Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 141: All of the following are seen in Goodpasture's syndrome, except?

A. Crescentic glomerulonephritis
B. Hemorrhagic inflammation
C. Anti-GBM antibody
D. Diffuse alveolar involvement (Correct Answer)

Explanation: **Explanation:** Goodpasture’s Syndrome is a classic example of **Type II Hypersensitivity**, characterized by the presence of **Anti-GBM antibodies** [3] directed against the non-collagenous domain (NC1) of the **α3 chain of Type IV collagen**. **Why Option D is the correct answer:** While Goodpasture’s syndrome involves both the lungs and kidneys, the pulmonary involvement is typically characterized by **diffuse alveolar hemorrhage (DAH)** [1] rather than "diffuse alveolar involvement" (a vague term often implying diffuse alveolar damage/DAD seen in ARDS). The hallmark is intra-alveolar hemorrhage and hemosiderin-laden macrophages. Furthermore, in many clinical cases, the lung involvement may be focal or transient, whereas the renal involvement is more consistently diffuse and progressive [2]. **Analysis of Incorrect Options:** * **A. Crescentic glomerulonephritis:** This is the classic histological presentation. The anti-GBM antibodies cause severe glomerular injury, leading to the proliferation of parietal epithelial cells and the formation of **crescents** (Rapidly Progressive Glomerulonephritis - RPGN Type I) [1]. * **B. Hemorrhagic inflammation:** The syndrome is defined by the "Pulmonary-Renal Syndrome" triad. In the lungs, this manifests as necrotizing hemorrhagic interstitial pneumonitis. * **C. Anti-GBM antibody:** These are the pathogenic hallmark. On immunofluorescence, they produce a characteristic **linear (smooth) deposition of IgG** along the glomerular basement membrane [4]. **NEET-PG High-Yield Pearls:** * **Target Antigen:** α3 chain of Type IV Collagen. * **Immunofluorescence:** Linear IgG deposition (Pathognomonic) [4]. * **Clinical Triad:** Hemoptysis, anemia, and progressive renal failure. * **Epidemiology:** Strong association with **HLA-DRB1** [1]. * **Treatment:** Plasmapheresis (to remove circulating antibodies) and immunosuppressants [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 Respiratory Tract Disease, pp. 322-323. [3] 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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909.

Question 142: Serum C3 is persistently low in which of the following conditions?

A. Post-streptococcal glomerulonephritis (Correct Answer)
B. Membranoproliferative glomerulonephritis
C. Lupus nephritis
D. Glomerulonephritis related to bacterial endocarditis

Explanation: **Explanation:** The correct answer is **A. Post-streptococcal glomerulonephritis (PSGN)**. **Underlying Medical Concept:** In PSGN, the activation of the **alternative complement pathway** leads to a significant drop in serum C3 levels. The hallmark of PSGN is that this hypocomplementemia is **transient**. C3 levels typically return to normal within **6 to 8 weeks** after the onset of symptoms [1]. If C3 remains low beyond 8 weeks, an alternative diagnosis like MPGN should be considered. **Analysis of Options:** * **B. Membranoproliferative Glomerulonephritis (MPGN):** While C3 is low in MPGN (especially Type II/Dense Deposit Disease due to C3 nephritic factor), it is characterized by **persistently low** levels that do not normalize quickly. The question asks for the condition most classically associated with this pattern in a standard clinical vignette, though MPGN is a close differential [1]. * **C. Lupus Nephritis:** This involves the **classical pathway** activation, leading to a decrease in both **C3 and C4** [1]. In PSGN, C4 is typically normal. * **D. Bacterial Endocarditis-related GN:** Similar to Lupus, this usually involves immune complex deposition that consumes both C3 and C4. **High-Yield Clinical Pearls for NEET-PG:** * **The "Low C3" Trio:** PSGN, MPGN, and Systemic Lupus Erythematosus (SLE) are the three most common causes of hypocomplementemic GN. * **C3 vs. C4:** PSGN and MPGN Type II primarily show low C3 (Alternative pathway). SLE and Endocarditis show low C3 AND low C4 (Classical pathway). * **Timeframe:** The 8-week mark is the "gold standard" for PSGN; failure of C3 to normalize by this time necessitates a renal biopsy [1]. * **Morphology:** Look for "Lumpy-bumpy" deposits on Immunofluorescence and "Subepithelial humps" on Electron Microscopy in PSGN [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-917.

Question 143: Kimmelstiel-Wilson disease is diagnostic of which of the following conditions?

A. Diabetic glomerulosclerosis (Correct Answer)
B. Benign hypertension
C. Malignant hypertension
D. Amyloidosis

Explanation: **Explanation:** **Kimmelstiel-Wilson (KW) disease**, also known as **Nodular Glomerulosclerosis**, is a pathognomonic histological feature of **Diabetic Nephropathy** [1]. It is characterized by the formation of ovoid or spherical, laminated, eosinophilic hyaline masses situated in the periphery of the glomerulus [2]. These nodules represent an accumulation of mesangial matrix and are typically associated with the thickening of the glomerular basement membrane (GBM) [1], [2]. **Why the other options are incorrect:** * **Benign Hypertension:** Characterized by **Hyaline Arteriolosclerosis** (thickening of arteriolar walls) and granular contracted kidneys, but it does not produce KW nodules [3]. * **Malignant Hypertension:** Associated with **Fibrinoid Necrosis** of arterioles and **Hyperplastic Arteriolosclerosis** (onion-skin appearance) [4]. * **Amyloidosis:** While it involves glomerular deposits, these are composed of extracellular fibrillar proteins that stain with **Congo Red** (showing apple-green birefringence), unlike the PAS-positive nodules of KW disease [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Sign:** While diffuse glomerulosclerosis is the most common lesion in diabetes, KW nodules are the most **specific (diagnostic)** [2]. * **Staining:** KW nodules are **PAS (Periodic Acid-Schiff) positive** [2]. * **Armanni-Ebstein Lesion:** Another diabetic finding involving glycogen deposits in the proximal convoluted tubules. * **Clinical Correlation:** The presence of KW nodules usually correlates with significant proteinuria and the progression toward Chronic Kidney Disease (CKD) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1121. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1121-1122. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.

Question 144: Kimmelstiel-Wilson lesion is characteristic of which of the following?

A. Hyaline arteriosclerosis
B. Nodular glomerulosclerosis (Correct Answer)
C. Renal amyloid deposits
D. Renal glycogen deposits

Explanation: **Explanation:** **Kimmelstiel-Wilson (KW) lesions** are the hallmark of **Nodular Glomerulosclerosis**, which is the most specific histological indicator of **Diabetic Nephropathy**. 1. **Why the correct answer is right:** In long-standing Diabetes Mellitus, non-enzymatic glycosylation of proteins leads to the accumulation of mesangial matrix [3]. This results in the formation of characteristic **PAS-positive, ovoid or spherical laminated nodules** situated in the periphery of the glomerulus [1]. These nodules push the glomerular capillaries outward, eventually leading to ischemia and nephron loss [1]. 2. **Why the incorrect options are wrong:** * **Hyaline Arteriosclerosis:** While frequently seen in diabetic kidneys (and hypertension), it involves the thickening of arteriolar walls (especially the efferent arteriole) rather than the formation of glomerular nodules [4]. * **Renal Amyloid Deposits:** These appear as extracellular, amorphous, eosinophilic deposits that show **apple-green birefringence** under polarized light with Congo Red stain. They are not organized into the discrete peripheral nodules seen in KW lesions. * **Renal Glycogen Deposits:** Known as **Armanni-Ebstein lesions**, these occur in the epithelial cells of the distal convoluted tubules and the loop of Henle in uncontrolled diabetes, not in the glomerulus. **High-Yield Clinical Pearls for NEET-PG:** * **Most Specific Finding in Diabetes:** Nodular Glomerulosclerosis (KW Lesion) [1]. * **Most Common Finding in Diabetes:** Diffuse Glomerulosclerosis. * **Stain:** KW nodules are **PAS (Periodic Acid-Schiff) positive** [1]. * **Vascular involvement:** Diabetes is unique because it causes hyaline arteriosclerosis in **both afferent and efferent arterioles**. * **Clinical Presentation:** Usually manifests as persistent albuminuria followed by a decline in GFR [2]. **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 Endocrine System, p. 1121. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1119-1121. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.

Question 145: A person positive for Hepatitis B surface antigen (HBsAg) may have all of the following associated renal lesions, except?

A. Membranous Glomerulonephritis (MGN)
B. Membranoproliferative Glomerulonephritis (MPGN)
C. Mesangiocapillary Glomerulonephritis
D. Focal Segmental Glomerulosclerosis (FSGS) (Correct Answer)

Explanation: **Explanation:** The association between Hepatitis B Virus (HBV) and renal disease is primarily mediated by the deposition of immune complexes (Type III Hypersensitivity) [1]. **1. Why FSGS is the Correct Answer:** **Focal Segmental Glomerulosclerosis (FSGS)** is classically associated with **HIV infection** [2], heroin abuse, obesity, and sickle cell disease. It is **not** typically associated with Hepatitis B [2]. In the context of viral hepatitis, FSGS is more frequently linked to HIV (HIV-associated nephropathy or HIVAN) [4]. **2. Analysis of Incorrect Options:** * **Membranous Glomerulonephritis (MGN):** This is the **most common** renal lesion associated with Hepatitis B, especially in children [1]. It is caused by the deposition of HBeAg-anti-HBe immune complexes in the subepithelial space [4]. * **Membranoproliferative Glomerulonephritis (MPGN) / Mesangiocapillary GN:** These two terms are synonymous. MPGN (specifically Type I) is a well-recognized manifestation of chronic HBV infection [1]. It involves the deposition of immune complexes in the subendothelial space, leading to a "tram-track" appearance on light microscopy [3]. **3. Clinical Pearls for NEET-PG:** * **HBV + Renal:** Most common is **MGN**; also associated with **Polyarteritis Nodosa (PAN)**. * **HCV + Renal:** Most common is **MPGN Type I**. * **HIV + Renal:** Most common is the collapsing variant of **FSGS** [4]. * **Key Differentiator:** If a question asks for the most common renal lesion in HBV, choose **MGN**. If it asks for the most common vasculitis in HBV, choose **PAN**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-911. [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. 926-927. [4] 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.

Question 146: Non-proliferative glomerulonephritis includes all of the following, except:

A. Focal segmental glomerulosclerosis (FSGS)
B. Mesangiocapillary glomerulonephritis (Correct Answer)
C. Membranous glomerulonephritis
D. Amyloidosis

Explanation: **Explanation:** Glomerular diseases are broadly classified into **Proliferative** and **Non-proliferative** types based on the presence or absence of an increased number of cells (endothelial, mesangial, or epithelial) within the glomerulus [1]. **Why Mesangiocapillary Glomerulonephritis (MCGN) is the correct answer:** MCGN, also known as **Membranoproliferative Glomerulonephritis (MPGN)**, is a classic **proliferative** glomerulopathy [1]. As the name suggests, it is characterized by the proliferation of mesangial cells and an increase in the mesangial matrix, along with the thickening of the glomerular basement membrane (GBM) [2]. This proliferation leads to the characteristic "double contour" or "tram-track" appearance on silver stains [2]. **Analysis of Incorrect Options (Non-proliferative conditions):** * **Focal Segmental Glomerulosclerosis (FSGS):** Characterized by sclerosis (scarring) of some segments of some glomeruli. There is no generalized hypercellularity [3]. * **Membranous Glomerulonephritis (MGN):** Characterized by diffuse thickening of the capillary wall due to subepithelial immune complex deposits [4]. Despite the name "nephritis," there is **no** inflammatory cell proliferation. * **Amyloidosis:** This is an infiltrative disease where extracellular amyloid fibrils deposit in the mesangium and capillary walls, leading to obliteration of the glomerulus without cellular proliferation [4]. **NEET-PG High-Yield Pearls:** * **Non-proliferative GN** typically presents as **Nephrotic Syndrome** (Minimal Change Disease, FSGS, MGN, Amyloidosis) [4]. * **Proliferative GN** typically presents as **Nephritic Syndrome** (PSGN, MPGN, RPGN) [1]. * **MPGN Type II (Dense Deposit Disease)** is associated with **C3 Nephritic Factor** and hypocomplementemia. * **Tram-track appearance** in MPGN is due to the interposition of mesangial cell processes into the capillary basement membrane [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921.

Question 147: Crescentic glomerulonephritis with pauci-immune glomerulonephritis is associated with which of the following?

A. Post-infectious glomerulonephritis
B. Goodpasture's syndrome
C. Granulomatosis with polyangiitis (Correct Answer)
D. Membranous glomerulonephritis

Explanation: **Explanation:** **Crescentic Glomerulonephritis (CrGN)**, also known as Rapidly Progressive Glomerulonephritis (RPGN), is characterized by the formation of crescents in the Bowman’s space. It is classified into three types based on Immunofluorescence (IF) findings: 1. **Type I (Anti-GBM):** Linear IgG deposits (e.g., Goodpasture’s). 2. **Type II (Immune Complex):** Granular deposits (e.g., PSGN, SLE). 3. **Type III (Pauci-immune):** Little to no immune deposition, strongly associated with **ANCA-associated vasculitides.** [1] **Why Option C is Correct:** **Granulomatosis with polyangiitis (GPA)** is a classic cause of Type III Pauci-immune CrGN. [2] It is characterized by the presence of **c-ANCA (PR3-ANCA)**. The lack of significant immune deposits on IF is the hallmark of "pauci-immune" pathology. **Analysis of Incorrect Options:** * **A. Post-infectious GN:** This is a Type II RPGN. IF shows **granular** deposits of IgG and C3 (starry sky appearance) due to immune complex deposition. * **B. Goodpasture’s Syndrome:** This is Type I RPGN. IF shows characteristic **linear** IgG deposits along the glomerular basement membrane. * **D. Membranous GN:** This typically presents as Nephrotic syndrome, not CrGN. While it shows granular deposits on IF, it is not associated with pauci-immune crescent formation. **High-Yield Pearls for NEET-PG:** * **Crescents** are composed of proliferating parietal epithelial cells and migrating monocytes/macrophages. * **GPA (Wegener’s):** Triad of Upper respiratory tract, Lower respiratory tract (hemoptysis), and Renal involvement (pauci-immune GN). * **Microscopic Polyangiitis (MPA):** Another pauci-immune GN, but associated with **p-ANCA (MPO-ANCA)** and lacks granulomas. * **Rule of 3s for RPGN:** Type I (Linear), Type II (Granular), Type III (Negative/Pauci-immune). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [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 148: Renal cell carcinoma is associated with a gene located on which chromosome?

A. 3 (Correct Answer)
B. X
C. 22
D. 20

Explanation: **Explanation:** The correct answer is **A (Chromosome 3)**. Renal Cell Carcinoma (RCC), specifically the most common subtype **Clear Cell RCC (70-80%)**, is fundamentally linked to the loss or mutation of the **VHL (von Hippel-Lindau) gene**, which is located on the short arm of **chromosome 3 (3p25-26)** [1], [2]. This occurs in both sporadic cases (via somatic mutations or epigenetic silencing) and hereditary VHL syndrome. The loss of VHL leads to the stabilization of Hypoxia-Inducible Factor (HIF), resulting in the overexpression of VEGF and PDGF, which drives the characteristic hypervascularity of these tumors. **Analysis of Incorrect Options:** * **Option B (X):** While some rare pediatric renal tumors (like Xp11.2 translocation RCC) involve the X chromosome [1], it is not the primary association for classic RCC. * **Option C (22):** Chromosome 22 is associated with **NF2 (Merlin gene)** and meningiomas/schwannomas, or the Philadelphia chromosome (t(9;22)) in CML [3], but not typically with RCC. * **Option D (20):** Chromosome 20 abnormalities are seen in some colorectal cancers but have no primary diagnostic link to RCC. **High-Yield Clinical Pearls for NEET-PG:** * **Clear Cell RCC:** Most common; associated with **3p deletion** [2]. * **Papillary RCC:** Associated with **Trisomy 7 and 17** and **MET** proto-oncogene mutations [1]. * **Chromophobe RCC:** Associated with **multiple chromosome losses** (1, 2, 6, 10, 13, 17, 21) and carries a better prognosis [1]. * **Classic Triad:** Hematuria, flank pain, and palpable mass (seen in <10% of cases). * **Paraneoplastic Syndromes:** RCC is the "Great Mimicker," often producing EPO (polycythemia), Renin (hypertension), or PTHrP (hypercalcemia). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 325-326. [3] 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. 225-226.

Question 149: Membranous glomerulonephritis is associated with which of the following?

A. Renal venous thrombosis (Correct Answer)
B. Hodgkin's disease
C. Subepithelial immune deposits
D. Hematuria

Explanation: **Explanation:** **Membranous Nephropathy (MN)** is a leading cause of nephrotic syndrome in adults [2]. The correct answer is **Renal Venous Thrombosis (RVT)** because MN is the glomerular disease most strongly associated with a hypercoagulable state. 1. **Why RVT is correct:** Patients with MN lose massive amounts of endogenous anticoagulants (like Antithrombin III) and proteins of the fibrinolytic system in the urine. This creates a pro-thrombotic state. While RVT can occur in any nephrotic syndrome, its incidence is highest in MN (up to 25-30% of cases). 2. **Why other options are incorrect:** * **Hodgkin’s Disease:** This is classically associated with **Minimal Change Disease (MCD)**. MN is more commonly associated with solid tumors (lung, colon, breast). * **Subepithelial immune deposits:** While these *are* the hallmark of MN (forming the "Spike and Dome" pattern) [1], [2], the question asks for a clinical association/complication. In many standardized exams, if a clinical complication like RVT is listed against a structural feature, the complication is often the intended "association" being tested. *Note: In some contexts, C could be considered a feature, but RVT is the classic clinical association.* * **Hematuria:** MN typically presents with **massive proteinuria** (nephrotic range). While microscopic hematuria can occur, it is not a defining or highly specific association compared to RVT. **High-Yield NEET-PG Pearls:** * **Most common cause:** Primary MN is most often due to antibodies against the **PLA2R (Phospholipase A2 Receptor)** on podocytes. * **Morphology:** Thickened basement membrane with **"Spike and Dome"** appearance on Silver stain [3]. * **Immunofluorescence:** Granular IgG and C3 deposits [3]. * **Secondary causes:** Rule out "HBV, Gold/Penicillamine, and Malignancy." **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. 529-530. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 921.

Question 150: Haematuria is seen in all except:

A. IgA nephropathy
B. Alport syndrome
C. Thin basement membrane disease
D. Focal segmental glomerulosclerosis (FSGS) (Correct Answer)

Explanation: ### Explanation The key to answering this question lies in distinguishing between **Nephritic** and **Nephrotic** syndromes. **Why FSGS is the correct answer:** Focal Segmental Glomerulosclerosis (FSGS) is a classic **Nephrotic syndrome** [1]. Its hallmark clinical presentation is heavy proteinuria (usually >3.5 g/day), hypoalbuminemia, and edema [1, 2]. While microscopic hematuria can occasionally occur in FSGS, it is primarily characterized by podocyte injury and basement membrane integrity loss leading to protein leakage, rather than the inflammatory rupture of capillaries that causes gross or significant hematuria [1, 5]. **Analysis of Incorrect Options:** * **IgA Nephropathy (Berger’s Disease):** This is the most common cause of glomerulonephritis worldwide [3]. It typically presents as **recurrent gross hematuria** following an upper respiratory tract infection (synpharyngitic hematuria). * **Alport Syndrome:** A genetic defect in Type IV Collagen (COL4A3/4/5). It presents with a "Nephritic" picture, characterized by persistent microscopic hematuria, sensorineural deafness, and ocular defects. * **Thin Basement Membrane Disease (Benign Familial Hematuria):** As the name suggests, the primary clinical manifestation is **persistent microscopic hematuria** due to a diffuse thinning of the glomerular basement membrane. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy (EM) Findings:** * **FSGS:** Effacement (fusion) of podocyte foot processes [4]. * **Alport Syndrome:** "Basket-weave" appearance of the GBM. * **Thin BM Disease:** GBM thickness <250 nm (Normal is ~300-400 nm). * **IgA Nephropathy** is associated with Celiac disease and Henoch-Schönlein Purpura (HSP). * **FSGS** is the most common cause of Nephrotic syndrome in African Americans and is associated with HIV, Heroin use, and Obesity [4]. **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. 530-531. [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. 919-921. [4] 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.

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