Nephrology Practice Questions

Q: Which of the following is the most specific and sensitive screening test for renovascular hypertension?

CT Angiography. **Explanation:** Renovascular hypertension (RVH) is the most common cause of secondary hypertension, typically resulting from renal artery stenosis (RAS) due to atherosclerosis or fibromuscular dysplasia [1]. **Why CT Angiography (CTA) is correct:** CTA is currently considered the preferred screening modality for RVH because it offers high sensitivity (94-98%) and specificity (90-94%). It provides excellent anatomical visualization of the renal arteries, accessory arteries, and the degree of stenosis [1]. With multi-detector rows, it can reconstruct 3D images that are nearly comparable to the "gold standard" invasive digital subtraction angiography (DSA). **Analysis of Incorrect Options:** * **HRCT:** High-Resolution CT is used primarily for lung parenchyma evaluation; it does not involve the contrast enhancement necessary to visualize vascular structures. * **Captopril Radionucleotide Scan:** Once a popular screening tool, its utility has declined due to low sensitivity in patients with bilateral disease or renal insufficiency. It is a functional test, not an anatomical one [1]. * **Doppler Ultrasound:** While non-invasive and cost-effective, it is highly operator-dependent and technically difficult in obese patients or those with overlying bowel gas [2]. It is often the *initial* test but is less sensitive than CTA. **Clinical Pearls for NEET-PG:** * **Gold Standard:** Invasive Digital Subtraction Angiography (DSA) remains the definitive "gold standard" for diagnosis and planning intervention. * **MRA (Magnetic Resonance Angiography):** An alternative to CTA, especially when avoiding ionizing radiation, but contraindicated in patients with metallic implants or severe renal failure due to the risk of Nephrogenic Systemic Fibrosis [3]. * **Screening Choice:** In patients with renal failure (CrCl <30 ml/min), Doppler is preferred over CTA/MRA to avoid contrast-induced nephropathy.

Q: A patient with chronic kidney disease presents with severe anemia. Laboratory tests reveal normocytic, normochromic anemia. What is the most appropriate treatment to manage this patient's anemia?

Darbepoetin alfa. ***Darbepoetin alfa*** - Anemia in **Chronic Kidney Disease (CKD)** is predominantly caused by decreased production of **erythropoietin** by the failing kidneys, resulting in normocytic, normochromic anemia [1] - **Darbepoetin alfa** is a long-acting **Erythropoiesis-Stimulating Agent (ESA)** that replaces the deficient hormone, directly correcting the underlying cause of anemia in CKD - This is the **standard of care** for managing anemia in CKD patients with normocytic, normochromic presentation *Folic acid supplementation* - Indicated for **megaloblastic anemia** due to **folate deficiency**, which presents as macrocytic anemia (high MCV) [2] - Does not stimulate red blood cell production directly and is ineffective against the primary defect of **erythropoietin deficiency** in CKD - The patient's normocytic anemia excludes folate deficiency [2] *Vitamin B12 injection* - Standard treatment for Vitamin B12 deficiency (e.g., **pernicious anemia**), which causes macrocytic, megaloblastic anemia [2] - The patient presents with **normocytic** anemia, indicating the deficiency is not related to B12 or folate metabolism - No indication for B12 supplementation in this clinical scenario *Iron chelation therapy* - **Iron chelation** is used to treat severe **iron overload** (hemochromatosis) or toxicity, not to treat anemia - Patients with CKD-related anemia often require supplemental **iron** to enhance their response to ESAs like Darbepoetin alfa - Using chelation would be counterproductive and worsen the anemia

Q: A patient after RTA had a renal shut down. Work-up shows: FeNa: $< 1\%$ , Urine osmolality: 300 mOsm/kg, Urinary sodium: 40 mEq/L. Most likely diagnosis?

Pre-renal AKI. Correct: Pre-renal AKI - **FeNa 500), and urinary sodium (40 mEq/L) is at the borderline, **FeNa remains the gold standard** differentiating parameter *Incorrect: Acute Tubular Necrosis (Renal AKI)* - ATN would show **FeNa >2%** due to tubular dysfunction and inability to reabsorb sodium [1] - Urinary sodium would typically be **>40 mEq/L** (here it's exactly 40, borderline) - Urine osmolality would be ** 2%, not <1% [1] *Incorrect: Post-renal AKI* - Implies obstruction (bladder, ureter, urethra) - Not suggested by the clinical scenario of post-trauma renal shutdown - Laboratory parameters don't help differentiate obstruction; needs imaging **Key Teaching Point:** When laboratory values seem mixed, **FeNa <1% is the most reliable indicator of pre-renal azotemia**, especially in trauma settings with likely hypovolemia.

Q: A patient with road traffic accident (RTA) is passing red color urine due to myoglobinuria. Which of the following will most likely be seen in this patient?

Hyperkalemia. ***Hyperkalemia***- Rhabdomyolysis involves massive breakdown of muscle cells, leading to the rapid release of intracellular contents, primarily **potassium (K+)**, into the circulation [1].- The associated **acute kidney injury (AKI)**, caused by myoglobin toxicity and sludge formation in the renal tubules, severely impairs K+ excretion, thus exacerbating the **hyperkalemia** [1].*Hypernatremia*- This condition is typically associated with states of significant **free water deficit** or inadequate fluid intake, not the massive tissue injury seen in rhabdomyolysis.- Fluid management of trauma patients often involves isotonic fluids, which are unlikely to cause severe dehydration leading to **hypernatremia**.*Hyponatremia*- While aggressive hydration with hypotonic fluids during resuscitation *could* potentially cause dilutional hyponatremia, the direct metabolic consequence of rhabdomyolysis is not primarily a state of **low serum sodium**.- Severe trauma leading to rhabdomyolysis is often associated with the release of ADH due to volume depletion, but this is less characteristic than the rapid rise in potassium.*Hypokalemia*- Hypokalemia, or low serum potassium, is the opposite of the predictable metabolic consequence of rhabdomyolysis.- Muscle cell death releases K+, making **hypokalemia** extremely unlikely in the acute setting of severe muscle injury and subsequent AKI.

Q: 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?

Start an ACE inhibitor. ***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.

Q: 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?

Metabolic alkalosis. ***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.

Q: Which electrolyte abnormality will lead to cardiac arrhythmia in patients with severe vomiting?

Hypokalemia. ***Hypokalemia*** - Severe vomiting leads to significant loss of gastric acid and subsequent volume depletion, often resulting in **metabolic alkalosis** and substantial **potassium** loss (due to renal compensation and direct GI loss) [1]. - **Hypokalemia** directly affects cardiac muscle repolarization, predisposing the patient to various arrhythmias, including **ventricular tachycardia** (e.g., *Torsades de pointes*) [2], [3]. *Hyponatremia* - While severe vomiting can cause hyponatremia (due to volume loss and inappropriate ADH release), symptomatic effects are primarily **neurological** (e.g., seizures, confusion), not typically cardiac arrhythmias [2]. - The effect on the heart tends to be mild unless the drop is very rapid and severe; it primarily influences **myocardial contractility** through fluid shifts [2]. *Hyperkalemia* - Hyperkalemia causes severe and characteristic ECG changes (tall, peaked T waves, broadened QRS, possible asystole), but it is **not associated** with severe vomiting, which typically causes **hypokalemia** [2]. - Hyperkalemia is more commonly seen in conditions like **renal failure** or acidosis [4]. *Hypocalcemia* - Hypocalcemia primarily affects the heart by causing **prolongation of the QT interval**, which can increase the risk of *Torsades de pointes*, similar to hypokalemia. - However, calcium losses from simple gastric vomiting are generally **not as dramatic** or primary as the potassium losses, making hypokalemia the most direct and common cause of arrhythmia in this specific clinical scenario [1].

Q: 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?

Increased potassium levels. ***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.

Q: Which of the following is not a cause of high anion gap metabolic acidosis?

Diarrhea. 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 1

Which of the following is the most specific and sensitive screening test for renovascular hypertension?

Accepted Answer

CT Angiography

Answer

HRCT

Answer

Captopril enhanced radionucleotide scan

Answer

Doppler ultrasound of renal arteries

Question 2

A patient with chronic kidney disease presents with severe anemia. Laboratory tests reveal normocytic, normochromic anemia. What is the most appropriate treatment to manage this patient's anemia?

Accepted Answer

Darbepoetin alfa

Answer

Vitamin B12 injection

Answer

Folic acid supplementation

Answer

Iron chelation therapy

Question 3

A patient after RTA had a renal shut down. Work-up shows: FeNa: $< 1\%$ , Urine osmolality: 300 mOsm/kg, Urinary sodium: 40 mEq/L. Most likely diagnosis?

Accepted Answer

Pre-renal AKI

Answer

Renal AKI

Answer

Acute Tubular Necrosis

Answer

Post-renal AKI

Question 4

A patient with road traffic accident (RTA) is passing red color urine due to myoglobinuria. Which of the following will most likely be seen in this patient?

Accepted Answer

Hyperkalemia

Answer

Hypokalemia

Answer

Hyponatremia

Answer

Hypernatremia

Question 5

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?

Accepted Answer

Start an ACE inhibitor

Answer

Start insulin therapy

Answer

Stop Metformin and start a different OHA

Answer

Begin a thiazide diuretic

Question 6

Which factor is most useful for distinguishing Acute Kidney Injury (AKI) from Chronic Kidney Disease (CKD)?

Accepted Answer

Albumin levels

Answer

Blood urea nitrogen (BUN)

Answer

Urinary output

Answer

Creatinine levels

Question 7

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?

Accepted Answer

Metabolic alkalosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Answer

Metabolic acidosis

Question 8

Which electrolyte abnormality will lead to cardiac arrhythmia in patients with severe vomiting?

Accepted Answer

Hypokalemia

Answer

Hyponatremia

Answer

Hyperkalemia

Answer

Hypocalcemia

Question 9

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?

Accepted Answer

Increased potassium levels

Answer

Decreased hemoglobin levels

Answer

Increased creatinine levels

Answer

RBCs in urine

Question 10

Which of the following is not a cause of high anion gap metabolic acidosis?

Accepted Answer

Diarrhea

Answer

Ketoacidosis

Answer

Acute kidney injury

Answer

Toxins

Nephrology — MCQs

Nephrology — MCQs

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