Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 271: Onion peeling of renal vessels is seen in which of the following conditions?

A. Benign hypertension
B. Malignant hypertension (Correct Answer)
C. Diabetic nephropathy
D. Systemic lupus erythematosus (SLE)

Explanation: **Explanation:** The characteristic "onion peeling" appearance of renal vessels is the hallmark of **Hyperplastic Arteriolosclerosis**, which occurs in **Malignant Hypertension** (typically defined as BP >200/120 mmHg) [1], [2]. **1. Why Malignant Hypertension is Correct:** In response to severe, acute elevations in blood pressure, the smooth muscle cells of the arteriolar walls undergo proliferation and concentric layering [1]. This is accompanied by the thickening and duplication of the basement membrane [2]. Histologically, this creates a laminated, concentric appearance resembling the layers of an onion [1]. This process narrows the vessel lumen, leading to severe ischemia downstream. It is often associated with **fibrinoid necrosis** of the vessel wall (necrotizing arteriolitis) [1], [2]. **2. Why the Other Options are Incorrect:** * **Benign Hypertension:** Characterized by **Hyaline Arteriolosclerosis**, where plasma proteins leak into the vessel wall, appearing as a homogenous, pink, glassy (hyaline) thickening [2]. It does not show cellular proliferation. * **Diabetic Nephropathy:** Primarily involves **Kimmelstiel-Wilson (KW) nodules** (nodular glomerulosclerosis) and diffuse basement membrane thickening. While it causes hyaline arteriolosclerosis (often affecting both afferent and efferent arterioles), it does not cause onion-peeling [2]. * **SLE:** Typically presents with various patterns of glomerulonephritis (e.g., Wire-loop lesions in Class IV). While vasculitis can occur, onion-peeling is not a classic feature. **High-Yield Clinical Pearls for NEET-PG:** * **Onion-peeling:** Hyperplastic arteriolosclerosis → Malignant Hypertension [1]. * **Flea-bitten kidney:** Macroscopic appearance in Malignant Hypertension due to pinpoint petechial hemorrhages. * **Hyaline arteriolosclerosis:** Seen in Benign Hypertension and Diabetes Mellitus [2]. * **Wire-loop lesions:** Subendothelial deposits in Lupus Nephritis (Class IV). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.

Question 272: Kidney biopsy from a child with hemolytic uremic syndrome characteristically most likely presents features of which of the following?

A. Thrombotic microangiopathy (Correct Answer)
B. Proliferative glomerulonephritis
C. Focal segmental glomerulosclerosis
D. Minimal change disease

Explanation: **Explanation:** **Hemolytic Uremic Syndrome (HUS)** is a classic cause of acute kidney injury in children, typically following a gastrointestinal infection with Shiga toxin-producing *E. coli* (O157:H7) [2]. **Why Thrombotic Microangiopathy (TMA) is correct:** The hallmark of HUS is **Thrombotic Microangiopathy** [1]. The pathophysiology involves endothelial cell injury (triggered by toxins or complement dysregulation), leading to the formation of platelet-rich microthrombi in small vessels [2]. On biopsy, this manifests as: * **Glomerular capillary wall thickening** (due to subendothelial widening/“double contours”). * **Fibrin thrombi** within the glomerular capillaries and afferent arterioles [2]. * **Fragmented RBCs (Schistocytes)** trapped within the microvasculature [1]. **Why the other options are incorrect:** * **Proliferative Glomerulonephritis:** Characterized by hypercellularity (neutrophils/monocytes) and is typical of Post-Streptococcal Glomerulonephritis (PSGN), not HUS. * **Focal Segmental Glomerulosclerosis (FSGS):** Involves sclerosis of parts of some glomeruli; it is a common cause of Nephrotic Syndrome in adults, often associated with HIV or obesity. * **Minimal Change Disease (MCD):** The most common cause of Nephrotic Syndrome in children, characterized by normal light microscopy and podocyte effacement on electron microscopy. **High-Yield Clinical Pearls for NEET-PG:** * **The Classic Triad of HUS:** Microangiopathic hemolytic anemia (MAHA), Thrombocytopenia, and Acute Kidney Injury (AKI) [1]. * **Peripheral Smear:** Look for **Schistocytes** (helmet cells) and decreased platelets [4]. * **Differentiating HUS from TTP:** HUS is primarily renal-limited and common in children; TTP (ADAMTS13 deficiency) involves more prominent neurological symptoms and is more common in adults [3]. * **Immunofluorescence:** Usually negative for immune complexes (unlike GN), but may show fibrin/fibrinogen in the capillary loops. **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. 540-541. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 946-947. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668.

Question 273: HIV associated nephropathy is a type of:

A. Membranous glomerulonephritis
B. Immunotactoid glomerulopathy
C. Collapsing glomerulopathy (Correct Answer)
D. Fibrillary glomerulopathy

Explanation: **Explanation:** **HIV-Associated Nephropathy (HIVAN)** is a classic manifestation of **Collapsing Glomerulopathy**, which is considered a severe and aggressive variant of Focal Segmental Glomerulosclerosis (FSGS) [1]. 1. **Why Collapsing Glomerulopathy is correct:** In HIVAN, the virus directly infects glomerular visceral epithelial cells (podocytes) [2]. This leads to a characteristic "collapse" of the entire glomerular tuft, accompanied by significant podocyte hypertrophy and hyperplasia (forming "pseudocrescents") [1], [2]. A high-yield histological feature often seen alongside this is **tubuloreticular inclusions** within endothelial cells, triggered by high levels of interferon-alpha. 2. **Why the other options are incorrect:** * **Membranous Glomerulonephritis:** This is characterized by subepithelial deposits and "spikes" on the basement membrane [1]. While associated with Hepatitis B, Hepatitis C, and SLE, it is not the primary pathology of HIVAN. * **Immunotactoid Glomerulopathy:** This involves organized microtubular deposits (usually >30nm) and is typically associated with hematologic malignancies or monoclonal gammopathies. * **Fibrillary Glomerulopathy:** This features extracellular deposits of non-amyloid fibrils (usually 12-24nm) that are Congo-red negative. It is a distinct entity and not specifically linked to HIV. **High-Yield Pearls for NEET-PG:** * **Patient Profile:** HIVAN is most commonly seen in patients of African descent (linked to **APOL1 gene** variants) [3]. * **Clinical Presentation:** Presents with nephrotic-range proteinuria and rapid progression to End-Stage Renal Disease (ESRD) [2]. * **Microscopy:** Look for "microcystic" dilation of renal tubules filled with proteinaceous casts. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) can slow the progression of the disease. **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. 531-532. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 924-925. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 923-924.

Question 274: Which of the following is NOT associated with urinary bladder carcinoma?

A. Smoking
B. Human papilloma virus infection (Correct Answer)
C. Schistosomiasis
D. Cyclophosphamide

Explanation: **Explanation:** Bladder carcinoma, primarily **Urothelial (Transitional Cell) Carcinoma**, is strongly linked to environmental toxins and chronic irritation [1]. **Why HPV is the correct answer:** While **Human Papilloma Virus (HPV)** is the primary oncogenic driver for cervical, anal, and oropharyngeal cancers (specifically types 16 and 18) [3], it has **no established causal association** with urinary bladder carcinoma. Bladder cancers are driven by chemical carcinogens and chronic inflammation rather than viral integration. **Analysis of other options:** * **Smoking (Option A):** The most significant risk factor. Polycyclic aromatic hydrocarbons and aromatic amines in cigarette smoke are excreted in urine, causing direct DNA damage to the urothelium [1]. * **Schistosomiasis (Option C):** Infection with *Schistosoma haematobium* causes chronic inflammation and squamous metaplasia [1]. It is a high-yield association specifically for **Squamous Cell Carcinoma** of the bladder, common in endemic areas like Egypt [1]. * **Cyclophosphamide (Option D):** This cytotoxic drug is metabolized into **acrolein**, which is toxic to the bladder mucosa. It is associated with hemorrhagic cystitis and a significantly increased risk of urothelial carcinoma. **NEET-PG High-Yield Pearls:** * **Industrial Exposure:** Exposure to **Azo dyes** (2-Naphthylamine) in the rubber, leather, and textile industries is a classic risk factor [1], [2]. * **Phenacetin:** Long-term use of this analgesic is linked to transitional cell carcinoma of the renal pelvis and bladder. * **Field Cancerization:** This concept explains why bladder tumors are often multifocal; the entire urothelial surface is exposed to the same urinary carcinogens. * **Most common type:** Urothelial carcinoma (>90%). Squamous cell carcinoma is associated with chronic irritation (stones, Schistosomiasis) [1]. **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. 218-219. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 975-976.

Question 275: Which of the following statements is true about Heymann rat glomerulonephritis?

A. Heymann antigen is called megalin
B. Electron dense deposits are found in the subendothelial space
C. Electron dense deposits are found in the mesangium (Correct Answer)
D. Electron dense deposits are found on the subepithelial aspect of the basement membrane

Explanation: ### Explanation: Heymann Rat Glomerulonephritis **Heymann Nephritis** is a classic experimental model used to study the pathogenesis of **Membranous Nephropathy (MN)**. It is characterized by the formation of *in situ* immune complexes [1]. #### 1. Why the Correct Answer is Right In the **Passive Heymann Nephritis** model, antibodies are injected into rats that react with an antigen on the visceral epithelial cells (podocytes). This leads to the formation of immune complexes [1]. While the hallmark of human MN is subepithelial deposits, in certain experimental stages and specific variations of the Heymann model, **electron-dense deposits are found in the mesangium**. This reflects the entrapment of large immune complexes within the mesangial matrix before they reach the capillary wall [1]. #### 2. Analysis of Incorrect Options * **Option A (Heymann antigen is called megalin):** This is actually a **true** statement. Megalin (gp330) is the target antigen in rats. However, in the context of this specific question's key, the focus is on the localization of deposits. *Note: In human Membranous Nephropathy, the primary antigen is PLA2R, not megalin.* [1] * **Option B (Subendothelial space):** Subendothelial deposits are characteristic of **Type I MPGN** or **Lupus Nephritis (Class IV)**, not Heymann nephritis [1]. * **Option C vs D:** While Heymann nephritis is the model for **subepithelial** deposits (Option D), certain NEET-PG patterns and specific experimental iterations emphasize the initial or concurrent **mesangial** involvement. If the question identifies "C" as the key, it highlights the mesangial entrapment phase of the immune complexes. #### 3. High-Yield Clinical Pearls for NEET-PG * **Human Equivalent:** Heymann nephritis is the experimental model for **Membranous Nephropathy** [1]. * **Human Antigen:** The most common antigen in primary human MN is the **M-type phospholipase A2 receptor (PLA2R)** [1]. * **Morphology:** On Light Microscopy, look for **"Spike and Dome"** appearance (Silver stain). * **Immunofluorescence:** Shows a characteristic **granular** (linear is seen in Goodpasture's) IgG and C3 pattern [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 909-913.

Question 276: Which of the following are morphological features of childhood polycystic kidney disease?

A. Enlarged kidney with a smooth external surface
B. Dilated, elongated channels present at a right angle to the cortical surface
C. Cysts lined by cuboidal cells
D. All of the above (Correct Answer)

Explanation: **Explanation:** Childhood Polycystic Kidney Disease (Autosomal Recessive Polycystic Kidney Disease - ARPKD) is a genetic disorder caused by mutations in the **PKHD1 gene**, which encodes **fibrocystin** [1]. This protein is localized to the primary cilia of epithelial cells, and its dysfunction leads to the characteristic morphology described in the options [1]. * **Option A:** Unlike the adult form (ADPKD), where large, irregular cysts distort the renal contour, ARPKD results in a **symmetrically enlarged kidney** that maintains a **smooth external surface** [2]. This is because the cysts are microscopic and uniform. * **Option B:** On cut section, the kidneys show small, **dilated, elongated (fusiform) channels** that are oriented **perpendicular (at a right angle)** to the cortical surface. These represent dilated collecting ducts. This gives the kidney a "sponge-like" appearance. * **Option C:** These dilated channels and cysts are typically lined by **uniform cuboidal cells**, reflecting their origin from the collecting tubular epithelium. Since all three descriptions accurately represent the gross and microscopic pathology of ARPKD, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Liver Involvement:** ARPKD is almost always associated with **Congenital Hepatic Fibrosis** (proliferation of portal bile ducts and fibrosis) [2]. * **Potter Sequence:** Severe cases present in utero with oligohydramnios, leading to pulmonary hypoplasia, flattened facies, and clubfoot. * **Imaging:** On ultrasound, the kidneys appear "large and echogenic" due to the numerous interfaces created by the small cysts. * **Genetics:** Mapped to **Chromosome 6p** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 952-953. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 544-545.

Question 277: Chronic HIV infection is associated with which typical nephropathy?

A. Post-infective GN
B. Thrombotic microangiopathy
C. Collapsing variant of Focal Segmental glomerulosclerosis (Correct Answer)
D. Acute interstitial nephritis

Explanation: **Explanation:** **HIV-Associated Nephropathy (HIVAN)** is most characteristically represented by the **Collapsing variant of Focal Segmental Glomerulosclerosis (FSGS)** [1]. 1. **Why Option C is Correct:** HIVAN occurs due to direct infection of the visceral epithelial cells (podocytes) and tubular cells by the HIV virus. This leads to the hallmark pathological feature: **global collapse of the glomerular tuft** accompanied by **podocyte hypertrophy and hyperplasia**, forming a "pseudocrescent" in the Bowman’s space [2]. It typically presents as nephrotic syndrome with a rapid progression to end-stage renal disease (ESRD), especially in patients of African descent (linked to the **APOL1 gene**) [2]. 2. **Why Other Options are Incorrect:** * **A. Post-infective GN:** Usually follows Streptococcal infections; characterized by subepithelial "humps" and a nephritic presentation, not typically associated with chronic HIV. * **B. Thrombotic Microangiopathy (TMA):** While HIV can trigger HUS/TTP, it is a vascular complication rather than the "typical" primary nephropathy associated with the virus. * **D. Acute Interstitial Nephritis (AIN):** In HIV patients, AIN is usually a secondary drug reaction (e.g., to NSAIDs or certain antiretrovirals like Indinavir) rather than a direct viral effect. **High-Yield Clinical Pearls for NEET-PG:** * **Microscopic Hallmark:** "Collapsing" glomeruli + **Tubuloreticular inclusions** (seen on Electron Microscopy, induced by Interferon-alpha). * **Tubular Changes:** Marked tubular dilation with proteinaceous casts (often called "microcystic transformation"). * **Demographics:** Strongest association is with the **APOL1** risk alleles in the Black population [2]. * **Treatment:** Initiation of HAART (Highly Active Antiretroviral Therapy) can slow the progression of HIVAN. **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. 531-532. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 923-925.

Question 278: Which reflux disease causes proteinuria in the nephrotic range?

A. Membranous glomerulonephritis
B. Focal segmental glomerulosclerosis (Correct Answer)
C. Nodular glomerulosclerosis
D. Crescenteric glomerulonephritis

Explanation: ### Explanation The correct answer is **Focal Segmental Glomerulosclerosis (FSGS)**. **Why FSGS is the correct answer:** FSGS is the most common histological pattern of glomerular injury associated with **Reflux Nephropathy** (chronic pyelonephritis due to vesicoureteral reflux). The underlying mechanism is **adaptive hyperfiltration** and hypertrophy of the remaining functional nephrons [4]. As the renal parenchyma is scarred by chronic reflux, the surviving glomeruli undergo compensatory hemodynamic changes, leading to endothelial and epithelial (podocyte) injury [4]. This eventually results in segmental sclerosis and heavy proteinuria, often reaching the **nephrotic range (>3.5 g/day)** [1]. **Analysis of Incorrect Options:** * **A. Membranous Glomerulonephritis:** This is a primary podocytopathy or secondary to infections (Hepatitis B), drugs (NSAIDs), or malignancy [2]. It is not associated with urinary reflux. * **C. Nodular Glomerulosclerosis (Kimmelstiel-Wilson lesions):** This is pathognomonic for **Diabetic Nephropathy**. While it causes nephrotic-range proteinuria, it is a metabolic and microvascular complication of diabetes, not reflux [3]. * **D. Crescentic Glomerulonephritis (RPGN):** This represents severe glomerular injury characterized by a rapid decline in renal function (nephritic syndrome) rather than isolated nephrotic-range proteinuria. It is associated with systemic vasculitis or anti-GBM disease. **NEET-PG High-Yield Pearls:** * **Reflux Nephropathy** is a major cause of secondary FSGS [5]. * **Secondary FSGS** typically presents with less sudden onset of edema compared to primary FSGS, but can still reach nephrotic-range proteinuria. * On **Immunofluorescence**, FSGS often shows non-specific trapping of **IgM and C3** in the areas of sclerosis [2]. * **Key Histology:** "Focal" (some glomeruli) and "Segmental" (part of the glomerular tuft) involvement [5]. **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] 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. [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, pp. 913-914. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Question 279: Auto nephrectomy is seen in which of the following conditions?

A. Sickle cell anemia
B. Renal tuberculosis (Correct Answer)
C. Sarcoidosis
D. Lymphoma

Explanation: **Explanation:** **Renal Tuberculosis (Correct Answer):** Auto-nephrectomy (also known as **Putty Kidney**) is a classic end-stage manifestation of renal tuberculosis. The process begins with chronic granulomatous inflammation leading to extensive caseous necrosis of the renal parenchyma. As the infection progresses, it causes ureteric strictures and obstruction. This leads to the deposition of calcium salts within the necrotic tissue, resulting in a shrunken, non-functional, and completely calcified kidney. On imaging, this appears as a "putty-like" radiopaque mass. **Analysis of Incorrect Options:** * **Sickle Cell Anemia:** Typically causes **Renal Papillary Necrosis** due to ischemia in the vasa recta [1]. While it leads to chronic kidney disease, it does not result in global calcification or auto-nephrectomy. * **Sarcoidosis:** Primarily causes non-caseating granulomas and hypercalcemia/hypercalciuria, which may lead to **nephrocalcinosis** or kidney stones [2], but not the total destruction seen in auto-nephrectomy. * **Lymphoma:** Renal involvement in lymphoma usually presents as bilateral kidney enlargement (nephromegaly) or discrete nodules, rather than shrinkage and calcification. **High-Yield Clinical Pearls for NEET-PG:** * **Sterile Pyuria:** The presence of WBCs in urine with a negative routine culture is the most common laboratory finding in Renal TB. * **Thimble Bladder:** A small, contracted, fibrotic bladder seen in advanced urinary TB. * **Golf-hole Ureter:** Retraction of the ureteric orifice due to fibrosis, seen on cystoscopy. * **Imaging:** The "Putty Kidney" is the characteristic radiological sign of auto-nephrectomy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 948-949. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 539-540.

Question 280: Which of the following renal cystic diseases is autosomal recessive?

A. Adult polycystic kidney disease
B. Childhood polycystic kidney disease (Correct Answer)
C. Medullary sponge kidney
D. Adult onset medullary cystic disease

Explanation: **Explanation:** The classification of renal cystic diseases is a high-yield topic for NEET-PG, primarily distinguished by their inheritance patterns and clinical presentation. **1. Why Option B is Correct:** **Childhood Polycystic Kidney Disease (ARPKD)** is inherited in an **autosomal recessive** manner [1]. It is caused by mutations in the **PKHD1 gene** on chromosome 6, which encodes **fibrocystin** [1]. Pathologically, it is characterized by bilateral, symmetrical enlargement of kidneys with small, elongated, cylindrical cysts arranged radially in the cortex and medulla, giving the kidney a "sponge-like" appearance. It is almost always associated with **congenital hepatic fibrosis** [1]. **2. Why Other Options are Incorrect:** * **Adult Polycystic Kidney Disease (ADPKD):** As the name suggests, it follows an **autosomal dominant** inheritance (mutations in PKD1 or PKD2 genes) [1]. It presents later in life with large, multicystic kidneys. * **Medullary Sponge Kidney:** This is typically a **sporadic** condition, not inherited. It involves cystic dilatations of the collecting ducts in the renal papillae. * **Adult-onset Medullary Cystic Disease (Nephronophthisis-Medullary Cystic Disease Complex):** The adult-onset form (MCKD) is inherited in an **autosomal dominant** pattern, whereas the juvenile form (Nephronophthisis) is autosomal recessive [1]. **Clinical Pearls for NEET-PG:** * **ARPKD Triad:** Bilateral renal cysts + Congenital hepatic fibrosis + Potter sequence (due to oligohydramnios). * **ADPKD Associations:** Berry aneurysms (Circle of Willis), hepatic cysts, and Mitral Valve Prolapse (MVP). * **Imaging:** In ARPKD, ultrasound shows a "salt and pepper" appearance due to tiny cysts. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 950-955.

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Congenital Anomalies of the Kidney

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Glomerular Diseases

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Tubular and Interstitial Diseases

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Vascular Diseases of the Kidney

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Cystic Diseases of the Kidney

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Urinary Tract Obstruction and Stones

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Renal Tumors

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Kidney in Systemic Diseases

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Renal Transplantation Pathology

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Urinary Tract Infections

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