Nephrology Practice Questions

Q: All of the following are used for the management of hyperkalemia except?

Beta 2 antagonist. ### Explanation The management of hyperkalemia focuses on three goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing potassium from the body. **Why "Beta 2 antagonist" is the correct answer:** Beta-2 receptors play a crucial role in potassium homeostasis by stimulating the Na+/K+-ATPase pump, which drives potassium into the intracellular compartment [1]. Therefore, **Beta-2 agonists** (like Salbutamol) are used to treat hyperkalemia. A Beta-2 **antagonist** (blocker) would prevent this shift and could potentially worsen hyperkalemia; thus, it has no role in its management. **Analysis of Incorrect Options:** * **Calcium gluconate:** This is the first-line treatment for hyperkalemia with ECG changes. It does not lower serum potassium levels but **stabilizes the myocardial membrane** by antagonizing the membrane-excitability effects of potassium [1], preventing life-threatening arrhythmias. * **Insulin plus dextrose:** Insulin is a potent stimulator of the Na+/K+-ATPase pump, causing an **intracellular shift** of potassium. Dextrose is co-administered to prevent hypoglycemia. * **Dialysis:** This is the most definitive method for **potassium removal** from the body, especially in patients with renal failure or refractory hyperkalemia. **NEET-PG High-Yield Pearls:** 1. **"C Big K" Mnemonic:** **C**alcium gluconate (Stabilize), **B**icarbonate/Beta-agonists (Shift), **I**nsulin (Shift), **G**lucose, **K**ayexalate/Kidney dialysis (Remove). 2. **Calcium gluconate vs. Calcium chloride:** Calcium gluconate is preferred via peripheral lines as it is less caustic than calcium chloride. 3. **ECG Changes:** The earliest sign is **Tall Tented T-waves**, followed by PR prolongation, loss of P-wave, and eventually a **Sine wave pattern**.

Q: A 12-year-old girl complains of headaches and blurred vision. She has a history of high blood pressure but is not currently taking medication. Her blood pressure is 160/95 mm Hg and pulse is 95 per minute. Funduscopic examination reveals small retinal microaneurysms and cotton-like zones of retinal edema and necrosis. She is hospitalized for further evaluation. Renal arteriography shows segmental stenoses forming multiple ridges that project into the lumen. What is the most likely cause of secondary hypertension in this young patient?

Fibromuscular dysplasia. **Explanation:** The patient presents with **secondary hypertension** and hypertensive retinopathy (cotton-wool spots and microaneurysms) at a young age. The definitive clue lies in the renal arteriography, which shows "segmental stenoses forming multiple ridges," classically described as the **"string of beads" appearance**. **1. Why Fibromuscular Dysplasia (FMD) is correct:** FMD is a non-inflammatory, non-atherosclerotic vascular disease that leads to stenosis of medium-sized arteries. It most commonly affects the **renal arteries** (causing renovascular hypertension via the Renin-Angiotensin-Aldosterone System) and the internal carotid arteries. It is most prevalent in **young females**. The "string of beads" occurs due to areas of medial fibroplasia alternating with aneurysmal dilation. **2. Why other options are incorrect:** * **Buerger Disease (Thromboangiitis obliterans):** An inflammatory vasculitis strongly associated with **heavy smoking**. It typically affects small-to-medium vessels of the extremities, leading to gangrene, not renal-induced hypertension. * **Giant Cell Arteritis:** A large-vessel vasculitis that occurs almost exclusively in patients **over age 50**. It presents with jaw claudication, scalp tenderness, and a high ESR. * **Kawasaki Disease:** An acute febrile vasculitis of childhood. While it affects medium-sized vessels, its hallmark is **coronary artery aneurysms**, not renal artery stenosis leading to chronic hypertension. **NEET-PG High-Yield Pearls:** * **FMD Pathophysiology:** Most common type is **Medial Fibroplasia** (85%). * **Ocular Link:** Severe hypertension from FMD can lead to **Grade IV Hypertensive Retinopathy** (Elschnig spots, Siegrist streaks, and macular stars). * **Diagnosis:** Digital Subtraction Angiography (DSA) is the gold standard, showing the "string of beads." * **Treatment:** Percutaneous transluminal angioplasty (PTA) is often the preferred intervention.

Q: All are true for acute nephritic syndrome EXCEPT:

WBC cast in urine. Acute Nephritic Syndrome is a clinical syndrome characterized by the sudden onset of hematuria, proteinuria, hypertension, and edema, typically following an inflammatory process in the glomeruli. [1] **Why "WBC cast in urine" is the correct answer (the exception):** WBC casts are the hallmark of **Acute Pyelonephritis** or **Acute Tubulointerstitial Nephritis**. In Acute Nephritic Syndrome, the characteristic finding is **RBC casts** (dysmorphic RBCs), which indicate glomerular bleeding. While a few WBCs may be present due to inflammation, the presence of WBC casts specifically points toward an infectious or interstitial etiology rather than a primary nephritic process. **Analysis of other options:** * **Hypoproteinemia:** In nephritic syndrome, glomerular damage leads to proteinuria. While not as massive as in nephrotic syndrome, it can still lead to a decrease in serum albumin levels. * **Edema:** This is a cardinal feature caused by two mechanisms: salt and water retention (due to decreased GFR) and decreased oncotic pressure from proteinuria. [1] * **Hypertension:** This occurs due to fluid overload and the activation of the Renin-Angiotensin-Aldosterone System (RAAS) resulting from impaired sodium excretion. [1] **NEET-PG High-Yield Pearls:** * **Classic Triad of Nephritic Syndrome:** Hematuria (Cola-colored urine), Hypertension, and Edema. [1] * **Most common cause:** Post-Streptococcal Glomerulonephritis (PSGN). [1] * **Differentiating Casts:** * **RBC Casts:** Glomerulonephritis (Nephritic Syndrome). * **WBC Casts:** Pyelonephritis / Interstitial Nephritis. * **Fatty Casts ("Maltese Cross"):** Nephrotic Syndrome. * **Muddy Brown Casts:** Acute Tubular Necrosis (ATN). * **Waxy/Broad Casts:** Chronic Renal Failure.

Q: Rhabdomyolysis is characterized by:

Increased K+. **Explanation:** Rhabdomyolysis involves the rapid breakdown of skeletal muscle, leading to the release of intracellular contents into the systemic circulation. **1. Why Increased K+ is Correct:** Potassium is the primary intracellular cation [1]. When muscle cell membranes (sarcolemma) are damaged, massive amounts of **Potassium (K+)** are released into the extracellular space, leading to life-threatening **hyperkalemia**. This is often the most immediate and dangerous electrolyte derangement in rhabdomyolysis, potentially causing cardiac arrhythmias. **2. Analysis of Incorrect Options:** * **Proximal muscle weakness (A):** While muscle weakness occurs, it is typically **generalized or localized** to the affected muscle groups (often associated with pain and swelling) rather than a specific "proximal" distribution, which is more characteristic of inflammatory myopathies like dermatomyositis. * **Increased Mg++ (B):** While magnesium is intracellular, hypermagnesemia is less clinically hallmark than hyperkalemia and hyperphosphatemia in this condition. * **Increased Ca++ (C):** In the acute phase, rhabdomyolysis typically causes **Hypocalcemia**. This occurs because calcium enters the damaged muscle cells and deposits as calcium phosphate. Hypercalcemia may only occur later during the recovery phase as calcium is remobilized from the muscles. **3. NEET-PG High-Yield Pearls:** * **Classic Triad:** Muscle pain, weakness, and dark (tea-colored) urine. * **Diagnostic Gold Standard:** Serum **Creatine Kinase (CK)** levels (typically >5 times the upper limit of normal). * **Renal Impact:** Myoglobinuria leads to Acute Tubular Necrosis (ATN). On urinalysis, a **positive dipstick for blood but absence of RBCs** on microscopy suggests myoglobinuria. * **Electrolyte "Rule of Up":** Increased K+, Increased Phosphate, Increased Uric acid, and Increased Creatinine. The "Rule of Down" applies to Calcium (initially).

Q: A 65-year-old man has urine output of 10 mL/h following abdominal aortic aneurysmectomy. Acute tubular necrosis is suggested by the presence of which of the following?

Urine sodium of more than 40 mEq/L. **Explanation:** The clinical scenario describes oliguria following major surgery [1], suggesting a transition from **Prerenal Azotemia** (due to hypovolemia or cross-clamping of the aorta) to **Intrinsic Acute Kidney Injury (Acute Tubular Necrosis - ATN)**. **Why Option B is Correct:** In ATN, the tubular epithelial cells are damaged and lose their ability to reabsorb sodium and concentrate urine. Consequently, a large amount of sodium is "wasted" in the urine. A **Urine Sodium >40 mEq/L** is a hallmark of ATN, indicating tubular dysfunction. **Why the Other Options are Incorrect:** * **Option A (Urine Osmolality >500 mOsm/kg):** This indicates intact tubular concentrating ability, characteristic of **Prerenal Azotemia**. In ATN, the urine is iso-osmolar with plasma (typically 2%**. * **Option D (BUN:SCr Ratio >20):** A high ratio (>20:1) is seen in **Prerenal Azotemia** due to increased urea reabsorption in the proximal tubule alongside water. In ATN, the ratio is typically normal (**10-15:1**) because both BUN and Creatinine are handled similarly by the damaged tubules. **High-Yield Clinical Pearls for NEET-PG:** * **Microscopy:** Look for **"Muddy Brown" granular casts** or renal tubular epithelial cell casts in ATN. * **Exception to FE_Na:** FE_Na can be <1% in certain types of ATN, such as those induced by **contrast media, rhabdomyolysis, or sepsis**. * **Urine Specific Gravity:** In ATN, it is fixed at **1.010** (isosthenuria), reflecting the loss of concentrating capacity.

Q: Which of the following is NOT true regarding idiopathic edema of women?

It is due to estrogen-mediated sodium retention.. **Explanation:** **Idiopathic Edema** is a clinical syndrome characterized by periodic swelling, primarily affecting women in their childbearing years. **1. Why Option A is the Correct Answer (The False Statement):** Contrary to common belief, idiopathic edema is **not** primarily caused by estrogen-mediated sodium retention. While estrogen can influence fluid balance, the hallmark pathophysiology involves an **exaggerated orthostatic response**. When the patient stands, there is an abnormal increase in capillary permeability and excessive pooling of fluid in the lower extremities, leading to a significant decrease in effective arterial blood volume. This triggers the Renin-Angiotensin-Aldosterone System (RAAS) and ADH, causing secondary sodium and water retention. **2. Analysis of Other Options:** * **Option B:** It is **not related to the menstrual cycle**. This distinguishes it from premenstrual edema, which occurs specifically during the luteal phase. Idiopathic edema occurs throughout the month. * **Option C:** There is **increased water retention in the upright position**. Patients often demonstrate a weight gain of >0.7–1.4 kg from morning to evening due to orthostatic fluid sequestration. * **Option D:** **ACE inhibitors** can be useful because they block the secondary hyperaldosteronism (RAAS activation) triggered by standing. **Clinical Pearls for NEET-PG:** * **Diuretic Abuse:** Many patients develop "diuretic-induced edema." Chronic use of diuretics leads to chronic volume depletion, which causes permanent RAAS activation. When the diuretic is stopped, massive rebound edema occurs. * **Diagnosis:** Confirmed by the **"Weight-Gain Test"** (comparing morning and evening weights). * **Management:** Reduce salt intake, avoid prolonged standing, use compression stockings, and avoid the overuse of diuretics. Spironolactone or ACE inhibitors are preferred over loop diuretics.

Q: What is the complication of the diuretic phase of acute renal failure?

Increased sodium excretion in urine. ### Explanation In the recovery phase of Acute Kidney Injury (AKI), specifically the **diuretic phase**, the kidneys regain their ability to filter blood before they regain the ability to concentrate urine or reabsorb electrolytes effectively. **Why Option C is Correct:** During this phase, the glomerular filtration rate (GFR) begins to normalize, but the newly regenerated tubular epithelial cells are still immature and lack full resorptive capacity [1]. This leads to an "osmotic diuresis" driven by the high levels of accumulated urea and a failure of the tubules to reabsorb sodium [4]. Consequently, there is a massive loss of water and **increased sodium excretion in the urine**, which can lead to profound dehydration and hyponatremia [2]. **Analysis of Incorrect Options:** * **A. Convulsion:** While severe electrolyte imbalances can cause seizures, they are more commonly associated with the uremic state of the *oliguric phase* or rapid shifts during dialysis (Dialysis Disequilibrium Syndrome) [3]. * **B. Hyperkalemia:** This is a hallmark of the *oliguric phase*. In the diuretic phase, the primary risk is actually **hypokalemia** due to excessive potassium loss in the urine. * **D. Metabolic Alkalosis:** AKI typically presents with High Anion Gap Metabolic Acidosis (HAGMA) [3]. While recovery occurs, metabolic alkalosis is not a standard complication of the diuretic phase unless there is external intervention (like excessive bicarbonate therapy). **High-Yield Clinical Pearls for NEET-PG:** * **Diuretic Phase Risk:** The most common cause of death in this phase is **hypokalemia** and secondary infections. * **Urine Output:** Can reach 4–5 Liters/day. * **Sequence of Recovery:** GFR recovers first $\rightarrow$ Tubular function (concentration/dilution) recovers last. * **Management:** Meticulous fluid and electrolyte replacement (especially $K^+$ and $Na^+$) is critical during this transition [1].

Question 1

All of the following are used for the management of hyperkalemia except?

Accepted Answer

Beta 2 antagonist

Answer

Calcium gluconate

Answer

Insulin plus dextrose

Answer

Dialysis

Question 2

Hypokalemia causes the following except?

Accepted Answer

Paralytic ileus

Answer

Tetany

Answer

Orthostatic hypotension

Answer

Rhabdomyolysis

Question 3

A 12-year-old girl complains of headaches and blurred vision. She has a history of high blood pressure but is not currently taking medication. Her blood pressure is 160/95 mm Hg and pulse is 95 per minute. Funduscopic examination reveals small retinal microaneurysms and cotton-like zones of retinal edema and necrosis. She is hospitalized for further evaluation. Renal arteriography shows segmental stenoses forming multiple ridges that project into the lumen. What is the most likely cause of secondary hypertension in this young patient?

Accepted Answer

Fibromuscular dysplasia

Answer

Buerger disease

Answer

Giant cell arteritis

Answer

Kawasaki disease

Question 4

All are true for acute nephritic syndrome EXCEPT:

Accepted Answer

WBC cast in urine

Answer

Hypoproteinemia

Answer

Edema

Answer

Hypertension

Question 5

Hyperkalemia is a feature of which of the following conditions?

Accepted Answer

Pseudohypoaldosteronism type 2

Answer

Conn's syndrome

Answer

Gitelman's syndrome

Answer

Liddle syndrome

Question 6

Rhabdomyolysis is characterized by:

Accepted Answer

Increased K+

Answer

Proximal muscle weakness

Answer

Increased Mg++

Answer

Increased Ca++

Question 7

Which of the following is true about sepsis-related acute kidney injury?

Accepted Answer

Tubular injury is manifested by tubular debris and casts in urine.

Answer

AKI is seen in 20% of severe sepsis cases.

Answer

Overt hypotension is the cause of decreased GFR.

Answer

Generalized arterial vasoconstriction is present.

Question 8

A 65-year-old man has urine output of 10 mL/h following abdominal aortic aneurysmectomy. Acute tubular necrosis is suggested by the presence of which of the following?

Accepted Answer

Urine sodium of more than 40 mEq/L

Answer

Urine osmolality of more than 500 mOsm/kg

Answer

Fractional excretion of sodium of <1%

Answer

Blood urea nitrogen (BUN)-to-serum creatinine ratio (SCR) of more than 20

Question 9

Which of the following is NOT true regarding idiopathic edema of women?

Accepted Answer

It is due to estrogen-mediated sodium retention.

Answer

It is not related to the menstrual cycle.

Answer

There is increased water retention in the upright position.

Answer

ACE inhibitors can be useful in some cases.

Question 10

What is the complication of the diuretic phase of acute renal failure?

Accepted Answer

Increased sodium excretion in urine

Answer

Convulsion

Answer

Hyperkalemia

Answer

Metabolic Alkalosis

Nephrology — MCQs

Nephrology — MCQs

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