Nephrology Practice Questions

Q: Which one of the following is not a feature of adult polycystic kidney disease?

Massive proteinuria. **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD) is primarily a **tubulointerstitial disorder**, not a primary glomerular disease. Therefore, while mild to moderate proteinuria (usually 3.5 g/day or nephrotic range) is not a feature** of ADPKD. If present, it suggests a superimposed glomerular pathology. **Analysis of Options:** * **Hypertension (Option A):** This is the most common early manifestation (seen in 70-80% of patients). It results from intrarenal ischemia caused by cyst expansion, which triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. * **Intermittent Renal Colic (Option B):** This occurs frequently due to the passage of blood clots (following cyst rupture) or the high incidence of **nephrolithiasis** (calcium oxalate stones) seen in these patients [1]. * **Macroscopic Haematuria (Option C):** A classic feature often precipitated by minor trauma or strenuous exercise [1]. It occurs when a cyst ruptures into the renal collecting system. **High-Yield Clinical Pearls for NEET-PG:** 1. **Extra-renal Manifestations:** The most common is **Liver cysts** (Polycystic Liver Disease). The most serious is **Berry Aneurysms** (Circle of Willis), which can lead to Subarachnoid Hemorrhage (SAH). 2. **Genetics:** Most cases (85%) are due to **PKD1** mutation (Chromosome 16), which progresses to ESRD faster than **PKD2** (Chromosome 4) [1]. 3. **Diagnosis:** Ultrasonography is the screening modality of choice (Ravine’s criteria). 4. **Treatment:** Tolvaptan (V2-receptor antagonist) is used to slow cyst growth and disease progression.

Q: Hyperkalemia without ECG changes may be treated with all of the following except?

Calcium gluconate. ### Explanation The management of hyperkalemia is divided into three strategies: stabilizing the cardiac membrane, shifting potassium into cells, and removing potassium from the body [1]. **1. Why Calcium Gluconate is the Correct Answer:** Calcium gluconate (or calcium chloride) is used specifically to **stabilize the myocardial membrane** against the toxic effects of high potassium. It does not lower the serum potassium levels [1]. In clinical practice, calcium is indicated only when there are **ECG changes** (e.g., peaked T-waves, widened QRS) or severe hyperkalemia (>6.5 mEq/L). If a patient has hyperkalemia **without** ECG changes, calcium gluconate is not indicated as there is no immediate cardiac instability to counteract [1]. **2. Analysis of Incorrect Options (Potassium-Shifting Agents):** These agents are used to lower serum potassium levels by shifting it from the extracellular to the intracellular compartment [2]: * **Insulin with Dextrose:** The most reliable method to shift potassium into cells via the Na+/K+-ATPase pump. * **Salbutamol (Beta-2 Agonists):** Stimulates the Na+/K+-ATPase pump to promote intracellular potassium uptake. * **Sodium Bicarbonate:** Useful primarily in patients with concomitant metabolic acidosis; it shifts potassium into cells in exchange for hydrogen ions [2]. **3. NEET-PG High-Yield Pearls:** * **First-line for ECG changes:** Calcium gluconate (acts within 1–3 minutes; duration 30–60 mins) [1]. * **Most definitive treatment:** Hemodialysis (removes potassium from the body). * **Potassium removal agents:** Loop diuretics (Furosemide), Cation exchange resins (Patiromer, Sodium polystyrene sulfonate). * **"Pseudohyperkalemia":** Always rule this out (caused by hemolysis during blood draw or thrombocytosis) before aggressive treatment if the patient is asymptomatic with a normal ECG.

Q: The finding of urine sodium concentration <20 mmol/L in hypovolemic hyponatremia implies:

Trauma. The core concept in evaluating hyponatremia is determining the **effective arterial blood volume (EABV)** and the kidney's response to it. [1], [2] **1. Why Trauma is correct:** In hypovolemic hyponatremia, the body has lost both water and sodium. If the loss is **extra-renal** (e.g., trauma with hemorrhage, burns, vomiting, or diarrhea), the kidneys function normally to compensate for the volume depletion. [2] The activation of the Renin-Angiotensin-Aldosterone System (RAAS) leads to maximal sodium reabsorption in the tubules to preserve volume. [3] Consequently, the **Urinary Sodium (UNa) drops to <20 mmol/L**. [2] In the context of trauma, blood loss or "third-spacing" triggers this intense renal sodium conservation. **2. Why other options are incorrect:** * **Salt-wasting nephropathy (A), Diuretic therapy (B), and Hypoaldosteronism (C):** These are all causes of **renal** sodium loss. [2] In these conditions, the defect lies within the kidney or the hormonal control of the kidney (lack of aldosterone). Despite being hypovolemic, the kidney cannot "hold onto" sodium, resulting in a **Urinary Sodium >20 mmol/L**. [2] **High-Yield Clinical Pearls for NEET-PG:** * **UNa 20 mmol/L:** Suggests renal losses (Diuretics, ACE inhibitors, Mineralocorticoid deficiency, or intrinsic renal disease). [2] * **Fractional Excretion of Sodium (FeNa):** In oliguric states, FeNa 2% suggests intrinsic renal damage (ATN). * **The "Rule of Thumb":** If the source of fluid loss is *not* the kidney, the UNa should be low. If the source of loss *is* the kidney, the UNa will be high. [2]

Q: A 30-year-old male with NIDDM has a blood pressure of 150/90 mmHg and persistent albuminuria in traces on urine examination. What is the most appropriate line of treatment?

Administering lisinopril and restricting sodium intake. ### Explanation **1. Why Option C is Correct:** The patient presents with **Diabetic Nephropathy (DN)**, characterized by persistent albuminuria and hypertension (150/90 mmHg). In patients with diabetes and albuminuria, the standard of care is the initiation of an **ACE inhibitor (e.g., Lisinopril)** or an ARB [1]. * **Mechanism:** ACE inhibitors reduce intraglomerular pressure by causing vasodilation of the **efferent arteriole**. This slows the progression of renal damage and reduces proteinuria [1]. * **Sodium Restriction:** Reducing salt intake is essential as it enhances the antiproteinuric and antihypertensive effects of ACE inhibitors. **2. Why Other Options are Incorrect:** * **Option A & B:** These are passive approaches. Diabetic nephropathy is a progressive condition [2]; "watchful waiting" allows irreversible glomerular scarring (Kimmelstiel-Wilson lesions) to occur [2]. Early intervention is mandatory to prevent progression to End-Stage Renal Disease (ESRD) [1]. * **Option D:** While sodium restriction is beneficial, it is insufficient as a monotherapy. It does not address the hemodynamic changes (efferent vasoconstriction) driven by the Renin-Angiotensin-Aldosterone System (RAAS) in diabetic kidneys. **3. Clinical Pearls for NEET-PG:** * **Earliest Sign:** Microalbuminuria (30–300 mg/day) is the earliest clinical sign of DN [3]. * **Target BP:** For diabetic patients with proteinuria, the target BP is generally **<130/80 mmHg**. * **Drug of Choice:** ACE inhibitors/ARBs are the first-line agents regardless of baseline BP if albuminuria is present [1]. * **Screening:** Type 1 DM patients should be screened 5 years after diagnosis; Type 2 DM patients should be screened **at the time of diagnosis** [3]. * **Contraindication:** Never combine ACE inhibitors and ARBs due to the risk of hyperkalemia and acute kidney injury.

Q: Painless haematuria is found in all of the following conditions EXCEPT:

Cystitis. **Explanation:** The clinical distinction between painful and painless haematuria is a high-yield concept in NEET-PG nephrology. **Why Cystitis is the correct answer:** Cystitis (inflammation of the bladder, usually due to infection) is classically associated with **painful haematuria**. The inflammatory process irritates the bladder mucosa and trigone, leading to symptoms of dysuria, urgency, and suprapubic pain. In contrast, the question asks for conditions that present with *painless* haematuria. [1] **Analysis of Incorrect Options:** * **Renal Carcinoma (RCC):** Classically presents with "painless total haematuria." While the classic triad includes flank pain and a mass, the bleeding itself is typically painless unless clots cause ureteric colic. * **Chronic Glomerulonephritis:** Glomerular bleeding is typically painless [1]. It is often microscopic but can be macroscopic (smoky/cola-colored urine) without associated physical pain [2]. * **Polycystic Kidney Disease (ADPKD):** While cyst rupture can cause acute pain, ADPKD frequently presents with bouts of asymptomatic, painless gross haematuria due to the stretching of overlying vessels. **Clinical Pearls for NEET-PG:** 1. **Rule of Thumb:** Painless gross haematuria in an elderly patient is **Malignancy** (RCC or Bladder Cancer) until proven otherwise. 2. **Painful Haematuria Causes:** Think "Stones and Infections" (Urolithiasis, Cystitis, Urethritis) [1]. 3. **Glomerular vs. Post-Glomerular:** Look for dysmorphic RBCs or RBC casts to confirm a glomerular source (like GN), which is almost always painless [2]. 4. **IgA Nephropathy:** The most common cause of recurrent painless macroscopic haematuria synpharyngitically (coinciding with URTI).

Q: Metabolic alkalosis is seen in all of the following conditions except:

Uretero-sigmoidostomy. **Explanation:** The correct answer is **Uretero-sigmoidostomy**, as it typically results in **Hyperchloremic Metabolic Acidosis**, not alkalosis. **1. Why Uretero-sigmoidostomy causes Acidosis:** In this surgical procedure, the ureters are diverted into the sigmoid colon. The colonic mucosa is exposed to urine, leading to the active reabsorption of chloride (Cl⁻) in exchange for bicarbonate (HCO₃⁻) secretion into the bowel. This loss of bicarbonate results in a **Normal Anion Gap Metabolic Acidosis (NAGMA)**. **2. Analysis of Incorrect Options (Causes of Metabolic Alkalosis):** * **Prolonged Vomiting:** Leads to the loss of gastric HCl (hydrogen and chloride ions). The loss of H⁺ directly causes alkalosis, while the loss of Cl⁻ leads to "Chloride-responsive" metabolic alkalosis. * **Thiazide Diuretic Therapy:** These drugs inhibit the Na⁺/Cl⁻ symporter in the distal tubule. Increased delivery of Na⁺ to the collecting ducts enhances K⁺ and H⁺ excretion (via aldosterone stimulation), leading to **Hypokalemic Metabolic Alkalosis**. * **Cushing’s Disease:** Excess cortisol has mineralocorticoid activity, leading to increased H⁺ secretion in the distal nephron and potassium depletion, both of which drive metabolic alkalosis. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for NAGMA:** "USED CARP" (Uretero-sigmoidostomy, Small bowel fistula, Extra-chloride, Diarrhea, Carbonic anhydrase inhibitors, Renal tubular acidosis, Pancreatic fistula). * **Saline Responsiveness:** Metabolic alkalosis due to vomiting or diuretics is usually **chloride-responsive** (Urinary Cl⁻ 20 mmol/L). * **Potassium Link:** Alkalosis is almost always associated with **hypokalemia** as H⁺ shifts out of cells in exchange for K⁺ shifting in.

Q: A 19-year-old girl develops sudden-onset non-bloody diarrhea. She was previously well, is not taking any medications, and has not traveled recently. Her abdomen is soft and non-tender on examination, and the anion gap is normal. For this patient, what is the most likely acid-base disorder?

Metabolic acidosis. ### Explanation **Correct Option: A. Metabolic Acidosis** The primary mechanism behind acid-base disturbances in diarrhea is the **loss of bicarbonate (HCO₃⁻)**. Intestinal secretions below the stomach (pancreatic, biliary, and intestinal fluids) are rich in bicarbonate. When a patient has significant diarrhea, this bicarbonate is lost from the body, leading to a decrease in serum pH. Furthermore, the question specifies a **Normal Anion Gap (NAGMA)**. In diarrhea, as bicarbonate is lost, the kidneys retain Chloride (Cl⁻) to maintain electroneutrality. This results in a **Hyperchloremic Metabolic Acidosis**, which is the classic presentation of GI-related base loss. **Why Incorrect Options are Wrong:** * **B. Metabolic Alkalosis:** This occurs with the loss of acid (H⁺), typically seen in **persistent vomiting** or nasogastric suction, where gastric HCl is lost. * **C. Respiratory Acidosis:** This is caused by alveolar hypoventilation (e.g., COPD, opioid overdose) leading to CO₂ retention, not GI losses. * **D. Respiratory Alkalosis:** This results from hyperventilation (e.g., anxiety, high altitude) leading to excessive CO₂ washout. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for NAGMA (USED CARP):** **U**reterosigmoidostomy, **S**aline infusion, **E**ndocrine (Addison’s), **D**iarrhea, **C**arbonic anhydrase inhibitors, **A**mmonium chloride, **R**enal tubular acidosis (RTA), **P**ancreatic fistula. * **Anion Gap Calculation:** $Na^+ - (Cl^- + HCO_3^-)$. Normal range is 8–12 mEq/L. * **Vomiting vs. Diarrhea:** Vomiting = Metabolic Alkalosis (Loss of H⁺); Diarrhea = Metabolic Acidosis (Loss of HCO₃⁻).

Question 1

Which one of the following is not a feature of adult polycystic kidney disease?

Accepted Answer

Massive proteinuria

Answer

Hypertension

Answer

Intermittent renal colic

Answer

Macroscopic haematuria

Question 2

Routine use of recombinant erythropoietin in patients with chronic kidney disease obviates the need for which of the following?

Accepted Answer

Regular blood transfusions

Answer

Iron supplementation

Answer

Dialysis

Answer

Hyperkalemia

Question 3

Hyperkalemia without ECG changes may be treated with all of the following except?

Accepted Answer

Calcium gluconate

Answer

Salbutamol

Answer

Sodium bicarbonate

Answer

Insulin with dextrose

Question 4

The finding of urine sodium concentration <20 mmol/L in hypovolemic hyponatremia implies:

Accepted Answer

Trauma

Answer

Salt-wasting nephropathy

Answer

Diuretic therapy

Answer

Hypoaldosteronism

Question 5

In which of the following conditions is the formation of a calcium-containing kidney stone NOT likely?

Accepted Answer

Lesch-Nyhan syndrome.

Answer

Parathyroid adenoma.

Answer

Multiple myeloma.

Answer

Sarcoidosis.

Question 6

A 30-year-old male with NIDDM has a blood pressure of 150/90 mmHg and persistent albuminuria in traces on urine examination. What is the most appropriate line of treatment?

Accepted Answer

Administering lisinopril and restricting sodium intake

Answer

No treatment

Answer

Regular urine examination and monitoring of blood sugar

Answer

Restricting sodium intake only

Question 7

Painless haematuria is found in all of the following conditions EXCEPT:

Accepted Answer

Cystitis

Answer

Renal carcinoma

Answer

Chronic glomerulonephritis

Answer

Polycystic kidney disease

Question 8

Metabolic alkalosis is seen in all of the following conditions except:

Accepted Answer

Uretero-sigmoidostomy

Answer

Thiazide diuretic therapy

Answer

Prolonged vomiting

Answer

Cushing's disease

Question 9

A 19-year-old girl develops sudden-onset non-bloody diarrhea. She was previously well, is not taking any medications, and has not traveled recently. Her abdomen is soft and non-tender on examination, and the anion gap is normal. For this patient, what is the most likely acid-base disorder?

Accepted Answer

Metabolic acidosis

Answer

Metabolic alkalosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Question 10

What type of renal stone is typically formed in a patient with regional enteritis?

Accepted Answer

Calcium oxalate

Answer

Cysteine

Answer

Struvite

Answer

Urate

Nephrology — MCQs

Nephrology — MCQs

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