Nephrology Practice Questions

Q: Which of the following clinical findings is more likely to be associated with acute rather than chronic glomerulonephritis?

Preservation of concentrating ability. The distinction between acute and chronic glomerulonephritis (GN) lies in the extent of structural damage to the nephron. **Why "Preservation of concentrating ability" is correct:** In **Acute Glomerulonephritis (AGN)**, the primary pathology is glomerular inflammation and hypercellularity, which reduces the Glomerular Filtration Rate (GFR) [1]. However, the **renal tubules** often remain functionally intact during the early stages. Since the concentrating mechanism (counter-current multiplier system) is a tubular function, it is preserved in AGN. In contrast, **Chronic Glomerulonephritis (CGN)** involves progressive interstitial fibrosis and tubular atrophy, leading to "isosthenuria" (loss of concentrating ability) [3]. **Analysis of Incorrect Options:** * **A. Osteomalacia:** This is a feature of **Chronic Kidney Disease (CKD)**. It results from the failure of 1-alpha-hydroxylase to convert Vitamin D to its active form (Calcitriol) and secondary hyperparathyroidism, which takes months to years to develop. * **B. Increased anion gap metabolic acidosis:** While seen in acute kidney injury, it is a hallmark of **advanced CGN/CKD** where the kidney can no longer excrete fixed acids (phosphates, sulfates). * **C. Oliguria:** This can occur in both acute (e.g., RPGN) and end-stage chronic GN [2]. It is not a specific differentiator, though it is a classic component of the "Nephritic Syndrome" in acute presentations [1]. **NEET-PG High-Yield Pearls:** * **Isosthenuria:** Fixed specific gravity of urine (~1.010); it is one of the earliest signs of chronic renal failure [3]. * **Small, shrunken kidneys** on ultrasound are the most reliable indicator of CGN (except in Diabetes, Amyloidosis, and Polycystic Kidney Disease where kidneys may be enlarged). * **Broad Waxy Casts** in urine sediment are highly suggestive of chronic end-stage renal disease.

Q: Which of the following is a manifestation of nephritic syndrome?

Hematuria. Nephritic syndrome is characterized by an **inflammatory process** within the glomeruli, leading to a breakdown of the glomerular filtration barrier [2]. This allows red blood cells to leak into the urine, making **Hematuria** (often presenting as "cola-colored" or "smoky" urine) the hallmark clinical manifestation [3]. **Why the other options are incorrect:** * **Syphilis (Option A):** While secondary syphilis is associated with glomerular disease, it typically manifests as **Nephrotic syndrome** (specifically Membranous Nephropathy) due to immune complex deposition, rather than a primary nephritic picture [2]. * **Hypotension (Option B):** Nephritic syndrome is associated with **Hypertension**, not hypotension [4]. The decrease in Glomerular Filtration Rate (GFR) leads to fluid retention and activation of the Renin-Angiotensin-Aldosterone System (RAAS) [3]. * **Polyuria (Option C):** Patients with nephritic syndrome typically experience **Oliguria** (reduced urine output) due to the inflammatory reduction in GFR and subsequent salt and water retention [4]. **NEET-PG High-Yield Pearls:** * **The Nephritic Triad:** Hematuria (with RBC casts), Hypertension, and Oliguria/Azotemia [4]. * **Proteinuria:** In nephritic syndrome, proteinuria is present but usually in the **sub-nephrotic range** (<3.5 g/day). * **Common Causes:** Post-Streptococcal Glomerulonephritis (PSGN), IgA Nephropathy (Berger’s disease), and Rapidly Progressive Glomerulonephritis (RPGN) [3]. * **Differentiating Feature:** The presence of **RBC casts** in the urine sediment is pathognomonic for glomerular bleeding (nephritic origin) [1].

Q: Hepatorenal syndrome is characterized by all of the following except?

Presence of a precipitating cause. **Explanation:** Hepatorenal Syndrome (HRS) is a functional renal failure that occurs in patients with advanced chronic liver disease or acute liver failure [1]. It is primarily caused by extreme splanchnic vasodilation leading to severe renal vasoconstriction. **Why Option D is the correct answer:** While HRS can be triggered by precipitating factors (such as spontaneous bacterial peritonitis, GI bleeding, or over-diuresis), a **precipitating cause is NOT a requirement** for the diagnosis. HRS can occur spontaneously due to the progressive nature of portal hypertension. According to the International Club of Ascites (ICA) criteria, the diagnosis is based on the exclusion of other causes of kidney injury, not the presence of a trigger [1]. **Analysis of Incorrect Options:** * **Option A (Serum Creatinine >1.5 mg/dL):** Historically, this was a hallmark diagnostic threshold. While the newer ICA-AKI criteria focus on a rise in creatinine from baseline (≥0.3 mg/dL or 50% increase), a creatinine level >1.5 mg/dL remains a classic clinical indicator of significant renal impairment in HRS [1]. * **Option B (Intrinsically normal kidney):** HRS is a **functional** disorder. The kidneys are structurally intact and would function normally if transplanted into a patient with a healthy liver. * **Option C (Low or absent proteinuria):** Since the pathology is pre-renal (vasoconstrictive) rather than glomerular, there is typically no significant proteinuria (<500 mg/day) or hematuria [1]. **Clinical Pearls for NEET-PG:** * **Type 1 HRS:** Rapidly progressive; doubling of creatinine in <2 weeks [1]. * **Type 2 HRS:** Slowly progressive; associated with refractory ascites [1]. * **Urine Sodium:** Typically **<10 mEq/L** (due to intense sodium retention) [1]. * **Treatment of Choice:** Vasoconstrictors (**Terlipressin** is preferred) + **Albumin** [1]. * **Definitive Treatment:** Liver Transplantation [1].

Q: High urinary chloride is seen in all of the following conditions except?

Vomiting. This question tests the ability to differentiate causes of metabolic alkalosis based on **urinary chloride (UCl⁻)** levels, a high-yield concept for NEET-PG. [1] ### **Explanation of the Correct Answer** **Vomiting (Option C)** is characterized by **low urinary chloride (<10-20 mEq/L)**. When a patient vomits, they lose hydrochloric acid (HCl), leading to metabolic alkalosis and volume depletion [1]. The kidneys respond to volume depletion by activating the Renin-Angiotensin-Aldosterone System (RAAS), which increases proximal tubule reabsorption of sodium and water. To maintain electrical neutrality, chloride is avidly reabsorbed alongside sodium. Consequently, the urine is "chloride-depleted." This is termed **Chloride-Responsive** metabolic alkalosis because it corrects with saline infusion. ### **Analysis of Incorrect Options** All other options are causes of **Chloride-Resistant** metabolic alkalosis, where **urinary chloride is high (>20 mEq/L)**: * **Bartter Syndrome (Option A):** A genetic defect in the thick ascending limb (NKCC2 transporter), mimicking the effect of loop diuretics. It presents with salt wasting and high UCl⁻. * **Gitelman Syndrome (Option B):** A genetic defect in the distal convoluted tubule (NCCT transporter), mimicking thiazide diuretics. It presents with hypocalciuria and high UCl⁻. * **Thiazide Diuretics (Option D):** These drugs inhibit the Na-Cl symporter in the distal tubule, directly increasing the excretion of chloride into the urine. ### **NEET-PG High-Yield Pearls** * **UCl⁻ 20 mEq/L (Saline Resistant):** Bartter’s, Gitelman’s, Mineralocorticoid excess (Conn’s, Cushing’s), Current diuretic use. * **Differential Tip:** If the question mentions **hypocalciuria**, think **Gitelman’s**; if **hypercalciuria**, think **Bartter’s**.

Q: What is the investigation of choice to establish the diagnosis in adult nephrotic syndrome?

Renal biopsy. **Explanation:** In adults, nephrotic syndrome is most commonly caused by primary glomerulopathies (like Membranous Nephropathy or FSGS) or systemic diseases (like Diabetes or Amyloidosis) [1]. Unlike in children, where Minimal Change Disease is so prevalent that steroids are started empirically, the etiology in adults is highly variable [3]. Therefore, a **Renal Biopsy** is the investigation of choice (Gold Standard) to establish a definitive histological diagnosis, determine prognosis, and guide specific immunosuppressive therapy [2]. **Analysis of Options:** * **Renal Biopsy (Correct):** It allows for light microscopy, immunofluorescence, and electron microscopy, which are essential to differentiate between various types of glomerulonephritis [4]. * **DMSA Scan (Incorrect):** This is a nuclear medicine scan used primarily to detect cortical scarring (common in chronic pyelonephritis) or to evaluate functional renal mass. It has no role in diagnosing the cause of nephrotic syndrome. * **CT Scan & MRI (Incorrect):** These are structural imaging modalities. While they can identify tumors, stones, or renal vein thrombosis (a complication of nephrotic syndrome), they cannot visualize the microscopic glomerular changes required for a nephrotic diagnosis. **High-Yield Clinical Pearls for NEET-PG:** * **Indications for Biopsy in Children:** Unlike adults, children are biopsied only if they are "Steroid Resistant," have atypical features (age 12 years), or show low C3 levels. * **Most common cause of Nephrotic Syndrome:** * **Children:** Minimal Change Disease (MCD). * **Adults (Worldwide):** Focal Segmental Glomerulosclerosis (FSGS) [1]. * **Adults (Historically/Older texts):** Membranous Nephropathy. * **Contraindications for Renal Biopsy:** Solitary kidney (relative), uncontrolled hypertension, bleeding diathesis, and small echogenic kidneys (suggesting ESRD).

Q: All of the following are true about hepatorenal syndrome except:

Type II has a more serious prognosis than Type I. **Explanation:** Hepatorenal Syndrome (HRS) is a form of functional renal failure occurring in patients with advanced liver disease, characterized by intense renal vasoconstriction despite histologically normal kidneys [1]. **1. Why Option B is the correct answer (The Exception):** In HRS, **Type I is significantly more severe than Type II.** * **Type I HRS** is characterized by rapid, progressive renal failure (doubling of serum creatinine to >2.5 mg/dL in less than 2 weeks). It is often triggered by a precipitating event like SBP and has a very poor median survival (approx. 2 weeks) without treatment [1]. * **Type II HRS** is a more chronic, slowly progressive form, typically presenting as refractory ascites [1]. While it has a poor long-term prognosis, it is less acutely life-threatening than Type I. **2. Analysis of Incorrect Options:** * **Option A:** HRS is almost exclusively seen in patients with **advanced cirrhosis** and portal hypertension [1]. * **Option C:** The pathophysiology involves splanchnic vasodilation leading to decreased effective arterial blood volume. This triggers the RAAS and sympathetic nervous systems, causing **intense renal vasoconstriction and hypoperfusion.** * **Option D:** It is a **functional failure.** If the liver is transplanted or the patient recovers, renal function often returns to normal because there is no structural damage to the nephrons [1]. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Requires exclusion of shock, nephrotoxic drugs, and intrinsic kidney disease (proteinuria <500mg/day, normal ultrasound) [1]. * **Treatment of Choice:** **Terlipressin** (vasoconstrictor) plus **Albumin** (volume expansion) [1]. * **Definitive Treatment:** Liver Transplantation [1]. * **Key Trigger:** Spontaneous Bacterial Peritonitis (SBP) is the most common precipitant for Type I HRS.

Question 1

Which of the following clinical findings is more likely to be associated with acute rather than chronic glomerulonephritis?

Accepted Answer

Preservation of concentrating ability

Answer

Osteomalacia

Answer

Increased anion gap metabolic acidosis

Answer

Oliguria

Question 2

Which of the following is a manifestation of nephritic syndrome?

Accepted Answer

Hematuria

Answer

Syphilis

Answer

Hypotension

Answer

Polyuria

Question 3

What is the cause of renal failure in rhabdomyolysis?

Accepted Answer

Myoglobin

Answer

Increased potassium

Answer

Increased phosphate

Answer

Increased uric acid

Question 4

Hepatorenal syndrome is characterized by all of the following except?

Accepted Answer

Presence of a precipitating cause

Answer

Serum creatinine more than 1.5 mg/dL

Answer

An intrinsically normal kidney

Answer

Low or absent proteinuria

Question 5

High urinary chloride is seen in all of the following conditions except?

Accepted Answer

Vomiting

Answer

Baer syndrome

Answer

Gitelman syndrome

Answer

Thiazide diuretics

Question 6

What is the treatment of choice for Hepatorenal syndrome?

Accepted Answer

Liver transplant

Answer

ACE inhibitors

Answer

Calcium channel blockers

Answer

Peritoneal dialysis

Question 7

What is the investigation of choice to establish the diagnosis in adult nephrotic syndrome?

Accepted Answer

Renal biopsy

Answer

DMSA scan

Answer

CT Scan

Answer

MRI

Question 8

Which of the following is the most important factor in determining the development of diabetic nephropathy?

Accepted Answer

Duration of the disease

Answer

Hypertension

Answer

Pre-existing renal disease

Answer

Control with treatment

Question 9

All of the following may be associated with massive proteinuria except?

Accepted Answer

Polycystic kidneys

Answer

Amyloidosis

Answer

Renal vein thrombosis

Answer

All

Question 10

All of the following are true about hepatorenal syndrome except:

Accepted Answer

Type II has a more serious prognosis than Type I

Answer

Seen in advanced stage of cirrhosis

Answer

Caused by intense hypoperfusion of the kidney

Answer

A functional renal failure without intrinsic renal pathology

Nephrology — MCQs

Nephrology — MCQs

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