and mechanical**, not due to an intrinsic red cell defect [2]. The primary pathology occurs in the vascular endothelium (especially in the kidneys), where microthrombi form [1]. As red blood cells (RBCs) pass through these narrowed, fibrin-clotted vessels, they are mechanically shredded, leading to the formation of **schistocytes** (fragmented cells) [2]. The RBCs themselves are structurally normal until they encounter the damaged microvasculature. **2. Analysis of Incorrect Options (True statements about HUS):** * **Option A:** MAHA is a hallmark of HUS, characterized by non-immune hemolytic anemia, thrombocytopenia, and schistocytes on a peripheral smear [2]. * **Option C:** Atypical HUS (aHUS), which includes familial forms, is significantly more severe than typical (Shiga-toxin related) HUS [1]. It carries a high acute mortality rate (up to 15-25%) because it is driven by uncontrolled complement activation [1]. * **Option D:** Unlike typical HUS (which usually resolves), aHUS has a poor prognosis. Approximately 50% of patients progress to **End-Stage Renal Disease (ESRD)** or develop permanent neurological damage. **3. High-Yield Clinical Pearls for NEET-PG:** * **Etiology of aHUS:** Most familial cases are due to inherited mutations in **Complement Factor H (CFH)**, Factor I, or Membrane Cofactor Protein (MCP/CD46), leading to alternative complement pathway dysregulation [1]. * **Typical HUS:** Usually follows a prodrome of bloody diarrhea caused by **STEC (Shiga toxin-producing E. coli O157:H7)** [1]. * **Triad of HUS:** 1. Microangiopathic hemolytic anemia, 2. Thrombocytopenia, 3. Acute Kidney Injury (AKI) [2]. * **Treatment Note:** Eculizumab (a monoclonal antibody against C5) is the drug of choice for atypical HUS. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 946-947. [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.

Question 406: What is the hallmark of IgA nephropathy?

A. Oedema
B. Hematuria (Correct Answer)
C. Hypertension
D. Proteinuria

Explanation: **Explanation:** **IgA Nephropathy (Berger’s Disease)** is the most common cause of primary glomerulonephritis worldwide [1]. The hallmark clinical presentation is **recurrent episodes of gross or microscopic hematuria**, typically occurring within 1-2 days of an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria) [3]. **Why Hematuria is the Correct Answer:** The pathogenesis involves the deposition of abnormally glycosylated IgA1 in the **glomerular mesangium** [2]. This triggers an inflammatory response and mesangial cell proliferation, which compromises the integrity of the glomerular capillaries, leading to the leakage of red blood cells into the urine. **Analysis of Incorrect Options:** * **A. Oedema:** While oedema can occur if the condition progresses to nephrotic-range proteinuria or renal failure, it is not the defining hallmark. * **C. Hypertension:** Hypertension is a common complication and a poor prognostic indicator, but it is a secondary feature rather than the presenting hallmark [4]. * **D. Proteinuria:** Most patients have mild proteinuria. While some may develop nephrotic syndrome, hematuria remains the more consistent and characteristic finding [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Finding:** Immunofluorescence (IF) shows **granular mesangial deposits of IgA** and C3. * **Electron Microscopy:** Shows **electron-dense deposits** restricted to the mesangium. * **Association:** Frequently associated with **Henoch-Schönlein Purpura (HSP)**, which is considered the systemic version of the same disease process. * **Prognosis:** The most reliable histological predictor of progression is the **Oxford Classification (MEST-C score)** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 928-929. [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. 929-930. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 930-931.

Question 407: Which of the following features is NOT true about membranous glomerulopathy?

A. Heavy proteinuria
B. Hyperlipidemia
C. Early onset of renal failure (Correct Answer)
D. Responds to steroids

Explanation: **Explanation:** Membranous Glomerulopathy (MGN) is the most common cause of **Nephrotic Syndrome** in non-diabetic adults [1]. Understanding its clinical course is key to identifying the correct answer. **1. Why "Early onset of renal failure" is the correct answer (NOT true):** MGN is characterized by an **indolent, slowly progressive course** [1]. Unlike rapidly progressive glomerulonephritis (RPGN), renal failure in MGN develops very late, often over decades [1]. Approximately 1/3 of patients undergo spontaneous remission, 1/3 persist with proteinuria, and only the remaining 1/3 progress to chronic renal failure over 10–20 years [1]. Therefore, "early onset" is clinically inaccurate. **2. Analysis of Incorrect Options:** * **A & B (Heavy proteinuria & Hyperlipidemia):** These are cardinal features of Nephrotic Syndrome. MGN presents with massive proteinuria (>3.5g/day) due to the formation of subepithelial immune complexes that damage the glomerular basement membrane (GBM) charge and size selectivity. This leads to hypoalbuminemia, triggering the liver to increase lipoprotein synthesis, resulting in hyperlipidemia. * **D (Responds to steroids):** While the response is variable and often requires combination therapy (e.g., the Ponticelli regimen with cyclophosphamide), MGN is considered a steroid-responsive condition, particularly in children or when used to induce remission in progressive cases [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Diffuse thickening of the GBM; **"Spike and Dome"** appearance on Silver stain [1]. * **Immunofluorescence:** Granular deposits of IgG and C3. * **Primary Cause:** 70% of cases are associated with antibodies against the **Phospholipase A2 Receptor (PLA2R)** [1]. * **Secondary Causes:** Hepatitis B, SLE (Class V), gold/penicillamine, and occult malignancies (lung/colon). * **Complication:** MGN has the highest association with **Renal Vein Thrombosis** among all nephrotic syndromes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-922.

Question 408: What is the most common infectious agent associated with chronic pyelonephritis?

A. Proteus vulgaris
B. Klebsiella pneumoniae
C. Staphylococcus
D. Escherichia coli (Correct Answer)

Explanation: **Explanation:** **Escherichia coli (E. coli)** is the most common causative agent for both acute and chronic pyelonephritis [4]. Chronic pyelonephritis is a clinicopathologic entity characterized by interstitial inflammation and uneven scarring of the renal parenchyma, typically resulting from recurrent or persistent infections [3]. These infections are most commonly associated with **vesicoureteral reflux (VUR)** or **chronic urinary tract obstruction** [1]. Since E. coli is the predominant uropathogen in the fecal flora and possesses virulence factors like P-pili (which facilitate adherence to urothelium), it remains the leading cause of the underlying recurrent infections that progress to chronic disease [4]. **Analysis of Incorrect Options:** * **Proteus vulgaris:** While Proteus is a significant cause of UTIs, it is specifically associated with **struvite (staghorn) calculi** due to its urease-producing ability, which alkalizes the urine. It is less common than E. coli. * **Klebsiella pneumoniae:** This is a common Gram-negative uropathogen, often seen in hospital-acquired infections or diabetic patients, but its overall prevalence is lower than E. coli. * **Staphylococcus:** *S. saprophyticus* is a common cause of UTIs in young, sexually active females, and *S. aureus* may cause renal abscesses via hematogenous spread, but neither is the primary agent for chronic pyelonephritis [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Feature:** The presence of **"Thyroidization" of tubules** (colloid-filled dilated tubules) is a classic histological hallmark of chronic pyelonephritis [2]. * **Gross Appearance:** Characterized by **asymmetric, coarse cortical scars** overlying blunted or deformed calyces (U-shaped scars) [1]. * **Xanthogranulomatous Pyelonephritis:** A rare variant of chronic pyelonephritis often associated with **Proteus** infections, characterized by "foamy" lipid-laden macrophages [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 939. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-939. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 935-937.

Question 409: Crescent formation is characteristic of which glomerular disease?

A. Minimal change disease
B. Rapidly progressive glomerulonephritis (Correct Answer)
C. Focal and segmental glomerulonephritis
D. Rapidly non-progressive glomerulonephritis

Explanation: **Explanation:** **Rapidly Progressive Glomerulonephritis (RPGN)**, also known as **Crescentic Glomerulonephritis**, is a clinical syndrome characterized by a rapid decline in renal function [1]. The hallmark pathological feature is the presence of **crescents** in the majority of glomeruli. These crescents are formed by the proliferation of **parietal epithelial cells** of Bowman’s capsule and the infiltration of **monocytes/macrophages** into the urinary space, triggered by the leakage of fibrin through ruptured glomerular basement membranes [1]. **Analysis of Options:** * **Minimal Change Disease (MCD):** Glomeruli appear normal under light microscopy. The characteristic finding is the effacement of podocyte foot processes visible only on electron microscopy. * **Focal Segmental Glomerulosclerosis (FSGS):** Characterized by sclerosis (scarring) involving some (focal) glomeruli and only portions (segmental) of the affected glomerular tufts. * **Rapidly non-progressive glomerulonephritis:** This is not a standard pathological entity. Most glomerulonephritides are either acute, chronic, or rapidly progressive. **High-Yield Clinical Pearls for NEET-PG:** * **Classification of RPGN:** * **Type I (Anti-GBM):** Linear IgG deposits (e.g., Goodpasture Syndrome). * **Type II (Immune Complex):** "Lumpy-bumpy" granular deposits (e.g., SLE, PSGN). * **Type III (Pauci-immune):** No immune deposits; associated with ANCA (e.g., Granulomatosis with Polyangiitis) [2]. * **Definition:** To diagnose RPGN pathologically, crescents must usually involve >50% of the glomeruli. * **Key Mediator:** **Fibrin** is the most important component leading to the formation of the crescent [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. 528-529, 536-537. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918.

Question 410: Collapsing glomerulopathy is seen in which of the following conditions?

A. HIV (Correct Answer)
B. Nephropathy associated with Nephrin A gene mutation
C. Systemic vasculitis
D. Renal artery stenosis

Explanation: **Explanation:** **Collapsing Glomerulopathy (CG)** is a severe morphological variant of Focal Segmental Glomerulosclerosis (FSGS). It is characterized by the **collapse of the glomerular capillary tuft** accompanied by the **hypertrophy and hyperplasia of overlying podocytes**, which often contain protein resorption droplets [1][2]. 1. **Why HIV is Correct:** **HIV-Associated Nephropathy (HIVAN)** is the classic cause of collapsing glomerulopathy [1]. It occurs due to direct infection of renal tubular and glomerular cells by the virus [2]. The viral proteins (like *nef* and *vpr*) induce podocyte proliferation and loss of differentiation markers, leading to the characteristic "collapsed" appearance and rapid progression to end-stage renal disease (ESRD). 2. **Why Incorrect Options are Wrong:** * **Nephrin (NPHS1) Gene Mutation:** This mutation is associated with **Finnish-type Congenital Nephrotic Syndrome**, characterized by microcystic dilation of proximal tubules, not collapsing FSGS. * **Systemic Vasculitis:** Typically presents as **Crescentic Glomerulonephritis** (Pauci-immune) with necrotizing lesions, rather than podocyte-driven collapsing tufts. * **Renal Artery Stenosis:** Leads to ischemic atrophy of the kidney and renovascular hypertension, but does not cause the specific podocyte proliferative changes seen in CG. **High-Yield Clinical Pearls for NEET-PG:** * **Other Causes of CG:** Apart from HIV, it is associated with **Pamidronate** therapy, **COVAN** (COVID-19 Associated Nephropathy), and **APOL1 gene risk variants** (common in African Americans) [3]. * **Morphology:** Look for "pseudocrescents" formed by proliferating podocytes (unlike true crescents in vasculitis which are formed by parietal epithelial cells and inflammatory cells) [2]. * **Prognosis:** Collapsing FSGS has the **worst prognosis** among all FSGS variants [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 531-532. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 924-925. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 923-924.

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