Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 31: Which of the following is true about Wegener's granulomatosis?

A. Large vessel vasculitis
B. Granulomas in GBM
C. Nephrosclerosis
D. Focal necrotizing GN (Correct Answer)

Explanation: **Explanation:** **Wegener’s Granulomatosis** (now known as Granulomatosis with Polyangiitis or GPA) is a systemic necrotizing vasculitis that typically affects the upper respiratory tract, lungs, and kidneys [1]. 1. **Why Focal Necrotizing GN is correct:** In the kidneys, GPA characteristically presents as a **Pauci-immune Crescentic Glomerulonephritis** [2]. In its early or milder stages, the light microscopy shows **focal necrotizing glomerulonephritis** (segmental fibrinoid necrosis without significant immune deposits) [1]. As the disease progresses, it leads to diffuse crescent formation and rapidly progressive renal failure [2]. 2. **Why the other options are incorrect:** * **A. Large vessel vasculitis:** GPA is a **small-vessel vasculitis** (affecting capillaries, venules, and arterioles) [1]. Large vessel vasculitis includes conditions like Takayasu arteritis and Giant Cell Arteritis. * **B. Granulomas in GBM:** While GPA is characterized by granulomatous inflammation, these granulomas occur in the **perivascular or extravascular lung/respiratory tissue**, not within the Glomerular Basement Membrane (GBM) itself. * **C. Nephrosclerosis:** This refers to hyaline or hyperplastic changes in renal arterioles typically associated with chronic hypertension, not the acute necrotizing inflammation seen in GPA. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Upper respiratory tract involvement (sinusitis/saddle nose), Lower respiratory tract (hemoptysis/cavities), and Renal involvement. * **Serology:** Highly associated with **c-ANCA** (anti-PR3 antibodies) [1]. * **Immunofluorescence:** Characterized as **"Pauci-immune"** (minimal to no Ig or complement deposition), distinguishing it from Goodpasture syndrome or SLE [2]. * **Treatment:** Cyclophosphamide and Corticosteroids are the mainstays. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-520. [2] 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.

Question 32: Which type of glomerulonephritis is least likely to cause chronic renal failure?

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

Explanation: ### Explanation The correct answer is **Post-streptococcal glomerulonephritis (PSGN)**. **Why PSGN is the correct answer:** PSGN is a classic example of **Acute Nephritic Syndrome** that typically follows a skin (impetigo) or throat (pharyngitis) infection with Group A Beta-hemolytic Streptococci [1]. The hallmark of PSGN is its **excellent prognosis**, especially in children. More than 95% of children recover completely with conservative management (fluid and electrolyte balance) [1]. Because the glomerular injury is usually transient and resolves once the immune complexes are cleared, it is the least likely among the given options to progress to Chronic Renal Failure (CRF). **Why the other options are incorrect:** * **Membranous Glomerulonephritis (MGN):** This is a common cause of Nephrotic Syndrome in adults. It follows a "rule of thirds": 1/3 remit spontaneously, 1/3 persist, and **1/3 progress to ESRD/CRF** [2]. * **Focal Segmental Glomerulosclerosis (FSGS):** This is a highly aggressive lesion characterized by podocyte injury. It is notorious for poor response to steroids and a **high rate of progression to CRF**. * **Membranoproliferative Glomerulonephritis (MPGN):** Both Type I and Type II (Dense Deposit Disease) have a poor prognosis, with approximately **50% of patients developing CRF** within 10 years [3]. **High-Yield Clinical Pearls for NEET-PG:** * **LMP Findings in PSGN:** "Starry sky" or "lumpy-bumpy" appearance on Immunofluorescence (IgG and C3 deposits) and **subepithelial humps** on Electron Microscopy [1]. * **Serology:** Low C3 levels are characteristic (normalize within 6–8 weeks); ASLO titers are elevated in post-pharyngeal cases. * **Prognosis:** While children have a >95% recovery rate, adults have a worse prognosis, with up to 15-20% potentially developing chronic disease [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-917. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 921-922. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927.

Question 33: Periglomerular fibrosis is considered typical of:

A. Chronic pyelonephritis (Correct Answer)
B. Chronic glomerulonephritis
C. Arterionephrosclerosis
D. Malignant hypertension

Explanation: ### Explanation **Correct Answer: A. Chronic pyelonephritis** **Why it is correct:** Periglomerular fibrosis is a hallmark histopathological feature of **Chronic Pyelonephritis (CPN)** [1]. In CPN, chronic inflammation and scarring primarily affect the renal interstitium and tubules. The inflammatory process leads to the deposition of concentric layers of collagen around the Bowman’s capsule, known as **periglomerular fibrosis**. Importantly, the underlying glomerulus often remains relatively preserved or undergoes secondary ischemic shrinkage, distinguishing it from primary glomerular diseases. **Analysis of Incorrect Options:** * **B. Chronic glomerulonephritis:** This condition is characterized by primary damage to the glomeruli, leading to global glomerulosclerosis (obliteration of the capillary tuft). While fibrosis occurs, it is typically **intraglomerular** rather than periglomerular. * **C. Arterionephrosclerosis (Benign Nephrosclerosis):** This is associated with long-standing hypertension. It shows hyaline arteriolosclerosis and "wedge-shaped" areas of cortical scarring, but periglomerular fibrosis is not a defining feature. * **D. Malignant hypertension:** This is characterized by **fibrinoid necrosis** of arterioles and **"onion-skin"** thickening of the vessel walls (hyperplastic arteriolosclerosis). It is an acute, aggressive process rather than the chronic scarring pattern seen in CPN. **High-Yield Facts for NEET-PG:** * **Thyroidization of Kidney:** A classic feature of CPN where tubules are dilated and filled with eosinophilic casts, resembling thyroid follicles [1]. * **U-shaped Scars:** CPN typically presents with coarse, discrete, U-shaped corticomedullary scars overlying dilated/blunted calyces [1]. * **Vesicoureteral Reflux (VUR):** The most common cause of chronic pyelonephritis in children [1]. * **Key Distinction:** Periglomerular fibrosis = Chronic Pyelonephritis; Onion-skinning = Malignant Hypertension; Wire-loop lesions = SLE (Lupus Nephritis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-940.

Question 34: What is true regarding IgA nephropathy?

A. Usually seen in children <10 years of age.
B. Microscopic hematuria is a common presentation.
C. Recurrent gross hematuria following respiratory infections. (Correct Answer)
D. Decreased serum IgA.

Explanation: **IgA Nephropathy (Berger’s Disease)** is the most common primary glomerulonephritis worldwide. It is characterized by the deposition of IgA in the glomerular mesangium. ### **Explanation of Options** * **Correct Answer (C):** The hallmark presentation is **synpharyngitic hematuria**—recurrent episodes of gross (visible) hematuria that occur concurrently or within 1–2 days of an upper respiratory tract infection (URTI) [2]. This happens because the mucosal infection triggers increased production of abnormally glycosylated IgA1, which deposits in the kidneys [1]. * **Option A:** While it can affect any age, it is most commonly seen in **older children and young adults** (2nd and 3rd decades), unlike Post-Streptococcal Glomerulonephritis (PSGN), which typically affects younger children [3]. * **Option B:** While microscopic hematuria can occur, the **classic, high-yield presentation** emphasized in exams is recurrent **gross hematuria** [2]. * **Option D:** Serum IgA levels are actually **increased** in about 50% of patients, not decreased. ### **High-Yield Clinical Pearls for NEET-PG** * **Pathogenesis:** "Multi-hit hypothesis" involving **galactose-deficient IgA1** (Gd-IgA1) [1]. * **Light Microscopy:** Shows **mesangial hypercellularity** and matrix expansion [2]. * **Immunofluorescence (Gold Standard):** Granular **mesangial deposits of IgA** and C3. * **Electron Microscopy:** Dense deposits restricted to the **mesangium** [1]. * **Differential Diagnosis:** Unlike PSGN (which has a 1–3 week latent period), IgA nephropathy has a very short latent period (<3 days) [3]. * **Systemic Form:** When IgA nephropathy occurs with systemic involvement (purpura, abdominal pain, arthritis), it is called **Henoch-Schönlein Purpura (HSP)**. **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. 535-536. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 928-929. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915.

Question 35: What is the most common type of renal cell carcinoma (RCC) associated with dialysis?

A. Clear cell carcinoma
B. Papillary carcinoma (Correct Answer)
C. Medullary carcinoma
D. Chromophobe carcinoma

Explanation: **Explanation:** The correct answer is **Papillary renal cell carcinoma (RCC)**. Patients with end-stage renal disease (ESRD) on long-term dialysis often develop **Acquired Cystic Kidney Disease (ACKD)**. In these patients, the risk of developing RCC is significantly higher (approximately 30–100 times) than in the general population. While clear cell RCC is the most common subtype in the general population, **Papillary RCC** is the most frequent subtype specifically associated with dialysis-related ACKD. **Analysis of Options:** * **B. Papillary RCC (Correct):** This is the most common histological subtype arising in the setting of acquired cysts [1]. These tumors are often multifocal and bilateral [1]. * **A. Clear Cell RCC:** This is the most common subtype of RCC overall (70-80%) and is associated with VHL gene mutations, but it is not the most common specifically linked to dialysis. * **C. Medullary Carcinoma:** This is a rare, highly aggressive tumor almost exclusively seen in patients with **Sickle Cell Trait**. * **D. Chromophobe RCC:** This subtype arises from intercalated cells of the collecting ducts and is associated with a better prognosis and Birt-Hogg-Dubé syndrome [1]. **NEET-PG High-Yield Pearls:** * **Acquired Cystic Kidney Disease (ACKD):** Defined as the presence of ≥4 cysts in each kidney in a patient with ESRD. * **Most common RCC in general:** Clear Cell RCC. * **Most common RCC in Dialysis/ACKD:** Papillary RCC. * **Specific variant:** "Acquired cystic disease-associated RCC" is a distinct entity recognized by the WHO, often showing a cribriform pattern and oxalate crystals. * **Genetics:** Papillary RCC is associated with trisomy 7 and 17 [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 957-959.

Question 36: What is the major cell type involved in interstitial nephritis?

A. Eosinophils
B. Neutrophils
C. Lymphocytes (Correct Answer)
D. Macrophage

Explanation: ### Explanation **Interstitial Nephritis (IN)**, specifically Acute Interstitial Nephritis (AIN), is an immunologically mediated tubulointerstitial injury [1]. The pathogenesis typically involves a Type IV (delayed-type) hypersensitivity reaction or a Type I reaction, triggered most commonly by drugs (e.g., NSAIDs, Penicillins, Diuretics) [2]. **Why Lymphocytes are the correct answer:** The hallmark of interstitial nephritis is a prominent inflammatory infiltrate within the renal interstitium. **T-lymphocytes** are the predominant cell type involved in the cell-mediated immune response that characterizes this condition [1]. While other cells may be present, the underlying process is primarily a lymphocytic infiltration leading to interstitial edema and tubular injury [2]. **Analysis of Incorrect Options:** * **Eosinophils:** While the presence of eosinophils in urine (eosinophiluria) and the interstitium is a **classic diagnostic clue** for drug-induced AIN, they are not the *major* or most numerous cell type [2]. They are transient and often absent in non-drug-induced cases. * **Neutrophils:** These are the hallmark of **Acute Pyelonephritis** (infectious tubulointerstitial nephritis). In AIN, neutrophils are typically absent or minimal. * **Macrophages:** These are often present as part of the chronic inflammatory milieu or in granulomatous interstitial nephritis (e.g., Sarcoidosis, TB), but they are secondary to the lymphocytic response [2]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Classic Triad:** Fever, Rash, and Arthralgia (seen in only 10-15% of drug-induced cases) [1]. 2. **Urinalysis:** Look for **sterile pyuria** (white blood cells without bacteria) and **white cell casts**. 3. **Drug Causes:** Remember the "5 P's": **P**ee (Diuretics), **P**ainkillers (NSAIDs), **P**enicillins/Cephalosporins, **P**roton Pump Inhibitors, and **P**ifampin (Rifampin) [1]. 4. **Gold Standard Diagnosis:** Renal Biopsy (shows interstitial edema and mononuclear/lymphocytic infiltrate) [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. 538-539. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 940-941.

Question 37: Physical examination of a two-year-old child reveals a large abdominal mass. CT studies show that the mass arises in the kidney. Which of the following is most likely a distinctive feature of this lesion?

A. Abundant clear cells
B. Embryonic glomerular structures (Correct Answer)
C. Eosinophilic cells packed with mitochondria
D. Hamartomatous blood vessels

Explanation: ### Explanation The clinical presentation of a **large abdominal mass** in a **two-year-old child** arising from the kidney is classic for **Wilms Tumor (Nephroblastoma)**. This is the most common primary renal tumor of childhood, typically presenting between ages 2 and 5 [1]. #### Why the Correct Answer is Right: Wilms tumor is characterized by a **triphasic histology** consisting of [2]: 1. **Blastema:** Sheets of small blue cells [2]. 2. **Stroma:** Fibrocytic or myxoid elements [2]. 3. **Epithelium:** This includes **abortive or embryonic glomerular and tubular structures** [2]. The presence of these primitive, "embryonic" structures is a hallmark of the tumor’s origin from the mesonephric blastema. #### Why Other Options are Incorrect: * **A. Abundant clear cells:** This describes **Clear Cell Renal Cell Carcinoma (RCC)**, which is the most common renal malignancy in adults, not children. * **C. Eosinophilic cells packed with mitochondria:** This is the classic description of an **Oncocytoma**, a benign renal tumor characterized by "mahogany brown" appearance and a central stellate scar. * **D. Hamartomatous blood vessels:** This refers to **Angiomyolipoma**, which consists of blood vessels, smooth muscle, and adipose tissue. It is strongly associated with **Tuberous Sclerosis**. #### High-Yield Clinical Pearls for NEET-PG: * **Genetics:** Associated with mutations in the **WT1 gene** (Chromosome 11p13) [1]. * **Syndromes:** * **WAGR Syndrome:** Wilms tumor, Aniridia, Genitourinary anomalies, and intellectual disability [1]. * **Denys-Drash Syndrome:** Wilms tumor, Gonadal dysgenesis, and early-onset nephropathy. * **Beckwith-Wiedemann Syndrome:** Wilms tumor, Macroglossia, Organomegaly, and Hemi-hypertrophy (WT2 gene/11p15.5). * **Prognosis:** The most important prognostic factor is **histology** (presence of **anaplasia** indicates a poor prognosis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 487-488. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 488-490.

Question 38: Mesangial deposits of monoclonal Kappa/Lambda light chains are indicative of which condition?

A. Mesangioproliferative glomerulonephritis
B. Focal and segmental glomerulosclerosis
C. Kimmelstiel-Wilson disease
D. Amyloidosis (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Amyloidosis** **Reasoning:** Amyloidosis (specifically **AL type**) is characterized by the extracellular deposition of misfolded monoclonal immunoglobulin light chains (Kappa or Lambda) [2], [5]. In the kidneys, these deposits typically begin in the **mesangium** and capillary basement membranes [1], [4]. Under light microscopy, they appear as acellular, eosinophilic "waxy" material [4]. The definitive diagnosis is made using **Congo Red stain**, which shows **apple-green birefringence** under polarized light [3]. Immunofluorescence (IF) will specifically show "light chain restriction," meaning only one type (either Kappa or Lambda) is present, confirming the monoclonal nature of the plasma cell dyscrasia [2]. **Why other options are incorrect:** * **A. Mesangioproliferative GN:** This is a pattern of injury characterized by increased mesangial cellularity. While it involves deposits (like IgA in IgA Nephropathy), these are **polyclonal** (both light chains) rather than monoclonal. * **B. Focal and Segmental Glomerulosclerosis (FSGS):** This involves sclerosis (collagen scarring) and hyalinosis, not light chain deposition. IF is typically negative or shows non-specific IgM/C3 trapping. * **C. Kimmelstiel-Wilson (KW) disease:** This refers to the nodular glomerulosclerosis seen in **Diabetic Nephropathy**. While it presents with mesangial expansion (KW nodules), the material is composed of Type IV collagen and matrix proteins, not monoclonal light chains. **High-Yield Clinical Pearls for NEET-PG:** * **AL Amyloidosis:** Most common systemic amyloidosis; associated with Multiple Myeloma [2]. * **Electron Microscopy (EM):** Amyloid appears as **non-branching, randomly oriented fibrils** (7–12 nm diameter) [3], [4]. * **Monoclonal Immunoglobulin Deposition Disease (MIDD):** If the light chains do not form fibrils (Congo Red negative) but deposit in the mesangium, it is called **Light Chain Deposition Disease (LCDD)** [1], [4]. * **Stain of choice:** Congo Red is the gold standard; Thioflavin T is a sensitive fluorescent alternative [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-266.

Question 39: What is the most widely accepted mechanism associated with nephropathy in chronic HBV patients?

A. Cytopathic collisions induced by cellular virus infection
B. Deposition of immune complex particles attributed to viral antigens and host antibodies (Correct Answer)
C. Virus-induced specific immunological mechanisms damaging the kidney
D. Indirect adverse effects of virus-induced cytokines or mediators in renal tissue.

Explanation: **Explanation:** The primary mechanism of renal injury in chronic Hepatitis B Virus (HBV) infection is a **Type III Hypersensitivity reaction** [1]. This involves the formation of circulating immune complexes consisting of viral antigens (HBeAg, HBsAg, or HBcAg) and host-specific antibodies. These complexes deposit in the glomerular basement membrane, activating the complement cascade and leading to inflammatory damage [2]. The most common clinical manifestation is **Membranous Nephropathy (MN)**, particularly in children, followed by Membranoproliferative Glomerulonephritis (MPGN) [2]. **Analysis of Options:** * **Option B (Correct):** Immune complex deposition is the gold standard mechanism. In HBV-associated MN, the **HBeAg** is most frequently implicated due to its small size, allowing it to pass through the glomerular basement membrane [2]. * **Option A:** HBV is not typically a direct cytopathic virus for renal cells; it does not cause "collisions" or direct lysis of podocytes. * **Option C:** While immunological, this option is too vague. The damage is specifically mediated by "immune complexes" (Type III) rather than direct T-cell mediated cytotoxicity (Type IV) against renal tissue [1]. * **Option D:** While cytokines play a role in chronic inflammation, they are secondary mediators and not the primary initiating mechanism of HBV nephropathy. **High-Yield Clinical Pearls for NEET-PG:** * **Most common HBV-associated renal disease:** Membranous Nephropathy (MN). * **Most common HCV-associated renal disease:** Type I Membranoproliferative Glomerulonephritis (MPGN) and Mixed Cryoglobulinemia. * **Key Antigen:** HBeAg is the most common antigen found in glomerular deposits in HBV-MN [2]. * **Morphology:** On light microscopy, look for "spikes and domes" on Silver stain (Jones stain) and granular IgG/C3 deposits on Immunofluorescence [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-911. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 911-913.

Question 40: What is the cause of renal failure in rhabdomyolysis?

A. Increased potassium
B. Increased phosphate
C. Increased uric acid
D. Myoglobin (Correct Answer)

Explanation: **Explanation:** The primary cause of Acute Kidney Injury (AKI) in rhabdomyolysis is the release of **Myoglobin** from damaged skeletal muscle into the systemic circulation. Myoglobin causes renal failure through three main mechanisms: 1. **Intratubular Obstruction:** Myoglobin precipitates with Tamm-Horsfall protein in the distal tubules, forming obstructing casts (exacerbated by acidic urine) [2]. 2. **Direct Cytotoxicity:** The iron-containing heme group in myoglobin generates reactive oxygen species, leading to proximal tubular necrosis [1]. 3. **Renal Vasoconstriction:** Myoglobin scavenges Nitric Oxide (NO), leading to intrarenal ischemia [1]. **Analysis of Incorrect Options:** * **A & B (Increased Potassium & Phosphate):** These are common *consequences* of muscle cell lysis in rhabdomyolysis. While hyperkalemia is a life-threatening complication, it does not directly cause the structural renal damage seen in AKI. * **C (Increased Uric Acid):** Hyperuricemia occurs due to the release of purines from damaged cells. While it can contribute to tubular obstruction (Urate nephropathy), it is a secondary factor compared to the massive pigment load of myoglobin [3]. **High-Yield Facts for NEET-PG:** * **Classic Triad:** Muscle pain, weakness, and dark (tea-colored) urine. * **Urinalysis Paradox:** Urine dipstick shows "positive for blood," but microscopic examination reveals **no RBCs** (the dipstick detects the heme group in myoglobin). * **Biochemical Marker:** Serum **Creatine Kinase (CK)** levels >5 times the upper limit of normal is the most sensitive diagnostic indicator. * **Management:** Aggressive fluid resuscitation and urinary alkalinization to prevent myoglobin precipitation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 933. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 933-934. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 941-942.

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