Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 441: A 30-year-old man presents with generalized edema and hypertension. Urine examination shows subnephrotic proteinuria (< 2gm) and microscopic hematuria. Serum complement levels are decreased, and he is positive for anti-hepatitis C antibodies. What is the most likely diagnosis?

A. Post-streptococcal glomerulonephritis (PSGN)
B. Mixed cryoglobulinemia
C. Membranoproliferative glomerulonephritis (Correct Answer)
D. Focal segmental glomerulosclerosis (FSGS)

Explanation: ### Explanation The clinical presentation of edema, hypertension, hematuria, and subnephrotic proteinuria points toward a **nephritic-nephrotic overlap syndrome**. The key diagnostic clues here are the **decreased serum complement levels** and the association with **Hepatitis C virus (HCV)**. **1. Why Membranoproliferative Glomerulonephritis (MPGN) is correct:** MPGN (specifically Type I) is classically associated with chronic infections, most notably **Hepatitis C** [1]. HCV often triggers the formation of immune complexes or **mixed cryoglobulins** that deposit in the glomerulus, activating the classical complement pathway [2]. This leads to low C3 and C4 levels. Histologically, it is characterized by "tram-track" appearance due to GBM splitting and mesangial proliferation [1]. **2. Why the other options are incorrect:** * **Post-streptococcal glomerulonephritis (PSGN):** While it presents with low complement (C3) and hematuria, it typically follows a sore throat or skin infection in a younger age group. It is not associated with Hepatitis C. * **Mixed cryoglobulinemia:** While this is associated with HCV and low complement, it is a systemic vasculitis. When it affects the kidney, the resulting pathological lesion is specifically categorized as **MPGN Type I** [1]. MPGN is the definitive renal diagnosis. * **Focal segmental glomerulosclerosis (FSGS):** This typically presents with massive proteinuria (nephrotic range) and is associated with HIV, obesity, or heroin use, but **complement levels remain normal** [4]. **Clinical Pearls for NEET-PG:** * **MPGN + Hepatitis C:** Always look for this association in exams [1]. * **Complement Profile:** MPGN Type I (Low C3 & C4); MPGN Type II/Dense Deposit Disease (Low C3, Normal C4 due to C3 nephritic factor) [3]. * **Morphology:** "Tram-track" appearance on Silver stain and "lobular" appearance of the glomerulus [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926. [3] 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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 924-925.

Question 442: A linear pattern of immunoglobulin deposition along the glomerular basement membrane, demonstrated by immunofluorescence, is typical of which condition?

A. Lupus nephritis
B. Diabetic glomerulopathy
C. Goodpasture's syndrome (Correct Answer)
D. Renal vein thrombosis

Explanation: ### Explanation **Correct Answer: C. Goodpasture's syndrome** The hallmark of **Goodpasture’s syndrome** (Anti-GBM disease) is the presence of autoantibodies directed against the **non-collagenous (NC1) domain of the α3 chain of Type IV collagen** [1]. Because Type IV collagen is a structural component distributed evenly throughout the glomerular basement membrane (GBM), the binding of these antibodies creates a continuous, smooth, **linear pattern** on immunofluorescence (IF) [1, 2]. This is a Type II hypersensitivity reaction. **Analysis of Incorrect Options:** * **A. Lupus Nephritis:** Typically presents with a **"Full House" pattern** (IgG, IgM, IgA, C3, and C1q). On IF, it shows a **granular pattern** due to the deposition of immune complexes (Type III hypersensitivity), not a linear one [1]. * **B. Diabetic Glomerulopathy:** While it may occasionally show "pseudo-linear" staining due to non-specific trapping of albumin or IgG in thickened membranes, it is not the classic diagnostic feature. The hallmark is **Kimmelstiel-Wilson (KW) nodules** (nodular glomerulosclerosis). * **D. Renal Vein Thrombosis:** This is a vascular complication often secondary to Nephrotic syndrome (especially Membranous Nephropathy). It does not have a specific primary IF pattern; rather, it is a clinical consequence of altered hemodynamics. **High-Yield Clinical Pearls for NEET-PG:** * **Goodpasture’s Triad:** Glomerulonephritis (RPGN), Pulmonary hemorrhage (hemoptysis), and Anti-GBM antibodies [1]. * **Morphology:** On Light Microscopy, it typically presents as **Crescentic Glomerulonephritis** (RPGN Type I) [1]. * **Granular vs. Linear:** * **Linear** = Anti-GBM antibodies (Goodpasture’s) [2]. * **Granular ("Lumpy-Bumpy")** = Immune complex deposition (PSGN, SLE, Membranous) [2]. * **Target Antigen:** α3 chain of Type IV collagen is also found in pulmonary alveoli, explaining the lung-kidney involvement [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. 526-538. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909.

Question 443: Which of the following is NOT a characteristic feature of nephronophthisis?

A. Interstitial fibrosis
B. Cortical tubular hypertrophy (Correct Answer)
C. Cysts in the medulla
D. 20% of cases are non-familial

Explanation: **Explanation:** Nephronophthisis (NPHP) is an autosomal recessive tubulointerstitial cystic kidney disease and is the most common genetic cause of end-stage renal disease (ESRD) in children and adolescents. **Why Option B is correct:** In nephronophthisis, the kidneys are typically **shrunken and small** [1]. The hallmark pathological process is **cortical tubular atrophy**, not hypertrophy [1]. This atrophy, combined with widespread interstitial fibrosis, leads to the characteristic contraction of the renal parenchyma [1]. **Analysis of other options:** * **Option A (Interstitial fibrosis):** This is a cardinal feature of the disease [1]. Chronic tubulointerstitial nephritis leads to dense fibrosis, which eventually causes renal failure. * **Option C (Cysts in the medulla):** Small cysts (typically 1–15 mm) are characteristically found at the **corticomedullary junction** and in the medulla [1]. While essential for the name, they may be absent in early stages or visible only on biopsy/ultrasound [1]. * **Option D (20% non-familial):** While NPHP is primarily a genetic (autosomal recessive) disorder, approximately 20% of cases occur sporadically without a documented family history, often due to de novo mutations or small family sizes. **NEET-PG High-Yield Pearls:** 1. **Genetics:** Most common gene involved is **NPHP1** (encoding Nephrocystin-1). It is a **ciliopathy**. 2. **Clinical Presentation:** Polyuria and polydipsia (due to impaired urinary concentrating ability) are early signs. Unlike many other cystic diseases, hypertension is a late finding. 3. **Extra-renal associations:** Senior-Løken syndrome (NPHP + Retinitis pigmentosa) and Joubert syndrome (NPHP + Cerebellar ataxia). 4. **Imaging:** Small, shrunken kidneys with loss of corticomedullary differentiation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 953-954.

Question 444: Linear deposits along the glomerular basement membrane are seen in which condition?

A. Goodpasture syndrome (Correct Answer)
B. Systemic lupus erythematosus (SLE)
C. Drug reaction
D. Henoch-Schönlein purpura (HS purpura)

Explanation: **Explanation:** The correct answer is **Goodpasture syndrome**. This condition is characterized by the presence of anti-glomerular basement membrane (anti-GBM) antibodies directed against the non-collagenous domain of the **α3 chain of Type IV collagen** [2]. On Immunofluorescence (IF) microscopy, these antibodies bind uniformly along the entire length of the GBM, resulting in a characteristic **smooth, continuous, linear pattern** of IgG deposits [1], [2]. **Analysis of Options:** * **Systemic Lupus Erythematosus (SLE):** Typically presents with a **"lumpy-bumpy" or granular pattern** on IF due to the deposition of immune complexes [1]. In Class IV Lupus Nephritis, it often shows a "full house" pattern (IgG, IgA, IgM, C3, and C1q). * **Drug Reaction:** Acute interstitial nephritis (AIN) is the common renal manifestation of drug reactions. It primarily involves the interstitium, not the GBM, and typically does not show linear IF deposits. * **Henoch-Schönlein Purpura (HSP):** This is a systemic IgA vasculitis. Renal biopsy shows **granular mesangial deposits of IgA**, similar to IgA nephropathy (Berger’s disease). **High-Yield Clinical Pearls for NEET-PG:** * **Goodpasture Syndrome vs. Anti-GBM Disease:** "Goodpasture syndrome" refers to the combination of glomerulonephritis and pulmonary hemorrhage (hemoptysis), whereas "Anti-GBM disease" refers to renal involvement alone [3]. * **Morphology:** On light microscopy, it typically presents as **Crescentic Glomerulonephritis** (RPGN Type I) [3]. * **HLA Association:** Strongly associated with **HLA-DRB1** [3]. * **Treatment:** Urgent plasmapheresis is required to remove circulating antibodies, combined with corticosteroids and cyclophosphamide [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909. [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] 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.

Question 445: Xanthogranulomatous pyelonephritis is often associated with infection by which organism?

A. Proteus (Correct Answer)
B. E. coli
C. S. aureus
D. Klebsiella

Explanation: **Explanation:** **Xanthogranulomatous Pyelonephritis (XGP)** is a chronic, destructive form of pyelonephritis characterized by the replacement of renal parenchyma with lipid-laden macrophages (foamy cells or xanthoma cells) [1]. **Why Proteus is the correct answer:** The pathogenesis of XGP is typically linked to chronic urinary tract obstruction and recurrent infections [1]. **Proteus mirabilis** is the most common organism associated with XGP [1]. This is because *Proteus* is a **urease-producing organism** that increases urinary pH, leading to the formation of **Staghorn calculi** (struvite stones) [2]. These large stones cause the chronic obstruction and inflammation necessary for the development of XGP [1], [2]. **Analysis of Incorrect Options:** * **B. E. coli:** While *E. coli* is the most common cause of acute pyelonephritis, it is less frequently associated with the specific obstructive, stone-forming pathology of XGP compared to *Proteus*. * **C. S. aureus:** This organism typically causes renal abscesses via hematogenous spread rather than the chronic, obstructive granulomatous process seen in XGP. * **D. Klebsiella:** Although *Klebsiella* can produce urease and is sometimes isolated in XGP cases, it is statistically less common than *Proteus* in this specific clinical context. **High-Yield Clinical Pearls for NEET-PG:** * **Gross Appearance:** The kidney often shows large, orange-yellow nodules that can mimic **Renal Cell Carcinoma (RCC)**; hence, it is known as the "Great Mimicker" [1]. * **Microscopy:** Presence of **lipid-laden foamy macrophages** (Xanthoma cells) [1]. * **Radiology:** The **"Bear Paw Sign"** on CT scan is a classic finding. * **Association:** Strongly associated with **Staghorn calculi** and non-functioning kidneys [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 957.

Question 446: Increased levels of C3NeF are associated with which of the following conditions?

A. Type I MPGN
B. Type II MPGN (Correct Answer)
C. FSGS
D. Berger Disease

Explanation: **Explanation:** **Correct Answer: B. Type II MPGN (Dense Deposit Disease)** The underlying mechanism of **Type II Membranoproliferative Glomerulonephritis (MPGN)**, now commonly referred to as **Dense Deposit Disease**, involves the **alternative complement pathway** [1]. **C3 Nephritic Factor (C3NeF)** is an IgG autoantibody that binds to and stabilizes **C3 convertase (C3bBb)**. Normally, C3 convertase is short-lived; however, C3NeF prevents its degradation, leading to continuous, uncontrolled cleavage of C3 [1]. This results in profound hypocomplementemia (low serum C3) and the deposition of complement byproducts in the glomerular basement membrane (GBM), appearing as characteristic "ribbon-like" electron-dense deposits [2]. **Analysis of Incorrect Options:** * **Type I MPGN:** This is primarily an immune-complex-mediated disease (classical pathway activation) [3]. While C3 levels may be low, it is not specifically associated with C3NeF. It features subendothelial deposits and "tram-track" splitting of the GBM [2], [3]. * **FSGS (Focal Segmental Glomerulosclerosis):** This is a podocytopathy characterized by sclerosis of segments of some glomeruli. It is not a complement-mediated proliferative GN. * **Berger Disease (IgA Nephropathy):** This is characterized by IgA1 mesangial deposits [4]. While the alternative pathway is involved, it is due to galactose-deficient IgA1, not C3NeF [4]. **High-Yield Pearls for NEET-PG:** * **Morphology:** Type II MPGN is unique for its "dense deposits" within the lamina densa of the GBM [2]. * **Immunofluorescence:** Shows "starry sky" or linear-like C3 staining; notably, **Immunoglobulins (IgG) are usually absent** (unlike Type I) [1]. * **Clinical Association:** Type II MPGN is frequently associated with **partial lipodystrophy**. * **Key Difference:** Type I = Subendothelial deposits; Type II = Intramembranous (dense) deposits [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. 534-535. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 926-927. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926. [4] 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.

Question 447: Which of the following is NOT true about post-streptococcal glomerulonephritis?

A. Proliferative glomerulonephritis
B. PSGN can be seen in the elderly
C. More common in males
D. PSGN develops 1-3 weeks after a skin infection and 2-6 weeks after streptococcal pharyngitis (Correct Answer)

Explanation: **Explanation:** The correct answer is **D** because the latent periods mentioned are reversed. In Post-Streptococcal Glomerulonephritis (PSGN), the latent period after a **pharyngeal infection** is typically **1–3 weeks**, whereas the latent period after a **skin infection (impetigo)** is longer, usually **3–6 weeks** [1]. This timing is a classic diagnostic feature used to differentiate PSGN from IgA Nephropathy (which occurs within days of infection). **Analysis of other options:** * **Option A (True):** PSGN is a classic example of **diffuse proliferative glomerulonephritis** [2]. Light microscopy typically shows hypercellular glomeruli due to the proliferation of endothelial and mesangial cells, along with an influx of neutrophils and monocytes [3]. * **Option B (True):** While PSGN is most common in children (ages 6–10) [1], it can certainly occur in the **elderly**. In older patients, the presentation is often more severe, frequently manifesting as sudden onset of hypertension, edema, and azotemia [4]. * **Option C (True):** There is a documented **male predominance** in PSGN, with a male-to-female ratio of approximately 2:1. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Caused by Nephritogenic strains of Group A Beta-hemolytic Streptococci (e.g., Type 12 for pharyngitis, Type 49 for skin). * **Immunofluorescence:** Shows a characteristic **"Starry Sky"** or "Lumpy-Bumpy" appearance due to granular deposits of IgG and C3 [2]. * **Electron Microscopy:** Pathognomonic **"Subepithelial Humps"** (representing immune complexes) [2]. * **Serology:** Low C3 levels are characteristic; ASO titers are elevated in pharyngitis-associated PSGN, while Anti-DNase B is more sensitive for skin-associated PSGN. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 915-916. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 916-917.

Question 448: Post-streptococcal glomerulonephritis (PSGN) is characterized by which of the following clinical presentations?

A. Dense deposit disease
B. Rapidly progressive glomerulosclerosis
C. Nephrotic syndrome
D. Nephritic syndrome (Correct Answer)

Explanation: **Explanation:** **Post-streptococcal glomerulonephritis (PSGN)** is the classic prototype of **Acute Nephritic Syndrome** [1]. It typically occurs 1–4 weeks after a group A beta-hemolytic streptococcal infection (pharyngitis or impetigo). The underlying mechanism is a **Type III hypersensitivity reaction**, where immune complexes (containing the streptococcal antigen SpeB) deposit in the glomerular basement membrane, triggering inflammation, leukocyte infiltration, and mesangial cell proliferation [1]. This leads to the characteristic clinical triad of **hematuria (cola-colored urine), hypertension, and localized edema (periorbital).** **Analysis of Options:** * **Option A (Dense Deposit Disease):** This refers to **MPGN Type II**, characterized by continuous intramembranous ribbon-like deposits. It is driven by the alternative complement pathway (C3 nephritic factor) rather than post-infectious immune complexes. * **Option B (Rapidly Progressive Glomerulosclerosis):** While PSGN can rarely progress to RPGN (Crescentic GN), it is not the standard presentation. RPGN is a clinical syndrome of rapid renal failure, not a primary synonym for PSGN [1]. * **Option C (Nephrotic Syndrome):** Characterized by massive proteinuria (>3.5g/day), hypoalbuminemia, and generalized edema (e.g., Minimal Change Disease). While PSGN may show some proteinuria, it rarely reaches nephrotic ranges. **High-Yield Clinical Pearls for NEET-PG:** * **Light Microscopy:** Enlarged, hypercellular glomeruli ("Starry sky" appearance on IF) [1]. * **Electron Microscopy:** Pathognomonic **"Subepithelial humps"** (immune complexes) [1]. * **Serology:** Low C3 levels (normalized by 6–8 weeks) and elevated ASO titers (after pharyngitis) or Anti-DNase B (after skin infection). * **Prognosis:** Excellent in children (>95% recover); more likely to progress to chronic renal failure in adults. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915.

Question 449: What is the most common type of glomerulonephritis?

A. Membranous glomerulonephritis
B. IgA nephropathy (Correct Answer)
C. Post-streptococcal glomerulonephritis
D. Rapidly progressive glomerulonephritis

Explanation: **Explanation:** **IgA Nephropathy (Berger’s Disease)** is the most common primary glomerulonephritis worldwide [2]. The underlying pathophysiology involves the deposition of IgA1-containing immune complexes in the glomerular mesangium [1]. This occurs due to an overproduction of **galactose-deficient IgA1**, which the body treats as an antigen, leading to the formation of IgG autoantibodies and subsequent immune complex deposition [1]. **Analysis of Options:** * **IgA Nephropathy (Correct):** It is the leading cause of primary glomerulonephritis globally [2]. It typically presents as recurrent episodes of gross or microscopic hematuria, often following an upper respiratory or gastrointestinal infection (synpharyngitic hematuria) [2]. * **Membranous Glomerulonephritis:** While a common cause of Nephrotic Syndrome in adults, it is not the most common glomerulonephritis overall [3]. * **Post-streptococcal Glomerulonephritis (PSGN):** This is a common cause of acute nephritic syndrome in children following a skin or throat infection, but its global prevalence is lower than IgA nephropathy [4]. * **Rapidly Progressive Glomerulonephritis (RPGN):** This is a clinical syndrome (characterized by crescents on histology) rather than a single disease entity and is much rarer, representing a medical emergency [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Histology:** Mesangial hypercellularity and matrix expansion [1]. * **Immunofluorescence (IF):** Granular mesangial deposits of **IgA and C3**. * **Electron Microscopy (EM):** Electron-dense deposits in the **mesangium**. * **Association:** Frequently associated with Celiac disease and Henoch-Schönlein Purpura (HSP), which is considered the systemic version of IgA nephropathy [1], [2]. * **Prognosis:** The most reliable histological predictor of poor prognosis is the presence of glomerular crescents or segmental sclerosis (Oxford Classification/MEST-C score) [1], [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. 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. 919-921. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915.

Question 450: Renal papillary necrosis is seen in which of the following conditions?

A. Thalassemia
B. Diabetes Mellitus (Correct Answer)
C. Phenacetin abuse
D. Alcoholism

Explanation: **Explanation:** **Renal Papillary Necrosis (RPN)** is a clinicopathologic entity characterized by ischemic and/or toxic coagulative necrosis of the renal papillae. **1. Why Diabetes Mellitus is correct:** Diabetes Mellitus is the most common cause of RPN [1], [4]. The pathogenesis involves a combination of **ischemia** (due to diabetic microangiopathy/hyaline arteriolosclerosis of the vasa recta) [2] and an increased susceptibility to **Acute Pyelonephritis** [1], [4]. The renal papillae are physiologically hypoxic; thus, any further reduction in blood flow leads to infarction and sloughing of the papillae. **2. Analysis of other options:** * **Phenacetin abuse:** While analgesic abuse (specifically Phenacetin) is a classic cause of RPN, it is typically associated with chronic, heavy ingestion over years. In many modern contexts and standardized exams, Diabetes is prioritized as the leading systemic cause. (Note: If this were a "Multiple Correct" type question, Phenacetin would also be right, but in single-best-response formats, Diabetes is the primary association). * **Thalassemia:** This is not a recognized cause. However, **Sickle Cell Trait/Disease** is a high-yield cause of RPN due to sickling in the hypertonic, hypoxic medulla [3], [4]. * **Alcoholism:** Alcoholism is not directly linked to RPN; it is more commonly associated with hepatic-related renal issues like IgA nephropathy or Cirrhosis-related changes. **3. High-Yield Clinical Pearls (Mnemonic: POSTCARDS):** To remember the causes of Renal Papillary Necrosis, use the mnemonic **POSTCARDS**: * **P** - Pyelonephritis (Acute) [4] * **O** - Obstruction of the urinary tract [4] * **S** - **Sickle Cell Disease** [3], [4] * **T** - Tuberculosis * **C** - Chronic liver disease (rare) * **A** - **Analgesics (Phenacetin)** * **R** - Renal transplant rejection * **D** - **Diabetes Mellitus** [1], [4] * **S** - Systemic Vasculitis **Clinical Presentation:** Patients may present with gross hematuria and renal colic due to sloughed papillae obstructing the ureter ("Ring sign" on IVP) [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. 543-544. [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 Kidney, pp. 948-949. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 937.

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