Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 271: Increased BP, proteinuria, and RBC casts are the features of which type of Glomerulonephritis?

A. Rapidly progressive glomerulonephritis (RPGN) (Correct Answer)
B. Membranous glomerulonephritis (GN)
C. Membranoproliferative glomerulonephritis (GN)
D. Focal segmental glomerulosclerosis (FSGS)

Explanation: **Explanation:** The clinical triad of **Hypertension (Increased BP), Proteinuria, and RBC casts** is the hallmark of **Nephritic Syndrome** [1]. Among the given options, **Rapidly Progressive Glomerulonephritis (RPGN)** is the most severe clinical manifestation of nephritic syndrome, characterized by a rapid decline in GFR (usually >50% within weeks to months) and the presence of **crescents** on histology [1]. * **Why RPGN is correct:** RBC casts are pathognomonic for glomerular bleeding (nephritis). In RPGN, severe glomerular inflammation leads to the leakage of RBCs and proteins into the urine, while decreased salt/water excretion causes hypertension [1]. * **Why other options are incorrect:** * **Membranous GN:** This is a classic **Nephrotic Syndrome**. It presents with massive proteinuria (>3.5g/day) and edema, but typically lacks RBC casts and significant hypertension in early stages [1]. * **FSGS:** Another primary cause of **Nephrotic Syndrome**. While it can occasionally present with mild hematuria or hypertension, it is primarily characterized by heavy proteinuria rather than an active nephritic sediment (RBC casts) [1]. * **Membranoproliferative GN (MPGN):** This is a "mixed" pattern that can present with both nephritic and nephrotic features. However, RPGN is the more definitive answer when focusing on the acute presentation of RBC casts and rapid clinical deterioration. **Clinical Pearls for NEET-PG:** * **RBC Casts:** Always signify **Glomerulonephritis** (not lower urinary tract bleeding). * **RPGN Histology:** Characterized by **Crescents** (formed by proliferation of parietal epithelial cells and infiltration of monocytes/fibrin) [1]. * **Classification:** RPGN is divided into Type I (Anti-GBM/Goodpasture), Type II (Immune complex), and Type III (Pauci-immune/ANCA-associated) [1].

Question 272: Which of the following is the most likely cause of Acute Renal Failure (ARF) in a patient with a renal failure index less than 1?

A. Acute glomerulonephritis
B. Congestive cardiac failure (Correct Answer)
C. Bilateral acute pyelonephritis
D. Thrombotic thrombocytopenic purpura (TTP)

Explanation: ### Explanation The **Renal Failure Index (RFI)** is a diagnostic tool used to differentiate between **Prerenal Azotemia** and **Intrinsic Acute Tubular Necrosis (ATN)**. It is calculated as: $RFI = \frac{Urine\ Sodium\ (U_{Na})}{Urine\ Creatinine / Plasma\ Creatinine\ (U_{Cr}/P_{Cr})}$ #### 1. Why Congestive Cardiac Failure (CCF) is Correct An **RFI < 1** (along with a Fractional Excretion of Sodium, $FE_{Na} < 1\%$) indicates **Prerenal Azotemia**. In CCF, there is a decrease in effective arterial blood volume and cardiac output. This leads to renal hypoperfusion [1]. The kidneys, being structurally intact, respond by maximally activating the Renin-Angiotensin-Aldosterone System (RAAS), leading to avid reabsorption of sodium and water. This results in low urinary sodium ($U_{Na} < 20$ mEq/L) and a low RFI. #### 2. Why Other Options are Incorrect * **Acute Glomerulonephritis:** While some cases of early glomerulonephritis can present with low $FE_{Na}$, it is primarily an intrinsic renal pathology [1]. * **Bilateral Acute Pyelonephritis:** This is an inflammatory/infective condition of the renal parenchyma. Once it causes ARF, the tubular ability to concentrate urine and reabsorb sodium is usually impaired, leading to an **RFI > 1**. * **TTP:** This causes renal failure via microangiopathic hemolytic anemia and microthrombi in the renal vasculature (intrinsic damage), typically resulting in an **RFI > 1**. #### 3. Clinical Pearls for NEET-PG * **RFI < 1 / $FE_{Na} < 1\%$:** Prerenal causes (Dehydration, CCF, Hepatorenal Syndrome) and Acute Glomerulonephritis. * **RFI > 1 / $FE_{Na} > 2\%$:** Intrinsic causes (Acute Tubular Necrosis). * **Urine Osmolality:** In Prerenal ARF, urine is concentrated (>500 mOsm/kg); in ATN, it is isosthenuric (~300 mOsm/kg). * **BUN/Creatinine Ratio:** Typically **>20:1** in Prerenal Azotemia due to increased urea reabsorption.

Question 273: Hepatorenal syndrome is characterized by all of the following except?

A. Reduction in creatinine clearance
B. Managed effectively by renal vasodilating agents. (Correct Answer)
C. Proteinuria less than 500 mg/d
D. Normal intrinsic kidney

Explanation: **Explanation:** Hepatorenal Syndrome (HRS) is a form of functional renal failure that occurs in patients with advanced liver disease (cirrhosis or fulminant hepatic failure) [1]. It is primarily caused by **splanchnic vasodilation**, which leads to a decrease in effective arterial blood volume, triggering intense **compensatory renal vasoconstriction** [1]. **Why Option B is the Correct Answer (The Exception):** Contrary to what might seem intuitive, **renal vasodilators** (like dopamine or prostaglandins) are **not effective** in managing HRS. The pathophysiology is driven by systemic/splanchnic vasodilation; therefore, the standard of care involves using **systemic vasoconstrictors** (e.g., Terlipressin, Midodrine, or Noradrenaline) in combination with **Albumin** [1]. This therapy aims to increase effective arterial pressure and suppress the overactive renin-angiotensin-sympathetic systems that are causing renal ischemia. **Analysis of Other Options:** * **Option A (Reduction in creatinine clearance):** HRS is defined by progressive renal failure; thus, a rising serum creatinine and a corresponding drop in creatinine clearance are hallmark features [1]. * **Option C (Proteinuria < 500 mg/d):** Since HRS is a functional/pre-renal failure rather than structural damage, the urine sediment is typically "bland." Significant proteinuria (>500 mg/d) or hematuria suggests intrinsic renal disease rather than HRS [1]. * **Option D (Normal intrinsic kidney):** The kidneys in HRS are histologically normal [1]. This is proven by the fact that these kidneys function perfectly if transplanted into a patient with a healthy liver, or if the patient receives a liver transplant. **Clinical Pearls for NEET-PG:** * **Diagnosis of Exclusion:** Always rule out shock, nephrotoxic drugs, and organic kidney disease first [1]. * **Urine Sodium:** Typically **< 10 mmol/L** (reflecting intense sodium retention), similar to pre-renal azotemia [1]. * **Definitive Treatment:** Liver Transplantation is the only curative treatment [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 274: A condition presenting as nephritic syndrome with features of loss of foot processes on electron microscopy and poor response to corticosteroid therapy is:

A. Postinfectious glomerulonephritis
B. Membranoproliferative glomerulonephritis type I
C. Minimal change disease
D. Focal segmental glomerulosclerosis (Correct Answer)

Explanation: ### Explanation The correct answer is **Focal Segmental Glomerulosclerosis (FSGS)**. **Why FSGS is correct:** FSGS is a common cause of nephrotic syndrome in adults, but it frequently presents with **nephritic features** such as hypertension, hematuria, and azotemia. On **Electron Microscopy (EM)**, it characteristically shows the **effacement (loss) of podocyte foot processes**, similar to Minimal Change Disease (MCD) [1]. However, unlike MCD, FSGS is notorious for its **poor response to corticosteroid therapy**, often progressing to chronic kidney disease [1]. **Why the other options are incorrect:** * **Postinfectious Glomerulonephritis (PSGN):** While it presents with nephritic syndrome, EM shows characteristic **subepithelial "humps"** (immune complexes), not simple foot process effacement [1]. * **Membranoproliferative Glomerulonephritis (MPGN) Type I:** This presents with a mixed nephritic/nephrotic picture, but EM shows **subendothelial deposits** and a "tram-track" appearance on light microscopy due to mesangial interposition. * **Minimal Change Disease (MCD):** Although MCD shows loss of foot processes on EM, it presents as a **pure nephrotic syndrome** (no hematuria/hypertension) and is highly **corticosteroid-sensitive**, especially in children [1]. **High-Yield Clinical Pearls for NEET-PG:** * **FSGS Hallmark:** Segmental sclerosis in some (focal) glomeruli on Light Microscopy; Foot process effacement on EM [1]. * **Collapsing Variant:** The most severe form of FSGS, strongly associated with **HIV infection** and IV drug use. * **Genetic Mutation:** Mutations in the **NPHS2 gene** (encoding podocin) are associated with steroid-resistant FSGS. * **Recurrence:** FSGS has a high rate of recurrence in renal transplants (up to 30-50%).

Question 275: A 45-year-old man experienced a subarachnoid hemorrhage from an intracranial aneurysm 6 years ago. He also developed progressive renal impairment associated with hematuria. What is the likely diagnosis?

A. Polycystic Kidney Disease (PCKD) (Correct Answer)
B. Medullary Sponge Kidney
C. Liddle syndrome
D. Fanconi syndrome

Explanation: ### Explanation The correct diagnosis is **Autosomal Dominant Polycystic Kidney Disease (ADPKD)**. **1. Why ADPKD is correct:** ADPKD is a multisystemic disorder characterized by the growth of numerous cysts in the kidneys, leading to progressive renal failure and hematuria (often due to cyst rupture or stones) [1]. A classic extra-renal manifestation of ADPKD is **intracranial "berry" aneurysms**, typically located in the Circle of Willis. Rupture of these aneurysms leads to **subarachnoid hemorrhage (SAH)**. The combination of progressive renal impairment, hematuria, and a history of SAH is a classic clinical triad for ADPKD in medical examinations [1]. **2. Why the other options are incorrect:** * **Medullary Sponge Kidney:** This involves cystic dilatation of collecting ducts [2]. While it can cause hematuria and stones, it rarely leads to progressive renal failure and has no association with intracranial aneurysms [2]. * **Liddle Syndrome:** A rare genetic disorder causing hypertension and hypokalemia due to overactive epithelial sodium channels (ENaC). It does not cause renal failure or intracranial aneurysms. * **Fanconi Syndrome:** A generalized dysfunction of the proximal tubule leading to the loss of glucose, amino acids, and phosphates in the urine. It presents with rickets/osteomalacia and electrolyte imbalances, not SAH. **3. NEET-PG High-Yield Pearls:** * **Genetics:** Most common cause is a mutation in the **PKD1 gene** (Chromosome 16), which is more severe than PKD2 (Chromosome 4) [1]. * **Extra-renal manifestations:** Hepatic cysts (most common), Berry aneurysms, Mitral Valve Prolapse (MVP), and diverticulosis. * **Diagnosis:** Ultrasonography is the initial screening modality of choice. * **Management:** Tolvaptan (Vasopressin V2 receptor antagonist) can be used to slow disease progression in certain patients.

Question 276: Primary peritonitis with pneumococcus is associated with which of the following conditions?

A. Lymphomas
B. Nephrotic syndrome (Correct Answer)
C. Carcinoids
D. None of the above

Explanation: **Explanation:** **Primary Peritonitis (Spontaneous Bacterial Peritonitis)** in the context of renal disease is a classic association with **Nephrotic Syndrome**, particularly in the pediatric population. [1] **Why Nephrotic Syndrome is the correct answer:** Patients with Nephrotic Syndrome are highly susceptible to infections due to several pathophysiological mechanisms: 1. **Hypogammaglobulinemia:** Massive urinary loss of Immunoglobulin G (IgG). 2. **Complement Deficiency:** Loss of Factor B and Factor D (alternative complement pathway components) in the urine, which impairs the **opsonization** of encapsulated bacteria. [1] 3. **Ascites:** The presence of ascitic fluid acts as a culture medium for bacterial growth. [1] *Streptococcus pneumoniae* (Pneumococcus) is the most common causative organism in these patients, followed by Gram-negative organisms like *E. coli*. **Why other options are incorrect:** * **Lymphomas:** While lymphoma patients are immunocompromised, they are more prone to infections related to T-cell dysfunction or neutropenia (e.g., fungal infections, viral reactivations). They do not typically present with primary pneumococcal peritonitis unless there is associated massive ascites or secondary hypogammaglobulinemia. * **Carcinoids:** Carcinoid tumors primarily cause symptoms via hormone secretion (serotonin). While they can cause "Carcinoid Heart Disease" or fibrosis, they do not have a direct association with pneumococcal peritonitis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common organism overall in SBP (Adult Cirrhosis):** *E. coli*. * **Most common organism in SBP (Nephrotic Syndrome):** *Streptococcus pneumoniae*. * **Diagnostic Gold Standard:** Ascitic fluid absolute neutrophil count (ANC) **>250 cells/mm³**. * **Prophylaxis:** In certain high-risk nephrotic patients, pneumococcal vaccination is recommended to mitigate this specific risk.

Question 277: Which of the following conditions is associated with high blood pressure, metabolic alkalosis, and hypokalemia?

A. Liddle’s syndrome (Correct Answer)
B. Gitelman syndrome
C. Barter syndrome
D. Fanconi’s syndrome

Explanation: ### Explanation The clinical triad of **Hypertension, Hypokalemia, and Metabolic Alkalosis** indicates an state of mineralocorticoid excess [1]. **1. Why Liddle’s Syndrome is Correct:** Liddle’s syndrome is an autosomal dominant disorder caused by a "gain-of-function" mutation in the genes encoding the **ENaC (Epithelial Sodium Channel)** in the collecting duct. This leads to constitutive sodium reabsorption regardless of aldosterone levels. The excessive sodium retention causes **hypertension** and volume expansion, which suppresses renin and aldosterone (Pseudohyperaldosteronism). The increased sodium delivery to the distal tubule promotes potassium and hydrogen ion secretion, resulting in **hypokalemia and metabolic alkalosis** [1]. **2. Why the Other Options are Incorrect:** * **Gitelman Syndrome:** A "loss-of-function" mutation in the thiazide-sensitive NaCl cotransporter (NCCT). It presents with hypokalemia and metabolic alkalosis but is associated with **low or normal blood pressure** and hypomagnesemia. * **Bartter Syndrome:** A "loss-of-function" mutation in the thick ascending limb (NKCC2/ROMK). It mimics loop diuretic use, presenting with hypokalemia, metabolic alkalosis, and hypercalciuria, but with **low or normal blood pressure**. * **Fanconi’s Syndrome:** A generalized dysfunction of the proximal tubule. It leads to the loss of glucose, amino acids, and bicarbonate (Type 2 RTA), typically causing **metabolic acidosis** and normal-to-low blood pressure. **3. Clinical Pearls for NEET-PG:** * **Liddle’s Syndrome Treatment:** Amiloride or Triamterene (ENaC blockers). Note: Spironolactone is **ineffective** because the defect is distal to the aldosterone receptor. * **Differential for Hypertension + Hypokalemia:** * *High Renin, High Aldo:* Renal artery stenosis. * *Low Renin, High Aldo:* Conn’s syndrome (Primary Hyperaldosteronism) [2]. * *Low Renin, Low Aldo:* Liddle’s syndrome, Cushing’s syndrome, or Licorice ingestion [2].

Question 278: All are features of renal tubular acidosis type I, except?

A. Stone in kidney
B. No anion gap
C. Hypokalemia
D. Fanconi syndrome (Correct Answer)

Explanation: Renal Tubular Acidosis (RTA) Type I, also known as **Distal RTA**, is characterized by a failure of the alpha-intercalated cells in the distal tubule to secrete hydrogen ions ($H^+$). This leads to an inability to acidify the urine (Urine pH > 5.5) [1]. **Why Fanconi Syndrome is the Correct Answer:** Fanconi syndrome is a generalized dysfunction of the **proximal tubule**, leading to the wasting of glucose, amino acids, uric acid, phosphate, and bicarbonate. It is the hallmark of **RTA Type II (Proximal RTA)**, not Type I. In Type I RTA, the proximal tubule functions normally. **Analysis of Incorrect Options:** * **Stone in kidney:** Type I RTA is strongly associated with **nephrocalcinosis and calcium phosphate stones**. The alkaline urine promotes calcium phosphate precipitation, and the systemic acidosis leads to hypocitraturia (citrate normally inhibits stone formation). * **No anion gap:** All primary RTAs are characterized by a **Normal Anion Gap Metabolic Acidosis (NAGMA)** [1]. The loss of bicarbonate (or failure to excrete $H^+$) is compensated by an increase in chloride, leading to hyperchloremic metabolic acidosis. * **Hypokalemia:** In Type I RTA, the body attempts to retain $H^+$ at the expense of excreting potassium ($K^+$) in the distal tubule [2]. This results in significant hypokalemia, which can manifest as muscle weakness. **High-Yield Clinical Pearls for NEET-PG:** * **Urine pH:** In Type I RTA, urine pH is **always > 5.5** (cannot acidify) [1]. In Type II, urine pH can be < 5.5 if systemic bicarbonate levels are very low. * **Type IV RTA:** The only RTA associated with **Hyperkalemia** (due to hypoaldosteronism or resistance). * **Association:** Type I RTA is often associated with autoimmune diseases like **Sjögren’s syndrome**.

Question 279: What is the most common cause of chronic kidney disease (CKD) in adults?

A. Hypertension
B. Diabetes Mellitus (Correct Answer)
C. Heart disease
D. Cystic tubule interstitial disease

Explanation: **Explanation:** **Diabetes Mellitus (DM)** is the leading cause of Chronic Kidney Disease (CKD) and End-Stage Renal Disease (ESRD) worldwide [1], accounting for approximately 40–50% of all cases. The underlying pathophysiology involves **Diabetic Nephropathy**, characterized by glomerular hyperfiltration, basement membrane thickening, and mesangial expansion leading to progressive glomerulosclerosis [2]. In the Indian context, as well as globally, the rising prevalence of Type 2 DM has solidified its position as the primary driver of CKD. **Analysis of Incorrect Options:** * **Hypertension (A):** This is the **second** most common cause of CKD [1]. While it frequently coexists with diabetes, hypertensive nephrosclerosis (damage to small blood vessels in the kidney) is statistically secondary to diabetes in terms of total disease burden. * **Heart Disease (C):** While there is a strong bidirectional link (Cardiorenal Syndrome), heart disease is typically a *complication* or a comorbidity of CKD rather than a primary cause of the renal failure itself. * **Cystic/Tubulointerstitial Disease (D):** These represent significant but less frequent causes. Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common *inherited* cause, but it does not match the epidemiological scale of metabolic diseases like diabetes. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of CKD:** Diabetes Mellitus (Type 2 > Type 1) [1]. * **Earliest clinical sign of Diabetic Nephropathy:** Microalbuminuria (30–300 mg/day) [2]. * **First structural change:** Thickening of the Glomerular Basement Membrane (GBM) [2]. * **Pathognomonic histological finding:** Kimmelstiel-Wilson (KW) nodules (nodular glomerulosclerosis) [2]. * **Most common cause of death in CKD patients:** Cardiovascular disease (not renal failure itself) [1].

Question 280: Which one of the following is NOT a novel biomarker of acute kidney injury?

A. NGAL
B. KIM-1
C. Cystatin C
D. β-Trace protein (Correct Answer)

Explanation: The diagnosis of Acute Kidney Injury (AKI) has traditionally relied on Serum Creatinine; however, creatinine is a "lagging" marker that only rises after significant loss of GFR [1]. To detect "subclinical AKI" or early tubular damage, several **novel biomarkers** have been identified. [2] **Why β-Trace Protein is the correct answer:** While β-Trace protein (also known as Prostaglandin D2 synthase) is a marker used to estimate GFR and detect CSF leaks, it is primarily considered a marker of **chronic kidney disease (CKD)** and stable renal function rather than an acute marker of tubular injury. It does not rise rapidly enough or specifically enough in response to acute insults to be classified as a "novel biomarker of AKI" in the same category as NGAL or KIM-1. **Analysis of Incorrect Options:** * **NGAL (Neutrophil Gelatinase-Associated Lipocalin):** Often called the "troponin of the kidney," it is the most well-studied novel biomarker. It is produced by thick ascending limb and collecting duct cells and rises within 2–4 hours of injury. * **KIM-1 (Kidney Injury Molecule-1):** A transmembrane protein highly expressed in proximal tubular cells specifically after ischemic or toxic injury. It is an excellent marker for acute tubular necrosis (ATN). * **Cystatin C:** A protease inhibitor produced by all nucleated cells. It is filtered freely and not secreted, making it a more sensitive marker for early changes in GFR than creatinine in the acute setting. **High-Yield Clinical Pearls for NEET-PG:** * **Functional Markers (GFR):** Cystatin C, Proenkephalin A. * **Damage Markers (Tubular):** NGAL, KIM-1, IL-18, L-FABP. * **Cell Cycle Arrest Markers:** [TIMP-2] × [IGFBP7] (marketed as NephroCheck) are the newest markers used to predict the development of moderate-to-severe AKI. * **NGAL** is the earliest marker to rise in post-cardiac surgery AKI.

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?