Nephrology — MCQs
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A child with 22-25 stool/day, 3 day old pneumonitis, no passage of urine from 36 hours. low B.P. Blood pH – 7.21. Urine Na+–18 meq/L, S. Urea 120, serum Creatinine 1.2 indicate –
What does the term 'anion gap' refer to in clinical medicine?
Chromosomes associated with autosomal dominant polycystic kidney disease (ADPKD).
Alport syndrome - all are true except?
Which of the following is associated with pauci-immune glomerulonephritis?
Which of these is the Renal feed for CKD patients?
Among the following conditions, which is most likely to cause type 4 renal tubular acidosis?
Most sensitive indicator of iron deficiency in chronic kidney disease?
A diabetic patient presents with painful hemorrhagic bullae on legs. Investigations show raised creatinine. Most likely diagnosis:
A CKD patient develops serum K+ 7.2 mEq/L without ECG changes. Best initial management?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 701: A child with 22-25 stool/day, 3 day old pneumonitis, no passage of urine from 36 hours. low B.P. Blood pH – 7.21. Urine Na+–18 meq/L, S. Urea 120, serum Creatinine 1.2 indicate –
- A. Acute tubular necrosis
- B. Acute cortical necrosis
- C. Acute medullary necrosis
- D. Pre–renal Azotemia (Correct Answer)
Explanation: ***Pre–renal Azotemia*** - Pre-renal azotemia is characterized by **reduced renal perfusion**, leading to decreased glomerular filtration rate and increased reabsorption of water and urea due to activation of the renin-angiotensin-aldosterone system. - The combination of **low blood pressure**, no urine output for 36 hours, metabolic acidosis (pH 7.21), elevated urea (120) and creatinine (1.2), and a relatively normal urine sodium (18 meq/L) despite severe dehydration (22-25 stools/day) is highly indicative of pre-renal azotemia as the kidneys are attempting to conserve sodium and water in response to hypovolemia. *Acute tubular necrosis* - **Acute tubular necrosis (ATN)** typically presents with a **high urine sodium** (>40 meq/L) due to damaged tubules failing to reabsorb sodium effectively, which contradicts the given urine sodium of 18 meq/L. - Although it can cause acute kidney injury with elevated BUN/creatinine and acidosis, the clinical picture here is more consistent with pre-renal causes due to the preserved tubular function indicated by low urine Na+ and oliguria in the setting of severe hypovolemia. *Acute cortical necrosis* - **Acute cortical necrosis** is a rare and severe form of acute kidney injury involving widespread necrosis of the renal cortex, often leading to **irreversible renal failure** and anuria. - While it can present with anuria, it is less common in children with gastroenteritis and hypovolemia, and the initial presentation of preserved tubular function (low urine sodium) points away from significant intrinsic damage. *Acute medullary necrosis* - **Acute medullary necrosis**, also known as **renal papillary necrosis**, primarily affects the renal medulla and papillae, often associated with conditions like sickle cell disease, diabetes, or NSAID abuse. - This condition is unlikely in a child presenting with severe dehydration and hypovolemia from gastroenteritis.
Question 702: What does the term 'anion gap' refer to in clinical medicine?
- A. Imbalance in serum anion levels.
- B. Calculation used to identify metabolic acidosis.
- C. Unmeasured ions
- D. Calculated difference between measured cations and measured anions. (Correct Answer)
Explanation: The term 'anion gap' refers to the calculated difference between measured cations and measured anions in clinical medicine. The anion gap represents the difference between the primary measured cations (sodium and potassium) and primary measured anions (chloride and bicarbonate) in the blood [1]. This calculation helps account for unmeasured anions (e.g., phosphates, sulfates, proteins) and is crucial in evaluating acid-base balance. While the anion gap can reflect an imbalance in anions, this description is too broad. The term specifically refers to a calculated value, not just a general imbalance. The anion gap is primarily used to classify metabolic acidosis into high anion gap or normal anion gap types [1], but its definition itself is not about identifying acidosis. It is a tool for differential diagnosis within metabolic acidosis, not the definition of the gap itself. The anion gap is influenced by unmeasured ions, but it is not synonymous with them. Rather, it's a calculated value that provides an indirect measure or estimate of the concentration of these unmeasured ions [2].
Question 703: Chromosomes associated with autosomal dominant polycystic kidney disease (ADPKD).
- A. 12 and 16
- B. 4 and 16 (Correct Answer)
- C. 6 and 14
- D. 12 and 14
Explanation: ***4 and 16*** - **ADPKD** is primarily associated with mutations in two genes: **PKD1** on chromosome **16** and **PKD2** on chromosome **4** [1]. - Mutations in **PKD1** account for approximately 85% of cases and are associated with a more severe disease course, while mutations in **PKD2** lead to a milder phenotype [1]. *12 and 16* - While chromosome 16 is involved in ADPKD through the **PKD1** gene, chromosome 12 is not typically associated with the primary genes causing this condition. - No major genes for ADPKD have been identified on chromosome 12. *6 and 14* - Neither chromosome 6 nor chromosome 14 harbor the primary gene mutations **(PKD1 or PKD2)** responsible for autosomal dominant polycystic kidney disease. - These chromosomes are known to be associated with other genetic conditions but not ADPKD. *12 and 14* - Similar to the previous option, neither chromosome 12 nor chromosome 14 are linked to the major genetic causes of **ADPKD**. - The key genes **PKD1** and **PKD2** are specifically located on chromosomes 16 and 4, respectively.
Question 704: Alport syndrome - all are true except?
- A. Nerve deafness
- B. X-linked
- C. Cardiac hypertrophy (Correct Answer)
- D. Glomerulonephritis
Explanation: ***Cardiac hypertrophy*** - While patients with **Alport syndrome** can have various systemic manifestations, **cardiac hypertrophy** is not a typical or primary feature of the disease. - The disease primarily affects the **kidneys, ears, and eyes** due to defects in type IV collagen [1]. *Nerve deafness* - **Sensorineural hearing loss** is a common and characteristic extrarenal manifestation of Alport syndrome, often progressive. - This hearing impairment results from structural abnormalities in the **cochlear basement membranes** due to defective **type IV collagen** [1]. *X-linked* - The most common and severe form of Alport syndrome is **X-linked dominant**, accounting for approximately 85% of cases. - This inheritance pattern means that males are typically more severely affected than females. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark of Alport syndrome, leading to **hematuria, proteinuria**, and eventually **end-stage renal disease (ESRD)**. - The glomerular basement membrane (GBM) is abnormally thin and prone to splitting, which impairs its filtering function [1].
Question 705: Which of the following is associated with pauci-immune glomerulonephritis?
- A. Anti-GBM glomerulonephritis
- B. SLE nephritis
- C. IgA nephropathy
- D. Granulomatosis with polyangiitis (GPA) (Correct Answer)
Explanation: ***Granulomatosis with polyangiitis (GPA)*** - **Pauci-immune glomerulonephritis** is characterized by the absence or scarcity of immune complex deposits in the glomeruli. - This is typical of **ANCA-associated vasculitides**, such as GPA (formerly Wegener's granulomatosis), which cause severe necrotising glomerulonephritis with few immune deposits [1]. *Anti-GBM glomerulonephritis* - This condition is characterized by **linear deposition of anti-GBM antibodies** along the glomerular basement membrane, making it an **immune complex-mediated disease**, not pauci-immune [1]. - It involves autoantibodies attacking the **collagen type IV** in the GBM. *SLE nephritis* - Systemic lupus erythematosus (SLE) nephritis is a classic example of **immune complex-mediated glomerulonephritis**, with abundant immune deposits containing immunoglobulins and complement [1]. - The pathology often shows **full-house immunofluorescence** with IgG, IgA, IgM, C3, and C1q. *IgA nephropathy* - This is characterized by prominent **mesangial deposition of IgA immune complexes**, which is clearly an immune complex-mediated process [1]. - While it can present with different histological patterns, the presence of **IgA deposition** means it is not pauci-immune [1].
Question 706: Which of these is the Renal feed for CKD patients?
- A. High calorie low volume (Correct Answer)
- B. High calorie high volume
- C. Low calorie high volume
- D. Low calorie low volume
Explanation: High calorie low volume - This is the ideal feeding approach for CKD patients as it provides adequate energy without stressing the kidneys with excess fluid. - Calorie density is important to meet metabolic needs, while fluid restriction helps manage fluid balance and prevent complications like edema and hypertension. High calorie high volume - While meeting calorie needs, a high volume of fluid can worsen fluid overload, particularly in patients with impaired renal function who struggle to excrete excess water. - This approach can lead to peripheral edema, pulmonary congestion, and elevated blood pressure. Low calorie high volume - A low calorie intake fails to meet the nutritional demands of CKD patients, potentially leading to malnutrition and catabolism. - High fluid volume still poses risks of fluid overload, making this an unsuitable combination for renal patients. Low calorie low volume - Both low calorie and low volume intake can severely compromise the nutritional status of CKD patients. - This would lead to rapid weight loss, muscle wasting, and overall deterioration in health outcomes without adequate energy or fluid balance considerations.
Question 707: Among the following conditions, which is most likely to cause type 4 renal tubular acidosis?
- A. Chronic pyelonephritis
- B. Diabetic nephropathy (Correct Answer)
- C. Systemic lupus
- D. Multiple myeloma
Explanation: ***Diabetic nephropathy*** - **Diabetic nephropathy** is a common cause of **type 4 renal tubular acidosis (RTA)** due to damage to the **juxtaglomerular apparatus** affecting **renin production** and subsequent aldosterone levels. - The resulting **hypoaldosteronism** or **aldosterone resistance** [1] leads to impaired potassium and hydrogen secretion in the **distal tubules**, causing **hyperkalemia** and **metabolic acidosis**. [1] *Chronic pyelonephritis* - While chronic pyelonephritis can lead to **renal scarring** and **chronic kidney disease**, it typically does not directly cause type 4 RTA. - It is more commonly associated with a variety of tubular defects, but not specifically the **hypoaldosteronism** characteristic of type 4 RTA unless severe general renal failure is present. *Systemic lupus* - **Systemic lupus erythematosus (SLE)** can cause **lupus nephritis**, leading to various forms of kidney damage, but it is more commonly associated with **type 1 (distal)** or **type 2 (proximal) RTA**, rather than type 4. - Type 1 RTA in SLE is often due to an **autoimmune attack** on the **distal tubule's ability** to secrete hydrogen ions. *Multiple myeloma* - **Multiple myeloma** is known to cause **renal impairment** primarily through the deposition of **light chains** in the tubules, often leading to **proximal tubular dysfunction** (Fanconi syndrome) or **cast nephropathy**. - This typically results in **type 2 RTA** (proximal RTA) characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate, rather than the distal tubular and aldosterone-related issues seen in type 4 RTA.
Question 708: Most sensitive indicator of iron deficiency in chronic kidney disease?
- A. Transferrin saturation (Correct Answer)
- B. TIBC
- C. Serum iron
- D. Serum ferritin
Explanation: ***Transferrin saturation*** - **Transferrin saturation (TSAT)** is the most sensitive indicator of iron deficiency in chronic kidney disease (CKD) because it reflects the amount of iron available for **erythropoiesis**. - A TSAT below **20%** is usually indicative of **functional iron deficiency**, even if ferritin levels appear normal due to inflammation. *TIBC* - **Total iron-binding capacity (TIBC)** measures the total amount of iron that can be bound by proteins in the blood, primarily transferrin. - While it generally increases in iron deficiency, in CKD, **inflammation** can suppress transferrin synthesis, leading to normal or even decreased TIBC, making it less reliable [2]. *Serum iron* - **Serum iron** levels fluctuate significantly throughout the day and are highly influenced by recent iron intake, making them a **poor indicator** of overall iron stores. - In CKD, systemic inflammation can also lead to **iron sequestration** within macrophages, lowering serum iron despite adequate total body iron [1]. *Serum ferritin* - **Serum ferritin** is a good indicator of overall iron stores but is often **elevated in CKD** due to inflammation, which is common in these patients. - This elevation can **mask true iron deficiency**, as ferritin can be high even when there isn't enough iron available for erythropoiesis (functional iron deficiency) [2].
Question 709: A diabetic patient presents with painful hemorrhagic bullae on legs. Investigations show raised creatinine. Most likely diagnosis:
- A. PCT
- B. Diabetic bullae
- C. Calciphylaxis (Correct Answer)
- D. Bullous pemphigoid
Explanation: ***Calciphylaxis*** - Characterized by **painful hemorrhagic bullae** and ulcers, often on the lower extremities, especially in patients with **end-stage renal disease** or **diabetes**. - **Raised creatinine** indicates kidney dysfunction, which is a significant risk factor for calciphylaxis due to abnormalities in calcium and phosphorus metabolism. *PCT (Porphyria Cutanea Tarda)* - Presents with **fragile skin, blistering, hyperpigmentation**, and **hirsutism** on sun-exposed areas, typically triggered by iron overload or hepatitis C [1]. - While it can cause bullae, the painful hemorrhagic nature and association with severe kidney disease are less typical features compared to calciphylaxis. 'Uraemic porphyria' in renal failure presents similarly but is due to impaired porphyrin elimination [1]. *Diabetic bullae* - Also known as **bullosis diabeticorum**, these are **tense, non-inflammatory, painless blisters** that appear on acral (hands, feet) or non-acral skin. - Unlike the painful hemorrhagic bullae seen here, diabetic bullae are typically non-hemorrhagic and not usually associated with advanced renal failure as a direct cause. *Bullous pemphigoid* - An **autoimmune subepidermal blistering disease** that usually presents as large, **tense bullae** on an erythematous base on the trunk and flexural areas. - Although it presents with bullae, it is typically **pruritic** rather than painful and hemorrhagic, and its association with elevated creatinine is not a primary diagnostic feature.
Question 710: A CKD patient develops serum K+ 7.2 mEq/L without ECG changes. Best initial management?
- A. Emergency dialysis
- B. Sodium polystyrene
- C. Insulin with glucose
- D. Calcium gluconate (Correct Answer)
Explanation: **Calcium gluconate** - **Calcium gluconate** is the best initial management for severe hyperkalemia, particularly when the potassium level is very high (above 6.5 mEq/L) even without ECG changes [1]. It acts quickly to directly stabilize the cardiac membrane by **antagonizing the effects of potassium on myocardial excitability**, thereby preventing life-threatening arrhythmias [1]. - It provides immediate cardioprotection, buying time for other therapies to shift potassium into cells or remove it from the body. *Emergency dialysis* - While **dialysis** is the most effective way to remove potassium from the body, it is typically reserved for cases of severe, refractory hyperkalemia, or when other therapies have failed [3]. - It is not the *initial* management for immediate cardiac stabilization, especially if no ECG changes are present and calcium can be administered more rapidly. *Sodium polystyrene* - **Sodium polystyrene sulfonate (Kayexalate)** is a potassium-binding resin that works in the gastrointestinal tract to exchange sodium for potassium, thus removing potassium from the body. - Its onset of action is slow (hours to days), making it inappropriate for acute, severe hyperkalemia requiring immediate intervention. *Insulin with glucose* - **Insulin with glucose** therapy promotes the intracellular shift of potassium, temporarily lowering serum potassium levels [2]. - While effective, its onset of action is typically 15-30 minutes, and it functions as a temporary measure to redistribute potassium, not to acutely stabilize the cardiac membrane, which is the primary concern when potassium is severely elevated.
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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