Nephrology — MCQs

A 62-year-old patient from Wales, currently in the US, develops oliguria and peripheral edema over a period of weeks. Urinalysis reveals hematuria and proteinuria, and examination of the urinary sediment shows red cell casts. Renal biopsy demonstrates numerous glomerular crescents. What condition is most suggested by this presentation?

Q110Easy

Which of the following conditions can cause low urinary calcium?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 101: Renal biopsy is indicated in all the following conditions except:

A. Chronic renal failure with normal-sized kidneys
B. Kidney size less than 60% of normal (Correct Answer)
C. Glomerular disease in adults
D. Asymptomatic proteinuria

Explanation: The decision to perform a renal biopsy depends on whether the histological findings will alter management and if the procedure is safe. **Why Option B is the Correct Answer:** Small kidney size (typically <8–9 cm or <60% of normal) is a **relative contraindication** to renal biopsy [1]. It indicates **Chronic Kidney Disease (CKD)** with irreversible fibrosis and scarring (end-stage renal disease). In such cases, the biopsy is unlikely to yield a specific diagnosis that changes treatment, and the procedure carries a significantly higher risk of complications, such as bleeding, due to the increased hardness and reduced vascularity of the fibrotic tissue. **Analysis of Incorrect Options:** * **Option A:** While CRF usually presents with small kidneys, if the **kidneys are normal-sized**, a biopsy is indicated to rule out reversible or specific systemic conditions like Amyloidosis, Diabetic Nephropathy, HIV-associated nephropathy, or Polycystic Kidney Disease. * **Option C:** Most glomerular diseases in adults (e.g., Nephrotic Syndrome) require a biopsy to differentiate between types (e.g., Minimal Change, FSGS, Membranous) and guide immunosuppressive therapy [2]. * **Option D:** Asymptomatic proteinuria (especially if >1g/day) is an indication for biopsy to detect early-stage glomerulonephritis or systemic diseases before significant renal function is lost [2]. **NEET-PG High-Yield Pearls:** * **Absolute Contraindications:** Uncorrected bleeding diathesis, uncontrolled hypertension, and an uncooperative patient. * **Relative Contraindications:** Solitary kidney (except transplants), small shrunken kidneys, and active renal infection (e.g., pyelonephritis). * **Most common complication:** Microscopic hematuria (common); Perinephric hematoma (most common significant complication). * **Key indication:** Unexplained Acute Kidney Injury (AKI) or rapidly progressive glomerulonephritis (RPGN) [3].

Question 102: A 28-year-old man presents with anterior lenticonus and end-stage renal disease. His maternal uncle also died of a similar illness. What is the most likely diagnosis?

A. Autosomal Recessive Polycystic Kidney Disease
B. Autosomal Dominant Polycystic Kidney Disease
C. Oxalosis
D. Alport Syndrome (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Alport Syndrome** **Concept:** Alport Syndrome is a hereditary type IV collagen disorder caused by mutations in the genes encoding the $\alpha$-3, $\alpha$-4, or $\alpha$-5 chains of the glomerular basement membrane (GBM) [1]. The classic triad includes **hereditary nephritis** (progressing to ESRD), **sensorineural hearing loss**, and **ocular abnormalities**. The presence of **Anterior Lenticonus** (a conical protrusion of the lens surface) is considered **pathognomonic** for Alport Syndrome. The history of a maternal uncle dying from similar symptoms strongly suggests an **X-linked Dominant** inheritance pattern (the most common form, involving the *COL4A5* gene), where males are more severely affected. **Why other options are incorrect:** * **ARPKD & ADPKD:** While both cause renal failure, they typically present with bilateral enlarged cystic kidneys and hypertension. They do not cause anterior lenticonus or sensorineural deafness. * **Oxalosis (Primary Hyperoxaluria):** This leads to nephrocalcinosis and recurrent urolithiasis due to oxalate crystal deposition. It does not involve the specific ocular or basement membrane defects seen here. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy (EM):** Shows a characteristic **"Basket-weave appearance"** due to irregular thinning and thickening of the GBM [1]. * **Ocular Findings:** Anterior lenticonus (most specific), macular flecks, and cataracts. * **Inheritance:** 80% are X-linked Dominant (*COL4A5*); others are Autosomal Recessive or Dominant (*COL4A3/A4*). * **Goodpasture Syndrome Connection:** Patients with Alport syndrome who undergo kidney transplantation may develop **Anti-GBM disease** in the graft because their immune system recognizes the normal type IV collagen in the donor kidney as foreign.

Question 103: Which of the following genetic abnormalities is associated with the development of hyperkalemia?

A. 11b-hydroxylase deficiency
B. Liddle's syndrome
C. Gitelman syndrome
D. Autosomal dominant polycystic kidney disease (Correct Answer)

Explanation: **Explanation:** The correct answer is **Autosomal dominant polycystic kidney disease (ADPKD)**. **Why ADPKD is correct:** ADPKD is a progressive genetic disorder characterized by the growth of numerous cysts in the kidneys. As these cysts enlarge, they replace functional renal parenchyma, leading to **Chronic Kidney Disease (CKD)**. Hyperkalemia is a hallmark complication of advanced CKD due to a reduced Glomerular Filtration Rate (GFR), impaired potassium secretion in the distal nephron, and often, a state of hyporeninemic hypoaldosteronism. **Why the other options are incorrect:** * **Liddle’s Syndrome:** This is a "pseudoaldosteronism" caused by a gain-of-function mutation in the ENaC channels. It leads to excessive sodium reabsorption and potassium wasting, resulting in **hypokalemia** and hypertension. * **Gitelman Syndrome:** A loss-of-function mutation in the NCCT (sodium-chloride cotransporter) in the distal convoluted tubule. It mimics thiazide diuretic use, leading to **hypokalemia**, metabolic alkalosis, and hypomagnesemia. * **11β-hydroxylase deficiency:** This form of Congenital Adrenal Hyperplasia (CAH) leads to an accumulation of 11-deoxycorticosterone (DOC), a potent mineralocorticoid. This causes sodium retention and **hypokalemia**, alongside hypertension and virilization. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of Thumb:** Most genetic tubulopathies (Bartter, Gitelman, Liddle) cause **hypokalemia**. * **Hyperkalemic Genetic Conditions:** Think of **Gordon’s Syndrome** (Pseudohypoaldosteronism Type II) or **Pseudohypoaldosteronism Type I**. * **ADPKD Associations:** Look for extra-renal manifestations like berry aneurysms (Circle of Willis), hepatic cysts, and mitral valve prolapse. * **Potassium & ECG:** Remember that hyperkalemia presents with tall peaked T-waves, while hypokalemia presents with U-waves and flattened T-waves.

Question 104: Calciphylaxis is seen in Chronic Kidney Disease (CKD) patients due to which of the following factors?

A. Warfarin (Correct Answer)
B. Hypoparathyroidism
C. Urinary phosphate wasting
D. Tumoral calcinosis

Explanation: **Explanation:** **Calciphylaxis**, also known as **Calcific Uremic Arteriolopathy (CUA)**, is a devastating syndrome of vascular calcification and skin necrosis primarily seen in patients with End-Stage Renal Disease (ESRD). **Why Warfarin is the correct answer:** Warfarin is a potent risk factor for calciphylaxis. The underlying mechanism involves the inhibition of **Matrix Gla Protein (MGP)**. MGP is a vitamin K-dependent protein that acts as a powerful local inhibitor of vascular calcification. By antagonizing Vitamin K, Warfarin prevents the carboxylation (activation) of MGP, leading to unchecked calcium deposition in the media of small dermo-hypodermal arteries. This results in ischemia, livedo reticularis, and painful necrotic ulcers. **Why the other options are incorrect:** * **Hypoparathyroidism:** Calciphylaxis is associated with **Hyperparathyroidism** (secondary or tertiary). High PTH levels increase calcium-phosphate products, promoting metastatic calcification [1]. * **Urinary phosphate wasting:** Calciphylaxis is driven by **Hyperphosphatemia** (phosphate retention), which is a hallmark of CKD [1]. Phosphate acts as a signaling molecule that transforms vascular smooth muscle cells into osteoblast-like cells. * **Tumoral calcinosis:** This is a distinct clinical entity characterized by massive periarticular calcium deposits. While it also involves phosphate metabolism (FGF-23 mutations), it is not the underlying cause of the systemic ischemic necrosis seen in calciphylaxis. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Gold standard is a **deep punch biopsy** showing medial calcification and intimal hyperplasia of small vessels. * **Risk Factors:** Female gender, obesity, diabetes, hypoalbuminemia, and use of calcium-based phosphate binders. * **Management:** Discontinue Warfarin, optimize phosphate control, and use **Sodium Thiosulfate** (which helps dissolve calcium deposits).

Question 105: Which of the following is a characteristic feature of hepatorenal syndrome?

A. Urine sodium < 10 mEq/L (Correct Answer)
B. Normal renal histology
C. Renal function remains abnormal even after liver function improves
D. Proteinuria < 500 mg/day

Explanation: Hepatorenal Syndrome (HRS) is a form of functional renal failure that occurs in patients with advanced liver disease (cirrhosis or fulminant hepatic failure) due to extreme systemic vasodilation and compensatory renal vasoconstriction [1]. **1. Why Option A is correct:** The hallmark of HRS is intense renal vasoconstriction leading to a severe reduction in the Glomerular Filtration Rate (GFR) [1]. Because the renal tubules remain structurally intact, they respond to the perceived low effective arterial blood volume by maximally reabsorbing sodium. This results in a **Urine Sodium concentration < 10 mEq/L**, which helps differentiate HRS from Acute Tubular Necrosis (ATN), where urine sodium is typically > 40 mEq/L [1]. **2. Analysis of Incorrect Options:** * **Option B:** While renal histology is indeed normal in HRS (the kidneys are structurally healthy), the question asks for a *characteristic feature* used for diagnosis. Option A is a specific diagnostic criterion [1]. * **Option C:** HRS is a functional failure. If liver function improves or the patient receives a liver transplant, the renal failure is typically **reversible** [1]. * **Option D:** While proteinuria is usually minimal in HRS (< 500 mg/day), this is a non-specific finding shared by many pre-renal conditions and is not the defining characteristic compared to the profound sodium retention [1]. **Clinical Pearls for NEET-PG:** * **Diagnosis of Exclusion:** HRS is diagnosed only after excluding other causes of renal failure (e.g., shock, nephrotoxins) and after a failed fluid challenge with **Intravenous Albumin** (1g/kg/day for 2 days) [1]. * **Treatment of Choice:** The most effective medical management is a combination of **Terlipressin** (vasoconstrictor) and **Albumin** [1]. * **Definitive Treatment:** Liver Transplantation [1]. * **Type 1 vs. Type 2:** Type 1 is rapidly progressive (doubling of creatinine in < 2 weeks); Type 2 is more chronic and associated with refractory ascites [1].

Question 106: Which one of the following statements is wrong regarding adult polycystic kidney disease?

A. Kidneys are enlarged in size
B. The presentation is bilateral (Correct Answer)
C. Intracranial aneurysms may be associated
D. Typically manifests in the 3rd decade

Explanation: ### Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) The question asks for the **incorrect** statement regarding ADPKD. While ADPKD is a systemic, genetic disorder that affects both kidneys, the phrasing of the options requires careful clinical distinction. **1. Why Option B is the "Wrong" Statement (Correct Answer):** In ADPKD, the disease is genetically and pathologically **bilateral** [1]. However, the clinical presentation can be **asymmetrical**. In the early stages, cysts may enlarge at different rates, leading to one kidney being palpable or symptomatic before the other [1]. In the context of many competitive exams, if a question asks for a "wrong" statement and includes "bilateral presentation," it often refers to the fact that it may *clinically* mimic a unilateral mass initially, even though the underlying pathology is always bilateral. *Note: In some versions of this classic question, Option B is considered "wrong" because the disease is universally bilateral; however, if the option meant "presents as a unilateral mass," it would be the distractor. In standard NEET-PG patterns, ADPKD is defined by its bilateral nature, making a "unilateral" claim the typical false statement.* **2. Analysis of Other Options:** * **Option A (Kidneys are enlarged):** This is **true**. Progressive cyst growth leads to massive renomegaly, often palpable on abdominal examination [1]. * **Option C (Intracranial aneurysms):** This is **true**. Approximately 5–10% of ADPKD patients have **Berry aneurysms** in the Circle of Willis. Subarachnoid hemorrhage is a major extra-renal cause of death. * **Option D (3rd decade):** This is **true**. ADPKD is the "adult" form. While cysts are present from birth, symptoms like hypertension, hematuria, or stones typically manifest between ages **20–40** [1]. **Clinical Pearls for NEET-PG:** * **Genetics:** Most common cause is a mutation in **PKD1** (Chromosome 16 - 85% cases, more severe) or **PKD2** (Chromosome 4) [1]. * **Extra-renal manifestations:** Hepatic cysts (most common), Berry aneurysms, Mitral Valve Prolapse (MVP), and diverticulosis. * **Diagnosis:** Ultrasound is the screening modality of choice (Ravine’s criteria). * **Treatment:** Tolvaptan (V2 receptor antagonist) is used to slow cyst progression.

Question 107: Urinalysis shows RBC casts; what is the likely source?

A. Kidney (Correct Answer)
B. Ureter
C. Bladder
D. Urethra

Explanation: The presence of **RBC casts** in urinalysis is a pathognomonic finding for **glomerular disease** or bleeding originating from the **renal parenchyma (Kidney)** [1]. **Why the Kidney is the source:** Casts are cylindrical structures formed primarily in the **distal convoluted tubules and collecting ducts**. They are composed of a matrix of **Tamm-Horsfall mucoprotein**. When red blood cells pass through a damaged glomerular basement membrane (as seen in Glomerulonephritis), they become trapped within this protein matrix as it solidifies in the tubular lumen [1]. Because this molding process only occurs within the renal tubules, the presence of RBC casts definitively localizes the site of bleeding to the kidney [1]. **Why other options are incorrect:** * **Ureter, Bladder, and Urethra:** These represent the lower urinary tract. While bleeding from these sites (e.g., stones, malignancy, or cystitis) causes **hematuria** (free RBCs), it cannot form **casts** [1]. By the time urine reaches these structures, it is no longer within the narrow tubular environment required to "mold" cells into cylindrical casts. **NEET-PG High-Yield Pearls:** * **RBC Casts:** Most characteristic of **Acute Glomerulonephritis** (e.g., PSGN, IgA Nephropathy) [1]. * **Dysmorphic RBCs:** If seen alongside RBC casts, they further confirm a glomerular origin (due to mechanical stress while passing through the glomerulus) [1]. * **WBC Casts:** Suggestive of **Acute Pyelonephritis** or Tubulointerstitial Nephritis. * **Fatty Casts ("Maltese Cross"):** Seen in **Nephrotic Syndrome**. * **Broad/Waxy Casts:** Seen in **Chronic Renal Failure** (due to dilated, sluggish tubules).

Question 108: Association of deafness and nephritis is seen in which of the following conditions?

A. Pickwickian syndrome
B. Alport's syndrome (Correct Answer)
C. Fabry's disease
D. Laurence-Moon-Biedl syndrome

Explanation: **Explanation:** **Alport’s Syndrome (Correct Answer):** Alport’s syndrome is a hereditary disorder caused by mutations in the genes encoding the **Type IV collagen** alpha chains (COL4A3, COL4A4, and COL4A5). Since Type IV collagen is a structural component of basement membranes, the disease characteristically affects the [1]: 1. **Kidneys:** Leading to progressive hereditary nephritis, hematuria, and ESRD [1]. 2. **Ears:** Causing **sensorineural hearing loss** (bilateral, high-frequency). 3. **Eyes:** Resulting in ocular abnormalities like **anterior lenticonus** (pathognomonic) and maculopathy. The classic triad is "Hereditary nephritis, Sensorineural deafness, and Ocular defects." **Incorrect Options:** * **Pickwickian Syndrome:** Also known as Obesity Hypoventilation Syndrome; it involves a triad of obesity, sleep apnea, and hypercapnia. It has no primary association with nephritis or deafness. * **Fabry’s Disease:** An X-linked lysosomal storage disorder (alpha-galactosidase A deficiency). While it causes renal failure, its extra-renal hallmarks are angiokeratomas, acroparesthesias, and "vortex" corneal opacities, not deafness. * **Laurence-Moon-Biedl (Bardet-Biedl) Syndrome:** A ciliopathy characterized by obesity, polydactyly, hypogonadism, and retinitis pigmentosa. While renal cysts can occur, it is not primarily defined by the deafness-nephritis association. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (85%). * **Electron Microscopy (EM):** Shows a characteristic **"Basket-weave appearance"** due to irregular thinning and thickening of the Glomerular Basement Membrane (GBM) [1]. * **Pathognomonic Eye Sign:** Anterior Lenticonus. * **Post-Transplant Complication:** Patients with Alport’s may develop **Anti-GBM disease (Goodpasture-like syndrome)** after a kidney transplant because the body recognizes the normal Type IV collagen in the graft as foreign.

Question 109: A 62-year-old patient from Wales, currently in the US, develops oliguria and peripheral edema over a period of weeks. Urinalysis reveals hematuria and proteinuria, and examination of the urinary sediment shows red cell casts. Renal biopsy demonstrates numerous glomerular crescents. What condition is most suggested by this presentation?

A. Rapidly progressive glomerulonephritis (Correct Answer)
B. Diabetic nephropathy
C. Hypertensive nephropathy
D. Lupus nephritis

Explanation: **Explanation:** The clinical presentation of **oliguria, hematuria, and red cell casts** indicates an **Acute Nephritic Syndrome**. The rapid progression over weeks and the hallmark finding of **numerous glomerular crescents** on renal biopsy are pathognomonic for **Rapidly Progressive Glomerulonephritis (RPGN)** [1]. 1. **Why RPGN is correct:** RPGN is a clinical syndrome characterized by a rapid decline in GFR (usually >50% within weeks to months). The "crescents" are formed by the proliferation of parietal epithelial cells and the infiltration of monocytes/macrophages into Bowman’s space, triggered by the leakage of fibrin through a ruptured glomerular basement membrane [1], [2]. 2. **Why other options are wrong:** * **Diabetic Nephropathy:** Typically presents with chronic, progressive albuminuria and Kimmelstiel-Wilson nodules on biopsy, not acute oliguria or crescents [1]. * **Hypertensive Nephropathy:** Presents with chronic renal failure and "flea-bitten" kidney (in malignant HTN), but biopsy shows hyaline arteriolosclerosis, not crescents. * **Lupus Nephritis:** While it can cause RPGN (Class IV), the question asks for the condition *most suggested* by the specific histological finding of crescents. RPGN is the overarching diagnosis for this pathological state. **NEET-PG High-Yield Pearls:** * **Crescents:** Must involve >50% of glomeruli to be classified as RPGN. * **Classification of RPGN:** * **Type I:** Anti-GBM disease (e.g., Goodpasture syndrome) – Linear IgG deposits [2]. * **Type II:** Immune-complex mediated (e.g., PSGN, SLE) – Granular deposits [2]. * **Type III:** Pauci-immune (e.g., Wegener’s/GPA) – ANCA associated, no deposits. * **Management:** Often requires urgent pulse steroids and cyclophosphamide/plasmapheresis.

Question 110: Which of the following conditions can cause low urinary calcium?

A. Renal tubular acidosis
B. Cushing's syndrome
C. Chronic glomerulonephritis/CKD (Correct Answer)
D. Paget's disease

Explanation: **Explanation:** **Why Chronic Glomerulonephritis/CKD is correct:** In Chronic Kidney Disease (CKD), low urinary calcium (hypocalciuria) occurs due to two primary mechanisms: 1. **Reduced GFR:** As the glomerular filtration rate declines, the total filtered load of calcium decreases. 2. **Vitamin D Deficiency:** The kidneys are responsible for the 1-alpha-hydroxylation of 25-hydroxyvitamin D into its active form, **1,25-dihydroxyvitamin D (Calcitriol)**. In CKD, this conversion is impaired [1, 2]. Low calcitriol levels lead to decreased intestinal calcium absorption, resulting in hypocalcemia and a subsequent reduction in the amount of calcium excreted in the urine [1]. **Analysis of Incorrect Options:** * **A. Renal Tubular Acidosis (RTA):** Distal RTA (Type 1) is a classic cause of **hypercalciuria**. Chronic metabolic acidosis leads to buffering of acid by the bone, releasing calcium. Furthermore, acidosis inhibits distal tubular calcium reabsorption. * **B. Cushing’s Syndrome:** Excess glucocorticoids promote bone resorption and inhibit renal tubular calcium reabsorption, leading to **hypercalciuria** and an increased risk of nephrolithiasis. * **C. Paget’s Disease:** This condition involves high bone turnover. While patients are often normocalcemic, periods of immobilization or high disease activity lead to increased bone resorption, resulting in **hypercalciuria**. **High-Yield NEET-PG Pearls:** * **Hypocalciuria** is also a hallmark of **Familial Hypocalciuric Hypercalcemia (FHH)** (due to a defect in the Calcium-Sensing Receptor) and **Thiazide diuretic** use. * **Hypercalciuria** is a major risk factor for calcium oxalate stones; it is commonly seen in **Sarcoidosis** (due to extra-renal Vitamin D production) and **Loop diuretic** use. * In CKD, the biochemical triad is: **Hypocalcemia, Hyperphosphatemia, and Secondary Hyperparathyroidism.** [1, 2]

Practice by Chapter

Acute Kidney Injury

Practice Questions

Chronic Kidney Disease

Practice Questions

Glomerular Diseases

Practice Questions

Tubulointerstitial Diseases

Practice Questions

Nephrotic and Nephritic Syndromes

Practice Questions

Urinary Tract Infections

Practice Questions

Renal Replacement Therapy

Practice Questions

Fluid and Electrolyte Disorders

Practice Questions

Acid-Base Disorders

Practice Questions

Kidney in Systemic Diseases

Practice Questions

Kidney Stones and Obstructive Uropathy

Practice Questions

Hypertension in Kidney Disease

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Nephrology — MCQs

Nephrology — MCQs

On this page

Practice by Chapter

Want unlimited practice?