Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 81: A characteristic electron microscopic feature of minimal change disease is:

A. Mesangial deposits
B. Splitting of basement membrane
C. Fusion of foot processes and their effacement (Correct Answer)
D. Subepithelial deposits

Explanation: ### Explanation **Minimal Change Disease (MCD)** is the most common cause of nephrotic syndrome in children [1]. The hallmark of this condition is that the kidney appears normal under Light Microscopy (LM) and Immunofluorescence (IF), but reveals diagnostic changes under Electron Microscopy (EM) [1]. **Why Option C is Correct:** The primary pathology in MCD is **podocyte injury** (podocytopathy). On EM, the most characteristic feature is the **diffuse effacement (flattening) and fusion of the foot processes** of visceral epithelial cells (podocytes) [1]. This leads to the loss of the anionic charge barrier (polyatomic charge), resulting in selective proteinuria (mainly albuminuria) [1]. **Analysis of Incorrect Options:** * **Option A (Mesangial deposits):** These are characteristic of **IgA Nephropathy** or certain stages of Lupus Nephritis, not MCD. * **Option B (Splitting of basement membrane):** This "tram-track" appearance is a classic feature of **Membranoproliferative Glomerulonephritis (MPGN)** or Alport Syndrome [1]. * **Option C (Subepithelial deposits):** These "humps" or "spikes" are seen in **Post-Streptococcal Glomerulonephritis (PSGN)** or **Membranous Nephropathy**, respectively. MCD is characterized by the *absence* of electron-dense deposits [1]. **NEET-PG High-Yield Pearls:** * **Light Microscopy:** Glomeruli appear completely normal (hence the name "Minimal Change") [1]. * **Immunofluorescence:** Negative (no immune complex deposits) [1]. * **Clinical Presentation:** Sudden onset of massive edema; **highly steroid-responsive.** * **Association:** Can be associated with **Hodgkin Lymphoma** in adults (due to T-cell dysfunction/cytokine release). * **Proteinuria:** Classically described as **highly selective** (albumin only) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Question 82: In which of the following conditions are linear IgA deposits in the mesangium noted?

A. Henoch Schonlein purpura (Correct Answer)
B. Malaria
C. Good Pasture's syndrome
D. Wegener's granulomatosis

Explanation: **Henoch-Schönlein Purpura (HSP)**, also known as IgA Vasculitis, is a systemic small-vessel vasculitis characterized by the deposition of IgA-dominant immune complexes [1]. In the kidneys (HSP Nephritis), these immune complexes deposit primarily in the **mesangium** [2]. On Immunofluorescence (IF) microscopy, this manifests as **granular to linear IgA deposits** along with C3. While IgA Nephropathy (Berger’s disease) also shows mesangial IgA, HSP is distinguished by its systemic involvement (purpura, arthritis, and abdominal pain) [1]. **Analysis of Incorrect Options:** * **Malaria:** Renal involvement in Malaria (especially *P. falciparum*) typically presents as Acute Tubular Necrosis (ATN) or Quartan Malarial Nephropathy (*P. malariae*), which shows **subendothelial** deposits of IgG and IgM, not IgA. * **Goodpasture’s Syndrome:** This is characterized by **linear IgG deposits** along the Glomerular Basement Membrane (GBM) due to anti-GBM antibodies [2]. It does not involve IgA or the mesangium. * **Wegener’s Granulomatosis (GPA):** This is a **Pauci-immune** glomerulonephritis. The hallmark finding on IF is the **absence** or scarcity of immunoglobulin/complement deposits. It is associated with c-ANCA (PR3-ANCA). **NEET-PG High-Yield Pearls:** * **HSP Triad:** Non-thrombocytopenic purpura (buttocks/legs), arthralgia, and abdominal pain. * **IgA Nephropathy vs. HSP:** Both are histologically identical in the kidney; HSP is the systemic version of the same pathology. * **Linear vs. Granular:** Linear deposits usually signify anti-GBM disease (Goodpasture’s) [2], while granular deposits signify immune-complex mediated diseases (PSGN, SLE). HSP is unique as its mesangial IgA can sometimes appear pseudo-linear. **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. 911-915.

Question 83: Papillary necrosis is most commonly seen in?

A. Diabetes Mellitus
B. Sickle cell anemia
C. Acute pyelonephritis
D. Analgesic nephropathy (Correct Answer)

Explanation: **Explanation:** **Renal Papillary Necrosis (RPN)** is a clinicopathologic entity characterized by ischemic necrosis of the renal papillae. While all the listed options are recognized causes of RPN, **Analgesic Nephropathy** is classically cited as the most common cause in many clinical contexts, particularly due to the synergistic effect of phenacetin, aspirin, and acetaminophen. **Why Analgesic Nephropathy is the Correct Answer:** Analgesics cause RPN through two mechanisms: 1. **Ischemia:** They inhibit prostaglandin synthesis (vasodilators), leading to vasoconstriction of the vasa recta. 2. **Direct Toxicity:** Acetaminophen metabolites accumulate in the papilla, causing oxidative damage. In analgesic abuse, the necrosis is typically **chronic and bilateral**, involving all papillae at different stages of development. **Analysis of Other Options:** * **Diabetes Mellitus:** A very common cause, but usually associated with concurrent infection (pyelonephritis) [2]. In DM, the necrosis is often more acute and severe. * **Sickle Cell Anemia:** Causes RPN due to sickling in the hypoxic, hypertonic environment of the renal medulla, leading to micro-infarctions [1]. It is a common cause in children/young adults. * **Acute Pyelonephritis:** RPN occurs as a complication of severe infection, especially when combined with urinary tract obstruction [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for RPN Causes (POSTCARDS):** **P**yelonephritis, **O**bstruction, **S**ickle cell, **T**uberculosis, **C**irrhosis, **A**nalgesics, **R**enal vein thrombosis, **D**iabetes, **S**ystemic vasculitis. * **IVP Finding:** The **"Ring Shadow"** sign (sloughed papilla surrounded by contrast). * **Gross Appearance:** The papillae appear "shrunken" or "mummified." * **Clinical Presentation:** Often presents with gross hematuria and renal colic (due to sloughed papillae obstructing the ureter) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 948-949. [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.

Question 84: Which of the following is NOT a feature of Potter syndrome?

A. Bilateral renal agenesis
B. Polyhydramnios (Correct Answer)
C. Pulmonary hypoplasia
D. Flattened facies

Explanation: **Explanation:** **Potter Syndrome** (or Potter Sequence) is a constellation of physical findings resulting from a severe lack of amniotic fluid (**Oligohydramnios**), not polyhydramnios [1]. **1. Why Polyhydramnios is the Correct Answer (The "NOT" feature):** The fundamental pathophysiology of Potter syndrome is **Oligohydramnios**. In a normal pregnancy, fetal urine is the primary source of amniotic fluid. When there is a lack of urine production (due to renal issues), the volume of amniotic fluid drops significantly. This leads to mechanical compression of the fetus and a lack of fluid for lung expansion [1]. **Polyhydramnios** (excess fluid) is typically associated with GI obstructions (e.g., esophageal atresia) or maternal diabetes, not renal agenesis. **2. Analysis of Other Options:** * **Bilateral Renal Agenesis (Option A):** This is the most common cause of Potter syndrome. Without kidneys, no urine is produced, initiating the sequence. * **Pulmonary Hypoplasia (Option C):** This is the **most common cause of death** in these neonates. Amniotic fluid is essential for the mechanical expansion of the developing lungs; without it, the lungs remain underdeveloped. * **Flattened Facies (Option D):** Due to the lack of cushioning fluid, the fetus is compressed against the uterine wall, leading to "Potter Facies" (flattened nose, recessed chin, and low-set ears) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (POTTER):** **P**ulmonary hypoplasia, **O**ligohydramnios, **T**wisted skin (wrinkly), **T**wisted face (Potter facies), **E**xtremity defects (clubbed feet), **R**enal agenesis [1]. * **Other Causes:** Besides bilateral renal agenesis, it can be caused by **Autosomal Recessive Polycystic Kidney Disease (ARPKD)** or obstructive uropathy (e.g., Posterior Urethral Valves) [2]. * **Key Association:** Look for **Amnion nodosum** (small nodules on the fetal surface of the amnion) on placental examination. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 460-462. [2] 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.

Question 85: Broad cast is a feature of which of the following conditions?

A. Acute Renal failure
B. Chronic Renal failure (Correct Answer)
C. Acute glomerulonephritis
D. Chronic glomerulonephritis

Explanation: **Explanation:** **Broad casts** (also known as "Renal Failure Casts") are significantly wider than standard urinary casts. They are formed in the **collecting ducts** that have become dilated due to compensatory hypertrophy or severe atrophy of the surrounding nephrons. 1. **Why Chronic Renal Failure (CRF) is correct:** In CRF, there is a progressive loss of functioning nephrons [3]. To compensate, the remaining viable nephrons undergo hypertrophy and their tubules (specifically the collecting ducts) dilate [4]. When urinary flow is severely sluggish in these wide, damaged ducts, proteins and cellular debris precipitate to form wide-diameter casts. Therefore, the presence of broad casts is a hallmark of **end-stage renal disease (ESRD)** or advanced CRF [3]. 2. **Why other options are incorrect:** * **Acute Renal Failure (ARF):** Typically characterized by **Muddy Brown (Granular) casts** due to Acute Tubular Necrosis (ATN) [2], but the tubules have not yet undergone the chronic dilation required to form "broad" casts. * **Acute Glomerulonephritis:** Characterized by **RBC casts**, indicating glomerular capillary damage [2]. * **Chronic Glomerulonephritis:** While this can lead to CRF, "Chronic Renal Failure" is the more specific clinical state associated with the broad cast. Broad casts represent the final common pathway of tubular dilation regardless of the initial cause. **High-Yield Clinical Pearls for NEET-PG:** * **Broad Waxy Casts:** These are the most specific type of broad casts found in CRF, indicating extremely low urine flow and chronic chronicity. * **Tamm-Horsfall Protein:** The mucoprotein matrix that forms the "stent" for all urinary casts; it is secreted by the thick ascending limb of the Loop of Henle [1]. * **Hyaline Casts:** Can be normal (seen after exercise or dehydration) [2]. * **RBC Casts:** Pathognomonic for Nephritic Syndrome/Glomerulonephritis [2]. * **WBC Casts:** Pathognomonic for Pyelonephritis or Tubulointerstitial nephritis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 520-521. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 903-905. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 949-950.

Question 86: What is an example of Pauci-immune Rapidly Progressive Glomerulonephritis (RPGN)?

A. Goodpasture syndrome
B. Membranoproliferative Glomerulonephritis (MPGN)
C. Wegener granulomatosis (Granulomatosis with polyangiitis) (Correct Answer)
D. Alport's syndrome

Explanation: **Explanation:** Rapidly Progressive Glomerulonephritis (RPGN) is a clinical syndrome characterized by a rapid decline in renal function and the presence of **crescents** in most glomeruli. It is classified into three types based on immunofluorescence (IF) findings: 1. **Type I (Anti-GBM):** Linear IgG deposits (e.g., Goodpasture syndrome) [4]. 2. **Type II (Immune Complex):** Granular deposits (e.g., PSGN, SLE, MPGN). 3. **Type III (Pauci-immune):** Characterized by a **lack of significant immune deposits** (negative or "pauci" IF) and an association with **ANCA** (Anti-Neutrophil Cytoplasmic Antibodies) [1]. **Why Option C is Correct:** **Wegener Granulomatosis (Granulomatosis with polyangiitis)** is a classic example of Type III Pauci-immune RPGN [2]. It is typically associated with **c-ANCA (PR3-ANCA)** and involves the upper/lower respiratory tracts along with the kidneys [3]. Other examples include Microscopic Polyangiitis (p-ANCA) and Churg-Strauss syndrome [5]. **Analysis of Incorrect Options:** * **A. Goodpasture Syndrome:** This is Type I RPGN. It features **linear** deposition of antibodies against the α3 chain of Type IV collagen [4]. * **B. MPGN:** This is a Type II (Immune Complex) mediated glomerulonephritis showing a **granular** pattern on IF and a "tram-track" appearance on light microscopy. * **D. Alport’s Syndrome:** This is a hereditary nephritis caused by mutations in Type IV collagen. It presents with thinning/splitting of the GBM (basket-weave appearance) but is **not** an immunologically mediated RPGN. **NEET-PG High-Yield Pearls:** * **Crescents** are formed by the proliferation of parietal epithelial cells and the migration of monocytes/macrophages into Bowman’s space. * **c-ANCA** = Granulomatosis with polyangiitis (Wegener's). * **p-ANCA** = Microscopic polyangiitis and Churg-Strauss. * The most common cause of death in Wegener’s is renal failure if left untreated [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 931-933. [3] 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. [4] 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. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519.

Question 87: Hypercoagulation in nephrotic syndrome is caused by?

A. Loss of antithrombin III (Correct Answer)
B. Decreased fibrinogen
C. Decreased metabolism of Vitamin K
D. Increase in protein C

Explanation: **Explanation:** Nephrotic syndrome is characterized by massive proteinuria (>3.5g/day) due to increased glomerular permeability. This leads to a **hypercoagulable state**, significantly increasing the risk of venous thromboembolism (e.g., Renal Vein Thrombosis). **1. Why Option A is Correct:** The primary mechanism for hypercoagulation is the **urinary loss of low-molecular-weight anticoagulant proteins**, most notably **Antithrombin III (ATIII)**. ATIII is a natural anticoagulant that inhibits thrombin and factors IXa, Xa, XIa, and XIIa. Its depletion shifts the hemostatic balance toward thrombosis. Additionally, the liver increases the synthesis of pro-coagulant factors (like Factor V and Fibrinogen) in a compensatory response to low oncotic pressure. **2. Why the other options are incorrect:** * **Option B:** Fibrinogen levels are actually **increased** (not decreased) in nephrotic syndrome due to reactive hepatic synthesis, contributing to hyperviscosity. * **Option C:** Vitamin K metabolism is not directly affected by the pathophysiology of nephrotic syndrome. * **Option D:** Levels of **Protein C and Protein S** are typically **decreased** (due to urinary loss), not increased [1]. An increase in these proteins would provide an anticoagulant effect, which contradicts the clinical presentation. **NEET-PG High-Yield Pearls:** * **Renal Vein Thrombosis (RVT):** Most commonly associated with **Membranous Nephropathy** in adults. * **Clinical Sign:** Sudden onset of flank pain and hematuria in a nephrotic patient suggests RVT. * **Other factors:** Hyperlipidemia and increased platelet aggregation also contribute to the pro-thrombotic state in these patients. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Question 88: Electron microscopy is diagnostic in which of the following conditions?

A. Goodpasture's syndrome (Correct Answer)
B. Wegener's granulomatosis
C. Polyarteritis nodosa (PAN)
D. Anti-GBM disease

Explanation: **Explanation:** In renal pathology, Electron Microscopy (EM) is a critical diagnostic tool used to identify specific ultrastructural changes in the glomerular basement membrane (GBM) and the presence/location of immune deposits [1]. **Why Goodpasture’s Syndrome is the Correct Answer:** Goodpasture’s syndrome is characterized by the presence of circulating **anti-GBM antibodies** that target the non-collagenous domain of the α3 chain of Type IV collagen [1]. While Immunofluorescence (IF) shows the classic **"linear" IgG deposition**, Electron Microscopy is considered diagnostic because it reveals specific, diffuse thickening of the GBM and, more importantly, can rule out other "pauci-immune" or "complex-mediated" glomerulonephritides [1]. In a clinical context where pulmonary hemorrhage and glomerulonephritis coexist, EM confirms the primary basement membrane pathology [2]. **Analysis of Incorrect Options:** * **Wegener’s Granulomatosis (GPA) & Polyarteritis Nodosa (PAN):** These are **Pauci-immune** conditions [3]. This means that on EM and IF, there are little to no immune deposits. Diagnosis relies primarily on clinical presentation, serology (c-ANCA for GPA), and light microscopy (necrotizing vasculitis) [3]. * **Anti-GBM Disease:** While closely related to Goodpasture’s, "Anti-GBM disease" refers specifically to renal involvement. Goodpasture’s *Syndrome* implies the clinical triad of anti-GBM antibodies, glomerulonephritis, and pulmonary hemorrhage, making it the more comprehensive clinical entity where EM confirms the underlying membrane damage [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Linear IF Pattern:** Pathognomonic for Goodpasture’s/Anti-GBM disease [1]. * **Lumpy-Bumpy/Granular IF Pattern:** Seen in Post-Streptococcal Glomerulonephritis (PSGN). * **Alport Syndrome:** Another condition where EM is diagnostic (shows "Basket-weave" appearance of GBM). * **Minimal Change Disease:** EM is the *only* way to see the diagnostic effacement of podocyte foot processes. **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. 526-527. [2] 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. [3] 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 89: Dense deposit disease is a characteristic finding in which of the following conditions?

A. Membranous Glomerulopathy
B. Membranoproliferative Glomerulonephritis (Correct Answer)
C. Mesangioproliferative Glomerulonephritis
D. No specific lesion

Explanation: **Explanation:** **Dense Deposit Disease (DDD)** is the hallmark of **Membranoproliferative Glomerulonephritis (MPGN) Type II** [1]. It is characterized by the presence of highly electron-dense, ribbon-like deposits within the lamina densa of the glomerular basement membrane (GBM) [1]. 1. **Why Option B is Correct:** MPGN is historically classified into three types. While Type I involves subendothelial deposits, **Type II (Dense Deposit Disease)** is unique because the deposits are intramembranous [1]. The underlying pathophysiology involves the **alternative complement pathway** dysregulation, often due to **C3 Nephritic Factor (C3NeF)**, an autoantibody that stabilizes C3 convertase, leading to continuous C3 consumption [2]. 2. **Why Other Options are Incorrect:** * **Option A (Membranous Glomerulopathy):** Characterized by subepithelial "spikes" and domes, not dense intramembranous ribbons. It involves diffuse thickening of the GBM due to immune complex deposition. * **Option C (Mesangioproliferative GN):** Defined by an increase in mesangial cells and matrix (often seen in IgA Nephropathy), without the characteristic dense GBM deposits. * **Option D:** Incorrect, as DDD is a distinct pathological entity with specific light, immunofluorescence (C3 positive, IgG negative), and electron microscopy findings [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy:** The "Gold Standard" for diagnosing DDD (ribbon-like deposits) [1]. * **Immunofluorescence:** Shows "starry sky" or linear C3 staining; notably **IgG is usually absent** [2] (distinguishing it from MPGN Type I). * **C3 Nephritic Factor:** Frequently positive in DDD; leads to hypocomplementemia (low C3, normal C4). * **Clinical Association:** DDD is uniquely associated with **partial lipodystrophy**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927. [2] 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.

Question 90: Selective proteinuria is typically seen in which of the following conditions?

A. Nil lesion (Correct Answer)
B. Diabetic nephropathy
C. Focal segmental glomerulosclerosis
D. Mesangioproliferative glomerulonephritis

Explanation: ### Explanation **Correct Option: A. Nil lesion (Minimal Change Disease)** Selective proteinuria refers to the loss of low-molecular-weight proteins (primarily **Albumin**) in the urine, while higher-molecular-weight proteins (like IgG) are retained [1]. In **Nil lesion (Minimal Change Disease)**, the primary pathology is the **loss of the glomerular polyanion (negative charge)** due to T-cell-mediated cytokine injury [3]. Since the basement membrane's size barrier remains intact but the charge barrier is lost, only small, negatively charged molecules like albumin leak through [3]. This is a hallmark of MCD, especially in children [1]. **Incorrect Options:** * **B. Diabetic nephropathy:** This involves structural damage to the glomerular basement membrane (GBM) and mesangial expansion. As the disease progresses, the size barrier is compromised, leading to **non-selective proteinuria** (loss of both albumin and globulins). * **C. Focal segmental glomerulosclerosis (FSGS):** FSGS involves physical scarring and sclerosis of glomerular segments [2]. This structural destruction leads to a breakdown of the size-selective barrier, resulting in **non-selective proteinuria**. * **D. Mesangioproliferative GN:** This condition involves the proliferation of mesangial cells and matrix. Like most inflammatory glomerulonephritides, the damage is structural rather than purely charge-based, leading to non-selective protein loss. **High-Yield Clinical Pearls for NEET-PG:** * **Selectivity Index:** Calculated as (Clearance of IgG / Clearance of Albumin). A ratio **< 0.1** indicates highly selective proteinuria (MCD), while **> 0.2** indicates non-selective proteinuria. * **Electron Microscopy (EM):** In Nil lesion, Light Microscopy is normal, but EM shows **effacement (fusion) of podocyte foot processes** [2]. * **Treatment:** Minimal Change Disease is highly steroid-responsive, which correlates with the "selective" nature of the damage [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 905-907.

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