Nephrology Practice Questions

Q: 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 –

Pre–renal Azotemia. ***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.

Q: Chromosomes associated with autosomal dominant polycystic kidney disease (ADPKD).

4 and 16. ***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.

Q: Alport syndrome - all are true except?

Cardiac hypertrophy. ***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].

Q: Which of the following is associated with pauci-immune glomerulonephritis?

Granulomatosis with polyangiitis (GPA). ***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].

Q: Which of these is the Renal feed for CKD patients?

High calorie low volume. 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.

Q: Among the following conditions, which is most likely to cause type 4 renal tubular acidosis?

Diabetic nephropathy. ***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.

Q: Most sensitive indicator of iron deficiency in chronic kidney disease?

Transferrin saturation. ***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].

Q: A diabetic patient presents with painful hemorrhagic bullae on legs. Investigations show raised creatinine. Most likely diagnosis:

Calciphylaxis. ***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.

Q: A CKD patient develops serum K+ 7.2 mEq/L without ECG changes. Best initial management?

Calcium gluconate. **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.

Question 1

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 –

Accepted Answer

Pre–renal Azotemia

Answer

Acute tubular necrosis

Answer

Acute cortical necrosis

Answer

Acute medullary necrosis

Question 2

What does the term 'anion gap' refer to in clinical medicine?

Accepted Answer

Calculated difference between measured cations and measured anions.

Answer

Imbalance in serum anion levels.

Answer

Calculation used to identify metabolic acidosis.

Answer

Unmeasured ions

Question 3

Chromosomes associated with autosomal dominant polycystic kidney disease (ADPKD).

Accepted Answer

4 and 16

Answer

12 and 16

Answer

6 and 14

Answer

12 and 14

Question 4

Alport syndrome - all are true except?

Accepted Answer

Cardiac hypertrophy

Answer

Nerve deafness

Answer

X-linked

Answer

Glomerulonephritis

Question 5

Which of the following is associated with pauci-immune glomerulonephritis?

Accepted Answer

Granulomatosis with polyangiitis (GPA)

Answer

Anti-GBM glomerulonephritis

Answer

SLE nephritis

Answer

IgA nephropathy

Question 6

Which of these is the Renal feed for CKD patients?

Accepted Answer

High calorie low volume

Answer

High calorie high volume

Answer

Low calorie high volume

Answer

Low calorie low volume

Question 7

Among the following conditions, which is most likely to cause type 4 renal tubular acidosis?

Accepted Answer

Diabetic nephropathy

Answer

Chronic pyelonephritis

Answer

Systemic lupus

Answer

Multiple myeloma

Question 8

Most sensitive indicator of iron deficiency in chronic kidney disease?

Accepted Answer

Transferrin saturation

Answer

TIBC

Answer

Serum iron

Answer

Serum ferritin

Question 9

A diabetic patient presents with painful hemorrhagic bullae on legs. Investigations show raised creatinine. Most likely diagnosis:

Accepted Answer

Calciphylaxis

Answer

PCT

Answer

Diabetic bullae

Answer

Bullous pemphigoid

Question 10

A CKD patient develops serum K+ 7.2 mEq/L without ECG changes. Best initial management?

Accepted Answer

Calcium gluconate

Answer

Emergency dialysis

Answer

Sodium polystyrene

Answer

Insulin with glucose

Nephrology — MCQs

Nephrology — MCQs

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