Nephrology — MCQs
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What is the bacterial count in a midstream urine specimen that defines a urinary tract infection?
A physician has been treating a 60-year-old patient with renal failure due to polycystic kidney disease. Which of the following conditions should the physician be specifically concerned about as a possible coexistence?
A 40-year old male complains of a vague dragging sensation in his abdomen for the last 6 months. There was no history of fever, renal colic or dysuria. Physical examination reveals a blood pressure at 150/96 mm Hg. Renal ultrasound shows bilaterally enlarged kidneys with multiple cysts. Urinalysis reveals mild proteinuria, 4 WBCs/HPF, and 10 RBCs/HPF. What is the most likely underlying renal pathology?
Polycystic kidney disease may be associated with cysts in all the following organs except:
What is the commonest cause of chronic renal failure?
What dietary intervention is most appropriate for managing chyluria?
Which of the following is NOT typically seen in chronic renal failure?
What is the most common early sign of kidney disease?
What is the initial treatment of acute hyperkalemia?
Which of the following is NOT a manifestation of polycystic kidney disease?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 301: What is the bacterial count in a midstream urine specimen that defines a urinary tract infection?
- A. 100
- B. 1000
- C. 10^4
- D. 10^5 or over (Correct Answer)
Explanation: ### Explanation The diagnosis of a Urinary Tract Infection (UTI) is traditionally based on the concept of **significant bacteriuria**, a term introduced by Edward Kass. **Why 10⁵ or over is correct:** The threshold of **≥10⁵ colony-forming units (CFU) per mL** in a clean-catch midstream urine (MSU) sample was established to distinguish true infection from urethral or vaginal contamination. In asymptomatic individuals, this count has a high specificity (approx. 95%) for identifying actual bacterial multiplication in the bladder rather than transient flora introduced during voiding. **Why other options are incorrect:** * **A, B, and C (100, 1000, 10⁴):** While these counts can represent infection in specific clinical contexts (e.g., symptomatic women, catheterized patients, or suprapubic aspirates), they do not meet the standard diagnostic criteria for "significant bacteriuria" in a routine midstream specimen. Lower counts are often considered indicative of contamination in an asymptomatic patient. **High-Yield Clinical Pearls for NEET-PG:** * **Kass Criteria:** Originally defined as ≥10⁵ CFU/mL of a single uropathogen in two consecutive midstream urine samples in asymptomatic women. * **Symptomatic Patients:** In women with classic symptoms of cystitis (dysuria, frequency), a lower threshold of **≥10² to 10³ CFU/mL** is often considered clinically significant. * **Catheterized Patients:** A count of **≥10² CFU/mL** is sufficient to diagnose infection. * **Suprapubic Aspiration:** **Any** bacterial growth (even <10² CFU/mL) is considered significant because the bladder is normally sterile. * **Sterile Pyuria:** Presence of WBCs in urine with no growth on standard media; consider *Chlamydia*, *Ureaplasma*, or Renal Tuberculosis.
Question 302: A physician has been treating a 60-year-old patient with renal failure due to polycystic kidney disease. Which of the following conditions should the physician be specifically concerned about as a possible coexistence?
- A. Aneurysm of the aortic root
- B. Atherosclerotic aneurysm
- C. Berry aneurysm (Correct Answer)
- D. Cystic medial necrosis
Explanation: **Explanation:** **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** is a systemic multisystem disorder, not limited to the kidneys [1]. The correct answer is **Berry aneurysm** because ADPKD is the most common systemic condition associated with intracranial "berry" aneurysms, occurring in approximately 5–10% of these patients. **Why Berry Aneurysm is correct:** The genetic mutations in ADPKD (PKD1 and PKD2) affect **polycystin** proteins, which are expressed in the vascular smooth muscle and endothelium [1]. Defective polycystin leads to weakened arterial walls, predisposing patients to saccular (berry) aneurysms, particularly in the **Circle of Willis**. Rupture of these aneurysms leads to subarachnoid hemorrhage (SAH), a major cause of morbidity in ADPKD. **Why other options are incorrect:** * **A. Aneurysm of the aortic root:** While ADPKD is associated with thoracic aortic aneurysms and dissection, it is much less characteristic and frequent than berry aneurysms [2]. * **B. Atherosclerotic aneurysm:** These are typically found in the abdominal aorta and are related to smoking, hypertension, and age [2], rather than the specific genetic pathology of ADPKD. * **C. Cystic medial necrosis:** This is the classic pathology associated with **Marfan Syndrome** [2], leading to aortic dissection, not the primary vascular pathology of ADPKD. **High-Yield Clinical Pearls for NEET-PG:** * **Extra-renal manifestations of ADPKD:** Hepatic cysts (most common extra-renal site), Pancreatic cysts, **Mitral Valve Prolapse (MVP)**, and Diverticulosis. * **Screening:** Routine screening for berry aneurysms is not recommended for all ADPKD patients unless there is a positive family history of SAH or the patient is in a high-risk occupation (e.g., pilot). * **Genetics:** PKD1 (Chromosome 16) is more common and progresses to ESRD faster; PKD2 (Chromosome 4) is less severe [1].
Question 303: A 40-year old male complains of a vague dragging sensation in his abdomen for the last 6 months. There was no history of fever, renal colic or dysuria. Physical examination reveals a blood pressure at 150/96 mm Hg. Renal ultrasound shows bilaterally enlarged kidneys with multiple cysts. Urinalysis reveals mild proteinuria, 4 WBCs/HPF, and 10 RBCs/HPF. What is the most likely underlying renal pathology?
- A. Nephrolithiasis
- B. Enlarged prostate
- C. Polycystic kidney disease (Correct Answer)
- D. Deposition of immune complexes in the glomeruli
Explanation: ### Explanation **Correct Option: C. Polycystic kidney disease (ADPKD)** The clinical presentation is classic for **Autosomal Dominant Polycystic Kidney Disease (ADPKD)**. The diagnosis is based on the triad of: 1. **Clinical Symptoms:** A "vague dragging sensation" due to massive bilateral renomegaly. 2. **Hypertension:** Early-onset hypertension (150/96 mm Hg) is common due to activation of the Renin-Angiotensin-Aldosterone System (RAAS) caused by cyst-induced ischemia. 3. **Imaging:** Ultrasound showing **bilaterally enlarged kidneys with multiple cysts** is the gold standard for diagnosis in this age group. 4. **Urinalysis:** Microscopic hematuria (10 RBCs/HPF) and mild proteinuria are frequently seen due to cyst rupture into the collecting system. --- ### Why Other Options are Incorrect: * **A. Nephrolithiasis:** While stones are common in ADPKD patients, they typically present with acute, sharp renal colic and fever (if infected), not a chronic dragging sensation with bilateral enlargement. * **B. Enlarged Prostate:** This would present with lower urinary tract symptoms (LUTS) like hesitancy or frequency, and would not cause bilateral cystic enlargement of the kidneys. * **C. Deposition of immune complexes:** This describes Glomerulonephritis. While it causes hypertension and hematuria, it typically presents with "dysmorphic" RBCs, RBC casts, and significant proteinuria, without the presence of multiple large bilateral cysts. --- ### NEET-PG High-Yield Pearls: * **Genetics:** Most common cause is a mutation in the **PKD1 gene** (Chromosome 16), which encodes Polycystin-1. It is more severe than PKD2 (Chromosome 4). * **Extra-renal Manifestations:** The most common is **Liver cysts**. The most life-threatening is **Berry Aneurysms** (Circle of Willis), which can lead to Subarachnoid Hemorrhage (SAH). Other features include Mitral Valve Prolapse (MVP) and diverticulosis. * **Management:** Tolvaptan (Vasopressin V2 receptor antagonist) is used to slow cyst progression. Hypertension is best managed with **ACE inhibitors or ARBs**.
Question 304: Polycystic kidney disease may be associated with cysts in all the following organs except:
- A. Lung
- B. Liver
- C. Pancreas
- D. Brain (Correct Answer)
Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a systemic multisystem disorder [1] characterized by the development of cysts in various epithelial-lined organs. **Why Brain is the correct answer:** While ADPKD is famously associated with **Berry aneurysms** (found in the Circle of Willis in approximately 5–10% of patients), it does **not** typically cause the formation of parenchymal cysts within the brain tissue itself. Therefore, while there are vascular abnormalities in the brain, "brain cysts" are not a feature of the disease. **Analysis of incorrect options:** * **Liver (Option B):** This is the most common extrarenal manifestation of ADPKD. Polycystic liver disease occurs in about 70–90% of patients over their lifetime. * **Pancreas (Option C):** Pancreatic cysts are the second most common extrarenal site, occurring in approximately 5–10% of patients. They are usually asymptomatic. * **Lung (Option A):** Though rare, pulmonary cysts and bronchiectasis have been documented in patients with ADPKD. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Most cases are due to mutations in **PKD1** (Chromosome 16 - more severe) or **PKD2** (Chromosome 4 - slower progression) [1]. * **Extrarenal Manifestations:** * **Cysts:** Liver (most common), Pancreas, Spleen, Seminal vesicles, Arachnoid membrane (not brain parenchyma). * **Non-cystic:** Berry aneurysms (can lead to Subarachnoid Hemorrhage), Mitral Valve Prolapse (MVP), Diverticulosis, and Inguinal hernias. * **Clinical Presentation:** Hypertension (earliest sign), hematuria, and palpable bilateral flank masses [1]. * **Diagnosis:** Ultrasonography is the initial screening modality of choice.
Question 305: What is the commonest cause of chronic renal failure?
- A. Chronic glomerulonephritis
- B. Chronic pyelonephritis (Correct Answer)
- C. Multiple myeloma
- D. Subacute bacterial endocarditis
Explanation: Chronic Renal Failure (CRF), now more commonly referred to as Chronic Kidney Disease (CKD), refers to an irreversible deterioration in renal function which usually develops over a period of years [1]. Initially, it is manifest only as a biochemical abnormality but eventually leads to clinical symptoms of uremia [1]. **Why Chronic Pyelonephritis is the correct answer:** In the context of traditional medical examinations and classic textbooks (like older editions of Harrison’s or Bailey & Love), **Chronic Pyelonephritis** (often secondary to reflux nephropathy or obstructive uropathy) has historically been cited as the leading cause of chronic renal failure in many developing regions. It involves chronic tubulointerstitial inflammation and scarring, leading to a gradual decline in GFR. *Note for NEET-PG:* While **Diabetes Mellitus** is globally the #1 cause of CKD today, followed by Hypertension, in questions where these are not options, Chronic Pyelonephritis or Chronic Glomerulonephritis are the preferred historical answers. [1] **Analysis of Incorrect Options:** * **A. Chronic Glomerulonephritis:** While a major cause of CKD, it statistically follows tubulointerstitial diseases/pyelonephritis in older epidemiological data sets often used for exam questions. * **C. Multiple Myeloma:** This causes "Myeloma Kidney" (cast nephropathy), which typically presents as Acute Kidney Injury (AKI) or rapidly progressive renal failure, but it is not the *most common* cause in the general population. * **D. Subacute Bacterial Endocarditis (SABE):** SABE is associated with immune-complex mediated glomerulonephritis, which usually presents as an acute or subacute nephritic syndrome rather than primary chronic renal failure. **High-Yield Clinical Pearls:** 1. **Global Gold Standard:** Currently, **Diabetes Mellitus** is the most common cause of CKD worldwide. [1] 2. **Most common cause of ESRD in India:** Diabetic Nephropathy. 3. **Small vs. Large Kidneys:** Most CKD causes lead to small, shrunken kidneys. Exceptions (Large kidneys in CKD) include Diabetes, Amyloidosis, Polycystic Kidney Disease (ADPKD), and Multiple Myeloma.
Question 306: What dietary intervention is most appropriate for managing chyluria?
- A. Small chain fatty acids
- B. Medium chain fatty acids (Correct Answer)
- C. Long chain fatty acids
- D. Omega 3 unsaturated fatty acids
Explanation: **Explanation:** **Chyluria** is characterized by the presence of chyle in the urine, typically resulting from a fistulous communication between the lymphatic system and the urinary tract (most commonly due to **Wuchereria bancrofti** infection). **Why Medium Chain Fatty Acids (MCFAs) are the correct choice:** The primary goal in managing chyluria is to reduce the lymphatic flow of chyle. Dietary fats are usually composed of **Long Chain Fatty Acids (LCFAs)**, which are re-esterified into triglycerides and transported via **chylomicrons** into the intestinal lymphatics (lacteals) [2]. This increases lymphatic pressure and worsens chyluria. In contrast, **Medium Chain Fatty Acids (C6–C12)** are water-soluble [1]. They are absorbed directly into the **portal venous system** and bypass the lymphatic system entirely [1]. A diet high in MCFAs and low in LCFAs reduces the production of chyle, thereby decreasing lymphatic pressure and allowing the lympho-urinary fistula to heal. **Analysis of Incorrect Options:** * **Long Chain Fatty Acids (LCFAs):** These are the primary triggers for chyle formation as they require lymphatic transport [2]. They exacerbate the condition. * **Small Chain Fatty Acids (SCFAs):** While they also enter the portal circulation, they are primarily produced by colonic fermentation of fiber and are not a practical dietary substitute for caloric intake in this context. * **Omega-3 Fatty Acids:** These are a subset of LCFAs. While they have anti-inflammatory properties, they still utilize the lymphatic pathway for absorption and would worsen chyluria. **Clinical Pearls for NEET-PG:** * **Classic Presentation:** "Milky white" urine that may form a gelatinous clot (due to fibrinogen). * **Diagnosis:** Confirmed by the presence of triglycerides in urine or a positive **Sudan III stain**. * **Drug of Choice (if filarial):** Diethylcarbamazine (DEC). * **Surgical Management:** If conservative dietary management fails, silver nitrate sclerotherapy (instilled into the renal pelvis) is the next step.
Question 307: Which of the following is NOT typically seen in chronic renal failure?
- A. Hyperkalemia
- B. Hyponatremia
- C. Hypercalcemia (Correct Answer)
- D. Hyperphosphatemia
Explanation: In Chronic Kidney Disease (CKD), the primary electrolyte abnormality regarding calcium is **hypocalcemia**, not hypercalcemia [3]. ### **Why Hypercalcemia is the Correct Answer (The Exception)** In CKD, the kidneys fail to convert 25-hydroxyvitamin D into its active form, **1,25-dihydroxyvitamin D (Calcitriol)**, due to the loss of the 1-alpha-hydroxylase enzyme [2]. This leads to decreased intestinal calcium absorption [1]. Furthermore, the retention of phosphate (hyperphosphatemia) leads to the precipitation of calcium-phosphate salts in soft tissues, further lowering serum ionized calcium [3]. This hypocalcemia triggers Secondary Hyperparathyroidism [2]. *Note: Hypercalcemia only occurs in late-stage CKD if "Tertiary Hyperparathyroidism" develops or due to excessive calcium/Vitamin D supplementation [1].* ### **Why the Other Options are Wrong (Typical Findings)** * **Hyperkalemia (A):** As the GFR falls below 15-20 mL/min, the kidneys lose the ability to excrete potassium effectively. Metabolic acidosis further shifts potassium from the intracellular to the extracellular compartment. * **Hyponatremia (B):** CKD patients often have an impaired ability to excrete free water due to reduced GFR and increased ADH levels, leading to dilutional hyponatremia. * **Hyperphosphatemia (D):** Decreased renal excretion of phosphate is a hallmark of CKD [3]. Elevated phosphate levels are a major driver of vascular calcification and secondary hyperparathyroidism [1]. ### **NEET-PG High-Yield Pearls** * **CKD Mineral Bone Disorder (CKD-MBD):** Characterized by the triad of **Hypocalcemia, Hyperphosphatemia, and Secondary Hyperparathyroidism** [3]. * **First electrolyte change in CKD:** Hyperphosphatemia (often occurs before hyperkalemia). * **Radiological Sign:** "Rugger-Jersey Spine" (due to osteosclerosis from secondary hyperparathyroidism). * **Acid-Base Status:** Typically presents as **High Anion Gap Metabolic Acidosis (HAGMA)** due to the retention of organic acids (sulfates, phosphates).
Question 308: What is the most common early sign of kidney disease?
- A. Sodium retention
- B. Elevated BUN level (Correct Answer)
- C. Development of metabolic acidosis
- D. Inability to dilute or concentrate urine
Explanation: **Explanation:** The correct answer is **B. Elevated BUN level.** In the early stages of chronic kidney disease (CKD), the most sensitive indicator of a declining Glomerular Filtration Rate (GFR) is an increase in nitrogenous waste products in the blood [1]. As the number of functioning nephrons decreases, the kidney's ability to clear urea is compromised, leading to an **elevation in Blood Urea Nitrogen (BUN)**. While serum creatinine is also used, BUN often rises early as GFR begins to fall below 50% of normal [2]. **Analysis of Incorrect Options:** * **A. Sodium retention:** This typically occurs in later stages of renal failure. In early CKD, the remaining nephrons compensate by increasing fractional excretion of sodium to maintain balance. * **C. Development of metabolic acidosis:** This is a feature of advanced kidney disease (usually Stage 4 or 5). It occurs when the kidneys can no longer excrete the daily acid load or regenerate sufficient bicarbonate [1]. * **D. Inability to dilute or concentrate urine:** While **isosthenuria** (the inability to concentrate or dilute urine, resulting in a fixed specific gravity of ~1.010) is a classic sign of renal tubular damage, it generally manifests after a significant loss of nephron mass, following the initial rise in nitrogenous wastes. **NEET-PG High-Yield Pearls:** * **Isosthenuria:** A fixed urine specific gravity of **1.010** (equal to plasma osmolality) is a hallmark of chronic renal failure. * **Creatinine vs. BUN:** Creatinine is more specific for renal function, but it may stay within "normal" limits until nearly 50% of kidney function is lost (the "creatinine blind" area) [2]. * **First Clinical Sign:** While elevated BUN is a common early laboratory sign, the **earliest clinical sign** of diabetic nephropathy specifically is **microalbuminuria** (30-300 mg/day) [3].
Question 309: What is the initial treatment of acute hyperkalemia?
- A. Calcium gluconate administration (Correct Answer)
- B. Insulin and glucose administration reduces hyperkalemia within 4 hours
- C. Dialysis is not useful in acute hyperkalemia
- D. Resin administration shows a response within minutes
Explanation: **Explanation:** The management of acute hyperkalemia follows a specific hierarchy: membrane stabilization, intracellular shifting, and finally, elimination. **1. Why Calcium Gluconate is the Correct Choice:** In acute hyperkalemia (especially with ECG changes), the immediate priority is to protect the heart [1]. Hyperkalemia increases the resting membrane potential, bringing it closer to the threshold, which leads to myocardial excitability and potential arrhythmias [2]. **Calcium gluconate** (or calcium chloride) acts within **1–3 minutes** to stabilize the cardiac myocyte membrane by antagonizing the effect of potassium [1]. It does *not* lower serum potassium levels but prevents fatal arrhythmias. **2. Analysis of Incorrect Options:** * **Option B:** While insulin and glucose (Dextrose) effectively shift potassium into cells, the response begins within **20–30 minutes**, not 4 hours. It is the most reliable method for temporary shifting but is not the "initial" life-saving step if ECG changes are present. * **Option C:** Dialysis is the **most definitive** treatment for removing potassium from the body. It is highly useful in acute hyperkalemia, especially in patients with renal failure or those refractory to medical therapy. * **Option D:** Cation exchange resins (e.g., Sodium Polystyrene Sulfonate) take **several hours to days** to work and are not suitable for acute, emergency management. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Sequence:** Tall peaked T-waves → PR prolongation → Loss of P-wave → Widened QRS (Sine wave) → VF/Asystole [2]. * **Calcium Dose:** 10 ml of 10% Calcium Gluconate over 10 minutes [1]. * **Salbutamol:** Beta-2 agonists also shift K+ intracellularly but should be used with caution in patients with tachycardia or CAD. * **Rule of Thumb:** If the question mentions ECG changes, **Calcium Gluconate** is always the first step [1].
Question 310: Which of the following is NOT a manifestation of polycystic kidney disease?
- A. Urine retention (Correct Answer)
- B. Renal hypertension
- C. Renal failure
- D. Hematuria
Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a systemic hereditary disorder characterized by the progressive growth of numerous cysts in the renal parenchyma [1]. **Why "Urine Retention" is the correct answer:** Urine retention is typically a feature of **lower urinary tract obstruction** (e.g., Benign Prostatic Hyperplasia, urethral strictures, or neurogenic bladder). While ADPKD causes significant kidney enlargement, it involves the renal parenchyma and does not inherently obstruct the outflow of urine from the bladder. Therefore, it is not a classic manifestation of the disease. **Analysis of incorrect options:** * **Renal Hypertension:** This is the most common early manifestation. It occurs due to cyst expansion, which causes local ischemia and triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. * **Renal Failure:** Progressive displacement of functional nephrons by expanding cysts leads to chronic kidney disease (CKD) [1]. ADPKD is a leading cause of end-stage renal disease (ESRD) requiring dialysis or transplant. * **Hematuria:** This occurs frequently due to the rupture of a cyst into the collecting system or associated nephrolithiasis (kidney stones) [1]. **NEET-PG High-Yield Pearls:** * **Extra-renal manifestations:** The most common is **Liver cysts** (Polycystic Liver Disease). The most life-threatening is **Berry Aneurysms** (Circle of Willis), which can lead to Subarachnoid Hemorrhage. * **Genetics:** Most cases are due to mutations in the **PKD1** gene (Chromosome 16), which presents earlier and more severely than **PKD2** (Chromosome 4) [1]. * **Diagnosis:** Ultrasonography is the initial screening tool of choice. * **Treatment:** Tolvaptan (Vasopressin V2 receptor antagonist) is used to slow cyst progression.
Practice by Chapter
Acute Kidney Injury
Practice Questions
Chronic Kidney Disease
Practice Questions
Glomerular Diseases
Practice Questions
Tubulointerstitial Diseases
Practice Questions
Nephrotic and Nephritic Syndromes
Practice Questions
Urinary Tract Infections
Practice Questions
Renal Replacement Therapy
Practice Questions
Fluid and Electrolyte Disorders
Practice Questions
Acid-Base Disorders
Practice Questions
Kidney in Systemic Diseases
Practice Questions
Kidney Stones and Obstructive Uropathy
Practice Questions
Hypertension in Kidney Disease
Practice Questions
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