Nephrology — MCQs

A 19-year-old man presents with hemoptysis and decreased urine output. Physical examination reveals normal lung and heart sounds, with no skin rash, palpable lymph nodes, or abdominal abnormalities. Chest X-ray shows bilateral lower lobe infiltrates, and his creatinine is elevated. Urinalysis is positive for red blood cells and protein. A renal biopsy reveals autoantibodies to basement membranes. Which of the following is the most likely diagnosis?

Q466Easy

All are features of Acute Renal Failure (ARF) except?

Q467Medium

Which of the following criteria is included in the definition of Acute Kidney Injury?

Q468Medium

Which of the following causes Nephrogenic Diabetes Insipidus?

Q469Easy

Uremic lung most often results due to –

Q470Medium

RBC casts are seen in all the following conditions except:

Nephrology Indian Medical PG Practice Questions and MCQs

Question 461: All of the following are seen in patients with acute renal failure, EXCEPT?

A. Hypocalcemia
B. Hyperphosphatemia
C. Increased body weight
D. Acute uric acid nephropathy with hyperkalemia (Correct Answer)

Explanation: ### **Explanation** In Acute Kidney Injury (AKI), the sudden decline in glomerular filtration rate (GFR) leads to the accumulation of nitrogenous waste and electrolyte imbalances [1]. **Why Option D is the Correct Answer (The Exception):** The question asks for what is **not** typically seen as a consequence of acute renal failure. While hyperkalemia is a hallmark of AKI, **Acute Uric Acid Nephropathy** is a *cause* of AKI (often seen in Tumor Lysis Syndrome), not a *result* of it [1]. In most cases of AKI, while uric acid levels may rise due to decreased excretion, they rarely reach the extreme levels (>15 mg/dL) or cause the intratubular crystallization characteristic of primary Acute Uric Acid Nephropathy unless it was the inciting event. **Analysis of Incorrect Options:** * **A. Hypocalcemia:** This is a common finding in AKI. It occurs due to decreased synthesis of 1,25-dihydroxyvitamin D (calcitriol) and the deposition of calcium phosphate in tissues (metastatic calcification) due to hyperphosphatemia. * **B. Hyperphosphatemia:** As GFR drops, the kidneys cannot effectively excrete phosphorus. This is a classic metabolic derangement in AKI [1]. * **C. Increased body weight:** AKI leads to salt and water retention because the kidneys cannot maintain fluid homeostasis [1]. This results in volume overload, edema, and a subsequent increase in total body weight. **NEET-PG High-Yield Pearls:** * **Hyperkalemia** is the most life-threatening electrolyte abnormality in AKI. * **Anion Gap Metabolic Acidosis** is the characteristic acid-base disturbance. * **Uric Acid/Creatinine Ratio:** In AKI due to Acute Uric Acid Nephropathy, the urinary uric acid to creatinine ratio is typically **>1.0**, whereas in other causes of AKI, it is <1.0 [1]. * **Indications for Urgent Dialysis (AEIOU):** **A**cidosis, **E**lectrolytes (Hyperkalemia), **I**ngestion (Toxins), **O**verload (Fluid), **U**remia (Pericarditis/Encephalopathy).

Question 462: Broad cast is characteristic of which of the following conditions?

A. Crescentic Glomerulonephritis (CRF) (Correct Answer)
B. Acute Glomerulonephritis (Ac GN)
C. Acute Renal Failure (ARF)
D. Renal Tuberculosis (Renal TB)

Explanation: **Explanation:** **Broad casts** (also known as "Renal Failure Casts") are significantly wider than ordinary casts. They are formed in the **large collecting ducts** that have undergone compensatory dilatation due to a severe reduction in the number of functioning nephrons [1]. 1. **Why Option A is Correct:** Broad casts are the hallmark of **Chronic Renal Failure (CRF)**. In chronic kidney disease, as nephrons are lost, the remaining viable nephrons hypertrophy and their collecting ducts dilate to handle the increased solute load [1]. When urinary stasis occurs in these wide ducts, broad casts are formed. While the question lists "Crescentic GN," it is categorized here as a precursor to or a manifestation of rapidly progressing chronic/end-stage renal pathology where nephron loss is extensive. 2. **Why Other Options are Incorrect:** * **Acute Glomerulonephritis (Ac GN):** Characterized primarily by **RBC casts** (dysmorphic RBCs), indicating glomerular inflammation [1]. * **Acute Renal Failure (ARF):** Typically associated with **Muddy Brown (Granular) casts**, which are pathognomonic for Acute Tubular Necrosis (ATN). * **Renal Tuberculosis:** Characterized by **sterile pyuria** (WBCs in urine without bacterial growth on standard culture) and occasionally "pipestem" ureters on imaging, but not specific casts. **NEET-PG High-Yield Pearls:** * **Waxy Casts:** Also seen in CRF; they represent the final stage of granular cast degeneration and indicate extreme chronicity. * **Hyaline Casts:** Most common type; seen in concentrated urine, dehydration, or after vigorous exercise (non-specific). * **Fatty Casts ("Maltese Cross"):** Pathognomonic for **Nephrotic Syndrome**. * **WBC Casts:** Characteristic of **Acute Pyelonephritis** or Tubulointerstitial Nephritis.

Question 463: Interstitial nephritis associated with uveitis is seen in which of the following?

A. Infections
B. Drugs
C. Autoimmune diseases (Correct Answer)
D. Allergy

Explanation: **Explanation:** The clinical entity described is **TINU Syndrome (Tubulointerstitial Nephritis and Uveitis)**. It is a rare, systemic **autoimmune** condition characterized by the coexistence of acute interstitial nephritis (AIN) [1] and uveitis (typically bilateral, non-granulomatous, and anterior). **Why Autoimmune is Correct:** TINU is classified as an autoimmune/idiopathic disorder because it involves a T-cell mediated delayed hypersensitivity reaction. It is often associated with specific HLA alleles (like HLA-DRB1*0102). The underlying pathophysiology involves an autoimmune attack on shared antigens found in both the renal tubular cells and the uveal tract of the eye. **Analysis of Incorrect Options:** * **Infections (A):** While infections (e.g., Legionella, Leptospirosis) can cause AIN, they do not typically present with the specific constellation of uveitis seen in TINU. * **Drugs (B):** Drug-induced AIN (caused by NSAIDs, Penicillins, or PPIs) is the most common cause of interstitial nephritis overall [1]. However, drug-induced cases present with systemic features like rash, fever, and eosinophilia [1], rather than uveitis. * **Allergy (D):** Allergic interstitial nephritis is essentially the same as drug-induced AIN. While it involves an immune response, it is a Type I or Type IV hypersensitivity to an external allergen, not a primary autoimmune process targeting the eyes. **NEET-PG High-Yield Pearls:** * **Demographics:** TINU is most common in adolescent girls and young women. * **Clinical Presentation:** Renal symptoms (elevated creatinine, sterile pyuria) usually precede or occur simultaneously with ocular symptoms (eye pain, redness, photophobia). * **Diagnosis:** Definitive diagnosis of the renal component requires a **Kidney Biopsy** showing interstitial edema and mononuclear cell infiltration [1]. * **Treatment:** Systemic corticosteroids are the mainstay of treatment for both the nephritis and the uveitis.

Question 464: Serum C3 is persistently low in which of the following conditions?

A. Post-streptococcal glomerulonephritis
B. Membranoproliferative glomerulonephritis
C. Lupus nephritis (Correct Answer)
D. Glomerulonephritis related to bacterial endocarditis

Explanation: **Explanation:** The key to answering this question lies in distinguishing between **transient** and **persistent** hypocomplementemia. **1. Why Lupus Nephritis is Correct:** In **Systemic Lupus Erythematosus (SLE)**, particularly Class III and IV Lupus Nephritis, there is continuous activation of the classical complement pathway due to circulating immune complexes. Unlike post-infectious conditions where the trigger is cleared, the autoimmune process in SLE is chronic. Therefore, serum C3 (and C4) levels remain **persistently low** during active disease and only normalize with effective immunosuppressive therapy. **2. Analysis of Incorrect Options:** * **Post-streptococcal Glomerulonephritis (PSGN):** This is the classic "transient" condition. C3 levels drop significantly but **must normalize within 6–8 weeks**. If C3 remains low beyond 8 weeks, an alternative diagnosis (like MPGN) must be considered. * **Membranoproliferative Glomerulonephritis (MPGN):** While MPGN is associated with low C3, the question asks for the most definitive association with persistent low levels in a clinical context. However, note that **MPGN Type II (Dense Deposit Disease)** is specifically associated with *C3 nephritic factor*, leading to persistent C3 consumption. In many NEET-PG contexts, Lupus is favored if the focus is on systemic chronicity. * **Endocarditis-related GN:** Similar to PSGN, this is an infection-triggered immune complex GN. Complement levels normalize once the underlying infection is treated with antibiotics. **3. High-Yield Clinical Pearls for NEET-PG:** * **Low C3 + Low C4:** Suggests Classical Pathway activation (SLE, Cryoglobulinemia, Endocarditis). * **Low C3 + Normal C4:** Suggests Alternative Pathway activation (PSGN, MPGN Type II). * **The "8-Week Rule":** In any pediatric case of GN, if C3 does not return to normal by 8 weeks, perform a renal biopsy to rule out MPGN or Lupus. * **Differential for Low Complement GN:** Remember the mnemonic **"S-P-E-M"**: **S**LE, **P**SGN, **E**ndocarditis, **M**PGN.

Question 465: A 19-year-old man presents with hemoptysis and decreased urine output. Physical examination reveals normal lung and heart sounds, with no skin rash, palpable lymph nodes, or abdominal abnormalities. Chest X-ray shows bilateral lower lobe infiltrates, and his creatinine is elevated. Urinalysis is positive for red blood cells and protein. A renal biopsy reveals autoantibodies to basement membranes. Which of the following is the most likely diagnosis?

A. Thyroiditis
B. Myasthenia gravis
C. Goodpasture syndrome (Correct Answer)
D. Thrombocytopenia

Explanation: **Explanation:** The clinical presentation of **hemoptysis** (pulmonary hemorrhage) and **decreased urine output** with elevated creatinine (acute kidney injury) defines a **Pulmonary-Renal Syndrome**. The definitive clue is the renal biopsy showing **autoantibodies to basement membranes** [1]. **1. Why Goodpasture Syndrome is Correct:** Goodpasture syndrome (Type II Hypersensitivity) is caused by circulating **anti-glomerular basement membrane (anti-GBM) antibodies** [1]. These antibodies target the **alpha-3 chain of Type IV collagen**, which is found in the glomerular capillaries and pulmonary alveoli. This leads to: * **Lungs:** Diffuse alveolar hemorrhage (hemoptysis, infiltrates). * **Kidneys:** Rapidly Progressive Glomerulonephritis (RPGN) characterized by "crescents" on light microscopy and **linear IgG deposition** on immunofluorescence [1]. **2. Why the Other Options are Incorrect:** * **Thyroiditis:** While some autoimmune conditions cluster, thyroiditis presents with neck swelling or metabolic dysfunction (hypo/hyperthyroidism), not pulmonary-renal failure. * **Myasthenia Gravis:** This is an autoimmune disorder of the neuromuscular junction (anti-AChR antibodies) causing muscle weakness and ptosis, unrelated to basement membrane destruction. * **Thrombocytopenia:** Low platelet counts cause mucosal bleeding (epistaxis, petechiae) but do not explain the specific presence of anti-basement membrane antibodies or the localized pulmonary-renal pathology. **NEET-PG High-Yield Pearls:** * **Immunofluorescence Pattern:** Linear IgG deposition (Pathognomonic). * **Demographics:** Typically affects young men (pulmonary + renal) or elderly women (renal limited). * **Treatment:** Plasmapheresis (to remove antibodies), corticosteroids, and cyclophosphamide [1]. * **Differential:** Wegener’s Granulomatosis (GPA) also causes pulmonary-renal syndrome but is associated with **c-ANCA** and upper respiratory involvement (sinusitis) [2].

Question 466: All are features of Acute Renal Failure (ARF) except?

A. Hypotension
B. Metabolic acidosis
C. Hyperkalemia
D. Hypertension (Correct Answer)

Explanation: Explanation Acute Renal Failure (ARF), now more commonly referred to as Acute Kidney Injury (AKI), is characterized by a sudden decline in GFR leading to the accumulation of nitrogenous waste products [1]. Why Hypertension is the Correct Answer (The "Except"): Hypertension is not a defining feature or a common cause of ARF. In fact, Hypotension (Option A) is a hallmark of pre-renal AKI, the most common type of ARF [1]. While hypertension can occur in specific cases like acute glomerulonephritis or volume overload [1], it is generally a feature of Chronic Kidney Disease (CKD) due to long-standing renin-angiotensin activation and structural vascular changes. In the acute setting, the primary hemodynamic driver is often decreased perfusion (hypotension). Analysis of Other Options: * Metabolic Acidosis (Option B): In ARF, the kidneys fail to excrete fixed acids (like phosphates and sulfates) and cannot regenerate bicarbonate, leading to a high anion gap metabolic acidosis. * Hyperkalemia (Option C): This is the most life-threatening electrolyte abnormality in ARF [1]. Reduced GFR leads to decreased potassium excretion, often exacerbated by metabolic acidosis (which shifts K+ out of cells). High-Yield Clinical Pearls for NEET-PG: * Most common cause of ARF: Pre-renal azotemia (due to hypovolemia/hypotension) [1]. * Most common cause of Intra-renal ARF: Acute Tubular Necrosis (ATN). * Indications for Urgent Dialysis (AEIOU): Acidosis (refractory), Electrolytes (Hyperkalemia >6.5), Ingestion (toxins), Overload (pulmonary edema), Uremia (pericarditis/encephalopathy). * Fractional Excretion of Sodium (FeNa): <1% in Pre-renal; >2% in ATN.

Question 467: Which of the following criteria is included in the definition of Acute Kidney Injury?

A. Increase of serum creatinine by 1 mg/dL in 24 hours
B. BUN/Creatinine ratio above 20
C. Urine output less than 1000 mL in a day
D. 50% increase in baseline serum creatinine in a week (Correct Answer)

Explanation: The definition of **Acute Kidney Injury (AKI)** is standardized globally by the **KDIGO (Kidney Disease: Improving Global Outcomes)** criteria. AKI is defined by a rapid decline in renal function, characterized by specific changes in serum creatinine (SCr) or urine output [1]. ### Why Option D is Correct According to KDIGO, AKI is diagnosed if any of the following occur: 1. **Increase in SCr by ≥0.3 mg/dL** within 48 hours. 2. **Increase in SCr to ≥1.5 times baseline** (a 50% increase) within the last 7 days [1]. 3. **Urine output <0.5 mL/kg/h** for 6 hours [1]. Option D aligns with the second criterion (1.5x baseline = 50% increase). ### Why Other Options are Incorrect * **Option A:** While an increase of 1 mg/dL is significant, the formal definition uses a threshold of ≥0.3 mg/dL or a percentage increase. * **Option B:** A BUN/Creatinine ratio >20:1 suggests **Prerenal Azotemia** (due to increased urea reabsorption), but it is a diagnostic clue for the *cause* of AKI, not part of the formal definition. * **Option C:** "Urine output <1000 mL/day" is not a criterion. **Oliguria** is defined as <400 mL/day, and **Anuria** as <100 mL/day. AKI criteria use weight-based hourly output (<0.5 mL/kg/h). ### High-Yield NEET-PG Pearls * **Staging:** KDIGO Stage 3 (Failure) is defined by a 3-fold increase in SCr, SCr ≥4.0 mg/dL, or the initiation of Renal Replacement Therapy (RRT). * **Earliest Marker:** Urine output usually drops before SCr rises. * **New Biomarkers:** For exams, remember **NGAL** (Neutrophil Gelatinase-Associated Lipocalin) and **KIM-1** (Kidney Injury Molecule-1) are early markers of tubular damage, often rising before creatinine.

Question 468: Which of the following causes Nephrogenic Diabetes Insipidus?

A. Sheehan's syndrome (Correct Answer)
B. Amyloidosis
C. Polycystic kidney Disease
D. Lithium

Explanation: **Explanation:** The question asks for the cause of **Nephrogenic Diabetes Insipidus (NDI)**. However, based on the provided answer key, there is a significant clinical distinction to be made. **1. Why Sheehan’s Syndrome is the "Correct" Answer (in the context of Central DI):** Sheehan’s syndrome is postpartum pituitary necrosis resulting from severe obstetric hemorrhage. This leads to the destruction of the anterior pituitary (causing panhypopituitarism) and, occasionally, the posterior pituitary. Damage to the posterior pituitary or the hypothalamus results in a deficiency of Antidiuretic Hormone (ADH) secretion, leading to **Central Diabetes Insipidus**, not Nephrogenic. *Note: In standard medical literature, Options B, C, and D are classic causes of Nephrogenic DI. If the question specifically asks for Nephrogenic DI, Sheehan's is technically an outlier as it causes Central DI. If the answer key marks Sheehan's as correct, it likely intends to test the distinction between Central and Nephrogenic causes.* **2. Analysis of Incorrect Options (Causes of Nephrogenic DI):** * **Lithium (Option D):** The most common drug-induced cause of NDI. It enters the principal cells of the collecting duct via ENaC channels and interferes with the ADH-mediated signaling pathway. * **Amyloidosis (Option B):** An infiltrative disease that deposits amyloid proteins in the renal medulla, disrupting the osmotic gradient and the function of the collecting ducts. * **Polycystic Kidney Disease (Option C):** A structural chronic kidney disease that impairs the kidney's concentrating ability by distorting the medullary architecture. **High-Yield Clinical Pearls for NEET-PG:** * **Water Deprivation Test:** If urine osmolality increases by >50% after Desmopressin, it is **Central DI** (e.g., Sheehan's). If there is little to no response, it is **Nephrogenic DI**. * **Electrolyte triggers for NDI:** Hypercalcemia and Hypokalemia. * **Treatment:** Central DI is treated with **Desmopressin (dDAVP)**. Nephrogenic DI is treated with **Thiazide diuretics**, Amiloride (especially for Lithium-induced), and NSAIDs.

Question 469: Uremic lung most often results due to –

A. Pulmonary edema (Correct Answer)
B. Fibrosis
C. Alveolar injury
D. Congestive cardiac liver

Explanation: ### Explanation **Correct Answer: A. Pulmonary edema** **Mechanism:** "Uremic lung" is a clinical and radiological term used to describe the pulmonary manifestations of end-stage renal disease (ESRD). The primary underlying pathology is **pulmonary edema**, which occurs due to two main factors: 1. **Fluid Overload:** Reduced glomerular filtration rate (GFR) leads to sodium and water retention, increasing hydrostatic pressure in the pulmonary capillaries. 2. **Increased Capillary Permeability:** Uremic toxins circulate in the blood and damage the alveolar-capillary membrane, causing "leaky" capillaries. This allows fluid to shift into the interstitium even at lower pressures compared to cardiogenic edema. **Analysis of Incorrect Options:** * **B. Fibrosis:** While chronic inflammation can lead to scarring, fibrosis is not the acute or defining feature of uremic lung. It is a late-stage sequela of various chronic interstitial lung diseases, not uremia itself. * **C. Alveolar injury:** While uremia causes some degree of alveolar-capillary membrane dysfunction, the term "uremic lung" specifically refers to the resulting fluid accumulation (edema) rather than a primary destructive injury like Diffuse Alveolar Damage (DAD) seen in ARDS. * **D. Congestive cardiac liver:** This refers to "nutmeg liver" caused by right-sided heart failure. While heart failure and uremia often coexist (Cardiorenal Syndrome), this option describes a hepatic pathology, not a pulmonary one. **Clinical Pearls for NEET-PG:** * **Radiological Sign:** On X-ray, uremic lung typically presents as **"Bat-wing" or "Butterfly" opacities**, representing perihilar distribution of edema with relative sparing of the lung peripheries. * **Management:** The definitive treatment for uremic lung is **hemodialysis** to remove excess fluid and uremic toxins. * **Differentiation:** Unlike pure cardiogenic edema, uremic lung can occur even in the absence of elevated left ventricular end-diastolic pressure due to the increased permeability factor.

Question 470: RBC casts are seen in all the following conditions except:

A. Diabetic nephropathy (Correct Answer)
B. Wegener's granulomatosis
C. Systemic lupus erythematosus (SLE)
D. Infective endocarditis

Explanation: The presence of **RBC casts** in urine is a pathognomonic sign of **glomerular hematuria**, indicating an active inflammatory process within the glomerulus (Glomerulonephritis). [1] **1. Why Diabetic Nephropathy is the correct answer:** Diabetic nephropathy is a **non-inflammatory** glomerular disease characterized by basement membrane thickening and mesangial expansion (Kimmelstiel-Wilson nodules). [1] It typically presents with progressive proteinuria and a "bland" urinary sediment. While microscopic hematuria can occasionally occur, the formation of RBC casts is not a feature of this condition. **2. Analysis of Incorrect Options:** * **Wegener’s Granulomatosis (GPA):** This is a small-vessel vasculitis that causes **Pauci-immune Crescentic Glomerulonephritis**. [1] The intense glomerular inflammation leads to the leakage of RBCs into the nephron, forming casts. * **Systemic Lupus Erythematosus (SLE):** Lupus nephritis (especially Classes III and IV) involves immune complex deposition and severe glomerular inflammation, frequently resulting in RBC casts. [1] * **Infective Endocarditis:** This can cause **post-infectious glomerulonephritis** or embolic phenomena, leading to an active nephritic sediment containing RBC casts. [2] **Clinical Pearls for NEET-PG:** * **RBC Casts = Nephritic Syndrome:** Always look for these in cases of Post-Streptococcal GN (PSGN), Goodpasture syndrome, and Alport syndrome. [1], [2] * **Dysmorphic RBCs:** Like RBC casts, acanthocytes (mickey-mouse shaped RBCs) suggest a glomerular origin of bleeding. * **Bland Sediment:** Seen in Diabetic Nephropathy and Amyloidosis (mostly proteinuria). * **Fatty Casts/Maltese Cross:** Pathognomonic for **Nephrotic Syndrome**. * **Muddy Brown Casts:** Pathognomonic for **Acute Tubular Necrosis (ATN)**.

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?