Renal Pathology — MCQs
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A young child presented with a history of dark-colored urine and reduced urine output. The child had a past history of abdominal pain, fever, and bloody diarrhea for 4 days, which resolved spontaneously. There was no peripheral edema or rashes. Investigations revealed anemia, thrombocytopenia, and elevated blood urea nitrogen and serum creatinine. Which of the following findings is most expected in this patient?
A wire loop lesion seen in lupus nephritis is due to which of the following?
Hypercalcemia is a known complication in which type of cancer?
Transitional cell carcinoma of the bladder is associated with which of the following?
Glomerulonephritis is due to what mechanism?
Loss of foot processes of podocytes is characteristically seen in which condition?
Hobnail pattern is seen in which type of Renal Cell Carcinoma?
Type I RPGN is seen in which of the following conditions?
Nephrotic syndrome is characterised by which of the following?
According to the WHO classification, which class of membranous glomerulonephritis is typically seen in Systemic Lupus Erythematosus (SLE)?
Renal Pathology Indian Medical PG Practice Questions and MCQs
Question 511: A young child presented with a history of dark-colored urine and reduced urine output. The child had a past history of abdominal pain, fever, and bloody diarrhea for 4 days, which resolved spontaneously. There was no peripheral edema or rashes. Investigations revealed anemia, thrombocytopenia, and elevated blood urea nitrogen and serum creatinine. Which of the following findings is most expected in this patient?
- A. Elevated haptoglobin level
- B. Elevated serum indirect bilirubin (Correct Answer)
- C. Elevated thrombin and prothrombin time
- D. Low fibrinogen and elevated D-dimer level
Explanation: ### **Explanation** **Diagnosis: Hemolytic Uremic Syndrome (HUS)** The clinical triad of **Microangiopathic Hemolytic Anemia (MAHA)**, **Thrombocytopenia**, and **Acute Kidney Injury (AKI)** following an episode of bloody diarrhea (typically caused by Shiga toxin-producing *E. coli* O157:H7) is pathognomonic for **Typical HUS** [2], [3]. **1. Why the Correct Answer is Right:** In HUS, the formation of microthrombi in small vessels leads to the mechanical shearing of RBCs (schistocytes). This intravascular hemolysis results in the release of unconjugated bilirubin [1]. Therefore, **elevated serum indirect bilirubin** is a hallmark finding of the hemolytic process occurring in this patient. **2. Analysis of Incorrect Options:** * **Option A (Elevated haptoglobin):** In intravascular hemolysis, haptoglobin binds to free hemoglobin and is subsequently cleared by the liver [1]. Therefore, haptoglobin levels are **decreased**, not elevated. * **Options C & D (Coagulation Profile):** HUS is characterized by platelet consumption in microthrombi, but the **coagulation cascade is not activated** [2]. Thus, PT, aPTT, Thrombin Time, and Fibrinogen levels remain **normal**. Elevated D-dimers and prolonged PT/aPTT would instead point toward **Disseminated Intravascular Coagulation (DIC)** [2]. **3. Clinical Pearls for NEET-PG:** * **Classic Presentation:** "D+ HUS" (Diarrhea-associated) usually follows *E. coli* or *Shigella* infection [3]. * **Peripheral Smear:** Must show **Schistocytes** (helmet cells). * **Key Distinction:** Unlike DIC, HUS and TTP (Thrombotic Thrombocytopenic Purpura) have **normal coagulation studies** [2]. * **Renal Pathology:** Characterized by **Glomerular Thrombotic Microangiopathy (TMA)** [3]. * **Management:** Primarily supportive; antibiotics are generally avoided as they may increase toxin release. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 946-947.
Question 512: A wire loop lesion seen in lupus nephritis is due to which of the following?
- A. Capillary wall thickening (Correct Answer)
- B. Basement membrane thickening
- C. Subepithelial deposits
- D. Sclerosis of mesangium
Explanation: **Explanation:** **1. Why Option A is Correct:** The "wire loop" lesion is a hallmark histological feature of **Systemic Lupus Erythematosus (SLE) Nephritis**, specifically **Class IV (Diffuse Proliferative Glomerulonephritis)**. It is caused by extensive **subendothelial immune complex deposits** (DNA-anti-DNA complexes) that accumulate between the endothelial cells and the glomerular basement membrane (GBM) [1]. These bulky deposits, along with associated endothelial proliferation, lead to a rigid, uniform thickening of the capillary wall [2]. Under a light microscope (H&E stain), these thickened walls resemble loops of stiff wire. **2. Why the Other Options are Incorrect:** * **Option B (Basement Membrane Thickening):** While the capillary wall appears thick, the primary pathology is the *deposition* of complexes, not the intrinsic thickening of the GBM itself (which is more characteristic of Membranous Nephropathy). * **Option C (Subepithelial Deposits):** Subepithelial deposits are characteristic of **Class V (Membranous) Lupus Nephritis** and result in "spikes and domes" on silver stain, not wire loops. Wire loops are specifically due to *subendothelial* deposits [1]. * **Option D (Sclerosis of Mesangium):** Mesangial sclerosis is a feature of chronic, irreversible damage (Class VI) or diabetic nephropathy (Kimmelstiel-Wilson nodules), rather than the active inflammatory phase represented by wire loops. **3. Clinical Pearls for NEET-PG:** * **Most Common & Most Severe Type:** Class IV (Diffuse Proliferative) is the most common and carries the worst prognosis. * **Immunofluorescence:** Shows a **"Full House" pattern** (positive for IgG, IgA, IgM, C3, and C1q). * **Electron Microscopy:** Subendothelial deposits are the ultrastructural equivalent of wire loops [1]. * **Associated Finding:** Look for **Hematoxylin bodies** (hyaline thrombi) in the capillary lumens, which are also characteristic of SLE. **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. 528-529.
Question 513: Hypercalcemia is a known complication in which type of cancer?
- A. Renal cell carcinoma (Correct Answer)
- B. Carcinoma of the stomach
- C. Small cell carcinoma of the lung
- D. Hepatocellular carcinoma
Explanation: **Explanation:** **Renal Cell Carcinoma (RCC)** is the correct answer because it is one of the most common tumors associated with **Paraneoplastic Syndromes**. The primary mechanism for hypercalcemia in RCC is the secretion of **Parathyroid Hormone-related Protein (PTHrP)**, which mimics PTH by increasing bone resorption and renal calcium reabsorption [2]. RCC is often nicknamed the "internist's tumor" because of its diverse systemic manifestations [1]. **Analysis of Options:** * **Renal cell carcinoma (A):** Correct. PTHrP production is a classic paraneoplastic feature of RCC (specifically the Clear Cell subtype) [2]. Other mechanisms include lytic bone metastases [1]. * **Carcinoma of the stomach (B):** Incorrect. Gastric cancer is more commonly associated with dermatological paraneoplastic syndromes like the Sign of Leser-Trélat or Acanthosis Nigricans. * **Small cell carcinoma of the lung (C):** Incorrect. While SCLC causes many paraneoplastic syndromes (SIADH, ACTH production, Lambert-Eaton syndrome), hypercalcemia is specifically associated with **Squamous Cell Carcinoma** of the lung (via PTHrP) [2]. * **Hepatocellular carcinoma (D):** Incorrect. While HCC can rarely cause hypercalcemia, it is much more characteristically associated with erythrocytosis (due to EPO production) or hypoglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **PTHrP-mediated hypercalcemia** is most commonly seen in: Squamous cell CA (Lung, Head/Neck), RCC, and Breast CA [2]. * **RCC Paraneoplastic Syndromes:** Hypercalcemia (PTHrP), Polycythemia (Erythropoietin), Hypertension (Renin), and Cushing’s Syndrome (ACTH). * **Stauffer Syndrome:** A unique paraneoplastic manifestation of RCC involving reversible hepatic dysfunction (elevated ALP) without liver metastases. **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. 492-493. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 338-339.
Question 514: Transitional cell carcinoma of the bladder is associated with which of the following?
- A. Schistosomiasis
- B. Naphthylamine
- C. Smoking
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Transitional Cell Carcinoma (TCC), now more commonly referred to as **Urothelial Carcinoma**, is the most common primary tumor of the urinary bladder [1]. Its etiology is multifactorial, involving chronic irritation and exposure to environmental carcinogens. 1. **Smoking (Option C):** This is the **most significant risk factor** for TCC [1]. Cigarette smoke contains aromatic amines and polycyclic aromatic hydrocarbons (like nitrosamines) which are filtered by the kidneys and concentrated in the urine, leading to direct DNA damage of the urothelium. 2. **Naphthylamine (Option B):** Industrial exposure to aromatic amines, specifically **2-Naphthylamine** and benzidine (used in dye, rubber, and leather industries), is a classic high-yield risk factor [1], [2]. These chemicals are potent carcinogens that undergo metabolic activation in the liver and are excreted in the urine. 3. **Schistosomiasis (Option A):** Infection with *Schistosoma haematobium* causes chronic inflammation and irritation [1]. While it is most classically associated with **Squamous Cell Carcinoma (SCC)** of the bladder, it also significantly increases the risk of **Transitional Cell Carcinoma**. **Clinical Pearls for NEET-PG:** * **Most common presentation:** Painless gross hematuria. * **Field Cancerization:** The entire urothelial lining (from renal pelvis to urethra) is at risk due to "field effect" exposure to carcinogens; hence, these tumors are often multifocal [3]. * **Cyclophosphamide:** A chemotherapy agent associated with hemorrhagic cystitis and an increased risk of bladder TCC. * **Phenacetin:** Chronic abuse of this analgesic is linked to TCC of the renal pelvis. * **Genetic Marker:** Deletions of **Chromosome 9** (9p and 9q) are frequently seen in superficial papillary tumors. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 968-970. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 217-218. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 964-966.
Question 515: Glomerulonephritis is due to what mechanism?
- A. Type I hypersensitivity reaction
- B. Type IV hypersensitivity reaction
- C. Immune complex deposition (Correct Answer)
- D. Type V hypersensitivity reaction
Explanation: ### Explanation **Correct Answer: C. Immune complex deposition** Glomerulonephritis (GN) is primarily an **immunologically mediated** injury [1]. The most common mechanism is **Type III hypersensitivity**, characterized by the deposition of antigen-antibody complexes within the glomeruli [1]. These complexes can either be formed in the circulation and trapped in the glomerular basement membrane (e.g., SLE, Post-streptococcal GN) or formed *in situ* by antibodies reacting against planted antigens [2]. Once deposited, these complexes activate the **complement system** (classical pathway), leading to leukocyte recruitment and the release of inflammatory mediators that damage the glomerular filtration barrier [1]. **Why other options are incorrect:** * **Option A (Type I):** This involves IgE-mediated mast cell degranulation (e.g., anaphylaxis, asthma). It does not play a primary role in the pathogenesis of GN. * **Option B (Type IV):** This is cell-mediated immunity (T-cells). While T-cells contribute to the progression of chronic renal scarring, the primary initiating mechanism for most GN is humoral (antibody-mediated). * **Option D (Type V):** This is an older classification sometimes used for stimulatory hypersensitivity (like Graves' disease). It is not a recognized mechanism for glomerulonephritis. **High-Yield Clinical Pearls for NEET-PG:** * **Type II Hypersensitivity** is also a cause of GN, specifically in **Goodpasture Syndrome**, where antibodies are directed against the fixed antigens in the GBM (Anti-GBM disease) [2]. * **Low Complement Levels (C3):** Characteristically seen in PSGN, MPGN, and Systemic Lupus Erythematosus (SLE) due to consumption during immune complex activation [2]. * **Immunofluorescence (IF) Patterns:** * *Granular:* Suggests Immune Complex deposition (Type III) [2]. * *Linear:* Suggests Anti-GBM disease (Type II) [2]. **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. 911-913.
Question 516: Loss of foot processes of podocytes is characteristically seen in which condition?
- A. Goodpasture syndrome
- B. Lipoid nephrosis (Correct Answer)
- C. Post-streptococcal glomerulonephritis (PSGN)
- D. Lupus nephritis
Explanation: **Explanation:** **Lipoid nephrosis**, also known as **Minimal Change Disease (MCD)**, is the most common cause of nephrotic syndrome in children [1]. The hallmark of this condition is the **effacement (loss/fusion) of foot processes of podocytes**, which is visible only under **Electron Microscopy (EM)** [1]. Light microscopy typically appears normal, and Immunofluorescence (IF) is negative [1]. The loss of these foot processes leads to the disappearance of the slit diaphragm, resulting in massive selective proteinuria (primarily albumin) [1]. **Analysis of Incorrect Options:** * **Goodpasture Syndrome:** Characterized by anti-GBM antibodies. Light microscopy shows **crescentic formation** (RPGN), and IF shows **linear IgG deposits** along the basement membrane. * **Post-streptococcal Glomerulonephritis (PSGN):** An immune-complex mediated disease. EM characteristically shows **subepithelial "humps"**, and IF shows a "starry sky" or granular pattern. * **Lupus Nephritis:** A complex systemic condition where EM typically shows **subendothelial deposits** (Wire-loop lesions in Class IV) and a "Full House" pattern on IF. **High-Yield Clinical Pearls for NEET-PG:** * **MCD** is the most common nephrotic syndrome in children; **FSGS** is the most common in adults (though FSGS also shows foot process effacement, it is focal and segmental). * MCD is highly responsive to **Corticosteroids** [1]. * The proteinuria in MCD is **highly selective** (Albuminuria) [1]. * Association: MCD can be associated with **Hodgkin Lymphoma** in adults (due to cytokine release). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.
Question 517: Hobnail pattern is seen in which type of Renal Cell Carcinoma?
- A. Clear cell
- B. Papillary
- C. Chromophobe
- D. Collecting duct (Correct Answer)
Explanation: **Explanation:** The **Collecting Duct Carcinoma (CDC)**, also known as Bellini duct carcinoma, is a rare but highly aggressive subtype of Renal Cell Carcinoma (RCC) arising from the distal segment of the collecting ducts. **Why the correct answer is right:** The characteristic histological feature of CDC is a **tubulopapillary architecture** lined by highly atypical cells. These cells exhibit a **"Hobnail appearance,"** where the nuclei bulge into the lumen of the tubules or papillae due to a high nuclear-to-cytoplasmic ratio and apical displacement. This pattern is a classic morphologic hallmark used to differentiate it from other renal tumors. **Why the incorrect options are wrong:** * **Clear cell RCC:** The most common type; characterized by cells with clear cytoplasm (due to glycogen and lipid) and a prominent delicate vascular network ("chicken-wire" pattern) [1]. * **Papillary RCC:** Characterized by papillae with fibrovascular cores containing **foamy macrophages** and psammoma bodies [1]. * **Chromophobe RCC:** Features large polygonal cells with prominent cell membranes (**"vegetable cell" appearance**), perinuclear halos, and "raisinoid" nuclei [1]. It stains positive with **Hale’s Colloidal Iron**. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** Medulla (unlike Clear cell/Papillary which arise from the Proximal Convoluted Tubule). * **Prognosis:** Extremely poor; most patients present with metastatic disease. * **Immunohistochemistry:** CDC is often positive for **High Molecular Weight Cytokeratin (HMWK)** and Ulex europaeus agglutinin-1 (UEA-1). * **Differential Diagnosis:** Medullary carcinoma (associated with Sickle Cell Trait) also shows hobnailing but is distinguished by its association with hemoglobinopathies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 959-961.
Question 518: Type I RPGN is seen in which of the following conditions?
- A. Cryoglobulinemia
- B. SLE
- C. Goodpasture's syndrome (Correct Answer)
- D. Wegner's granulomatosis
Explanation: **Explanation:** Rapidly Progressive Glomerulonephritis (RPGN) is a clinical syndrome characterized by a rapid decline in renal function and the histological presence of **crescents** in most glomeruli [3]. It is classified into three types based on immunofluorescence (IF) findings: **1. Why Goodpasture’s Syndrome is Correct:** **Type I RPGN** is characterized by **Anti-Glomerular Basement Membrane (Anti-GBM) antibodies** [1]. These antibodies are directed against the non-collagenous domain of the ̱3 chain of Type IV collagen [2]. On immunofluorescence, this results in a classic **linear deposition** of IgG and C3 along the GBM [2]. When this is associated with pulmonary hemorrhage (hemoptysis), it is termed **Goodpasture’s syndrome** [1]. **2. Analysis of Incorrect Options:** * **Option A (Cryoglobulinemia) & Option B (SLE):** These are causes of **Type II RPGN (Immune-complex mediated)**. This type is characterized by a **granular pattern** on IF due to the deposition of antigen-antibody complexes [2]. Other examples include Post-streptococcal GN and IgA nephropathy. * **Option D (Wegener’s Granulomatosis/GPA):** This is a cause of **Type III RPGN (Pauci-immune)** [1]. It is characterized by the absence of significant antibody deposition (negative IF) and is strongly associated with **ANCA** (c-ANCA in Wegener’s) [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Histology Hallmark:** "Crescents" are formed by the proliferation of parietal epithelial cells and the migration of monocytes/macrophages into Bowman’s space. * **Type I (Anti-GBM):** Linear IF pattern [2]. * **Type II (Immune Complex):** Granular IF pattern [2]. * **Type III (Pauci-immune):** Negative IF; associated with Vasculitis (GPA, MPA, Churg-Strauss) [4]. * **Treatment:** Plasmapheresis is specifically indicated in Type I RPGN to remove circulating anti-GBM antibodies [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. 537-538. [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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 931-933. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918.
Question 519: Nephrotic syndrome is characterised by which of the following?
- A. Proteinuria
- B. Hyperlipidemia
- C. Oedema
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Nephrotic syndrome is a clinical complex resulting from a massive increase in glomerular permeability to plasma proteins [2]. The correct answer is **All of the above** because the syndrome is defined by a specific tetrad of clinical and biochemical findings. **1. Why "All of the above" is correct:** The underlying pathophysiology begins with **massive proteinuria** (typically >3.5 g/24 hours). The loss of albumin leads to **hypoalbuminemia**, which decreases the plasma oncotic pressure. This shift of fluid from the intravascular space to the interstitium results in generalized **oedema** (anasarca). To compensate for low plasma protein, the liver increases the synthesis of lipoproteins, leading to **hyperlipidemia** and lipiduria (fatty casts). **2. Analysis of Options:** * **Proteinuria:** This is the hallmark and initiating event [2]. It is usually "heavy" or "nephrotic range." * **Hyperlipidemia:** Occurs due to increased hepatic synthesis of LDL and VLDL and decreased catabolism of circulating lipids. * **Oedema:** Classically starts as puffiness around the eyes (periorbital) and progresses to pitting pedal oedema and ascites. **Clinical Pearls for NEET-PG:** * **Most common cause:** In children, it is **Minimal Change Disease** (effacement of podocyte foot processes); in adults, it is often **Membranous Nephropathy** or **FSGS** [1]. * **Hypercoagulability:** Patients are at high risk for venous thrombosis (especially **Renal Vein Thrombosis**) due to the loss of Antithrombin III in urine. * **Infection Risk:** Increased susceptibility to staphylococcal and pneumococcal infections due to loss of low-molecular-weight complement components and immunoglobulins. * **Mnemonic:** Remember **"PHO"** (Proteinuria, Hypoalbuminemia, Hyperlipidemia, Oedema). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-923. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 527-531.
Question 520: According to the WHO classification, which class of membranous glomerulonephritis is typically seen in Systemic Lupus Erythematosus (SLE)?
- A. Class II
- B. Class III
- C. Class IV
- D. Class V (Correct Answer)
Explanation: **Explanation:** The classification of Lupus Nephritis is based on the **ISN/RPS (International Society of Nephrology/Renal Pathology Society)** criteria, which is the standard used in WHO classifications. **Why Class V is Correct:** **Class V Lupus Nephritis** is specifically defined as **Membranous Lupus Nephritis** [1]. It is characterized by the global or segmental subepithelial immune complex deposits, often accompanied by basement membrane thickening (spikes) [2]. Clinically, patients typically present with nephrotic-range proteinuria, similar to idiopathic membranous nephropathy [3]. **Analysis of Incorrect Options:** * **Class II (Mesangial Proliferative LN):** Characterized by purely mesangial hypercellularity and immune deposits. It usually presents with mild hematuria or proteinuria. * **Class III (Focal LN):** Involves less than 50% of all glomeruli. It shows active or inactive focal, segmental, or global endo- or extracapillary glomerulonephritis. * **Class IV (Diffuse LN):** This is the **most common and most severe form** [4]. It involves more than 50% of glomeruli. It typically presents with "wire-loop" lesions (subendothelial deposits) and carries the worst prognosis if untreated [4]. **NEET-PG High-Yield Pearls:** * **Most Common Class:** Class IV (Diffuse Proliferative) [4]. * **Most Severe/Worst Prognosis:** Class IV [4]. * **Wire-loop lesions:** Characteristic of Class IV (due to massive subendothelial deposits) [4]. * **Full House Immunofluorescence:** SLE is classic for showing "Full House" positivity (IgG, IgA, IgM, C3, and C1q) [1]. * **Fingerprint pattern:** Often seen on Electron Microscopy in SLE. * **Class VI:** Represents Advanced Sclerotic Lupus Nephritis (>90% sclerosed glomeruli). **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. 532-533. [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. 919-921. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 232.
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