Renal Pathology — MCQs
On this page
Goodpasture syndrome is characterized by antibodies against which component?
Striped fibrosis of the kidney is seen in which of the following conditions?
A 12-year-old boy complains of swelling of his feet for the past 3 weeks. He is otherwise healthy, with no known previous illness. Vital signs are normal. Physical examination reveals pitting edema of the lower legs and a swollen abdomen. Urinalysis shows 4+ protein but no RBCs or WBCs. Which of the following are the most likely diagnoses to consider in your evaluation of this patient?
What is the primary pathogenic mechanism of acute proliferative glomerulonephritis?
Renal vein thrombosis is most commonly associated with which of the following conditions?
Linear deposition of IgG on glomerular basement membrane is seen in which of the following conditions?
A 25-year-old woman presents with new symptoms of decreased urine output, leg edema, and facial swelling. Laboratory investigations reveal acute kidney injury. A renal biopsy shows a granular pattern of immune complex-mediated glomerulonephritis on immunofluorescence. Which of the following conditions is most likely to cause this pattern of renal injury?
All among the following are markers of Wilms' tumor except?
A 33-year-old woman in her third trimester of pregnancy (gravida I, para 0) is rushed to the emergency room after suffering a seizure. The patient is hypertensive and laboratory studies show that the patient manifests nephritic syndrome. What is the appropriate diagnosis?
What are the histological features of acute rejection of a renal transplant?
Renal Pathology Indian Medical PG Practice Questions and MCQs
Question 241: Goodpasture syndrome is characterized by antibodies against which component?
- A. Collagen 1
- B. G-y or x-y of Collagen
- C. Collagen 4 (Correct Answer)
- D. Collagen 2
Explanation: **Explanation:** **Goodpasture Syndrome** (Anti-GBM Disease) is a type II hypersensitivity reaction characterized by the formation of autoantibodies against the glomerular basement membrane (GBM) [1] and alveolar basement membrane [2]. **Why Option C is correct:** The specific target of these autoantibodies is the **non-collagenous domain (NC1)** of the **alpha-3 chain of Type 4 Collagen**. Type 4 collagen is the primary structural component of basement membranes [1]. When antibodies bind to these chains in the kidneys and lungs, it triggers an inflammatory cascade leading to **Rapidly Progressive Glomerulonephritis (RPGN)** and pulmonary hemorrhage [2]. **Why other options are incorrect:** * **Option A (Collagen 1):** This is the most abundant collagen, found in bone, skin, and tendons. It is not the target in Goodpasture syndrome. * **Option B (G-y or x-y):** This refers to the repeating amino acid sequence (Glycine-X-Y) found in all collagen triple helices. Antibodies in Goodpasture are specific to the NC1 domain, not the general triple-helical repeat. * **Option D (Collagen 2):** This is primarily found in hyaline cartilage and vitreous humor. **High-Yield Clinical Pearls for NEET-PG:** * **Immunofluorescence (IF):** Shows a characteristic **Linear IgG deposition** along the GBM (Pathognomonic) [1], [3]. * **Clinical Triad:** Hematuria (Glomerulonephritis), Hemoptysis (Pulmonary hemorrhage), and Iron deficiency anemia [2]. * **HLA Association:** Strongly associated with **HLA-DRB1** (specifically DR15 and DR4) [2]. * **Morphology:** On light microscopy, it typically presents as **Crescentic Glomerulonephritis**. * **Treatment:** Plasmapheresis (to remove circulating antibodies), corticosteroids, and cyclophosphamide [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. 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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909.
Question 242: Striped fibrosis of the kidney is seen in which of the following conditions?
- A. Chronic rejection
- B. Diabetes mellitus
- C. Malignant hypertension
- D. Cyclosporin toxicity (Correct Answer)
Explanation: **Explanation:** **Cyclosporine toxicity** is the classic cause of **striped fibrosis** in the kidney. This pattern occurs due to the drug’s potent vasoconstrictive effect on the afferent arterioles. Chronic exposure leads to permanent narrowing of these vessels, resulting in downstream tubular atrophy and interstitial fibrosis. Because the blood supply is affected in a focal, linear distribution corresponding to the medullary rays, the resulting fibrosis appears as "stripes" under the microscope. **Analysis of Incorrect Options:** * **Chronic Rejection:** Typically presents with **interstitial fibrosis and tubular atrophy (IFTA)** that is more diffuse or patchy, often accompanied by "transplant glomerulopathy" and vascular intimal thickening (obliterative arteriopathy) [2]. * **Diabetes Mellitus:** Characterized by diffuse or nodular glomerulosclerosis (**Kimmelstiel-Wilson lesions**), diffuse thickening of the glomerular basement membrane, and hyaline arteriolosclerosis. * **Malignant Hypertension:** Associated with **fibrinoid necrosis** of arterioles and "onion-skin" hypertrophy of the vessel walls [1], leading to petechial hemorrhages (flea-bitten kidney) rather than striped fibrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Cyclosporine vs. Tacrolimus:** Both Calcineurin Inhibitors (CNIs) can cause striped fibrosis, but it is more classically associated with Cyclosporine. * **Acute CNI Toxicity:** Presents with isometric vacuolization of the tubular epithelial cells (reversible). * **Chronic CNI Toxicity:** Presents with striped fibrosis and hyaline arteriolosclerosis (irreversible). * **Key Histological Clue:** When you see "striped fibrosis" in a transplant biopsy, think of CNI nephrotoxicity first. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 546-549.
Question 243: A 12-year-old boy complains of swelling of his feet for the past 3 weeks. He is otherwise healthy, with no known previous illness. Vital signs are normal. Physical examination reveals pitting edema of the lower legs and a swollen abdomen. Urinalysis shows 4+ protein but no RBCs or WBCs. Which of the following are the most likely diagnoses to consider in your evaluation of this patient?
- A. Henoch-Schonlein purpura, lupus nephritis
- B. Malignant hypertension, renal vein thrombosis
- C. Minimal change disease, focal segmental glomerulosclerosis (Correct Answer)
- D. Pyelonephritis, acute tubular necrosis
Explanation: ### Explanation **1. Why the Correct Answer is Right:** The clinical presentation describes a classic case of **Nephrotic Syndrome** in a pediatric patient [2]. Key indicators include: * **Age (12 years):** The most common cause of nephrotic syndrome in children is Minimal Change Disease (MCD) [1]. * **Clinical Signs:** Pitting edema and ascites (swollen abdomen) due to severe hypoalbuminemia. * **Urinalysis:** 4+ proteinuria (massive protein loss) with a **"bland" sediment** (absence of RBCs and WBCs) [3]. This absence of hematuria or pyuria distinguishes nephrotic syndrome from nephritic syndrome [2]. In the pediatric age group, **Minimal Change Disease (MCD)** is the most common cause (80-90%), followed by **Focal Segmental Glomerulosclerosis (FSGS)** [1]. Both present with heavy proteinuria and podocyte effacement on electron microscopy [1]. **2. Why the Other Options are Wrong:** * **Option A (HSP, Lupus Nephritis):** These typically present as **Nephritic Syndrome**, characterized by hematuria (RBC casts), hypertension, and active urinary sediment [2]. * **Option B (Malignant HTN, Renal Vein Thrombosis):** Malignant hypertension presents with severe BP elevation and end-organ damage. While Renal Vein Thrombosis can cause nephrotic-range proteinuria, it is usually a *complication* of nephrotic syndrome (especially Membranous Nephropathy) rather than the primary cause in a healthy child. * **Option D (Pyelonephritis, ATN):** Pyelonephritis presents with fever, flank pain, and WBCs/bacteria in urine. Acute Tubular Necrosis (ATN) presents with acute renal failure and "muddy brown" granular casts, not isolated massive proteinuria. **3. NEET-PG High-Yield Pearls:** * **MCD:** Most common cause of nephrotic syndrome in children; shows "nil" changes on Light Microscopy; **Effacement of podocyte foot processes** on Electron Microscopy; excellent response to steroids [1], [3]. * **FSGS:** Most common cause of nephrotic syndrome in **adults** in many regions (and African Americans); often steroid-resistant; progresses to ESRD [1]. * **Selective Proteinuria:** MCD is characterized by the loss of albumin only (due to loss of glomerular polyanion charge) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 527-528. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923.
Question 244: What is the primary pathogenic mechanism of acute proliferative glomerulonephritis?
- A. Cytotoxic T-cell mediated
- B. Immune complex mediated (Correct Answer)
- C. Antibody mediated
- D. Cell-mediated (Type IV hypersensitivity)
Explanation: **Explanation:** **Acute Proliferative Glomerulonephritis (APGN)**, most commonly seen as Post-Streptococcal Glomerulonephritis (PSGN), is a classic example of a **Type III Hypersensitivity reaction** [1]. 1. **Why Option B is Correct:** The primary mechanism involves the formation of **immune complexes** (antigen-antibody complexes) [1]. These complexes, formed either in the circulation or *in situ*, trap within the glomerular basement membrane (GBM) [3]. This triggers the complement cascade (classical and alternative pathways), leading to the recruitment of neutrophils and monocytes. This inflammatory influx results in the characteristic hypercellularity (proliferation of endothelial and mesangial cells) seen on light microscopy [2]. 2. **Why Other Options are Incorrect:** * **Option A & D:** While T-cells play a minor role in orchestrating the inflammatory response, APGN is not primarily a cell-mediated or cytotoxic T-cell disorder. Cell-mediated immunity is more characteristic of certain types of Crescentic Glomerulonephritis or transplant rejection. * **Option C:** "Antibody-mediated" usually refers to Type II Hypersensitivity, where antibodies are directed against fixed antigens on the GBM (e.g., Goodpasture Syndrome) [1]. In APGN, the damage is caused by the *complexes*, not direct anti-GBM antibodies. **NEET-PG High-Yield Pearls:** * **Immunofluorescence (IF):** Shows a characteristic **"Starry Sky"** or granular appearance due to IgG and C3 deposits [1]. * **Electron Microscopy (EM):** Reveals pathognomonic **"Subepithelial Humps"** (humps of immune complexes) [1]. * **Clinical Presentation:** Nephritic syndrome (hematuria, hypertension, edema) occurring 1–4 weeks after a streptococcal throat or skin infection [1]. * **Serology:** Low C3 levels are a hallmark; ASO titers are elevated in post-pharyngeal cases. **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. 915-916. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215.
Question 245: Renal vein thrombosis is most commonly associated with which of the following conditions?
- A. Diabetic nephropathy
- B. Membranous glomerulopathy (Correct Answer)
- C. Minimal change disease
- D. Membranoproliferative glomerulonephritis
Explanation: **Explanation** **Renal Vein Thrombosis (RVT)** is a well-known complication of **Nephrotic Syndrome**. While any condition causing heavy proteinuria can predispose a patient to thromboembolism, **Membranous Glomerulopathy (MGN)** carries the highest risk (up to 25–30% of cases). **1. Why Membranous Glomerulopathy is correct:** The underlying mechanism is the development of a **hypercoagulable state**. In MGN, there is a profound loss of endogenous anticoagulants (like **Antithrombin III**) and proteins of the fibrinolytic system (Plasminogen) through the leaky glomerular basement membrane. Simultaneously, there is an increase in pro-coagulant factors (Factor V, VIII) and increased platelet aggregation [1]. The renal vein is particularly susceptible because the blood leaving the kidney is most concentrated and depleted of Antithrombin III. **2. Why the other options are incorrect:** * **Diabetic Nephropathy:** While it is the most common cause of nephrotic syndrome overall, the specific incidence of RVT is significantly lower than in MGN [1]. * **Minimal Change Disease (MCD):** Although it causes massive proteinuria (especially in children), the risk of thromboembolic events is statistically lower compared to MGN [2]. * **Membranoproliferative Glomerulonephritis (MPGN):** This can present with nephrotic features and carries a risk of thrombosis, but it is less frequently associated with RVT than the classic association with MGN [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad of RVT:** Flank pain, hematuria, and an increase in kidney size (due to venous congestion). * **Left-sided preference:** RVT more commonly affects the left renal vein; in males, this may present as a **left-sided varicocele** because the left gonadal vein drains into the renal vein. * **Most common cause of Nephrotic Syndrome in adults:** Membranous Glomerulopathy (though Focal Segmental Glomerulosclerosis is now more common in certain demographics) [4]. * **Key Marker for MGN:** Phospholipase A2 receptor (**PLA2R**) antibodies [1]. **Note on Primary Glomerulopathy:** Membranous nephropathy is characterized by diffuse thickening of the glomerular capillary wall due to the accumulation of Ig deposits along the subepithelial side of the basement membrane [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 919-921. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 527-528. [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. 530-531.
Question 246: Linear deposition of IgG on glomerular basement membrane is seen in which of the following conditions?
- A. Chronic Renal Failure
- B. Goodpasture's syndrome (Correct Answer)
- C. Nephrotic syndrome
- D. Shunt nephritis
Explanation: ### Explanation **Correct Answer: B. Goodpasture's syndrome** The hallmark of **Goodpasture’s syndrome** (Type I 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 these antigens are intrinsic and uniformly distributed along the glomerular basement membrane (GBM), Immunofluorescence (IF) microscopy reveals a characteristic **continuous, smooth, linear deposition of IgG** [1][2]. #### Analysis of Options: * **A. Chronic Renal Failure:** This is a clinical end-stage state resulting from various etiologies. Pathologically, it is characterized by global glomerulosclerosis and interstitial fibrosis rather than a specific linear IF pattern. * **C. Nephrotic Syndrome:** This is a clinical complex (e.g., Minimal Change Disease, FSGS, Membranous Nephropathy). Membranous Nephropathy, a common cause, shows a **granular** (not linear) pattern due to subepithelial immune complex deposition [1]. * **D. Shunt Nephritis:** This is a type of Type III hypersensitivity reaction (immune-complex mediated) occurring as a complication of infected ventriculoatrial shunts. It typically presents with a **granular** pattern of IgG and C3 on IF. #### NEET-PG High-Yield Pearls: * **Linear Pattern:** Exclusively seen in Anti-GBM diseases (Goodpasture’s) [2]. * **Granular Pattern ("Lumpy-Bumpy"):** Seen in immune-complex mediated GN (e.g., PSGN, SLE, Membranous GN) [1]. * **Pauci-immune (Negative IF):** Seen in ANCA-associated vasculitis (Wegener’s/GPA, Microscopic Polyangiitis). * **Goodpasture’s Triad:** Glomerulonephritis (RPGN), Pulmonary hemorrhage (hemoptysis), and Anti-GBM antibodies. * **Type IV Collagen:** Remember that Alport Syndrome involves a genetic defect in the same collagen (α3, α4, α5 chains), but presents with "basket-weave" appearance on EM, not linear IgG. **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.
Question 247: A 25-year-old woman presents with new symptoms of decreased urine output, leg edema, and facial swelling. Laboratory investigations reveal acute kidney injury. A renal biopsy shows a granular pattern of immune complex-mediated glomerulonephritis on immunofluorescence. Which of the following conditions is most likely to cause this pattern of renal injury?
- A. Acute tubular necrosis (ATN)
- B. Wegener granulomatosis
- C. Postinfectious glomerulonephritis (Correct Answer)
- D. Hemolytic uremic syndrome (HUS)
Explanation: ### Explanation **Correct Answer: C. Postinfectious glomerulonephritis (PSGN)** **Why it is correct:** Postinfectious glomerulonephritis is a classic example of a **Type III hypersensitivity reaction**. It is characterized by the deposition of immune complexes (antigen-antibody complexes) within the glomerular basement membrane [1]. On **immunofluorescence (IF)**, these deposits appear as a **"granular" or "starry sky" pattern**, primarily consisting of IgG and C3 [1], [2]. This leads to an inflammatory response (nephritic syndrome) resulting in decreased GFR, oliguria, and edema, as seen in this patient [1]. **Why the other options are incorrect:** * **A. Acute tubular necrosis (ATN):** This is caused by ischemic or toxic injury to tubular cells. It does not involve immune complex deposition; therefore, IF would be negative (pauci-immune). * **B. Wegener granulomatosis (GPA):** This is a small-vessel vasculitis associated with c-ANCA. On biopsy, it typically shows a crescentic glomerulonephritis with a **pauci-immune pattern** (minimal to no staining on IF), not a granular one [3]. * **C. Hemolytic uremic syndrome (HUS):** This is a thrombotic microangiopathy (TMA) characterized by microthrombi in capillaries. While it causes AKI, it does not involve granular immune complex deposition. **NEET-PG High-Yield Pearls:** * **IF Pattern:** Granular/Starry sky (PSGN, SLE, Membranous); Linear (Goodpasture syndrome); Pauci-immune (Wegener’s, Churg-Strauss, Microscopic Polyangiitis) [1], [2]. * **Electron Microscopy (EM):** PSGN is pathognomonic for **subepithelial "humps"** [1], [4]. * **Serology:** Low C3 levels are characteristic of PSGN; levels typically return to normal within 6–8 weeks. * **Clinical presentation:** Often follows a streptococcal pharyngitis (1-2 weeks) or skin infection/impetigo (3-6 weeks). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [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, p. 911.
Question 248: All among the following are markers of Wilms' tumor except?
- A. Desmin
- B. Vimentin
- C. TTF 1 (Correct Answer)
- D. Cytokeratin
Explanation: **Explanation:** Wilms' tumor (Nephroblastoma) is the most common primary renal tumor of childhood [3]. It is characterized by its **triphasic morphology**, consisting of three components: blastemal, stromal, and epithelial cells [2]. Because it originates from the primitive metanephric blastema, it expresses markers associated with these diverse lineages. **Why TTF-1 is the correct answer:** **TTF-1 (Thyroid Transcription Factor-1)** is a protein typically expressed in the thyroid and the epithelium of the lungs. It is a highly specific marker used to identify **adenocarcinomas of the lung** or thyroid tumors. It has no expression in renal blastemal or embryonic tissues, making it the "except" in this list. **Analysis of other options:** * **Vimentin:** This is a marker for mesenchymal/stromal cells. Since Wilms' tumor has a prominent **stromal component** (fibroblastic or myxoid), vimentin is characteristically positive [2]. * **Cytokeratin:** This is a marker for epithelial cells. Wilms' tumor contains an **epithelial component** (forming abortive tubules or glomeruli), which stains positive for cytokeratin [2]. * **Desmin:** Wilms' tumor often shows heterologous differentiation, most commonly **rhabdomyoblastic differentiation** (skeletal muscle). Desmin is a marker for muscle cells and is frequently positive in the stromal areas of these tumors [2]. **NEET-PG High-Yield Pearls:** * **WT1 Gene:** Located on chromosome **11p13**. Deletion is associated with WAGR syndrome [1]. * **Most common site of metastasis:** Lungs (presents as "cannonball" secondaries). * **Blastema:** The most primitive component; cells are small, round, and blue (making it a "Small Round Blue Cell Tumor" of childhood) [2]. * **NWTS Staging:** Unlike most tumors, Wilms' is staged based on both surgical and pathological findings. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 487-488. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 488-490. [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. 211-212.
Question 249: A 33-year-old woman in her third trimester of pregnancy (gravida I, para 0) is rushed to the emergency room after suffering a seizure. The patient is hypertensive and laboratory studies show that the patient manifests nephritic syndrome. What is the appropriate diagnosis?
- A. Acute tubular necrosis
- B. Crescentic glomerulonephritis
- C. Eclampsia (Correct Answer)
- D. Malignant nephrosclerosis
Explanation: **Explanation:** The clinical presentation of hypertension, seizures, and nephritic syndrome in a third-trimester pregnant woman is the classic triad of **Eclampsia** [3]. **Why Eclampsia is Correct:** Eclampsia is defined as the onset of seizures in a woman with pre-eclampsia (hypertension and proteinuria) [1]. In the kidneys, this manifests as **glomerular endotheliosis**—a characteristic lesion where endothelial cells swell and lose their fenestrations, leading to a reduced glomerular filtration rate (GFR) and clinical features of nephritic syndrome (hypertension, mild hematuria, and proteinuria) [1]. **Why Other Options are Incorrect:** * **Acute Tubular Necrosis (ATN):** Typically presents with acute kidney injury (oliguria/anuria) following ischemic or toxic insults. While it can occur post-partum due to hemorrhage, it does not explain the seizure and hypertension triad. * **Crescentic Glomerulonephritis (RPGN):** Characterized by a rapid decline in renal function and "crescents" on biopsy [4]. While it causes nephritic syndrome, it is not specifically associated with pregnancy-induced seizures. * **Malignant Nephrosclerosis:** Associated with malignant hypertension (BP >200/120 mmHg) and "onion-skinning" of arterioles. While it causes renal failure, Eclampsia is the more specific diagnosis given the obstetric context and seizure. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Renal Lesion:** Glomerular capillary endotheliosis (swelling of endothelial cells). * **Management:** The definitive treatment for Eclampsia is the delivery of the fetus and placenta. * **Drug of Choice:** Magnesium sulfate ($MgSO_4$) is used for seizure prophylaxis and control. * **HELLP Syndrome:** A severe variant of pre-eclampsia involving Hemolysis, Elevated Liver enzymes, and Low Platelets [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1041-1042. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1042-1043. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 872. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 527-528.
Question 250: What are the histological features of acute rejection of a renal transplant?
- A. Areolar hyalinosis
- B. Eosinophilic infiltration
- C. Glomerular vasodilation
- D. Neutrophilic infiltration (Correct Answer)
Explanation: **Explanation:** Renal transplant rejection is categorized into hyperacute, acute, and chronic phases based on the timing and underlying immune mechanism. **Why Neutrophilic Infiltration is Correct:** Acute rejection is primarily divided into **Acute Cellular Rejection (ACR)** and **Acute Antibody-Mediated Rejection (AMR)** [1]. While ACR is characterized by lymphocytic infiltration (T-cells) and tubulitis [3], **Acute AMR** involves the activation of the complement system. This leads to the recruitment of **neutrophils** and monocytes within the peritubular capillaries (**capillaritis**) and glomeruli (**glomerulitis**) [2]. In the context of this question, neutrophilic infiltration is a hallmark histological sign of the inflammatory response seen in acute humoral rejection. **Analysis of Incorrect Options:** * **A. Arteriolar hyalinosis:** This is a feature of **chronic** transplant rejection or chronic hypertension/calcineurin inhibitor (CNI) toxicity. It represents long-term vascular damage rather than acute inflammation. * **B. Eosinophilic infiltration:** While eosinophils can sometimes be seen, they are not the diagnostic hallmark of acute rejection. Their presence is more characteristic of **Acute Interstitial Nephritis (AIN)** caused by drug hypersensitivity. * **C. Glomerular vasodilation:** This is a non-specific finding and not a diagnostic histological feature of transplant rejection. **NEET-PG High-Yield Pearls:** * **Hyperacute Rejection:** Occurs within minutes; mediated by pre-formed antibodies; characterized by **fibrinoid necrosis** and widespread thrombosis [1]. * **Acute Cellular Rejection:** Most common; look for **"Tubulitis"** (lymphocytes invading tubular epithelium) [3]. * **C4d Deposition:** A crucial immunofluorescence marker for diagnosing **Antibody-Mediated Rejection (AMR)**. * **Banff Classification:** The standard international grading system used for renal transplant pathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 546-549. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242.
Practice by Chapter
Congenital Anomalies of the Kidney
Practice Questions
Glomerular Diseases
Practice Questions
Tubular and Interstitial Diseases
Practice Questions
Vascular Diseases of the Kidney
Practice Questions
Cystic Diseases of the Kidney
Practice Questions
Urinary Tract Obstruction and Stones
Practice Questions
Renal Tumors
Practice Questions
Kidney in Systemic Diseases
Practice Questions
Renal Transplantation Pathology
Practice Questions
Urinary Tract Infections
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free