Nephrology — MCQs
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Which of the following statements is FALSE regarding Autosomal dominant polycystic kidney disease (ADPKD)?
Which of the following is the most accurate method to assess decline in GFR during initial stages of renal insufficiency?
A patient undergoing hemodialysis becomes restless and complains of headache and nausea. Which complication do you suspect?
A 50-year-old man with a history of diabetes presents with a poor urinary stream, increased frequency of micturition, and hesitancy. What is the most likely diagnosis?
Proximal and distal renal tubular acidosis are differentiated by all except?
Recurrent gross hematuria is seen in which of the following conditions?
A 27-year-old alcoholic man presents with decreased appetite, mild generalized weakness, intermittent mild abdominal pain, perioral numbness, and some cramping of his hands and feet. His physical examination is initially normal. His laboratory results show a sodium level of 140 mEq/L, potassium 4.0 mEq/L, calcium 6.9 mg/dL, albumin 3.5 g/dL, magnesium 0.7 mg/dL, and phosphorus 2.0 mg/dL. You go back to the patient and find that he has both a positive Trousseau and a positive Chvostek sign. Which of the following is the most likely cause of the hypocalcemia?
All of the following are true about Prerenal Azotemia, EXCEPT:
A 70-year-old male, a known case of a certain malignancy, presents with elevated erythropoietin levels and a packed cell volume (PCV) of 52%. Which tumor is most likely responsible?
Isosthenuria is seen in which of the following conditions?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 91: Which of the following statements is FALSE regarding Autosomal dominant polycystic kidney disease (ADPKD)?
- A. Berry aneurysm is the most common central nervous system manifestation.
- B. There is an increased risk of subarachnoid hemorrhage from a ruptured intracranial aneurysm.
- C. The polyductin gene is involved in ADPKD. (Correct Answer)
- D. Saccular aneurysms may be detected in up to 10% of asymptomatic patients.
Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is primarily caused by mutations in the **PKD1** (Chromosome 16) or **PKD2** (Chromosome 4) genes [1], which encode the proteins polycystin-1 and polycystin-2, respectively. The **Polyductin** gene (also known as PKHD1) is associated with **Autosomal Recessive Polycystic Kidney Disease (ARPKD)**, not the dominant form. **Analysis of Incorrect Options (True statements):** * **Option A:** Berry (saccular) aneurysms are indeed the most common CNS manifestation of ADPKD. They occur due to defects in the arterial wall integrity associated with polycystin mutations. * **Option B:** Due to the prevalence of these aneurysms, patients with ADPKD have a significantly higher risk of subarachnoid hemorrhage (SAH) compared to the general population, especially if there is a positive family history of stroke or aneurysm. * **Option D:** Screening studies using MRA have shown that saccular aneurysms are present in approximately 5–10% of asymptomatic ADPKD patients. **High-Yield Clinical Pearls for NEET-PG:** * **Extra-renal manifestations:** Hepatic cysts (most common extra-renal site), Mitral Valve Prolapse (MVP), diverticulosis, and pancreatic cysts. * **Genetics:** PKD1 mutations (85% of cases) lead to earlier onset and faster progression to ESRD compared to PKD2 [1]. * **Diagnosis:** Ultrasonography is the primary screening tool; diagnostic criteria are based on the number of cysts relative to the patient's age. * **Management:** Tolvaptan (V2 receptor antagonist) is used to slow the increase in kidney volume and decline in GFR.
Question 92: Which of the following is the most accurate method to assess decline in GFR during initial stages of renal insufficiency?
- A. Serum creatinine
- B. Creatinine clearance (Correct Answer)
- C. Serum BUN
- D. Serum urea
Explanation: The Glomerular Filtration Rate (GFR) is the gold standard for assessing renal function. In the **initial stages** of renal insufficiency (early chronic kidney disease), **Creatinine Clearance (CrCl)** is the most accurate clinical method to detect a decline [2]. **Why Creatinine Clearance is correct:** Serum creatinine has a non-linear, hyperbolic relationship with GFR. In early stages of renal disease, a significant drop in GFR (up to 50%) can occur while the serum creatinine remains within the "normal" range (the "creatinine-blind" area) [1]. Creatinine clearance, which involves a 24-hour urine collection, accounts for both serum levels and urinary excretion, making it more sensitive than serum creatinine alone for detecting early functional loss [2]. **Why other options are incorrect:** * **Serum Creatinine:** It is an insensitive marker for early disease because it does not rise significantly until the GFR has fallen by approximately 50% [1]. It is affected by muscle mass, age, and gender. * **Serum BUN & Urea:** These are poor markers of GFR because they are heavily influenced by non-renal factors such as high-protein diet, dehydration, GI bleeding, and corticosteroid use [2]. Furthermore, urea undergoes significant tubular reabsorption. **High-Yield Pearls for NEET-PG:** * **Gold Standard:** Inulin Clearance is the absolute gold standard for measuring GFR but is rarely used clinically due to its exogenous nature and cost [2], [4]. * **Creatinine Secretion:** CrCl slightly **overestimates** GFR because a small amount of creatinine is secreted by the proximal tubules [5]. * **Best Formula:** The **CKD-EPI** formula is currently preferred over MDRD [3] for estimating GFR (eGFR) in clinical practice. * **Cystatin C:** An endogenous marker that is not affected by muscle mass and may be more sensitive than creatinine in early CKD.
Question 93: A patient undergoing hemodialysis becomes restless and complains of headache and nausea. Which complication do you suspect?
- A. Infection
- B. Disequilibrium syndrome (Correct Answer)
- C. Air embolism
- D. Acute hemolysis
Explanation: The patient is presenting with classic symptoms of **Dialysis Disequilibrium Syndrome (DDS)**. **1. Why the correct answer is right:** DDS is a neurological complication that typically occurs during or immediately after the first few sessions of hemodialysis. It is caused by the **rapid removal of urea** from the blood. Urea is an osmotically active solute; while it is cleared quickly from the plasma, it crosses the blood-brain barrier slowly. This creates an osmotic gradient that draws water into the brain cells, leading to **cerebral edema**. Clinical manifestations range from restlessness, headache, and nausea to more severe symptoms like seizures and coma. **2. Why the incorrect options are wrong:** * **Infection:** While common in dialysis patients (e.g., peritonitis or catheter-related sepsis), it usually presents with fever, chills, and localized pain rather than acute neurological symptoms during the procedure [1]. * **Air Embolism:** This is a sudden emergency characterized by acute dyspnea, chest pain, and hypotension (the "mill-wheel" murmur). It does not typically present with isolated restlessness and headache. * **Acute Hemolysis:** This presents with back pain, chest tightness, and a drop in hematocrit. The blood in the lines may appear "cherry red." **3. NEET-PG High-Yield Pearls:** * **Risk Factor:** Most common during the **first dialysis session** or when pre-dialysis BUN levels are extremely high (>150 mg/dL). * **Prevention:** Use a slower blood flow rate, shorter dialysis duration for the first session, or use osmotic agents like **Mannitol** to prevent rapid shifts. * **Management:** If DDS occurs, the dialysis should be slowed or stopped, and hypertonic solutions may be administered to reduce cerebral edema.
Question 94: A 50-year-old man with a history of diabetes presents with a poor urinary stream, increased frequency of micturition, and hesitancy. What is the most likely diagnosis?
- A. Benign prostatic hyperplasia (BPH) (Correct Answer)
- B. Urinary tract infection (UTI)
- C. Atonic bladder
- D. Autonomic neuropathy
Explanation: ### Explanation **Correct Option: A. Benign Prostatic Hyperplasia (BPH)** The clinical presentation of a poor urinary stream, increased frequency, and hesitancy constitutes classic **Lower Urinary Tract Symptoms (LUTS)**. These are categorized into **obstructive symptoms** (hesitancy, weak stream, straining, terminal dribbling) and **irritative symptoms** (frequency, urgency, nocturia) [1]. In a 50-year-old male, the most common cause of mechanical bladder outlet obstruction leading to these symptoms is BPH [1]. While the patient is diabetic, the mechanical nature of the "poor stream" and "hesitancy" points directly toward prostatic enlargement rather than a purely functional nerve issue. **Why other options are incorrect:** * **B. Urinary Tract Infection (UTI):** While UTI causes increased frequency and urgency, it typically presents with dysuria (painful micturition) and suprapubic pain [2]. It does not explain the mechanical obstructive symptoms like hesitancy or a poor stream. * **C. Atonic Bladder:** This refers to a large-capacity, non-contractile bladder. While it can cause overflow incontinence, it usually presents with a lack of sensation of fullness and is a late-stage complication of chronic obstruction or neurological injury. * **D. Autonomic Neuropathy:** In diabetics, this leads to a **"Diabetic Cystopathy."** It typically presents with a loss of bladder sensation and infrequent voiding (increased bladder capacity) rather than the classic obstructive symptoms of hesitancy and poor stream seen in BPH. **NEET-PG High-Yield Pearls:** * **Initial Investigation for BPH:** Digital Rectal Examination (DRE) and Uroflowmetry [1]. * **Gold Standard Investigation:** Pressure-flow studies (Urodynamics) [1]. * **Medical Management:** Alpha-blockers (e.g., Tamsulosin) for rapid symptom relief; 5-alpha-reductase inhibitors (e.g., Finasteride) to reduce prostate volume. * **Surgical Gold Standard:** TURP (Transurethral Resection of the Prostate). * **Diabetic Cystopathy:** Characterized by decreased bladder sensation, increased post-void residual volume, and impaired detrusor contractility.
Question 95: Proximal and distal renal tubular acidosis are differentiated by all except?
- A. Stones in kidney
- B. Hypokalemia (Correct Answer)
- C. Daily acid secretion
- D. Presence of Fanconi syndrome
Explanation: To differentiate between Proximal (Type 2) and Distal (Type 1) Renal Tubular Acidosis (RTA), one must identify the unique clinical and biochemical markers of each [1]. **Why Hypokalemia is the correct answer:** Hypokalemia is **not** a differentiating factor because it is a common feature of **both** Type 1 (Distal) and Type 2 (Proximal) RTA. In Type 1, it occurs due to the inability to secrete H+, leading to compensatory K+ secretion [1]. In Type 2, the failure to reabsorb bicarbonate leads to increased distal delivery of sodium bicarbonate, which promotes potassium excretion. Since both conditions present with low serum potassium, it cannot be used to distinguish between them. **Explanation of other options (Differentiating factors):** * **Stones in kidney (Nephrolithiasis/Nephrocalcinosis):** This is a hallmark of **Type 1 RTA** (due to alkaline urine and hypercalciuria). It is typically **absent in Type 2 RTA** because the distal acidification remains intact, keeping calcium soluble. * **Daily acid secretion:** In **Type 1 RTA**, the primary defect is the inability to secrete H+ ions, leading to a high urinary pH (>5.5) [1]. In **Type 2 RTA**, the distal tubule can still secrete acid once the plasma bicarbonate levels drop below the threshold, allowing for a low urinary pH (<5.5). * **Presence of Fanconi syndrome:** This is specifically associated with **Type 2 RTA**. It involves a generalized dysfunction of the proximal tubule, leading to glycosuria, phosphaturia, and aminoaciduria alongside bicarbonate loss. **High-Yield NEET-PG Pearls:** * **Type 1 (Distal):** Inability to secrete H+; associated with Sjögren’s syndrome and Amphotericin B. * **Type 2 (Proximal):** Inability to reabsorb HCO3-; associated with Multiple Myeloma and Wilson’s disease. * **Type 4 (Hyperkalemic):** Associated with Diabetes Mellitus and hypoaldosteronism; the **only** RTA with **high** potassium.
Question 96: Recurrent gross hematuria is seen in which of the following conditions?
- A. Alport's syndrome
- B. IgA nephropathy (Correct Answer)
- C. Focal segmental glomerulosclerosis
- D. Diabetes mellitus
Explanation: Explanation: **IgA Nephropathy (Berger’s Disease)** is the most common cause of primary glomerulonephritis worldwide and is the classic cause of **recurrent gross hematuria**. The underlying pathophysiology involves the deposition of IgA-dominant immune complexes in the glomerular mesangium [2][3]. Characteristically, episodes of gross hematuria are triggered by an upper respiratory tract infection (synpharyngitic hematuria), occurring within 24–48 hours of the onset of infection [2]. **Analysis of Incorrect Options:** * **Alport’s Syndrome:** While it presents with persistent microscopic hematuria and can have episodes of gross hematuria, it is primarily characterized by a family history of renal failure, sensorineural hearing loss, and ocular abnormalities (lenticonus). It is a basement membrane disorder (Type IV Collagen mutation), not typically defined by "recurrent gross" episodes as its hallmark. * **Focal Segmental Glomerulosclerosis (FSGS):** This typically presents with nephrotic syndrome (heavy proteinuria, edema) [1][4]. While microscopic hematuria can occur, recurrent gross hematuria is not a feature. * **Diabetes Mellitus:** Diabetic nephropathy presents with progressive albuminuria and a decline in GFR [4]. Hematuria is rare; if present, it usually warrants investigation for other causes like papillary necrosis or malignancy [5]. **High-Yield Clinical Pearls for NEET-PG:** * **Synpharyngitic Hematuria:** Hematuria occurs *with* the infection (IgA Nephropathy) [2]. * **Post-Streptococcal GN (PSGN):** Hematuria occurs 1–3 weeks *after* the infection (latent period) [1][2]. * **Diagnosis:** Gold standard is Renal Biopsy showing **mesangial IgA deposits** and mesangial hypercellularity [3]. * **Prognosis:** The most reliable predictor of poor prognosis is the degree of proteinuria and hypertension at presentation.
Question 97: A 27-year-old alcoholic man presents with decreased appetite, mild generalized weakness, intermittent mild abdominal pain, perioral numbness, and some cramping of his hands and feet. His physical examination is initially normal. His laboratory results show a sodium level of 140 mEq/L, potassium 4.0 mEq/L, calcium 6.9 mg/dL, albumin 3.5 g/dL, magnesium 0.7 mg/dL, and phosphorus 2.0 mg/dL. You go back to the patient and find that he has both a positive Trousseau and a positive Chvostek sign. Which of the following is the most likely cause of the hypocalcemia?
- A. Poor dietary intake
- B. Hypoalbuminemia
- C. Pancreatitis
- D. Decreased end-organ response to parathyroid hormone because of hypomagnesemia (Correct Answer)
Explanation: ### Explanation The patient presents with symptomatic hypocalcemia (Trousseau and Chvostek signs, perioral numbness, cramps) in the setting of chronic alcoholism and severe **hypomagnesemia** (0.7 mg/dL). **1. Why Option D is Correct:** Magnesium is a critical cofactor for the synthesis and release of Parathyroid Hormone (PTH), as well as for the responsiveness of target organs (bones and kidneys) to PTH. Severe hypomagnesemia (typically <1.0 mg/dL) causes hypocalcemia through two mechanisms: * **PTH Resistance:** It impairs the activation of adenylate cyclase, leading to decreased end-organ response to PTH. * **PTH Deficiency:** It inhibits the release of PTH from the parathyroid glands. In this patient, the hypocalcemia will not correct with calcium supplementation alone; magnesium must be replaced first to restore PTH functionality. **2. Why Other Options are Incorrect:** * **A. Poor dietary intake:** While common in alcoholics, the body has massive calcium stores in the bone. Dietary deficiency alone rarely causes symptomatic hypocalcemia unless accompanied by Vitamin D deficiency or malabsorption. * **B. Hypoalbuminemia:** The patient’s albumin is 3.5 g/dL (near normal). Since roughly 40% of calcium is protein-bound, low albumin causes "pseudohypocalcemia." However, this patient has *symptomatic* hypocalcemia, indicating low ionized (active) calcium, which albumin levels do not explain here. * **C. Pancreatitis:** While pancreatitis causes hypocalcemia (via saponification of fat), the clinical picture (lack of severe abdominal pain/vomiting) and the presence of profound hypomagnesemia make Option D the more specific underlying cause. **3. NEET-PG High-Yield Pearls:** * **Magnesium-Calcium Link:** Always check Magnesium levels in "refractory hypocalcemia" or "refractory hypokalemia." * **Chvostek Sign:** Facial twitching when tapping the facial nerve. * **Trousseau Sign:** Carpal spasm induced by inflating a BP cuff (more sensitive/specific than Chvostek). * **Alcoholism:** The most common cause of hypomagnesemia in clinical practice due to poor intake, decreased absorption, and ethanol-induced renal wasting.
Question 98: All of the following are true about Prerenal Azotemia, EXCEPT:
- A. Urinary Cr/Plasma Cr >40
- B. FENa < 1
- C. Urinary output < 400 ml/day
- D. Plasma BUN/Creatinine ratio <20 (Correct Answer)
Explanation: Prerenal azotemia is a state of renal hypoperfusion where the kidney's structural integrity is intact, but the glomerular filtration rate (GFR) decreases due to reduced blood flow [1]. **Why Option D is the Correct Answer (The False Statement):** In prerenal azotemia, the **BUN/Creatinine ratio is typically >20:1**. When renal perfusion decreases, the renin-angiotensin-aldosterone system (RAAS) is activated. This increases the reabsorption of sodium and water in the proximal tubule. Since urea follows sodium and water passively, urea reabsorption is significantly increased. Creatinine, however, is not reabsorbed. This leads to a disproportionate rise in blood urea nitrogen (BUN) relative to serum creatinine. A ratio **<20:1** (usually 10-15:1) is more characteristic of intrinsic renal failure (Acute Tubular Necrosis). **Analysis of Other Options:** * **Option A (Urinary Cr/Plasma Cr >40):** True. In prerenal states, the kidneys are highly efficient at reabsorbing water. This concentrates the urine, leading to a high concentration of non-reabsorbable solutes like creatinine in the urine compared to the plasma. * **Option B (FENa < 1%):** True. This is the most sensitive index to differentiate prerenal azotemia from ATN. Intact tubules respond to hypoperfusion by maximally conserving sodium. * **Option C (Urinary output < 400 ml/day):** True. Oliguria is a common clinical manifestation of prerenal azotemia as the body attempts to conserve volume [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Urine Osmolality:** In prerenal azotemia, it is typically **>500 mOsm/kg** (concentrated urine), whereas in ATN it is <350 mOsm/kg (isosthenuria). * **Urine Sodium:** Usually **<20 mEq/L** in prerenal states. * **Management:** Prerenal azotemia is reversible with prompt fluid resuscitation; failure to treat can lead to Intrinsic AKI (ATN) [1].
Question 99: A 70-year-old male, a known case of a certain malignancy, presents with elevated erythropoietin levels and a packed cell volume (PCV) of 52%. Which tumor is most likely responsible?
- A. Renal Cell Carcinoma (Correct Answer)
- B. Medullary thyroid carcinoma
- C. Gastric Carcinoma
- D. Colorectal Carcinoma
Explanation: ### **Explanation** **1. Why Renal Cell Carcinoma (RCC) is Correct:** The clinical presentation of elevated erythropoietin (EPO) and a high packed cell volume (PCV) in the presence of a malignancy points toward a **Paraneoplastic Syndrome**. RCC is the most common cause of **paraneoplastic erythrocytosis** [1], [3]. The tumor cells ectopically produce erythropoietin, which stimulates the bone marrow to increase red blood cell production, leading to secondary polycythemia (erythrocytosis) [3]. **2. Why the Other Options are Incorrect:** * **Medullary Thyroid Carcinoma:** Typically associated with the secretion of Calcitonin, CEA, or ACTH (leading to Cushing syndrome), but not EPO [2]. * **Gastric Carcinoma:** Often presents with iron deficiency anemia due to chronic occult blood loss, rather than erythrocytosis. * **Colorectal Carcinoma:** Similar to gastric cancer, it is a common cause of microcytic hypochromic anemia due to chronic GI bleeding. **3. High-Yield Clinical Pearls for NEET-PG:** * **Differential Diagnosis for Ectopic EPO Production:** Remember the mnemonic **"Potentially Really High Hematocrit"**: * **P**heochromocytoma * **R**enal Cell Carcinoma (Most common) [1] * **H**epatocellular Carcinoma (HCC) * **H**emangioblastoma (Cerebellar) * **U**terine Leiomyoma (Fibroids) * **Stauffer Syndrome:** A unique paraneoplastic syndrome in RCC characterized by reversible hepatic dysfunction (elevated ALP) without liver metastases. * **Classic Triad of RCC:** Hematuria, flank pain, and a palpable abdominal mass (seen in only 10% of cases). * **Investigation of Choice:** Contrast-Enhanced CT (CECT) of the abdomen [1].
Question 100: Isosthenuria is seen in which of the following conditions?
- A. Chronic renal failure (Correct Answer)
- B. Diabetes insipidus
- C. Congestive cardiac failure
- D. Weil's disease
Explanation: **Explanation:** **Isosthenuria** refers to the excretion of urine with a fixed specific gravity (typically **1.010**) that is identical to that of the plasma ultrafiltrate. This indicates that the renal tubules have lost their ability to either concentrate or dilute the urine. 1. **Why Chronic Renal Failure (CRF) is correct:** In CRF, there is a progressive loss of functioning nephrons. The remaining "survivor" nephrons undergo compensatory hypertrophy and experience an increased solute load per nephron (solute diuresis) [1]. This impairs the medullary osmotic gradient and renders the tubules unresponsive to Vasopressin (ADH). Consequently, the kidney cannot modify the filtrate, and urine is excreted at the same osmolality as plasma (~285–295 mOsm/kg) [2]. 2. **Why other options are incorrect:** * **Diabetes Insipidus:** Characterized by **Hyposthenuria** (specific gravity < 1.005). Due to a lack of ADH or resistance to it, the kidneys cannot reabsorb water, leading to very dilute urine. * **Congestive Cardiac Failure (CCF):** Results in **Hypersthenuria** (high specific gravity). Reduced renal perfusion activates the RAAS and ADH, causing the kidneys to conserve water and sodium, resulting in highly concentrated urine. * **Weil’s Disease (Leptospirosis):** While it causes renal failure, it is classically associated with non-oliguric renal failure and hypokalemia. Isosthenuria is a hallmark of established, chronic parenchymal damage rather than acute infectious insults. **High-Yield Clinical Pearls for NEET-PG:** * **Specific Gravity of 1.010:** This is the "magic number" for isosthenuria, reflecting a urine osmolality of ~300 mOsm/L. * **Hyposthenuria:** Seen in Diabetes Insipidus, Primary Polydipsia, and Sickle Cell Trait (early loss of concentrating ability). * **Fixed Specific Gravity:** Is often one of the earliest signs of chronic renal parenchymal disease, appearing before significant rises in BUN or Creatinine.
Practice by Chapter
Acute Kidney Injury
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Chronic Kidney Disease
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Glomerular Diseases
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Tubulointerstitial Diseases
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Nephrotic and Nephritic Syndromes
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Urinary Tract Infections
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Renal Replacement Therapy
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Fluid and Electrolyte Disorders
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Acid-Base Disorders
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Kidney in Systemic Diseases
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Kidney Stones and Obstructive Uropathy
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Hypertension in Kidney Disease
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