Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 791: Polyuria with low fixed specific gravity urine is seen in ?

A. Diabetes mellitus
B. Diabetes insipidus
C. Chronic glomerulonephritis (Correct Answer)
D. Potomania

Explanation: ***Chronic glomerulonephritis*** - Damage to the **renal tubules** in chronic glomerulonephritis impairs their ability to concentrate urine, leading to polyuria with a **low, fixed specific gravity**. [1] - This fixed specific gravity reflects the kidneys' inability to adjust urine concentration in response to hydration status, a hallmark of **chronic kidney disease**. [2] *Diabetes mellitus* - Polyuria in diabetes mellitus is caused by **osmotic diuresis** due to high glucose levels in the urine, leading to increased urinary volume. [2] - While there is polyuria, the specific gravity is not necessarily fixed and can vary, often being high due to the presence of glucose. *Diabetes insipidus* - Diabetes insipidus causes polyuria and dilute urine due to either a deficiency of **ADH (central DI)** or renal unresponsiveness to ADH **(nephrogenic DI)**. - While it causes polyuria with low specific gravity, it's typically *not* fixed; the urine specific gravity can still fluctuate to some extent depending on the patient's hydration, or in response to ADH if it's central DI. *Potomania* - Potomania, or **primary polydipsia**, is excessive water intake that leads to dilutional hyponatremia and polyuria. - The kidneys are otherwise healthy and can still concentrate urine to some extent if water intake is restricted, preventing a truly fixed low specific gravity.

Question 792: Which of the following is NOT a common cause of acute renal failure?

A. Chronic kidney disease due to analgesic nephropathy (Correct Answer)
B. Acute pyelonephritis
C. Acute kidney injury from snakebite
D. Acute kidney injury due to rhabdomyolysis

Explanation: Chronic kidney disease due to analgesic nephropathy - This is a cause of chronic kidney disease, characterized by gradual, irreversible kidney damage over a long period due to prolonged use of certain analgesics. [1] - It does not present as an acute, sudden decline in kidney function, which is the hallmark of acute renal failure. [1] Acute pyelonephritis - Severe cases of acute pyelonephritis (kidney infection) can lead to acute kidney injury due to sepsis, inflammation, and potential obstruction. [1] - The systemic inflammatory response and direct tissue damage can impair kidney function rapidly. [1] Acute kidney injury from snakebite - Snake envenomation can cause acute kidney injury through various mechanisms, including hemolysis, rhabdomyolysis, direct nephrotoxicity, and systemic hypotension. - These effects can lead to rapid and severe kidney damage. Acute kidney injury due to rhabdomyolysis - Rhabdomyolysis involves the breakdown of skeletal muscle tissue, releasing large amounts of myoglobin into the bloodstream. [1] - Myoglobin is toxic to the renal tubules, leading to acute tubular necrosis and rapid onset of acute kidney injury. [1]

Question 793: All are seen in Nephrotic syndrome except

A. Atherosclerosis
B. Thrombo-embolism
C. Lipiduria
D. Increased protein C levels (Correct Answer)

Explanation: ***Increased protein C levels*** - In **nephrotic syndrome**, there is an **increased urinary loss of anticoagulant proteins**, including **Protein C** and **Protein S**, leading to a state of **hypercoagulability**. [1] - Therefore, **Protein C levels are decreased**, not increased, making this the exception. *Atherosclerosis* - **Hyperlipidemia**, a hallmark of nephrotic syndrome, contributes significantly to **accelerated atherosclerosis** due to dysregulation of lipid metabolism. - The increased levels of **LDL cholesterol** and other lipoproteins promote plaque formation and arterial stiffening. *Thrombo-embolism* - Patients with nephrotic syndrome are at a significantly **increased risk of thromboembolic events**, such as deep vein thrombosis and pulmonary embolism, due to a **hypercoagulable state**. - This state results from the **urinary loss of anticoagulant proteins** (e.g., antithrombin III, Protein C, Protein S) and increased levels of procoagulant factors (e.g., fibrinogen, factor V, factor VIII). *Lipiduria* - **Lipiduria**, the presence of lipids in the urine, is a characteristic feature of nephrotic syndrome, often manifested as **oval fat bodies** and **fatty casts**. [1] - This occurs due to the increased glomerular permeability that allows lipoproteins to filter into the urine. [1]

Question 794: Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?

A. HTN
B. Increased urea
C. Increased creatinine
D. Normal C3 level (Correct Answer)

Explanation: ***Normal C3 level*** - In Post-streptococcal glomerulonephritis (PSGN), **C3 levels are typically decreased** due to complement consumption during the inflammatory process. [1] - A **normal C3 level** would not be consistent with PSGN, as it suggests no significant complement activation. *Increased urea* - Increased urea can occur due to **impaired renal function**, which is common in PSGN due to glomerular inflammation. [1] - It's a typical finding reflecting the kidneys' inability to excrete waste products properly. *HTN* - Hypertension is frequently associated with PSGN due to **volume overload** and activation of the renin-angiotensin system. [1] [2] - It is a common clinical feature that results from increased fluid retention. *Increased creatinine* - Increased creatinine levels indicate **renal impairment**, which is characteristic of PSGN as kidney function is affected during this condition. [1] - This finding highlights the reduction in glomerular filtration rate (GFR), typical in glomerulonephritis. [2]

Question 795: Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.

A. None of the above are correct causes.
B. I, II, and IV are correct causes.
C. I and III are correct causes.
D. All of the options are correct causes of post-transplantation hypertension. (Correct Answer)

Explanation: ***All of the options are correct causes of post-transplantation hypertension.*** - Post-transplantation hypertension often has a multifactorial etiology, with **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** all being significant contributors. - Each of these conditions can lead to mechanisms that elevate blood pressure, such as **renal ischemia**, activation of the **renin-angiotensin system**, and inflammatory responses affecting renal function. *I, II, and IV are correct causes.* - This option is incorrect because it excludes **renal transplant artery stenosis (RTAS)** (III), which is a well-established cause of secondary hypertension in transplant recipients due to reduced blood flow to the allograft. - **RTAS** activates the renin-angiotensin-aldosterone system (RAAS), leading to **vasoconstriction** and **sodium retention**, contributing to hypertension. *I and III are correct causes.* - This option is incorrect as it omits other crucial causes like **cyclosporine nephrotoxicity** (II) and **recurrent disease in the allograft** (IV), both of which are documented contributors to post-transplantation hypertension. - **Cyclosporine nephrotoxicity** causes afferent arteriolar vasoconstriction and glomerulosclerosis, directly increasing blood pressure. *None of the above are correct causes.* - This option is incorrect because **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** are all recognized and significant causes of post-transplantation hypertension. - Each condition has distinct pathological mechanisms that contribute to **elevated blood pressure** in transplant recipients.

Question 796: What does the measurement of Glomerular Filtration Rate (GFR) help determine in kidney function?

A. Heart rate
B. Recovery from shock
C. Stage of kidney disease (Correct Answer)
D. Blood volume

Explanation: Stage of kidney disease - A low GFR indicates impaired kidney function, helping to classify the severity and stage of chronic kidney disease (CKD) [1]. - Monitoring GFR over time is crucial for assessing disease progression and guiding treatment strategies [1]. *Heart rate* - Heart rate is a measure of cardiac function and is not directly assessed by GFR. - Kidney function can indirectly affect heart rate over time (e.g., in advanced kidney disease with fluid overload), but GFR itself doesn't measure it. *Recovery from shock* - While kidney function is important during shock, GFR primarily measures the kidney's filtration capacity at a given moment. - Recovery from shock involves many physiological parameters beyond just kidney filtration, such as blood pressure and organ perfusion. *Blood volume* - Blood volume is regulated by many mechanisms, including hormonal systems (e.g., renin-angiotensin-aldosterone system) and fluid intake/excretion. - Although kidneys play a role in fluid balance, GFR specifically measures the rate of filtration of blood plasma, not the overall blood volume [1].

Question 797: Which of the following is a sign of Bartter's syndrome?

A. High potassium levels
B. Acidic blood
C. Low potassium levels (Correct Answer)
D. High sodium levels

Explanation: ***Low potassium levels*** * Bartter's syndrome is characterized by **renal salt wasting** and subsequent volume depletion, which activates the **renin-angiotensin-aldosterone system** [1]. * This leads to increased aldosterone levels, causing increased potassium secretion in the collecting ducts, resulting in **hypokalemia** [2]. *High potassium levels* * **Hyperkalemia** is not a feature of Bartter's syndrome; instead, it is marked by persistent potassium loss [1]. * Conditions causing hyperkalemia typically involve impaired renal potassium excretion or increased potassium release from cells. *Acidic blood* * Bartter's syndrome usually presents with **metabolic alkalosis** due to hydrogen ion loss in the urine, not acidic blood [2]. * Acidic blood (**acidemia**) would imply a state of respiratory or metabolic acidosis. *High sodium levels* * Bartter's syndrome primarily involves **renal salt wasting**, leading to **normal or low sodium levels** rather than high sodium levels. * High sodium levels (**hypernatremia**) are usually due to inadequate water intake or excessive water loss.

Question 798: Interstitial nephritis is common with

A. Black water fever
B. Rhabdomyolysis
C. Tumor lysis syndrome
D. Nonsteroidal anti-inflammatory drugs (NSAIDs) (Correct Answer)

Explanation: ***Nonsteroidal anti-inflammatory drugs (NSAIDs)*** - **NSAIDs** are a known cause of **acute interstitial nephritis** (AIN), an inflammatory condition affecting the tubules and interstitium of the kidney [1]. - This adverse reaction often manifests as **fever**, **rash**, **eosinophilia**, and **acute kidney injury**, typically 7-10 days after drug exposure. *Black water fever* - **Blackwater fever** is a severe complication of **malaria**, characterized by massive hemolysis leading to **hemoglobinuria**, which darkens the urine. - It primarily causes **acute kidney injury** through **acute tubular necrosis** due to hemoglobin precipitation in the renal tubules, not interstitial nephritis. *Rhabdomyolysis* - **Rhabdomyolysis** involves the breakdown of muscle tissue, releasing myoglobin into the bloodstream, which is toxic to the kidneys. [1] - This condition leads to **acute kidney injury** predominantly through **acute tubular necrosis** due to myoglobin casts obstructing tubules and direct toxicity, not interstitial inflammation. *Tumor lysis syndrome* - **Tumor lysis syndrome** occurs when large numbers of cancer cells are rapidly destroyed, releasing intracellular contents like potassium, phosphate, and nucleic acids. - The high concentration of **uric acid** and **phosphate** in the renal tubules leads to crystal formation, causing **acute kidney injury** primarily through **acute uric acid nephropathy** and **phosphate nephropathy**, rather than interstitial nephritis [1].

Question 799: A diabetic patient presents with hyperkalemia and urinary pH < 5.5. What is the MOST likely underlying cause?

A. Uremia
B. Primary hyperaldosteronism
C. Type IV RTA (Correct Answer)
D. Type I Renal tubular acidosis

Explanation: ***Type IV RTA*** - Patients with **diabetes mellitus** frequently develop **hyporeninemic hypoaldosteronism**, leading to Type IV RTA [1]. - This condition is characterized by **hyperkalemia** and **acidosis** with a paradoxically low urinary pH (typically < 5.5). *Uremia* - **Uremia** can cause hyperkalemia and acidosis, but it is a broader term for severe kidney failure and not the most specific underlying cause for the given urinary findings. - While patients with uremia can have aciduria, the combination of **diabetic hyperkalemia** and acid urine points more directly to a specific tubular defect. *Primary hyperaldosteronism* - **Primary hyperaldosteronism** is characterized by **hypertension**, **hypokalemia**, and metabolic alkalosis, which is the opposite of the patient's presentation [1]. - This condition involves excessive aldosterone production, leading to increased potassium excretion [1]. *Type I Renal tubular acidosis* - **Type I RTA** (distal RTA) is characterized by the inability to acidify urine, resulting in a **urinary pH > 5.5** despite systemic acidosis [1]. - While it can cause hypokalemia (due to increased distal K+ secretion) and acidosis, the elevated urinary pH is a key differentiating factor from this patient's presentation [1].

Question 800: Hyperkalemia aciduria is seen in

A. Type I Renal Tubular Acidosis
B. Type IV Renal Tubular Acidosis (Correct Answer)
C. Sigmoidocolostomy procedure
D. Type II Renal Tubular Acidosis

Explanation: Type IV Renal Tubular Acidosis - This condition is characterized by **hyperkalemia** and **aciduria**, often due to a deficiency in aldosterone or a renal tubular insensitivity to aldosterone [1]. - The impaired aldosterone action leads to reduced potassium excretion and decreased ammonium production, both contributing to **hyperkalemia** and metabolic acidosis [1]. *Type I Renal Tubular Acidosis* - Type I RTA (distal RTA) is characterized by a defect in acid secretion in the distal tubule, leading to **hypokalemia** and metabolic acidosis with persistently high urine pH [2]. - Patients typically excrete an alkaline urine despite systemic acidosis, contrasting with the aciduria seen with hyperkalemia [2]. *Sigmoidocolostomy procedure* - A sigmoidocolostomy can lead to **hyperchloremic metabolic acidosis** due to the reabsorption of chloride and excretion of bicarbonate by the colonic mucosa. - However, it typically causes **hypokalemia** as potassium is secreted into the colonic lumen from the blood. *Type II Renal Tubular Acidosis* - Type II RTA (proximal RTA) involves a defect in bicarbonate reabsorption in the proximal tubule, resulting in **hypokalemia** and metabolic acidosis. - The kidney's ability to acidify urine is still largely intact in the distal nephron once the bicarbonate buffer system is overwhelmed.

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Acute Kidney Injury

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Chronic Kidney Disease

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Glomerular Diseases

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Tubulointerstitial Diseases

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Nephrotic and Nephritic Syndromes

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Urinary Tract Infections

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Renal Replacement Therapy

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Fluid and Electrolyte Disorders

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Acid-Base Disorders

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Kidney in Systemic Diseases

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Kidney Stones and Obstructive Uropathy

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Hypertension in Kidney Disease

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Nephrology — MCQs

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