Nephrology — MCQs
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A 55-year-old woman with a history of type 2 diabetes presents for a routine follow-up. Her serum creatinine and potassium levels are normal, but she has microalbuminuria and an HbA1c of 8%. Her blood pressure and pulse are within normal limits, and she is currently on metformin for diabetes management. What should be the next step in her management?
Which factor is most useful for distinguishing Acute Kidney Injury (AKI) from Chronic Kidney Disease (CKD)?
A patient presents with a history of vomiting. Arterial blood gas analysis reveals the following: - pH: 7.5 - pCO₂: 48 mm Hg - HCO₃⁻: 30 mEq/L What is the most likely acid-base abnormality?
In a patient with electric burns and stable vital signs, red-colored urine is observed. What is the most likely finding in the patient's blood work?
Which of the following is not a cause of high anion gap metabolic acidosis?
What is the cause of hyponatremia in diarrhea-induced hypovolemia?
A 60-year-old man with chronic kidney disease presents with complaints of increasing fatigue, dyspnea on exertion, and signs of congestive heart failure. On evaluation, he is found to have anemia. What is the most appropriate next step in management?
A 55-year-old man presents with altered sensorium and deep labored breathing. ABG is given below. What is the most likely acid-base disorder? pH: 7.20 pCO₂: 31 mmHg HCO₃⁻:16 mEq/L Na⁺: 130 mEq/L Cl⁻: 84 mEq/L PaO₂: 80 mmHg
A 68-year-old male with a history of COPD presents to the emergency room with severe dyspnea and altered mental status. An arterial blood gas (ABG) is drawn with the following results: pH: 7.28 PaCO2: 60 mmHg HCO3-: 28 mEq/L Na+: 142 mEq/L Cl-: 100 mEq/L Based on these results, what is the calculated anion gap?
Patient came with severe headache and seizures. Sodium on admission was 98 meq/L. We have started correction with 3 % saline and now after 24 hours of infusion sodium is 110 meq/L. Patient develops mutism and altered sensorium. Which investigation will you perform now?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 621: A 55-year-old woman with a history of type 2 diabetes presents for a routine follow-up. Her serum creatinine and potassium levels are normal, but she has microalbuminuria and an HbA1c of 8%. Her blood pressure and pulse are within normal limits, and she is currently on metformin for diabetes management. What should be the next step in her management?
- A. Start insulin therapy
- B. Stop Metformin and start a different OHA
- C. Begin a thiazide diuretic
- D. Start an ACE inhibitor (Correct Answer)
Explanation: ***Start an ACE inhibitor***- **ACE inhibitors** (or **ARBs**) are the cornerstone of treatment for **microalbuminuria** in patients with **Type 2 Diabetes Mellitus**, regardless of blood pressure, due to their **renoprotective** effects [2].- They are preferred because they reduce **glomerular capillary pressure** and mitigate the progression of early **diabetic nephropathy** (as indicated by microalbuminuria) [2].*Begin a thiazide diuretic*- Thiazide diuretics are primarily indicated for the management of **hypertension** and **edema**.- The patient is currently normotensive, and thiazides do not offer the specific **renoprotective benefits** mediated by **ACE inhibitors** in diabetic kidney disease.*Start insulin therapy*- Although the **HbA1c of 8%** indicates suboptimal glycemic control, initiating **ACE inhibition** is the most critical next step due to the presence of **microalbuminuria**.- Insulin therapy is usually reserved for higher A1c levels (e.g., >10%) or after failure of combination oral/injectable non-insulin therapy [1].*Stop Metformin and start a different OHA*- **Metformin** is the appropriate first-line drug of choice, and given her normal serum creatinine, there is no contraindication to its continuation [1].- The treatment strategy is usually to add a second agent (like the ACE inhibitor for kidney protection, and potentially another **OHA/SGLT-2 inhibitor/GLP-1 RA** for glycemic control) rather than discontinuing Metformin.
Question 622: Which factor is most useful for distinguishing Acute Kidney Injury (AKI) from Chronic Kidney Disease (CKD)?
- A. Blood urea nitrogen (BUN)
- B. Albumin levels (Correct Answer)
- C. Urinary output
- D. Creatinine levels
Explanation: ***Albumin levels (Persistent Albuminuria)*** - The presence of **persistent albuminuria** (albumin excretion in urine >30 mg/24 hours for ≥3 months) is one of the **defining criteria for Chronic Kidney Disease (CKD)** according to KDIGO guidelines [2]. - CKD is diagnosed when either **GFR <60 mL/min/1.73m²** OR **markers of kidney damage** (including albuminuria) persist for **≥3 months** [2]. - AKI typically involves acute tubular necrosis or prerenal azotemia without sustained, chronic albuminuria. While AKI may have transient proteinuria, it does not meet the chronicity criterion. - **Note:** In clinical practice, the **most useful distinguishing factors** are actually **kidney size on ultrasound** (small kidneys in CKD), **duration of elevated creatinine**, and **presence of complications of chronicity** (anemia, renal bone disease). Among the given laboratory markers, persistent albuminuria best indicates chronicity. *Creatinine levels* - Elevated serum **creatinine** reflects reduced GFR and is seen in **both AKI and CKD**. - A **single creatinine value** cannot distinguish between acute and chronic disease [1]. - **Serial measurements** showing trajectory (rapidly rising in AKI vs. chronically stable but elevated in CKD) are helpful, but a single level is not diagnostic [1]. *Urinary output* - Both severe AKI and advanced CKD can present with **oliguria** (<400 mL/day) or **anuria**. - Urinary output reflects current kidney function severity but does not indicate acuity versus chronicity. - **Non-oliguric AKI** is actually common, making urine output an unreliable distinguisher. *Blood urea nitrogen (BUN)* - **BUN** accumulates when GFR decreases and is elevated in **both AKI and CKD**. - A very high **BUN:Creatinine ratio (>20:1)** may suggest **prerenal AKI**, but this is not a reliable distinguisher between acute and chronic kidney disease. - BUN is also affected by non-renal factors (GI bleeding, catabolic states, protein intake).
Question 623: A patient presents with a history of vomiting. Arterial blood gas analysis reveals the following: - pH: 7.5 - pCO₂: 48 mm Hg - HCO₃⁻: 30 mEq/L What is the most likely acid-base abnormality?
- A. Metabolic alkalosis (Correct Answer)
- B. Respiratory acidosis
- C. Respiratory alkalosis
- D. Metabolic acidosis
Explanation: ***Metabolic alkalosis***- The high pH (7.5) indicates **alkalemia**, while the elevated **bicarbonate (HCO₃⁻)** of 30 mEq/L identifies the primary metabolic cause [3].- The mild elevation in **pCO₂ (48 mm Hg)** shows appropriate respiratory compensation via **hypoventilation**, attempting to normalize the pH [1, 2]. *Metabolic acidosis*- Requires a low **HCO₃⁻** level (< 22 mEq/L) and a low pH (< 7.35), directly contradicting the observed **high pH** (7.5) and high HCO₃⁻.- This state often arises from conditions like **lactic acidosis** or **diabetic ketoacidosis**, which are not supported by these blood gas results [4]. *Respiratory acidosis*- While the **pCO₂ is elevated (48 mm Hg)**, if this were the primary disorder, it would drive the pH toward an **acidemic** state (< 7.35), which is inconsistent with the pH of 7.5 [3].- Elevated pCO₂ in the context of alkalemia indicates that the respiratory change is a secondary, **compensatory response** to the primary metabolic alkalosis [1]. *Respiratory alkalosis*- This condition is characterized by a low **pCO₂** (< 35 mm Hg) leading to alkalemia, typically due to **hyperventilation** [1].- This diagnosis is ruled out because the patient’s pCO₂ is significantly elevated (48 mm Hg), not low.
Question 624: In a patient with electric burns and stable vital signs, red-colored urine is observed. What is the most likely finding in the patient's blood work?
- A. Decreased hemoglobin levels
- B. Increased potassium levels (Correct Answer)
- C. Increased creatinine levels
- D. RBCs in urine
Explanation: ***Increased potassium levels***- Electric burns cause extensive muscle breakdown (known as **rhabdomyolysis**), releasing high concentrations of intracellular contents, especially **potassium**.- This release results in **hyperkalemia**, which is the most immediate and life-threatening electrolyte abnormality observed after massive muscle injury. *Increased creatinine levels*- While rhabdomyolysis often leads to **acute kidney injury (AKI)** due to myoglobin deposition [1], causing increased creatinine, hyperkalemia is the earlier and more acutely dangerous serological derangement.- Increased creatinine reflects impaired renal function and usually develops hours to days after the initial injury. *RBCs in urine*- The red color in the urine is primarily due to **myoglobinuria** (free myoglobin released from damaged muscle) and not typically due to **hematuria** (intact red blood cells).- Urine dipstick tests will be positive for blood because myoglobin and hemoglobin are structurally similar, but microscopy shows few or no red blood cells [1]. *Decreased hemoglobin levels*- Decreased hemoglobin (anemia) is usually a consequence of severe hemorrhage, which is not the primary complication of electrical injury causing rhabdomyolysis.- In the acute burn phase, patients often experience fluid shifts that can lead to **hemoconcentration**, potentially resulting in a transient increase in relative hemoglobin levels.
Question 625: Which of the following is not a cause of high anion gap metabolic acidosis?
- A. Ketoacidosis
- B. Acute kidney injury
- C. Toxins
- D. Diarrhea (Correct Answer)
Explanation: Diarrhea causes non-anion gap metabolic acidosis (NAGMA) because the excessive loss of bicarbonate-rich fluid (HCO3-) from the lower GI tract requires the retention of chloride (Cl-) to maintain electrical neutrality, leading to hyperchloremia (HCO3- loss replaced by Cl-) [2]. The resulting acidosis has a normal anion gap because the lost bicarbonate is effectively replaced by another unmeasured ion (chloride), keeping the calculated gap ([Na+] - ([Cl-] + [HCO3-])) within the normal range [1]. Severe acute kidney injury (AKI) causes high anion gap metabolic acidosis (HAGMA) due to the retention of unmeasured organic acids resulting from decreased glomerular filtration rate (GFR) [2]. Ketoacidosis (Diabetic, Alcoholic, Starvation) is a classic cause of high anion gap metabolic acidosis (HAGMA) [3]. The metabolic acidosis results from the overproduction and accumulation of ketone bodies (beta-hydroxybutyrate and acetoacetate), which are unmeasured organic acids [3]. Many toxins, such as Methanol, Ethylene glycol, and high doses of Salicylates, cause high anion gap metabolic acidosis (HAGMA) [1].
Question 626: What is the cause of hyponatremia in diarrhea-induced hypovolemia?
- A. Decreased aldosterone (Correct Answer)
- B. Decreased ADH
- C. Decreased sodium absorption from gastrointestinal tract
- D. Increased sodium absorption from kidney
Explanation: ***Decreased aldosterone*** * In scenarios where salt loss (e.g., due to diarrhea) leads to hypovolemia, a relative or true deficiency of **aldosterone** prevents maximal sodium reabsorption in the distal tubules and collecting ducts. * This failure to maximally conserve sodium leads to **renal salt wasting**, which exacerbates the volume deficit and, when coupled with ADH-mediated water retention, results in hyponatremia. ***Decreased ADH*** * Hypovolemia (volume depletion) is the strongest non-osmotic trigger for the release of **Antidiuretic Hormone (ADH)** from the posterior pituitary, overriding low plasma osmolality [1]. * Therefore, in diarrhea-induced hypovolemia, **ADH levels are actually increased**, which drives powerful free water reabsorption in the kidney, resulting in dilutional hyponatremia [1]. ***Decreased sodium absorption from gastrointestinal tract*** * This is the primary mechanism by which diarrhea causes salt and water loss, leading to the state of **hypovolemia**. * However, the mechanism driving the *hyponatremia* (low plasma sodium concentration) involves the kidney's disproportionate reabsorption of water relative to sodium, mediated by **ADH**. ***Increased sodium absorption from kidney*** * System mechanisms like the Renin-Angiotensin-Aldosterone System (RAAS) are activated by hypovolemia to increase **sodium and water absorption** in an attempt to restore blood volume [2]. * Increased renal sodium absorption is a compensatory mechanism that works against hyponatremia; thus, it is not the cause of low plasma sodium.
Question 627: A 60-year-old man with chronic kidney disease presents with complaints of increasing fatigue, dyspnea on exertion, and signs of congestive heart failure. On evaluation, he is found to have anemia. What is the most appropriate next step in management?
- A. Blood transfusion
- B. Darbepoetin alfa
- C. Intravenous iron infusion (Correct Answer)
- D. Oral iron therapy
Explanation: Intravenous iron infusion - Patients with chronic kidney disease (CKD) and anemia often have associated iron deficiency, which is necessary to correct before starting erythropoiesis-stimulating agents (ESAs). [1] - Intravenous iron is strongly preferred over oral iron in CKD, especially in dialysis patients, due to poor gastrointestinal absorption and high risk of non-compliance. Oral iron therapy - Oral iron is less effective and poorly tolerated in patients with CKD due to altered absorption and potential for gastrointestinal side effects. - It is not the initial treatment of choice when a rapid and efficient iron correction is needed to prepare for ESA therapy. Blood transfusion - This is reserved for patients with symptomatic severe anemia (e.g., severe dyspnea, hemodynamic instability) that is refractory to other treatments or requires immediate intervention. - Transfusion carries risks like volume overload (especially in heart failure) and sensitization, making it unsuitable as a routine initial step. Darbepoetin alfa - Darbepoetin alfa (an ESA) is used to correct the underlying erythropoietin deficiency in CKD-related anemia. [1] - ESAs are typically initiated only after iron stores have been adequately replenished (target ferritin >500 ng/mL or transferrin saturation >30%) to maximize response and minimize dosing.
Question 628: A 55-year-old man presents with altered sensorium and deep labored breathing. ABG is given below. What is the most likely acid-base disorder? pH: 7.20 pCO₂: 31 mmHg HCO₃⁻:16 mEq/L Na⁺: 130 mEq/L Cl⁻: 84 mEq/L PaO₂: 80 mmHg
- A. Respiratory acidosis
- B. Respiratory alkalosis
- C. Metabolic alkalosis
- D. Metabolic acidosis (Correct Answer)
Explanation: ***Metabolic acidosis*** - The **low pH (7.20)** indicates **acidosis** [2]. The primary cause is low **bicarbonate (HCO₃⁻ 16 mEq/L)**, defining it as metabolic acidosis [1]. - This patient presents with **Kussmaul breathing** (deep, labored breathing) as a respiratory attempt to compensate (blowing off CO₂) for the underlying metabolic acidosis, suggested by the low **pCO₂ (31 mmHg)** [1]. *Metabolic alkalosis* - This would be characterized by a **high pH (>7.45)** and a **high HCO₃⁻** level, which is the opposite of the current findings [3]. - Commonly caused by conditions like **vomiting** or excessive intake of **alkali** substances [3]. *Respiratory acidosis* - This requires a **high pCO₂ (>45 mmHg)**, which is the cause of acidemia, typically due to **hypoventilation** or respiratory failure [2]. - The current pCO₂ (31 mmHg) is low, indicating **hyperventilation** (compensation). *Respiratory alkalosis* - This would show a **high pH (>7.45)** caused by a **low pCO₂ (<35 mmHg)** due to **hyperventilation** (e.g., anxiety, high altitude) [2]. - While pCO₂ is low, the pH is acidic (7.20), not alkaline, ruling out primary respiratory alkalosis [2].
Question 629: A 68-year-old male with a history of COPD presents to the emergency room with severe dyspnea and altered mental status. An arterial blood gas (ABG) is drawn with the following results: pH: 7.28 PaCO2: 60 mmHg HCO3-: 28 mEq/L Na+: 142 mEq/L Cl-: 100 mEq/L Based on these results, what is the calculated anion gap?
- A. A. 10 mEq/L
- B. D. 24 mEq/L
- C. C. 18 mEq/L
- D. B. 14 mEq/L (Correct Answer)
Explanation: ***14 mEq/L*** - The **anion gap (AG)** is calculated using the formula: $\text{AG} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$. [1] - Plugging in the patient's values: $142 - (100 + 28) = 142 - 128 = **14 \text{ mEq/L}**$. *10 mEq/L* - This value is below the calculated 14 mEq/L and would be considered low if the normal range upper limit is 12, suggesting a calculation error. [1] - An anion gap of 10 mEq/L is typically a normal value, but it is not the mathematically correct result based on the patient's **serum electrolyte** values. *18 mEq/L* - Obtaining this value would imply that $[\text{Cl}^-] + [\text{HCO}_3^-]$ equaled 124 mEq/L ($142 - 18$), which is incorrect as the sum is **128 mEq/L**. - An anion gap of 18 mEq/L indicates a **High Anion Gap Metabolic Acidosis (HAGMA)**, which is metabolically possible but mathematically inconsistent with the provided electrolyte numbers. [1] *24 mEq/L* - This value is significantly higher than 14 mEq/L and would suggest a severe uncompensated **HAGMA** (e.g., severe ketoacidosis or lactic acidosis). [1] - The calculation based on the given **plasma concentrations** of sodium, chloride, and bicarbonate simply does not support this result.
Question 630: Patient came with severe headache and seizures. Sodium on admission was 98 meq/L. We have started correction with 3 % saline and now after 24 hours of infusion sodium is 110 meq/L. Patient develops mutism and altered sensorium. Which investigation will you perform now?
- A. LP for CSF biochemistry
- B. MRI Head (Correct Answer)
- C. EEG
- D. Brainstem evoked potentials
Explanation: ***MRI Head*** - A rapid correction of **severe chronic hyponatremia** (from 98 to 110 mEq/L in 24 hours, exceeding the recommended limit of 8-10 mEq/L) puts the patient at very high risk for **Osmotic Demyelination Syndrome (ODS)** (previously Central Pontine Myelinolysis). [1] - The new onset of **mutism** and **altered sensorium** are classic, late symptoms of ODS, necessitating an **MRI head** to visualize characteristic **pontine** (and sometimes extrapontine) lesions. *LP for CSF biochemistry* - LP is primarily indicated for diagnosing infections or inflammatory conditions of the CNS, which is less likely given the clear history of electrolyte imbalance and complication following rapid correction. - While CSF analysis can reveal demyelination products, an **MRI** is the definitive, non-invasive imaging modality for diagnosing ODS. *Brainstem evoked potentials* - Brainstem auditory evoked potentials (BAEP) primarily assess the **integrity of the auditory pathways** through the brainstem. [2] - While ODS affects the brainstem, BAEP is not the standard or most sensitive first-line investigation for confirming demyelinating lesions in the pons. *EEG* - EEG measures the electrical activity of the cerebral cortex and is primarily useful for localizing seizure foci or assessing the severity of encephalopathy. [2] - The symptoms (mutism, altered sensorium) point strongly to a structural brainstem lesion (ODS), which is best confirmed by **MRI head**, not EEG.
Practice by Chapter
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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