Renal Pathology — MCQs
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A 49-year-old male who is a long-term smoker presents with frequency and hematuria. Histologic examination of sections taken from an exophytic lesion of the urinary bladder reveals groups of atypical cells with frequent mitoses forming finger-like projections that have thin, fibrovascular cores. These groups of atypical cells do not extend into the lamina propria and muscularis. No glands or keratin production are found. What is the most accurate diagnosis for this bladder tumor?
A 2 kg baby, born at 30 weeks gestation to an 18-year-old primigravida, died after 48 hours. The Apgar scores were 5 and 8 at 1 and 5 minutes, respectively. Autopsy revealed bilateral enlarged kidneys with multiple radially arranged cysts. Which of the following findings is expected to be associated with this condition?
All are true about infantile polycystic kidney disease except?
Immune complex-mediated glomerular damage is seen in all of the following except:
Which subtype of Renal Cell Carcinoma (RCC) has the best prognosis?
Casts are produced due to damage to which of the following structures?
What is the first manifestation of Alport syndrome?
Which of the following is NOT associated with Adult Polycystic Kidney Disease?
A specimen shows a nephrectomy. What is your diagnosis?
Which is the most characteristic glomerular nephritis (GN) in HIV patients?
Renal Pathology Indian Medical PG Practice Questions and MCQs
Question 211: A 49-year-old male who is a long-term smoker presents with frequency and hematuria. Histologic examination of sections taken from an exophytic lesion of the urinary bladder reveals groups of atypical cells with frequent mitoses forming finger-like projections that have thin, fibrovascular cores. These groups of atypical cells do not extend into the lamina propria and muscularis. No glands or keratin production are found. What is the most accurate diagnosis for this bladder tumor?
- A. Adenocarcinoma, noninvasive
- B. Inverted papilloma
- C. Transitional cell carcinoma in situ
- D. Papillary transitional cell carcinoma (TCC), noninvasive (Correct Answer)
Explanation: **Explanation:** The clinical presentation and histopathology point toward **Papillary Transitional Cell Carcinoma (TCC)**, also known as Urothelial Carcinoma. 1. **Why Option D is correct:** The description of "finger-like projections with thin fibrovascular cores" is the classic histological hallmark of a **papillary** growth pattern [2]. The presence of "atypical cells with frequent mitoses" confirms malignancy (carcinoma) rather than a benign papilloma [1]. Crucially, the fact that these cells "do not extend into the lamina propria and muscularis" defines the tumor as **noninvasive** (Stage Ta) [3]. Smoking is the most significant risk factor for urothelial tumors due to the excretion of carcinogens like beta-naphthylamine [4]. 2. **Why other options are incorrect:** * **Option A:** Adenocarcinomas are rare in the bladder and would show **glandular** differentiation, which is explicitly absent here [1]. * **Option B:** Inverted papilloma is a benign lesion characterized by an **endophytic** (downward) growth of urothelium into the lamina propria, not an exophytic papillary structure with atypia [2]. * **Option C:** Carcinoma in situ (CIS) refers to cytologically malignant cells limited to the surface epithelium; however, CIS is by definition a **flat** lesion, not a papillary/exophytic one [3]. **NEET-PG High-Yield Pearls:** * **Most common bladder cancer:** Urothelial (Transitional Cell) Carcinoma (>90%) [1]. * **Risk Factors:** Smoking (most common), Arylamines (dye industry), *Schistosoma haematobium* (linked to Squamous Cell CA), and Cyclophosphamide [4]. * **Field Effect:** The entire urothelium is at risk; these tumors are often multifocal and recurrent [1]. * **Painless hematuria** in an older smoker is bladder cancer until proven otherwise [3]. **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. 495-496. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, p. 970. [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. 971-972. [4] 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.
Question 212: A 2 kg baby, born at 30 weeks gestation to an 18-year-old primigravida, died after 48 hours. The Apgar scores were 5 and 8 at 1 and 5 minutes, respectively. Autopsy revealed bilateral enlarged kidneys with multiple radially arranged cysts. Which of the following findings is expected to be associated with this condition?
- A. Imperforate anus
- B. Hepatic cyst and fibrosis (Correct Answer)
- C. Absence of ureter
- D. Holoprosencephaly
Explanation: ### Explanation **Diagnosis: Autosomal Recessive Polycystic Kidney Disease (ARPKD)** The clinical presentation of bilateral enlarged kidneys with **radially arranged cysts** (extending from the medulla to the cortex) in a neonate is pathognomonic for **ARPKD** [1]. This condition is caused by mutations in the *PKHD1* gene, which encodes **fibrocystin**, a protein found in the primary cilia of epithelial cells in both the renal tubules and bile ducts [1]. **1. Why Option B is Correct:** In ARPKD, the genetic defect affects both the kidneys and the liver. Virtually all patients with ARPKD have associated **congenital hepatic fibrosis** and **biliary hamartomas** (Meyenburg complexes) [1], [2]. In older children, this manifests as portal hypertension and splenomegaly. The "radially arranged cysts" represent cylindrical dilation of the collecting ducts [1]. **2. Why Incorrect Options are Wrong:** * **Option A (Imperforate anus):** This is typically part of the VACTERL association, not linked to the *PKHD1* mutation. * **Option C (Absence of ureter):** This is seen in Renal Agenesis or Multicystic Dysplastic Kidney (MCDK). In ARPKD, the urinary tract anatomy (ureters and bladder) is structurally normal, though the kidneys are dysfunctional. * **Option D (Holoprosencephaly):** This midline brain defect is associated with Trisomy 13 or Shh gene mutations, not polycystic kidney disease. **Clinical Pearls for NEET-PG:** * **Potter Sequence:** ARPKD often leads to oligohydramnios in utero, resulting in pulmonary hypoplasia, flattened facies, and clubfeet (Potter facies). * **ADPKD vs. ARPKD:** ADPKD (Adult type) presents with spherical cysts and is associated with **berry aneurysms** and **liver cysts** (but rarely fibrosis). ARPKD (Infantile type) presents with elongated/radial cysts and **liver fibrosis** [2]. * **Imaging:** On ultrasound, ARPKD kidneys appear "large and echogenic" due to the numerous small interfaces of the microcysts. **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 213: All are true about infantile polycystic kidney disease except?
- A. Autosomal dominant (Correct Answer)
- B. Hepatic cysts
- C. Renal cysts are present at birth
- D. Periporal fibrosis
Explanation: **Explanation:** The correct answer is **A (Autosomal dominant)** because Infantile Polycystic Kidney Disease (IPKD) is inherited in an **Autosomal Recessive (AR)** pattern [1]. It is caused by mutations in the **PKHD1 gene** on chromosome 6, which encodes the protein **fibrocystin** [1]. In contrast, the adult form of the disease (ADPKD) is Autosomal Dominant. **Analysis of Options:** * **Option A (Incorrect Statement):** As stated, IPKD is AR, not AD. This makes it the correct "except" choice. * **Option B & D (True Statements):** IPKD is almost invariably associated with liver involvement [1]. This spectrum is known as **Fibrocystic Liver Disease**, characterized by **hepatic cysts** and **periportal fibrosis** (congenital hepatic fibrosis). In older children, this can lead to portal hypertension and splenomegaly. * **Option C (True Statement):** Unlike the adult form, where cysts develop over decades, in the infantile form, **renal cysts are present at birth** [1]. The kidneys are symmetrically enlarged with a "sponge-like" appearance due to cylindrical dilation of the collecting ducts. **NEET-PG High-Yield Pearls:** * **Morphology:** Grossly, the kidneys have a smooth external surface (unlike the bosselated surface in ADPKD) with elongated, fusiform cysts arranged radially. * **Potter Sequence:** Severe cases present in utero with oligohydramnios, leading to pulmonary hypoplasia, flattened facies, and clubfeet. * **Key Association:** The severity of renal disease is often inversely proportional to the severity of hepatic fibrosis. * **Gene:** Remember **PKHD1** for ARPKD and **PKD1/PKD2** for ADPKD [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 952-953.
Question 214: Immune complex-mediated glomerular damage is seen in all of the following except:
- A. Membranoproliferative GN
- B. Focal segmental GN (Correct Answer)
- C. Crescentic GN
- D. RPGN
Explanation: **Explanation:** The core concept in this question is distinguishing between **immune complex-mediated** diseases and those caused by **podocyte injury** or **pauci-immune** mechanisms. **Why Focal Segmental Glomerulosclerosis (FSGS) is the correct answer:** FSGS is primarily a **podocytopathy** [1]. The underlying pathology involves direct injury to the visceral epithelial cells (podocytes), leading to effacement of foot processes, hyalinosis, and sclerosis [2]. Unlike many other forms of glomerulonephritis (GN), FSGS is **not** typically mediated by the deposition of antigen-antibody immune complexes [1]. Immunofluorescence (IF) in FSGS is usually negative, though non-specific IgM and C3 trapping may occasionally be seen in sclerotic areas [1]. **Analysis of Incorrect Options:** * **Membranoproliferative GN (MPGN):** Type I MPGN is a classic example of immune complex-mediated damage, characterized by subendothelial deposits and a "tram-track" appearance on light microscopy [2]. * **Crescentic GN & RPGN:** Rapidly Progressive Glomerulonephritis (RPGN) is a clinical syndrome, and Crescentic GN is its histological hallmark. These are classified into three types [3]: * **Type I:** Anti-GBM (Linear deposits). * **Type II: Immune Complex-mediated** (Granular deposits; e.g., Post-streptococcal GN, SLE). * **Type III:** Pauci-immune (ANCA-associated). Since Type II is a major category of RPGN/Crescentic GN, these options are considered immune complex-mediated in this context. **High-Yield Clinical Pearls for NEET-PG:** * **FSGS** is the most common cause of Nephrotic Syndrome in adults in many regions and is frequently associated with HIV, Heroin use, and Obesity [1]. * **Pauci-immune GN** (Type III RPGN) is characterized by a lack of immune deposits on IF and is associated with Wegener’s (GPA) and Microscopic Polyangiitis. * **Rule of Thumb:** If the disease involves "Sclerosis" (FSGS, Diabetic Nephropathy, Amyloidosis), it is generally not immune complex-mediated. **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] 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 215: Which subtype of Renal Cell Carcinoma (RCC) has the best prognosis?
- A. Clear cell
- B. Papillary
- C. Chromophobe (Correct Answer)
- D. Collecting duct
Explanation: **Explanation:** Renal Cell Carcinoma (RCC) is a heterogeneous group of tumors with varying clinical behaviors. The prognosis is primarily determined by the histological subtype, stage, and grade. **Why Chromophobe RCC is the correct answer:** Chromophobe RCC (5% of cases) carries the **best prognosis** among the common subtypes [1]. It originates from the **intercalated cells of the collecting ducts**. These tumors are typically circumscribed, solid, and pale tan/brown. Microscopically, they feature large cells with prominent cell membranes ("vegetable cells"), perinuclear halos, and multiple chromosome losses (hypodiploidy) [1]. They have a low risk of metastasis and a high 5-year survival rate (>90%). **Analysis of Incorrect Options:** * **Clear Cell RCC (Option A):** The most common subtype (70-80%). It originates from the **proximal convoluted tubule**. While common, it is more aggressive than chromophobe and papillary types, frequently showing vascular invasion (renal vein). * **Papillary RCC (Option B):** The second most common subtype (10-15%). While it generally has a better prognosis than clear cell RCC, it is statistically slightly more aggressive than the chromophobe subtype [1]. It is often associated with the MET proto-oncogene [1]. * **Collecting Duct Carcinoma (Option D):** An extremely rare subtype (<1%) originating from the Medullary collecting ducts. It is highly aggressive, often presenting at an advanced stage with a **very poor prognosis**. **High-Yield Clinical Pearls for NEET-PG:** * **Best Prognosis:** Chromophobe RCC [1]. * **Worst Prognosis:** Collecting Duct (Bellini) Carcinoma. * **Most Common:** Clear Cell RCC (associated with **VHL gene** deletion on Chromosome 3p). * **Cytogenetics:** Chromophobe RCC is characterized by **extreme hypodiploidy** (loss of multiple chromosomes: 1, 2, 6, 10, 13, 17, 21) [1]. * **Stain:** Chromophobe RCC shows diffuse cytoplasmic positivity with **Hale’s Colloidal Iron stain**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959.
Question 216: Casts are produced due to damage to which of the following structures?
- A. Nephron
- B. Tubule
- C. Proximal convoluted tubule (PCT)
- D. Distal convoluted tubule (DCT) (Correct Answer)
Explanation: **Explanation:** Urinary casts are cylindrical structures formed by the precipitation of **Tamm-Horsfall mucoprotein** (also known as Uromodulin) [3]. **Why DCT is the correct answer:** The formation of casts occurs primarily in the **Distal Convoluted Tubule (DCT)** and the **Collecting Ducts** [1]. This is due to the specific physiological conditions present in these segments: 1. **Maximum Concentration:** The tubular fluid is most concentrated here, favoring protein precipitation. 2. **Acidic pH:** Low pH promotes the gelation of Tamm-Horsfall protein [3]. 3. **Tamm-Horsfall Protein Secretion:** This glycoprotein is specifically secreted by the cells of the Thick Ascending Limb of Henle and the DCT, acting as the "matrix" or "glue" for all casts. **Analysis of Incorrect Options:** * **Nephron:** This is too broad a term. While the DCT is part of the nephron, the question asks for the specific site of formation. * **Tubule:** Similar to "Nephron," this is an umbrella term. Casts do not form in all parts of the tubule (e.g., they do not form in the PCT). * **Proximal Convoluted Tubule (PCT):** Casts do not form here because the tubular fluid is still isotonic and the concentration of Tamm-Horsfall protein is insufficient to form a solid matrix. **High-Yield Clinical Pearls for NEET-PG:** * **Hyaline Casts:** Most common; seen in concentrated urine, fever, or strenuous exercise [2]. * **RBC Casts:** Pathognomonic for **Glomerulonephritis** (e.g., PSGN) [2]. * **WBC Casts:** Indicative of **Pyelonephritis** or Tubulointerstitial inflammation [2]. * **Fatty Casts ("Maltese Cross"):** Seen in **Nephrotic Syndrome**. * **Broad, Waxy Casts:** Characteristic of **Chronic Renal Failure** (formed in dilated, atrophic tubules). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 933-934. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 520-521. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943.
Question 217: What is the first manifestation of Alport syndrome?
- A. Microscopic hematuria (Correct Answer)
- B. Proteinuria
- C. Oliguria
- D. Sensorineural deafness
Explanation: **Explanation:** **Alport Syndrome** is a hereditary nephritis caused by mutations in the genes encoding the **α-chains of Type IV collagen** (most commonly *COL4A5*, X-linked). Since Type IV collagen is a structural component of the Glomerular Basement Membrane (GBM), its defect leads to progressive basement membrane thinning and splitting. 1. **Why Microscopic Hematuria is correct:** The earliest structural change in Alport syndrome is the thinning of the GBM. This structural fragility leads to the leakage of red blood cells into the urine. **Persistent microscopic hematuria** is the earliest and most common clinical manifestation, often appearing in early childhood (frequently before age 5) [1]. 2. **Why other options are incorrect:** * **Proteinuria:** This develops later in the disease course as the GBM undergoes further damage and "basket-weave" transformation, leading to secondary focal segmental glomerulosclerosis (FSGS) [1]. * **Oliguria:** This is a sign of advanced renal failure or acute kidney injury. In Alport syndrome, renal function declines gradually over decades, leading to End-Stage Renal Disease (ESRD) in early adulthood, rather than sudden oliguria [1]. * **Sensorineural deafness:** While a classic extra-renal feature of Alport syndrome, it typically manifests in late childhood or adolescence, following the onset of hematuria. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (80%). * **Electron Microscopy (Gold Standard):** Shows characteristic **"Basket-weave appearance"** due to irregular thinning, thickening, and splitting of the lamina densa. * **Clinical Triad:** Hereditary nephritis (hematuria/ESRD), Sensorineural deafness, and Ocular defects (e.g., **Anterior Lenticonus**). * **Rule of thumb:** If a pediatric patient has persistent hematuria and a family history of deafness or renal failure, think Alport Syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930.
Question 218: Which of the following is NOT associated with Adult Polycystic Kidney Disease?
- A. Autosomal dominant inheritance
- B. Mutations involving genes affecting cell-cell-matrix interaction
- C. Intracranial berry aneurysm may be present
- D. Tricuspid valve prolapse (Correct Answer)
Explanation: **Explanation:** **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** is a systemic multisystem disorder characterized by the formation of numerous expanding cysts in the renal parenchyma [1]. **Why Option D is the Correct Answer:** ADPKD is associated with cardiovascular abnormalities, most notably **Mitral Valve Prolapse (MVP)**, which occurs in about 20-25% of patients. While other valves can occasionally be involved (like the aortic root), **Tricuspid Valve Prolapse** is not a classic or recognized association of ADPKD. Therefore, it is the "incorrect" association in the list. **Analysis of Incorrect Options:** * **Option A:** ADPKD follows an **Autosomal Dominant** inheritance pattern (Adult type), whereas the infantile form (ARPKD) is Autosomal Recessive [2]. * **Option B:** The disease is caused by mutations in **PKD1** (85%, Polycystin-1) or **PKD2** (15%, Polycystin-2). These proteins are localized to the primary cilia of tubular epithelial cells and are crucial for sensing mechanical shear stress and maintaining **cell-cell and cell-matrix interactions** [1]. * **Option C:** Extra-renal manifestations are common. Approximately 5-10% of patients develop **intracranial berry aneurysms**, typically in the Circle of Willis, which can lead to subarachnoid hemorrhage. **NEET-PG High-Yield Pearls:** * **PKD1** is located on **Chromosome 16** (more severe, earlier onset). * **PKD2** is located on **Chromosome 4** (slower progression). * **Most common extra-renal site for cysts:** The **Liver** (Polycystic liver disease), followed by the pancreas and spleen. * **Other associations:** Diverticulosis of the colon and abdominal/inguinal hernias. * **Clinical presentation:** Often asymptomatic until the 4th decade; presents with hypertension, hematuria, and palpable bilateral flank masses [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 951-952. [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 219: A specimen shows a nephrectomy. What is your diagnosis?
- A. Renal cell carcinoma (Correct Answer)
- B. Renal papillary adenoma
- C. Urothelial cancer of renal pelvis
- D. Oncocytoma
Explanation: ***Renal cell carcinoma*** - Presents as a **golden-yellow variegated** mass in the **renal cortex** with areas of **hemorrhage and necrosis** on gross examination. - Typically shows **clear cell morphology** with abundant cytoplasm and is the most common primary renal malignancy requiring nephrectomy. *Renal papillary adenoma* - Usually **very small** (typically <5mm) **benign tumors** that rarely require nephrectomy due to their minimal size. - Characterized by **papillary architecture** with **bland cytology** and lack the aggressive features seen in larger masses. *Urothelial cancer of renal pelvis* - Arises from the **renal pelvis** and **collecting system**, not the cortical parenchyma like RCC. - Shows **white-tan** appearance with **papillary or solid growth** pattern extending into the pelviocalyceal system. *Oncocytoma* - Appears as a **well-circumscribed tan-brown mass** with a characteristic **central stellate scar** on cut surface. - **Benign tumor** composed of **oncocytes** with abundant eosinophilic cytoplasm, typically doesn't require nephrectomy unless large.
Question 220: Which is the most characteristic glomerular nephritis (GN) in HIV patients?
- A. Focal Segmental Glomerulosclerosis (FSGS) (Correct Answer)
- B. Membranoproliferative Glomerulonephritis (MPGN)
- C. Minimal Change Disease (MCD)
- D. Rapidly Progressive Glomerulonephritis (RPGN)
Explanation: The most characteristic renal manifestation of HIV infection is **HIV-Associated Nephropathy (HIVAN)**, which histologically presents as a specific variant of **Focal Segmental Glomerulosclerosis (FSGS)** [1], [2]. **1. Why FSGS is correct:** HIVAN typically manifests as the **collapsing variant** of FSGS [1], [2]. It is characterized by the global collapse of the glomerular tuft and hypertrophy/hyperplasia of overlying podocytes [1], [2]. This occurs due to direct infection of renal visceral epithelial cells by the HIV virus (via *vpr* and *nef* genes). It is most commonly seen in patients of African descent (linked to **APOL1 gene** variants) [3] and presents with nephrotic-range proteinuria and rapid progression to ESRD [2]. **2. Why other options are incorrect:** * **MPGN:** Usually associated with chronic infections like Hepatitis C or autoimmune diseases, not specifically characteristic of HIV [4]. * **Minimal Change Disease (MCD):** While it causes nephrotic syndrome, it lacks the segmental scarring and podocyte collapse seen in HIVAN [5]. * **RPGN:** This is a clinical syndrome of rapid renal decline with "crescents" on biopsy, typically seen in vasculitis or Goodpasture syndrome, rather than primary HIV infection. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Look for "collapsing" glomeruli and **microcystic dilation** of renal tubules filled with proteinaceous casts [1]. * **Electron Microscopy:** Presence of **Tubuloreticular inclusions (TRIs)** within endothelial cells (induced by high Interferon-alpha levels). * **Treatment:** Highly Active Antiretroviral Therapy (HAART) can significantly slow the progression of HIVAN. * **Demographics:** Strongest association is with the **APOL1 risk alleles** on chromosome 22 [3]. **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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923.
Practice by Chapter
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