Renal Pathology — MCQs

Renal Pathology Indian Medical PG Practice Questions and MCQs

Question 41: A pathologist examines a renal biopsy from a 45-year-old man with nephrotic syndrome and requests a Congo red stain to confirm the nature of amorphous acidophilic extracellular hyaline substances localized within the mesangial matrix of the glomeruli. A positive test confirms the presence of?

A. Alpha 1-antitrypsin
B. Amyloid (Correct Answer)
C. Copper
D. Glycogen

Explanation: ### Explanation **Correct Answer: B. Amyloid** The presence of **amorphous, acidophilic (eosinophilic), extracellular hyaline material** [1] in the glomerular mesangium is a classic histological description of **Amyloidosis** [2]. The definitive diagnostic test for amyloid is the **Congo red stain**, which demonstrates a characteristic **salmon-pink** color under light microscopy and **apple-green birefringence** when viewed under polarized light [1]. This occurs because amyloid proteins are arranged in a cross-beta-pleated sheet configuration, which binds the dye in a highly organized manner [1]. In the kidney, amyloid deposition leads to basement membrane thickening and mesangial expansion, eventually causing heavy proteinuria and nephrotic syndrome [2]. **Why other options are incorrect:** * **A. Alpha 1-antitrypsin:** This is typically identified in the liver (hepatocytes) as PAS-positive, diastase-resistant globules. It is not associated with Congo red staining or primary renal hyaline deposits. * **C. Copper:** Copper deposits (seen in Wilson’s disease) are identified using **Rhodanine stain** or Orcein stain, primarily in the liver and cornea (Kayser-Fleischer rings), not as mesangial hyaline. * **D. Glycogen:** Glycogen is identified using the **Periodic Acid-Schiff (PAS) stain** and is sensitive to diastase digestion. While glycogen can accumulate in tubular cells (Armanni-Ebstein lesions in diabetes), it does not stain with Congo red. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type of Renal Amyloidosis:** AL (Light chain) amyloidosis is most common in the West; AA (Secondary) amyloidosis is common in India due to chronic infections like TB [3]. * **Staining Mnemonic:** "Amyloid is **A**pple-green on **P**olarized light." * **Other Stains:** Thioflavin T (Fluorescence) is more sensitive but less specific than Congo red. * **Electron Microscopy:** Shows non-branching, random fibrils (7.5–10 nm diameter) [2]. **References:** [1] Kumar v, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-269. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534. [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. 135-136.

Question 42: All of the following are true statements about membranous nephropathy except?

A. Irregular 'spikes' on silver staining
B. Selective proteinuria
C. Granular subendothelial IgG accompanied by C3 deposits (Correct Answer)
D. SLE is a secondary cause

Explanation: **Explanation:** **Membranous Nephropathy (MN)** is characterized by the accumulation of immune complexes along the **subepithelial** side of the glomerular basement membrane (GBM) [1]. 1. **Why Option C is the correct (false) statement:** In MN, the immune deposits are **subepithelial** (between the podocytes and the GBM), not subendothelial [1]. On Immunofluorescence (IF), these deposits appear as **granular IgG and C3** [2]. Subendothelial deposits are characteristic of conditions like Lupus Nephritis (Class III/IV) or MPGN [1]. 2. **Analysis of other options:** * **Option A:** As the GBM grows around the subepithelial deposits to incorporate them, it creates protrusions. On Silver stain (Jones stain), these appear as **"spikes"** and "domes" [2]. * **Option B:** MN typically presents with **non-selective proteinuria** (loss of both albumin and higher molecular weight globulins) due to significant podocyte injury and GBM thickening [3]. *Note: While Minimal Change Disease is the classic example of selective proteinuria, MN is a prototype of nephrotic syndrome where proteinuria is usually non-selective.* * **Option D:** While 75% of cases are primary (linked to **PLA2R antibodies**), secondary causes include **SLE** (Class V Lupus Nephritis), Hepatitis B, NSAIDs, and solid tumors (lung/colon). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause** of Nephrotic Syndrome in elderly Caucasian adults. * **Electron Microscopy (Gold Standard):** Shows "Spike and Dome" appearance and podocyte foot process effacement [2]. * **Primary MN Marker:** Antibodies against **Phospholipase A2 Receptor (PLA2R)** are found in ~70% of idiopathic cases. * **Rule of Thirds:** 1/3rd undergo spontaneous remission, 1/3rd persist with proteinuria, and 1/3rd progress to ESRD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 911. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 921. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Question 43: Increased renin activity is seen in all of the following conditions, except:

A. Benign nephrosclerosis (Correct Answer)
B. Malignant nephrosclerosis
C. Hemolytic Uremic Syndrome
D. Juxtaglomerular cell tumor

Explanation: ### Explanation The Renin-Angiotensin-Aldosterone System (RAAS) is activated primarily by decreased renal perfusion or ischemia. The key to this question lies in distinguishing between conditions that cause significant renal ischemia versus those that do not. **1. Why Benign Nephrosclerosis is the Correct Answer:** In **Benign Nephrosclerosis**, the renal changes (hyaline arteriolosclerosis) are associated with long-standing, well-controlled hypertension [2]. While there is gradual narrowing of the lumen [3], it typically does **not** cause sufficient ischemia to trigger a significant rise in renin. In fact, most patients with essential hypertension (the precursor to benign nephrosclerosis) have **low or normal plasma renin levels**. **2. Analysis of Incorrect Options:** * **Malignant Nephrosclerosis:** Characterized by "flea-bitten" kidneys and hyperplastic arteriolosclerosis (onion-skinning). The severe narrowing of the lumen causes profound renal ischemia [4], leading to a massive release of renin and a self-perpetuating cycle of hypertension [1]. * **Hemolytic Uremic Syndrome (HUS):** This is a microangiopathic hemolytic anemia where microthrombi obstruct renal glomerular capillaries [5]. This acute obstruction causes significant renal ischemia, thereby stimulating renin production. * **Juxtaglomerular Cell Tumor (Reninoma):** This is a rare benign tumor of the JG cells themselves. These cells are the primary source of renin; hence, the tumor autonomously secretes high levels of renin, leading to secondary hyperaldosteronism. **Clinical Pearls for NEET-PG:** * **Goldblatt Kidney:** A classic experimental model of renin-dependent hypertension caused by renal artery stenosis [1]. * **Morphology:** Remember **Hyaline** arteriolosclerosis = Benign [3]; **Hyperplastic** (onion-skin) = Malignant [4]. * **Bartter Syndrome:** Another high-yield condition featuring JG cell hyperplasia and increased renin/aldosterone, but with normal blood pressure due to salt-wasting. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 945-946. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 541-542. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948.

Question 44: In minimal change disease, why does albumin first appear in the urine?

A. Albumin has a high affinity to the glomerular basement membrane.
B. Albumin has a lower molecular weight compared to globulins. (Correct Answer)
C. There is a high albumin:globulin ratio in plasma.
D. Albumin undergoes active excretion.

Explanation: **Explanation:** Minimal Change Disease (MCD) is characterized by the effacement of podocyte foot processes and the **loss of the glomerular polyanionic charge** (heparan sulfate) [1]. This loss of negative charge results in **selective proteinuria**, where smaller proteins are leaked into the urine while larger proteins are retained [2]. **1. Why Option B is Correct:** The glomerular filtration barrier restricts molecules based on both **charge** and **size** [1]. In MCD, the charge barrier is lost, but the size barrier remains partially functional. **Albumin**, having a relatively low molecular weight (~69 kDa) and a smaller molecular radius compared to globulins (which are much larger, >150 kDa), can easily pass through the filtration slits once the electrostatic repulsion is gone [1]. Therefore, albuminuria occurs first and most prominently [2]. **2. Why Other Options are Incorrect:** * **Option A:** Albumin is normally repelled by the GBM due to its negative charge; it does not have a high affinity for it. * **Option C:** While the A:G ratio in plasma is high, this is not the physiological reason for its selective filtration in renal disease; the filtration is governed by the physical properties of the barrier. * **Option D:** Albumin is filtered at the glomerulus, not actively secreted by the tubules. **High-Yield Clinical Pearls for NEET-PG:** * **Selectivity Index:** MCD shows a **high selectivity index** (<0.1), meaning mainly low-molecular-weight proteins (albumin) are excreted [2]. * **Light Microscopy:** Glomeruli appear **normal** [2]. * **Electron Microscopy (Gold Standard):** Shows **effacement (fusion) of podocyte foot processes** [3]. * **Treatment:** It is the most common cause of Nephrotic Syndrome in children and is highly **steroid-responsive** [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 905-907. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-923. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Question 45: Hereditary nephritis is seen in which of the following conditions?

A. Analgesic nephropathy
B. Balkan nephropathy
C. Alport syndrome (Correct Answer)
D. Eosinophilic nephritis

Explanation: **Explanation:** **Alport Syndrome (Correct Answer):** Alport syndrome is a classic example of **hereditary nephritis**. It is primarily an X-linked dominant disorder (85% of cases) caused by mutations in the **COL4A5 gene**, which encodes the α-5 chain of **Type IV collagen**. This collagen is a crucial structural component of the glomerular basement membrane (GBM), cochlea, and lens. Defective collagen leads to thinning and splitting of the GBM, clinically manifesting as the triad of **hereditary hematuria, sensorineural deafness, and ocular defects** (e.g., anterior lenticonus) [1]. **Analysis of Incorrect Options:** * **Analgesic Nephropathy:** An **acquired** chronic tubulointerstitial nephritis caused by the cumulative ingestion of large quantities of NSAIDs or phenacetin. It is characterized by renal papillary necrosis. * **Balkan Nephropathy:** An **acquired** environmental form of interstitial nephritis found in the Danube River basin. It is linked to the ingestion of **aristolochic acid** (from the plant *Aristolochia clematitis*) and carries a high risk of transitional cell carcinoma. * **Eosinophilic Nephritis:** Typically an **acquired** hypersensitivity reaction (Acute Interstitial Nephritis) often triggered by drugs like NSAIDs, antibiotics (penicillins), or diuretics. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy (EM):** The hallmark of Alport syndrome is a **"Basket-weave appearance"** due to irregular thickening, thinning, and splitting of the lamina densa. * **Immunofluorescence:** Shows a characteristic **negative staining** for Type IV collagen chains [1]. * **Goodpasture Syndrome vs. Alport:** While both involve Type IV collagen, Goodpasture is an autoimmune attack against the α-3 chain, whereas Alport is a genetic deficiency. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930.

Question 46: You are examining a nephrectomy specimen diagnosed as renal cell carcinoma. On microscopic examination, the tumor cells contain glycogen and lipids. What is the most likely diagnosis?

A. Clear cell carcinoma (Correct Answer)
B. Papillary carcinoma
C. Chromophobe renal carcinoma
D. Collecting duct carcinoma

Explanation: ### Explanation **1. Why Clear Cell Carcinoma is correct:** Clear cell carcinoma (RCC) is the most common histological subtype of renal cell carcinoma (70-80%). The characteristic "clear" appearance of the cytoplasm in routine H&E staining is an artifact of processing. In vivo, these cells are packed with **glycogen and lipids** [1]. During histological preparation, these substances are dissolved by solvents (like xylene and alcohol), leaving behind an optically empty, clear cytoplasm demarcated by a distinct cell membrane [1]. These tumors typically arise from the **proximal convoluted tubule**. **2. Why the other options are incorrect:** * **Papillary Carcinoma:** These cells typically show a cuboidal or columnar morphology arranged in finger-like projections (papillae) with fibrovascular cores [1]. They often contain **psammoma bodies** and foamy macrophages, but not the lipid-laden clear cytoplasm. * **Chromophobe Renal Carcinoma:** These cells have a "wrinkled" or "raisinoid" nucleus with a prominent **perinuclear halo** [1]. The cytoplasm is typically eosinophilic or pale but contains numerous microvesicles (detected by Hale’s colloidal iron stain), not primarily glycogen/lipids. * **Collecting Duct Carcinoma:** This is a rare, highly aggressive tumor arising from the medulla. It shows a **tubulopapillary pattern** with significant desmoplasia and "hobnail" cells; it does not feature clear cells. **3. NEET-PG High-Yield Pearls:** * **Genetics:** Clear cell RCC is associated with the loss of the **VHL gene** on **Chromosome 3p** [1]. * **Staining:** Glycogen can be demonstrated using a **PAS (Periodic Acid-Schiff) stain**. * **Gross Appearance:** Classically described as a **golden-yellow** cortical mass (due to high lipid content) with areas of hemorrhage and necrosis [1]. * **Paraneoplastic Syndromes:** RCC is the "Great Mimicker," often presenting with polycythemia (EPO), hypercalcemia (PTHrP), or Cushing’s (ACTH). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 959-961.

Question 47: The most characteristic finding in diabetic nephropathy is:

A. Diffuse glomerulosclerosis
B. Nodular glomerulosclerosis (Correct Answer)
C. Armanni-Ebstein reaction
D. Fibrin caps

Explanation: **Explanation:** **Nodular glomerulosclerosis**, also known as **Kimmelstiel-Wilson (KW) lesions**, is considered the most characteristic (pathognomonic) histological finding in diabetic nephropathy [1]. These are ovoid, laminated, hyaline eosinophilic masses located in the periphery of the glomerulus, resulting from increased mesangial matrix production and basement membrane thickening. **Analysis of Options:** * **A. Diffuse glomerulosclerosis:** This is actually the **most common** lesion in diabetic nephropathy [1]. It involves a generalized increase in mesangial matrix. While frequent, it is not as specific (characteristic) as the nodular form. * **C. Armanni-Ebstein reaction:** This refers to vacuolation and glycogen deposits in the epithelial cells of the **proximal convoluted tubules** (pars recta). While seen in diabetes, it is a tubular change, not a glomerular one, and is less common today due to better glycemic control. * **D. Fibrin caps:** These are hyaline accumulations on the surface of glomerular capillaries. Along with **Capsular drops**, they are features of diabetic nephropathy but are non-specific as they can occur in other glomerular diseases. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Clinical Sign:** Microalbuminuria (30-300 mg/day). * **Earliest Morphological Change:** Thickening of the Glomerular Basement Membrane (GBM) [2]. * **Pathogenesis:** Non-enzymatic glycosylation of proteins leading to Advanced Glycation End-products (AGEs). * **Vascular Change:** Hyaline arteriolosclerosis affecting **both** afferent and efferent arterioles (highly suggestive of diabetes). * **Kimmelstiel-Wilson nodules** are PAS-positive [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1121-1122. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1121.

Question 48: Crescents in renal pathology are derived from which of the following cellular components?

A. Epithelial cells, fibrin, and macrophages (Correct Answer)
B. Mesangial cells, fibrin, and macrophages
C. Tubular cells, mesangial cells, and fibrin
D. Neutrophils, tubular cells, and fibrin

Explanation: **Explanation:** **Crescent formation** is the hallmark of **Rapidly Progressive Glomerulonephritis (RPGN)** [1]. It represents a severe inflammatory response to glomerular basement membrane (GBM) injury. 1. **Why Option A is correct:** When the GBM is severely damaged, plasma proteins—specifically **fibrin**—leak into Bowman’s space. Fibrin acts as a potent stimulus for the proliferation of **parietal epithelial cells** (which line Bowman’s capsule) [1][2]. Simultaneously, **macrophages** and monocytes migrate from the blood into the urinary space. Therefore, a crescent is histologically composed of layers of proliferating parietal epithelial cells, infiltrating macrophages, and fibrin strands. Over time, these cellular crescents may undergo fibrosis. 2. **Why other options are incorrect:** * **Mesangial cells (Options B & C):** These are located within the glomerular tuft (central core). While they proliferate in conditions like IgA nephropathy or Membranoproliferative GN, they do not migrate into Bowman’s space to form crescents [2]. * **Tubular cells (Options C & D):** These line the renal tubules (proximal/distal). While they are involved in Acute Tubular Necrosis (ATN), they do not contribute to the structure of a glomerular crescent. * **Neutrophils (Option D):** While neutrophils are present in acute inflammation (like Post-Streptococcal GN), they are not the primary structural component of the crescentic mass. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** RPGN is defined by the presence of crescents in **>50% of glomeruli** on biopsy. * **Staining:** Fibrin within the crescents can be highlighted using **Masson’s Trichrome** or Immunofluorescence. * **Classification:** RPGN is divided into three types: * **Type I:** Anti-GBM disease (e.g., Goodpasture syndrome; Linear IF). * **Type II:** Immune-complex mediated (e.g., SLE, PSGN; Granular IF). * **Type III:** Pauci-immune (e.g., Wegener’s/GPA; ANCA associated). **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. 528-529. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926.

Question 49: Malakoplakia of the bladder is associated with which of the following?

A. Smoking
B. Aniline dye
C. Defect in phagocytosis (Correct Answer)
D. Contrast dye

Explanation: **Explanation:** **Malakoplakia** is a rare, chronic inflammatory condition most commonly affecting the urinary bladder. It is characterized by a **defect in phagocytosis**, specifically an acquired impairment in the bactericidal activity of macrophages. 1. **Why the correct answer is right:** In Malakoplakia, macrophages (known as **von Hansemann cells**) can ingest bacteria (most commonly *E. coli*) but are unable to digest them completely due to defective lysosomal function. This leads to the accumulation of partially digested bacterial components and calcium/iron salts within the cytoplasm. These calcified concentric inclusions are called **Michaelis-Gutmann bodies**, which are the pathognomonic histological hallmark of the disease. 2. **Why the incorrect options are wrong:** * **Smoking & Aniline dye:** These are major risk factors for **Urothelial (Transitional Cell) Carcinoma** of the bladder, not inflammatory conditions like Malakoplakia [1]. * **Contrast dye:** While contrast media can cause nephrotoxicity (Acute Tubular Necrosis), it has no association with the pathogenesis of Malakoplakia. **High-Yield Facts for NEET-PG:** * **Pathognomonic Feature:** Michaelis-Gutmann bodies (calcified siderotic granules). * **Stains:** These bodies are positive for **PAS**, **Von Kossa** (calcium), and **Prussian Blue** (iron). * **Common Organism:** *Escherichia coli* is implicated in 90% of cases. * **Clinical Presentation:** Often presents as soft, yellowish, slightly raised mucosal plaques on the bladder wall, mimicking a tumor. * **Patient Profile:** Often seen in immunosuppressed patients or those with chronic systemic diseases. **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.

Question 50: All are true about ANCA-associated crescentic glomerulonephritis, except?

A. Seen in Wegener's granulomatosis
B. Seen in microscopic polyangiitis
C. Seen in Henoch-Schönlein purpura (Correct Answer)
D. Is pauci-immune in nature

Explanation: Crescentic Glomerulonephritis (CrGN), or Rapidly Progressive Glomerulonephritis (RPGN), is classified into three types based on immunofluorescence (IF) findings. **ANCA-associated CrGN (Type III)** is characterized by a **pauci-immune** pattern, meaning there is little to no deposition of antibodies or complement in the glomeruli [1]. * **Why Option C is the correct answer:** Henoch-Schönlein Purpura (HSP), now known as IgA Vasculitis, is an **immune-complex mediated** disease (Type II RPGN) [5]. On IF, it shows prominent **granular IgA deposits** in the mesangium [3]. Since it involves significant immune deposition, it is not "pauci-immune" and is not associated with ANCA. * **Why Options A & B are incorrect:** Both Granulomatosis with Polyangiitis (formerly Wegener’s) and Microscopic Polyangiitis (MPA) are classic examples of pauci-immune Type III RPGN [2]. Wegener’s is typically associated with **c-ANCA (PR3-ANCA)**, while MPA is associated with **p-ANCA (MPO-ANCA)** [1]. * **Why Option D is incorrect:** "Pauci-immune" is the defining characteristic of ANCA-associated vasculitis, distinguishing it from Anti-GBM disease (linear deposits) and Immune-complex GN (granular deposits) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Type I RPGN:** Anti-GBM disease (e.g., Goodpasture Syndrome); Linear IF [3]. * **Type II RPGN:** Immune Complex mediated (e.g., PSGN, SLE, HSP); Granular IF [4]. * **Type III RPGN:** Pauci-immune (ANCA +ve); No deposits on IF [1]. * **Crescents** are formed by the proliferation of **parietal epithelial cells** and the migration of monocytes/macrophages into Bowman’s space, triggered by fibrin leakage [5]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 526-527. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 528-529.

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