Nephrology Practice Questions

Q: In chronic renal failure, what is the typical change in anion gap?

Increase in anion gap. **Explanation:** In Chronic Renal Failure (CRF), the primary acid-base disturbance is a **High Anion Gap Metabolic Acidosis (HAGMA)**. This occurs because, as the Glomerular Filtration Rate (GFR) declines (typically below 20–25 mL/min), the kidneys lose the ability to excrete "fixed" organic and inorganic acids [1]. These unmeasured anions—primarily **phosphates, sulfates, and organic acids**—accumulate in the blood, displacing bicarbonate and increasing the anion gap. **Analysis of Options:** * **Option C (Correct):** The retention of acid anions (phosphates/sulfates) that are not measured in the standard electrolyte panel leads to an increased anion gap. * **Option A:** A decreased anion gap is rare and usually associated with hypoalbuminemia, lithium toxicity, or multiple myeloma, but not CRF. * **Option B:** While early-stage Chronic Kidney Disease (CKD) can present with a Normal Anion Gap Metabolic Acidosis (due to impaired ammoniagenesis) [4], the **typical** and classic presentation of advanced CRF/Uremia is an increased anion gap [2]. * **Option D:** Metabolic alkalosis occurs with acid loss (e.g., vomiting) or bicarbonate gain, which is the opposite of the pathophysiology in renal failure. **High Yield Pearls for NEET-PG:** 1. **The "MUDPILES" Mnemonic:** Remember that **'U' stands for Uremia** (CRF) as a classic cause of High Anion Gap Metabolic Acidosis. 2. **Bicarbonate levels:** In CRF, the serum bicarbonate typically stabilizes between 12–20 mEq/L; a level below 10 mEq/L suggests an additional acute process. 3. **Early vs. Late CKD:** Early CKD (Stage 1-3) often shows a Normal Anion Gap (Hyperchloremic) Acidosis [4], but as it progresses to CRF (Stage 4-5), it converts to a High Anion Gap Acidosis [3].

Q: All of the following conditions are associated with hypokalemia, except?

Acute renal failure. The correct answer is **Acute Renal Failure (ARF)**. In ARF, particularly during the **oliguric phase**, the kidneys are unable to effectively excrete potassium due to a drastic reduction in the Glomerular Filtration Rate (GFR). This leads to **hyperkalemia**, which is one of the most life-threatening complications of renal failure [1]. **Why the other options are incorrect:** * **Adrenal Tumor:** Specifically, an aldosterone-secreting tumor (Conn’s Syndrome) causes primary hyperaldosteronism. Aldosterone acts on the distal tubules to reabsorb sodium and water while secreting potassium into the urine, leading to **hypokalemia** [1]. * **Thiazide Diuretics:** These inhibit the Na-Cl symporter in the distal convoluted tubule. The increased delivery of sodium to the collecting ducts stimulates sodium reabsorption in exchange for potassium secretion, resulting in **hypokalemia**. * **Diarrhea:** Lower gastrointestinal fluids are rich in potassium and bicarbonate. Excessive loss of these fluids leads to direct potassium depletion and metabolic acidosis (or contraction alkalosis in some cases), causing **hypokalemia** [1]. **NEET-PG High-Yield Pearls:** 1. **Phase Matters:** While the oliguric phase of ARF causes hyperkalemia, the **recovery (polyuric) phase** of ARF can actually cause hypokalemia due to osmotic diuresis. 2. **ECG in Hyperkalemia:** Look for tall "tented" T-waves, PR prolongation, and widening of the QRS complex (Sine wave pattern) [1]. 3. **Liddle’s Syndrome:** A rare genetic cause of hypokalemia that mimics hyperaldosteronism but with low renin and low aldosterone levels. 4. **Hypomagnesemia:** Always check magnesium levels in refractory hypokalemia, as potassium cannot be corrected until magnesium is replenished [1].

Q: Normal to increased kidney size is seen in all of the following conditions except?

Chronic glomerulonephritis. In clinical nephrology, the progression of Chronic Kidney Disease (CKD) typically leads to **bilateral small, shrunken kidneys** due to progressive fibrosis and loss of nephrons. However, certain conditions are classic exceptions where kidney size remains normal or becomes enlarged despite renal failure. **Why Option D is Correct:** **Chronic Glomerulonephritis (CGN)** is the prototypical cause of small, shrunken kidneys [1]. Long-standing inflammation leads to extensive glomerular scarring, tubular atrophy, and interstitial fibrosis, resulting in a significant reduction in renal cortical thickness and overall kidney size [1]. **Why Incorrect Options are Wrong:** * **Diabetic Nephropathy (A):** This is the most common cause of CKD with enlarged kidneys. Hyperfiltration, cellular hypertrophy, and the accumulation of extracellular matrix (Kimmelstiel-Wilson nodules) lead to increased renal volume. * **Polycystic Kidney Disease (B):** Autosomal Dominant PKD (ADPKD) causes massive bilateral kidney enlargement due to the progressive growth of thousands of fluid-filled cysts. * **AIDS-related Nephropathy (C):** HIV-associated nephropathy (HIVAN) typically presents with large, echogenic kidneys on ultrasound due to profound tubulointerstitial inflammation and "collapsing" focal segmental glomerulosclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Large Kidneys in CKD:** "SHAPE" * **S** – Systemic Amyloidosis * **H** – HIV-associated nephropathy * **A** – Autosomal Dominant Polycystic Kidney Disease * **P** – Progressive Diabetic Nephropathy * **E** – End-stage Multiple Myeloma (due to light chain deposition) * **Other causes:** Renal vein thrombosis, Hydronephrosis, and Acute Glomerulonephritis (due to edema). * **Ultrasound Tip:** A kidney size of **<9 cm** is generally indicative of irreversible chronic renal failure [1].

Q: All of the following are true about oliguric acute renal failure EXCEPT:

Hypercalcemia. In **Oliguric Acute Renal Failure (ARF)**, the sudden decline in glomerular filtration rate (GFR) leads to the accumulation of nitrogenous waste and electrolyte imbalances [1]. **Why Hypercalcemia is the Correct Answer (The Exception):** In the acute phase of renal failure, **Hypocalcemia** is the classic finding, not hypercalcemia. This occurs due to: 1. **Hyperphosphatemia:** Impaired phosphate excretion leads to phosphate binding with ionized calcium (metastatic calcification). 2. **Vitamin D Deficiency:** Reduced conversion of 25-OH Vitamin D to its active form (1,25-(OH)₂D₃) by the kidneys. 3. **Skeletal Resistance:** The bones become resistant to the action of Parathyroid Hormone (PTH). *Note: Hypercalcemia may only occur during the recovery (diuretic) phase if there is mobilization of calcium from tissues or underlying rhabdomyolysis.* **Explanation of Incorrect Options:** * **Anemia:** Common in ARF due to decreased erythropoietin production, hemodilution, and a shortened red cell life span caused by the uremic environment [2]. * **Metabolic Acidosis:** The kidney fails to excrete fixed acids (H⁺ ions) and cannot regenerate bicarbonate, leading to a High Anion Gap Metabolic Acidosis (HAGMA) [2]. * **Uremia:** The hallmark of ARF is the retention of nitrogenous waste products (Azotemia), which manifests clinically as Uremia (nausea, vomiting, encephalopathy) [2]. **NEET-PG High-Yield Pearls:** * **Most common electrolyte abnormality in ARF:** Hyperkalemia (Life-threatening). * **Fractional Excretion of Sodium (FeNa):** 2% in Acute Tubular Necrosis (ATN). * **Urinary Sediments:** "Muddy brown granular casts" are pathognomonic for ATN.

Q: Which of the following conditions can cause renal vein thrombosis?

Membranous nephropathy, Lupus nephritis, Renal amyloidosis. Renal Vein Thrombosis (RVT) is a well-known complication of **Nephrotic Syndrome**. The underlying pathophysiology involves a hypercoagulable state caused by the urinary loss of anticoagulant proteins (like Antithrombin III, Protein C, and S) and a concomitant increase in procoagmatic factors and platelet aggregation. **Why Option B is Correct:** While any cause of nephrotic syndrome can lead to RVT, it is most strongly associated with specific pathologies: 1. **Membranous Nephropathy (MN):** This is the most common cause of RVT in adults (incidence up to 30-50%) [1]. 2. **Membranoproliferative Glomerulonephritis (MPGN):** Also carries a high risk. 3. **Lupus Nephritis:** Particularly Class V (Membranous) lupus nephritis. 4. **Renal Amyloidosis:** A significant cause of heavy proteinuria and subsequent thrombosis. **Why Other Options are Incorrect:** * **Post-streptococcal Glomerulonephritis (PSGN):** This is primarily a **Nephritic Syndrome** [1]. While it involves glomerular injury, it typically does not present with the massive, sustained proteinuria required to create the profound hypercoagulable state seen in RVT. Options A, C, and D are incorrect because they include PSGN. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Selective Renal Venography (though CT Angiography is the preferred initial non-invasive test). * **Clinical Presentation:** Can be acute (flank pain, hematuria, sudden decline in GFR) or chronic (often asymptomatic, discovered during workup for pulmonary embolism). * **Left vs. Right:** The left renal vein is more commonly involved due to its more complex anatomical drainage (e.g., receiving the left gonadal vein). * **Most Common Cause:** Membranous Nephropathy is the single most high-yield association for RVT in exams [1].

Q: All are new markers for Acute Kidney Injury (AKI) except?

Plasma IL-18. ### Explanation The correct answer is **A. Plasma IL-18**. In the context of Acute Kidney Injury (AKI), the search for "renal troponins" has led to the discovery of several biomarkers that rise earlier than Serum Creatinine. [1] **1. Why Plasma IL-18 is the correct answer:** Interleukin-18 (IL-18) is a pro-inflammatory cytokine produced in the **proximal tubule** in response to injury. While **Urinary IL-18** is a highly specific and sensitive marker for ischemic acute tubular necrosis (ATN), **Plasma IL-18** is not considered a reliable or standard marker for AKI. Plasma levels of IL-18 are often influenced by systemic inflammatory conditions (like sepsis or liver disease), making it non-specific for primary renal insult. **2. Analysis of Incorrect Options:** * **Urinary IL-18:** It is a validated marker that increases significantly (up to 25-fold) in patients with ATN, typically peaking 12–48 hours before the rise in creatinine. * **NGAL (Neutrophil Gelatinase-Associated Lipocalin):** Often called the "gold standard" of new biomarkers. It is produced by nephrons in response to epithelial damage. * **Urinary NGAL:** Reflects decreased reabsorption and increased production by the distal nephron. * **Plasma NGAL:** Reflects both the systemic response and the "back-leak" from injured nephrons. Both are valid early markers for AKI. **3. High-Yield Clinical Pearls for NEET-PG:** * **Earliest Marker:** NGAL is generally considered the earliest marker to rise (within 2 hours of injury). * **KIM-1 (Kidney Injury Molecule-1):** Another high-yield urinary marker; it is a transmembrane protein specifically expressed in the proximal tubule after ischemic or toxic injury. * **Functional vs. Damage Markers:** Creatinine is a marker of *function* (GFR), whereas NGAL, IL-18, and KIM-1 are markers of *structural damage*. * **Cystatin C:** A marker of GFR that is not affected by muscle mass or age, unlike creatinine. [1]

Question 1

In chronic renal failure, what is the typical change in anion gap?

Accepted Answer

Increase in anion gap

Answer

Decrease in anion gap

Answer

Normal anion gap

Answer

Metabolic alkalosis

Question 2

All of the following conditions are associated with hypokalemia, except?

Accepted Answer

Acute renal failure

Answer

Adrenal tumor

Answer

Thiazide

Answer

Diarrhea

Question 3

Normal to increased kidney size is seen in all of the following conditions except?

Accepted Answer

Chronic glomerulonephritis

Answer

Diabetic nephropathy

Answer

Polycystic kidney disease

Answer

AIDS-related nephropathy

Question 4

All of the following are true about oliguric acute renal failure EXCEPT:

Accepted Answer

Hypercalcemia

Answer

Anemia

Answer

Metabolic Acidosis

Answer

Uremia

Question 5

Which of the following conditions can cause renal vein thrombosis?

Accepted Answer

Membranous nephropathy, Lupus nephritis, Renal amyloidosis

Answer

Membranous nephropathy, Lupus nephritis, Post-streptococcal glomerulonephritis

Answer

Membranoproliferative glomerulonephritis, Post-streptococcal glomerulonephritis, Renal amyloidosis

Answer

Membranous nephropathy, Post-streptococcal glomerulonephritis, Renal amyloidosis

Question 6

A patient has had calcium nephrocalcinosis for the past 10 years. Which of the following dietary recommendations should NOT be suggested?

Accepted Answer

Sodium Restriction

Answer

Protein Restriction

Answer

Fluid Intake Increase

Answer

All of the above

Question 7

All are new markers for Acute Kidney Injury (AKI) except?

Accepted Answer

Plasma IL-18

Answer

Urinary IL-18

Answer

Plasma NGAL

Answer

Urinary NGAL

Question 8

A 60-year-old woman presents with generalized edema, skin ulceration, and hypertension. Urine examination shows subnephrotic proteinuria (<2gm) and microscopic hematuria. Serum complement levels are decreased, and she is positive for anti-hepatitis C antibodies. What is the likely diagnosis?

Accepted Answer

Essential mixed cryoglobulinemia

Answer

Post-streptococcal glomerulonephritis (PSGN)

Answer

Membranoproliferative glomerulonephritis

Answer

Focal segmental glomerulosclerosis

Question 9

A 20-year-old male presents with features of acute renal failure. Blood examination reveals thrombocytopenia and Hb of 10 gm%. What is the likely cause?

Accepted Answer

Haemolytic uremic syndrome

Answer

Hereditary spherocytosis

Answer

Haemolytic crises

Answer

Chronic glomerulonephritis

Question 10

All of the following are indications for emergency dialysis, EXCEPT:

Accepted Answer

Azotemia

Answer

Uremic encephalopathy

Answer

Persistent hyperkalemia

Answer

Refractory volume overload

Nephrology — MCQs

Nephrology — MCQs

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