Nephrology — MCQs

A 58-year-old man with cirrhosis complains of worsening fatigue and confusion over the past 5 days. He also reports a declining urinary output over the past 48 hours. On examination, he is gaunt and jaundiced. He has tense ascites and a liver span of 7 cm in the midclavicular line. Lab results reveal a WBC 4600/mm3, Hb 9.4 g/dL, and PCB 29%. BUN of 34 mg/dL and a creatinine of 3.1 mg/dL. A urinary Na <10 mEq/L. What is the most appropriate treatment for his elevated BUN and creatinine?

Q536Medium

A 25-year-old man presents with a kidney stone. He is married to his first cousin, and six months earlier, his 8-year-old son also had a kidney stone. What is the most likely diagnosis?

Q537Medium

What is the cornerstone of therapy for chronic hyponatremia?

Q538Easy

Which of the following is the LEAST likely to be associated with gross hematuria?

Q539Medium

A patient presents with symptoms suggestive of stage IV kidney disease, including anemia and progressive malnutrition. Which of the following glomerular filtration rate (GFR) ranges would be most consistent with this stage of kidney disease?

Q540Easy

A client is diagnosed with chronic renal failure and must start hemodialysis. Client teaching would include which of the following instructions?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 531: The earliest clinical feature of diabetic nephropathy is:

A. Microalbuminuria (Correct Answer)
B. Increased serum creatinine
C. Nephritic syndrome
D. Hematuria

Explanation: **Explanation:** Diabetic Nephropathy (DN) follows a predictable clinical course known as the **Mogensen stages**. **1. Why Microalbuminuria is correct:** Microalbuminuria (30–300 mg/day) is the **earliest clinical sign** of diabetic nephropathy (Stage III) [1]. It represents the first detectable evidence of glomerular damage [3] and is a critical predictor of progression to overt renal failure and increased cardiovascular risk [1]. While Stage I involves glomerular hyperfiltration (increased GFR), this is a functional change often detected only by specialized clearance tests, making microalbuminuria the first identifiable *clinical* marker [1], [3]. **2. Why the other options are incorrect:** * **Increased serum creatinine:** This occurs much later in the disease (Stage IV or V) once the GFR has significantly declined [3]. By the time creatinine rises, substantial irreversible structural damage has already occurred. * **Nephritic syndrome:** DN typically presents as a **Nephrotic** picture (heavy proteinuria, edema), not nephritic [4]. Nephritic syndrome (hematuria, hypertension, oliguria) suggests an alternative diagnosis like post-streptococcal glomerulonephritis [4]. * **Hematuria:** While microscopic hematuria can occur in advanced DN, it is not a hallmark or early feature [2]. Its presence should prompt a search for non-diabetic renal diseases. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest functional change:** Increased GFR (Hyperfiltration). * **Earliest structural change:** Thickening of the Glomerular Basement Membrane (GBM) [3]. * **Most specific histological finding:** Kimmelstiel-Wilson (KW) nodules (nodular glomerulosclerosis) [3]. * **Screening:** Annual screening for microalbuminuria should start 5 years after diagnosis in Type 1 DM and at the time of diagnosis in Type 2 DM [1]. * **Management:** ACE inhibitors or ARBs are the drugs of choice as they reduce intraglomerular pressure.

Question 532: Which of the following is a true complication of hemodialysis?

A. Beta-amyloid deposition
B. Cardiovascular complications (Correct Answer)
C. Renal rickets
D. Metabolic acidosis

Explanation: **Explanation:** **Cardiovascular complications (Option B)** are the leading cause of morbidity and mortality in patients undergoing long-term hemodialysis (HD), accounting for nearly 50% of deaths. The underlying pathophysiology involves a combination of traditional risk factors (hypertension, diabetes) and uremia-specific factors (chronic fluid overload, electrolyte imbalances, and systemic inflammation). These lead to accelerated atherosclerosis, left ventricular hypertrophy (LVH), and arrhythmias. **Analysis of Incorrect Options:** * **Beta-amyloid deposition (Option A):** This is incorrect because the amyloidosis associated with long-term dialysis is specifically due to **Beta-2 Microglobulin ($\beta_2$M)** deposition, not Beta-amyloid (which is associated with Alzheimer’s disease). $eta_2$M is poorly cleared by standard dialysis membranes, leading to carpal tunnel syndrome and bone cysts. * **Renal rickets (Option C):** This is a manifestation of Chronic Kidney Disease (CKD) itself (part of CKD-Mineral Bone Disorder) due to Vitamin D deficiency and secondary hyperparathyroidism, rather than a complication *caused* by the dialysis procedure [1]. * **Metabolic acidosis (Option D):** Hemodialysis is a **treatment** for metabolic acidosis, not a complication [2]. Dialysate contains bicarbonate or acetate to buffer the acid load in uremic patients. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death in HD:** Cardiovascular disease (specifically sudden cardiac death). * **Dialysis Equilibrium Syndrome:** A serious neurological complication caused by the rapid removal of urea, leading to cerebral edema. * **First-use syndrome:** An anaphylactoid reaction (Type 1 hypersensitivity) often seen with ethylene oxide-sterilized membranes. * **Infection:** The second most common cause of death; Staphylococcus aureus is the most common pathogen related to vascular access [2].

Question 533: A patient presents with hyperkalemia and no ECG changes. Which of the following is used for treatment, EXCEPT?

A. Glucose + Insulin
B. Sodium bicarbonate
C. Calcium gluconate (Correct Answer)
D. Resins

Explanation: In the management of hyperkalemia, treatment is categorized into three goals: membrane stabilization, shifting potassium into cells, and removing potassium from the body [1]. **Why Calcium Gluconate is the correct answer:** Calcium gluconate (or calcium chloride) is used specifically for **membrane stabilization**. It antagonizes the cardiotoxic effects of high potassium by stabilizing the resting membrane potential of cardiomyocytes [1]. However, it does **not** lower serum potassium levels. It is strictly indicated only when there are **ECG changes** (e.g., peaked T-waves, PR prolongation, widened QRS) or severe hyperkalemia (>6.5 mEq/L) [1]. Since this patient has **no ECG changes**, calcium gluconate is not indicated [1]. **Explanation of other options (Incorrect because they DO treat hyperkalemia):** * **A. Glucose + Insulin:** Insulin promotes the shift of potassium from the extracellular to the intracellular fluid by stimulating the Na+/K+-ATPase pump. Glucose is co-administered to prevent hypoglycemia. * **B. Sodium Bicarbonate:** This induces alkalosis, which causes a hydrogen-potassium exchange, shifting potassium into the cells. It is particularly useful if the patient has underlying metabolic acidosis. * **C. Resins (e.g., Polystyrene sulfonate):** These are cation-exchange resins that bind potassium in the GI tract in exchange for sodium or calcium, facilitating the actual removal of potassium from the body. **NEET-PG High-Yield Pearls:** * **Earliest ECG change:** Tall, tented/peaked T-waves. * **Most definitive treatment:** Hemodialysis. * **Salbutamol (Nebulized):** Another "shifter" that can be used to lower serum potassium. * **Calcium Gluconate vs. Chloride:** Calcium gluconate is preferred for peripheral lines as it is less caustic than calcium chloride.

Question 534: Antibodies against phospholipase A2 receptors are seen in which of the following conditions?

A. Membranous GN (Correct Answer)
B. Membranoproliferative GN
C. Minimal change disease
D. Focal segmental glomerulosclerosis

Explanation: **Explanation:** **1. Why Membranous Glomerulonephritis (MGN) is correct:** The discovery of the **Phospholipase A2 Receptor (PLA2R)** antibody has revolutionized the diagnosis of Primary Membranous Nephropathy. In approximately **70-80% of cases of idiopathic (primary) MGN**, antibodies (mainly IgG4) are directed against the M-type phospholipase A2 receptor, which is a transmembrane protein located on the surface of **podocytes**. The binding of these antibodies leads to in-situ immune complex formation, complement activation, and the characteristic "spike and dome" basement membrane thickening. [1] **2. Why the other options are incorrect:** * **Membranoproliferative GN (MPGN):** This is characterized by the "tram-track" appearance due to mesangial interposition. It is associated with C3 nephritic factor (Type II) or chronic infections like Hepatitis C (Type I), not PLA2R antibodies. [1] * **Minimal Change Disease (MCD):** This involves the effacement of podocyte foot processes but lacks immune complex deposits. It is often associated with T-cell dysfunction and cytokine release. * **Focal Segmental Glomerulosclerosis (FSGS):** This is a pattern of injury caused by podocyte depletion or genetic mutations (e.g., NPHS1/nephrin). While it involves podocytes, it is not mediated by PLA2R antibodies. [1] **3. NEET-PG High-Yield Pearls:** * **Primary MGN:** Most common cause of Nephrotic Syndrome in elderly Caucasians. * **Secondary MGN:** Associated with **Rule of S**: **S**LE (Class V), **S**ol**i**d tumors (Lung/Colon/Breast), **S**yphilis/Hepatitis B, and Drug**s** (Penicillamine, Gold, NSAIDs). * **THSD7A:** Thrombospondin Type-1 Domain-Containing 7A is the *second* most common autoantibody in PLA2R-negative primary MGN. * **Biopsy finding:** Silver stain shows "Spikes"; Immunofluorescence shows granular IgG and C3. [1]

Question 535: A 58-year-old man with cirrhosis complains of worsening fatigue and confusion over the past 5 days. He also reports a declining urinary output over the past 48 hours. On examination, he is gaunt and jaundiced. He has tense ascites and a liver span of 7 cm in the midclavicular line. Lab results reveal a WBC 4600/mm3, Hb 9.4 g/dL, and PCB 29%. BUN of 34 mg/dL and a creatinine of 3.1 mg/dL. A urinary Na <10 mEq/L. What is the most appropriate treatment for his elevated BUN and creatinine?

A. Large volume paracentesis
B. Hemodialysis
C. Mesocaval shunt
D. Liver transplantation (Correct Answer)

Explanation: ### Explanation The clinical presentation of a patient with cirrhosis, tense ascites, worsening encephalopathy (confusion), and acute kidney injury (Creatinine >1.5 mg/dL) with a low urinary sodium (<10 mEq/L) is classic for **Hepatorenal Syndrome (HRS)** [1]. **1. Why Liver Transplantation is the Correct Answer:** HRS is a functional renal failure caused by intense renal vasoconstriction due to portal hypertension and systemic vasodilation. While medical management (Albumin + Terlipressin) can serve as a bridge, **Liver Transplantation** is the only definitive, curative treatment [1]. It reverses the underlying portal hypertension, thereby resolving the stimulus for renal vasoconstriction and restoring normal kidney function [1]. **2. Why the Other Options are Incorrect:** * **Large volume paracentesis (LVP):** While it may relieve abdominal tension, LVP without adequate volume expansion can actually worsen circulatory dysfunction and precipitate or aggravate HRS. * **Hemodialysis:** This is a supportive measure for end-stage renal failure or acute life-threatening electrolyte imbalances. It does not treat the underlying pathophysiology of HRS and is generally reserved for patients awaiting transplant [1]. * **Mesocaval shunt:** Portosystemic shunts (like TIPS or surgical shunts) can sometimes improve renal perfusion, but they carry a high risk of worsening hepatic encephalopathy, which this patient already exhibits [2]. **3. NEET-PG Clinical Pearls:** * **HRS Type 1:** Rapidly progressive (doubling of creatinine in <2 weeks); often triggered by Spontaneous Bacterial Peritonitis (SBP) [1]. * **Diagnostic Hallmark:** AKI in a cirrhotic patient that **fails to improve** after 48 hours of fluid resuscitation (Albumin 1g/kg/day) and the absence of parenchymal kidney disease (no proteinuria/hematuria). * **Urinary Sodium:** Characteristically **<10 mEq/L**, reflecting intact tubular function attempting to conserve volume despite renal ischemia [1].

Question 536: A 25-year-old man presents with a kidney stone. He is married to his first cousin, and six months earlier, his 8-year-old son also had a kidney stone. What is the most likely diagnosis?

A. Autosomal dominant polycystic kidney disease (ADPKD)
B. Medullary cystic kidney disease
C. Fanconi syndrome
D. Cystinuria (Correct Answer)

Explanation: The clinical presentation points toward **Cystinuria**, an autosomal recessive disorder characterized by a defect in the proximal renal tubular amino acid transporter for **COLA** (Cystine, Ornithine, Lysine, and Arginine). **Why Cystinuria is correct:** 1. **Inheritance Pattern:** The mention of a "first-cousin marriage" (consanguinity) strongly suggests an **autosomal recessive** inheritance. 2. **Early Onset:** Kidney stones in an 8-year-old child are highly suggestive of metabolic or genetic defects rather than lifestyle-related urolithiasis [1]. 3. **Pathophysiology:** In cystinuria, the failure to reabsorb cystine leads to high urinary concentrations. Because cystine is poorly soluble in acidic urine, it precipitates to form **hexagonal crystals** and radiolucent (or faintly radiopaque) stones. **Why other options are incorrect:** * **ADPKD:** Follows an autosomal dominant pattern (usually presents in the 3rd–4th decade) and is characterized by bilateral large cystic kidneys and hypertension, not isolated stones in childhood [2]. * **Medullary Cystic Kidney Disease:** Now known as ADTKD, it is autosomal dominant and typically presents with polyuria, salt wasting, and progression to ESRD, rather than recurrent nephrolithiasis [3]. * **Fanconi Syndrome:** Involves a generalized proximal tubule defect (loss of glucose, amino acids, phosphate, etc.). While it causes phosphaturia, it is not a classic cause of recurrent childhood stones. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The **Sodium Nitroprusside test** (Cyanide-nitroprusside test) turns urine purple/red in the presence of cystine. * **Microscopy:** Pathognomonic **hexagonal (benzene ring)** crystals. * **Management:** High fluid intake, **urinary alkalinization** (pH > 7.5), and chelating agents like **Penicillamine** or Tiopronin for refractory cases.

Question 537: What is the cornerstone of therapy for chronic hyponatremia?

A. Vasopressin antagonists
B. Hypertonic 3% saline
C. Water deprivation (Correct Answer)
D. Demeclocycline

Explanation: The cornerstone of therapy for chronic hyponatremia is **Water Deprivation (Fluid Restriction)** [1]. In chronic cases, the body has had time to adapt to lower osmolarity by shedding intracellular organic osmolytes. Rapid correction can lead to Osmotic Demyelination Syndrome (ODS) [1]. Fluid restriction (typically <800–1000 mL/day) is the safest and most effective first-line strategy, particularly in SIADH, as it forces the body to utilize and excrete existing free water, gradually raising serum sodium levels [1]. **Analysis of Options:** * **Hypertonic 3% Saline:** This is the treatment of choice for **acute symptomatic** hyponatremia or emergencies (seizures, coma). In chronic cases, it is avoided unless the patient is severely symptomatic due to the high risk of ODS. * **Vasopressin Antagonists (Vaptans):** While effective for euvolemic and hypervolemic hyponatremia, they are considered second-line therapy due to cost, potential hepatotoxicity (Tolvaptan), and the risk of over-correction. * **Demeclocycline:** This antibiotic induces a form of nephrogenic diabetes insipidus. It is used only in chronic SIADH when fluid restriction fails, but it is rarely a first-line choice due to nephrotoxicity [1]. **NEET-PG High-Yield Pearls:** * **Rate of Correction:** In chronic hyponatremia, do not exceed a correction rate of **8–10 mEq/L in 24 hours** (or <18 mEq/L in 48 hours) [1]. * **ODS Risk:** The pons is most susceptible (Central Pontine Myelinolysis). Clinical features include "locked-in syndrome," dysarthria, and dysphagia, appearing days after rapid correction [1]. * **Formula:** Use the Adrogue-Madias formula to calculate the change in serum sodium per liter of infusate.

Question 538: Which of the following is the LEAST likely to be associated with gross hematuria?

A. Acute glomerulonephritis (Correct Answer)
B. Renal trauma
C. Ureteral calculi
D. Acute cystitis

Explanation: The key to answering this question lies in distinguishing between **glomerular** and **extra-glomerular (urological)** causes of hematuria. **Why Option A is correct:** In **Acute Glomerulonephritis (AGN)**, red blood cells leak through the damaged glomerular basement membrane [1]. This process is typically slow and associated with significant transit time through the nephron, leading to **microscopic hematuria**. When the hematuria is visible, it classically presents as "cola-colored" or "smoky" urine due to the formation of acid hematin. While visible, it is rarely "gross" or bright red with clots, making it the least likely cause of frank, gross hematuria among the choices provided. **Why the other options are incorrect:** * **Renal Trauma (B):** Direct injury to the renal parenchyma or vasculature often leads to significant, bright red bleeding into the collecting system, frequently resulting in gross hematuria. * **Ureteral Calculi (C):** Stones cause mechanical trauma and mucosal erosion as they pass through the ureter. This is a classic cause of sudden-onset gross hematuria, often accompanied by renal colic. * **Acute Cystitis (D):** Severe inflammation of the bladder mucosa (especially in hemorrhagic cystitis) commonly leads to terminal or total gross hematuria [1]. **NEET-PG High-Yield Pearls:** 1. **Glomerular vs. Non-Glomerular:** Glomerular bleeding [1] is characterized by **dysmorphic RBCs** (acanthocytes) and **RBC casts**. Non-glomerular bleeding (trauma, stones, malignancy) features **monomorphic RBCs** and often includes **blood clots**. 2. **Clots:** The presence of blood clots *always* indicates a non-glomerular (urological) source, as urinary urokinase in the tubules inhibits clot formation in glomerular diseases. 3. **Initial vs. Terminal Hematuria:** Initial hematuria suggests a urethral source; terminal hematuria suggests the bladder neck or prostatic urethra.

Question 539: A patient presents with symptoms suggestive of stage IV kidney disease, including anemia and progressive malnutrition. Which of the following glomerular filtration rate (GFR) ranges would be most consistent with this stage of kidney disease?

A. GFR of 60-89 mL/min per 1.73 m2
B. GFR of 30-59 mL/min per 1.73 m2
C. GFR of 15-29 mL/min per 1.73 m2 (Correct Answer)
D. GFR less than 15 mL/min per 1.73 m2

Explanation: Chronic Kidney Disease (CKD) is classified into five stages based on the Glomerular Filtration Rate (GFR), as defined by the KDIGO guidelines. This classification is a high-yield topic for NEET-PG, as clinical manifestations often correlate with the degree of GFR decline [1]. **1. Why Option C is Correct:** **Stage IV CKD** is defined by a **GFR of 15–29 mL/min/1.73 m²**. This stage represents a "severely decreased" GFR [1]. At this point, patients frequently develop significant systemic complications, including **anemia** (due to decreased erythropoietin production), secondary hyperparathyroidism [3], and **progressive malnutrition** (often due to uremic toxins causing anorexia and metabolic acidosis) [2]. This stage is the critical period for preparing the patient for renal replacement therapy (RRT). **2. Analysis of Incorrect Options:** * **Option A (60–89 mL/min):** This corresponds to **Stage II CKD** (mildly decreased GFR). Patients are usually asymptomatic, and anemia or malnutrition at this stage would likely be due to other causes. * **Option B (30–59 mL/min):** This corresponds to **Stage III CKD** (moderately decreased) [1]. While some complications begin to emerge here, Stage IV is the classic presentation for the severity described in the stem. * **Option D (< 15 mL/min):** This corresponds to **Stage V CKD** (Kidney Failure) [1]. At this stage, RRT (dialysis or transplant) is usually indicated as the patient approaches end-stage renal disease (ESRD). **Clinical Pearls for NEET-PG:** * **Stage I:** GFR ≥ 90 (Normal GFR but with evidence of kidney damage, e.g., proteinuria). * **Stage III Split:** Stage IIIa (45–59) and Stage IIIb (30–44). * **Anemia of CKD:** Typically normocytic, normochromic [2]. Treatment involves Erythropoiesis-Stimulating Agents (ESAs) only after ensuring adequate iron stores. * **Diet:** Protein restriction (0.6–0.8 g/kg/day) is often recommended in Stage IV to slow progression, provided the patient is not severely malnourished.

Question 540: A client is diagnosed with chronic renal failure and must start hemodialysis. Client teaching would include which of the following instructions?

A. Follow a high potassium diet.
B. Strictly follow the hemodialysis schedule. (Correct Answer)
C. There will be few changes in your lifestyle.
D. Use alcohol on the skin and clean it due to integumentary changes.

Explanation: **Explanation:** **Why Option B is Correct:** In Chronic Kidney Disease (CKD) Stage 5 (End-Stage Renal Disease), the kidneys can no longer maintain electrolyte balance, fluid homeostasis, or waste excretion. Hemodialysis (HD) serves as a life-sustaining renal replacement therapy [1]. **Strict adherence to the HD schedule** (typically 3 times a week for 4 hours) is critical to prevent life-threatening complications such as hyperkalemia, metabolic acidosis, and pulmonary edema. Missing even a single session significantly increases the risk of cardiovascular mortality. **Why Other Options are Incorrect:** * **Option A:** Patients on HD must follow a **low-potassium diet**. Since the kidneys cannot excrete potassium, high intake can lead to fatal cardiac arrhythmias. * **Option C:** HD requires **massive lifestyle modifications**, including strict fluid restrictions, dietary changes (low sodium, potassium, and phosphorus), and the physical/temporal commitment to the dialysis center [1]. * **Option D:** CKD causes "Uremic Pruritus" and dry skin (xerosis) [1]. Using **alcohol** is contraindicated as it further dries the skin and exacerbates itching. Patients are instead advised to use emollient creams and mild, soap-free cleansers. **NEET-PG Clinical Pearls:** * **Most common cause of death in HD patients:** Cardiovascular disease (not renal failure itself). * **Dietary Protein:** Unlike pre-dialysis CKD (where protein is restricted), patients on HD require **increased protein intake** (1.2–1.3 g/kg/day) due to amino acid loss during the procedure. * **First-use Syndrome:** An anaphylactoid reaction occurring during the first few minutes of HD, often due to Ethylene Oxide used for membrane sterilization. * **Vascular Access:** The **AV Fistula** (Radiocephalic/Brescia-Cimino) is the gold standard due to lower infection and thrombosis rates compared to grafts or catheters [1].

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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Nephrology — MCQs

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