Acute Kidney Injury — MCQs

10 questions

The following are causes of hematuria in childhood except

Regarding FeNa, which of the following is true?

The most appropriate investigation to diagnose and determine the extent of renal injury in a 15-year-old boy who presents with hematuria and left-sided abdominal pain 48 hours after sustaining a blunt abdominal injury, with a pulse rate of 96/minute, blood pressure of 110/70 mmHg, hemoglobin of 10.8 gm%, and packed cell volume of 31%, would be-

The most common form of acute kidney injury is:

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 –

Hemolytic uremic syndrome is caused by:

Best immediate management of hyperkalemia includes all except?

All are used for management of hyperkalemia except?

Oliguria is defined as:-

Q10

A 75-year-old man with chronic kidney disease presents with worsening dyspnea and lower extremity edema. Which class of drugs should be used cautiously in this patient?

Acute Kidney Injury Indian Medical PG Practice Questions and MCQs

Question 1: The following are causes of hematuria in childhood except

A. Alpha thalassemia (Correct Answer)
B. Alport syndrome
C. Factor V Leiden mutation
D. E. coli O157

Explanation: ***Alpha thalassemia*** - **Alpha thalassemia** primarily affects **hemoglobin production**, leading to anemia. It does not directly cause hematuria. - While severe anemia can sometimes lead to organ dysfunction, hematuria is not a characteristic or direct symptom of alpha thalassemia itself. *Alport syndrome* - **Alport syndrome** is a genetic disorder affecting the **glomerular basement membrane**, leading to microscopic or macroscopic hematuria, proteinuria, and progressive renal failure. - It classically presents with **hematuria in childhood**, often accompanied by hearing loss and ocular abnormalities. *Factor V Leiden mutation* - The **Factor V Leiden mutation** increases the risk for **thrombophilia** and **venous thromboembolism**. - While it can lead to clots in renal veins, causing hematuria, its primary manifestation is not direct hematuria but rather a predisposition to thrombosis that can secondarily cause it. *E. coli O157* - **_E. coli_ O157 infection** can cause **hemolytic uremic syndrome (HUS)**, particularly in children. - HUS is characterized by a **microangiopathic hemolytic anemia**, thrombocytopenia, and acute kidney injury, which often manifests with hematuria due to glomerular damage.

Question 2: Regarding FeNa, which of the following is true?

A. Measurement of FeNa is NOT affected by use of diuretic
B. FeNa is higher in intrinsic renal failure than pre renal failure (Correct Answer)
C. FeNa is lower in neonates when compared to children
D. FeNa is similar in both pre term and term neonate

Explanation: ***FeNa is higher in intrinsic renal failure than pre renal failure*** - In **intrinsic renal failure**, the kidneys lose their ability to conserve sodium effectively, leading to a **higher fractional excretion of sodium (FeNa)**, typically > 2%. - Conversely, in **prerenal failure**, the kidneys avidly reabsorb sodium to compensate for decreased renal perfusion, resulting in a **low FeNa**, usually < 1%. *Measurement of FeNa is NOT affected by use of diuretic* - The use of **diuretics** significantly impacts FeNa by directly inhibiting sodium reabsorption, thus rendering FeNa values unreliable for distinguishing between prerenal and intrinsic acute kidney injury [1]. - When a patient is on diuretics, the FeNa will be artificially elevated, regardless of the underlying cause of kidney injury [1]. *FeNa is lower in neonates when compared to children* - **Neonates** generally have a **higher FeNa** compared to older children because their immature renal tubules are less efficient at reabsorbing sodium. - As the kidneys mature during infancy and childhood, sodium reabsorption improves, leading to lower FeNa values. *FeNa is similar in both pre term and term neonate* - **Preterm neonates** typically have a **higher FeNa** than full-term neonates due to even greater renal immaturity, particularly in tubular function. - Their kidneys are less developed, resulting in a reduced capacity for sodium reabsorption compared to full-term infants.

Question 3: The most appropriate investigation to diagnose and determine the extent of renal injury in a 15-year-old boy who presents with hematuria and left-sided abdominal pain 48 hours after sustaining a blunt abdominal injury, with a pulse rate of 96/minute, blood pressure of 110/70 mmHg, hemoglobin of 10.8 gm%, and packed cell volume of 31%, would be-

A. Sonographic evaluation of abdomen
B. Intravenous pyelography
C. Contrast enhanced computed tomography (Correct Answer)
D. MR urography

Explanation: ***Contrast enhanced computed tomography*** - **CT with intravenous contrast** is the gold standard for evaluating **renal trauma**, providing detailed anatomical information on the extent of injury, including lacerations, hematomas, and urinary extravasation, which might be missed by other modalities. - It rapidly assesses the **parenchyma**, **collecting system**, and surrounding structures, allowing for proper staging of the injury and guiding management decisions. *Sonographic evaluation of abdomen* - **Ultrasound** is useful for rapidly detecting **free fluid** (e.g., blood) in the abdomen and assessing major organ integrity, but its ability to characterize renal parenchymal injuries or urinary extravasation is limited. - It is **operator-dependent** and often insufficient for detailed staging of renal trauma compared to CT. *Intravenous pyelography* - **IVP** primarily evaluates the **collecting system** and ureteral patency but has limited sensitivity for assessing renal parenchymal injuries or perinephric hematomas. - It involves radiation exposure and a contrast load, and generally provides **less anatomical detail** than modern CT scans. *MR urography* - **MR urography** provides excellent soft tissue contrast without ionizing radiation, but it is typically **less readily available** in an emergency setting and takes longer to perform than CT. - Its role in acute trauma is usually reserved for cases where **iodinated contrast is contraindicated** (e.g., severe allergy, renal insufficiency) or when specific soft-tissue detail is crucial for follow-up.

Question 4: The most common form of acute kidney injury is:

A. Prerenal azotemia (Correct Answer)
B. Acute tubular injury
C. Acute interstitial nephritis
D. Acute glomerular disease

Explanation: ***Prerenal azotemia*** - This is the most prevalent form of **acute kidney injury (AKI)**, accounting for approximately 50-60% of all cases [1]. - It results from **decreased renal perfusion**, leading to reduced glomerular filtration without direct damage to the kidney parenchyma [1]. *Acute tubular injury* - This is an **intrinsic form of AKI** characterized by damage to the renal tubules, often due to ischemia or nephrotoxins [1]. - While common, it is usually a consequence of prolonged or severe prerenal AKI, and thus not the *most* common initial cause [1]. *Acute interstitial nephritis* - This involves inflammation of the kidney's **interstitial tissue**, often triggered by **allergic reactions to medications** or infections [2]. - It represents a smaller percentage of AKI cases compared to prerenal causes. *Acute glomerular disease* - This form of AKI involves direct injury to the **glomeruli**, such as in glomerulonephritis [2]. - While serious, glomerular diseases are significantly less common as a cause of overall AKI compared to prerenal factors.

Question 5: 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 6: Hemolytic uremic syndrome is caused by:

A. Streptococcus pneumoniae
B. Shiga toxin-producing E. coli and complement dysregulation (Correct Answer)
C. Streptococcus pneumoniae and complement dysregulation
D. Streptococcus pneumoniae and adenovirus
E. Enteroinvasive E. coli

Explanation: Shiga toxin-producing E. coli and complement dysregulation - The most common cause of **hemolytic uremic syndrome (HUS)** is infection with **Shiga toxin-producing E. coli (STEC)**, typically O157:H7, leading to typical HUS [1]. - Atypical HUS (aHUS) is primarily caused by **complement dysregulation**, often due to genetic mutations in complement regulatory proteins [1]. *Streptococcus pneumoniae* - *Streptococcus pneumoniae* can cause HUS, but it is typically associated with **pneumococcal-associated HUS**, a less common form. - The mechanism involves neuraminidase production by the bacteria, which exposes T-antigen on red blood cells, leading to their destruction. *Streptococcus pneumoniae and complement dysregulation* - While both can cause HUS, *Streptococcus pneumoniae* and **complement dysregulation** are typically distinct causes, leading to different forms of the syndrome. - This option incorrectly combines the primary causes of two different subtypes of HUS. *Streptococcus pneumoniae and adenovirus* - *Streptococcus pneumoniae* can cause HUS, but **adenovirus** is not a generally recognized cause of HUS. - HUS is primarily linked to bacterial toxins or genetic complement defects, not typically viral infections like adenovirus. *Enteroinvasive E. coli* - **Enteroinvasive E. coli (EIEC)** causes a dysentery-like illness but does not produce Shiga toxin. - HUS is specifically triggered by toxins that damage endothelial cells, which EIEC does not produce.

Question 7: Best immediate management of hyperkalemia includes all except?

A. Salbutamol nebulization
B. Insulin drip
C. Calcium gluconate
D. MgSO4 (Correct Answer)

Explanation: ***MgSO4*** - **Magnesium sulfate** is not used for the immediate management of **hyperkalemia**; its primary uses include treating hypomagnesemia, eclampsia, and certain arrhythmias. - While magnesium can have effects on electrolyte balance, it directly addresses calcium or potassium levels in an acute hyperkalemic crisis. *Calcium gluconate* - **Calcium gluconate** is crucial for **cardiac stabilization** in hyperkalemia by protecting the myocardium from potassium's effects [1]. - It does not lower potassium levels but prevents life-threatening arrhythmias by antagonizing the cardiac membrane effects of potassium [1]. *Insulin drip* - An **insulin drip** (often with dextrose) shifts potassium **intracellularly**, thereby lowering serum potassium levels [1]. - This effect is rapid, making it an effective measure for immediate management. *Salbutamol nebulization* - **Salbutamol (albuterol)** nebulization can also help shift potassium into cells, thus reducing serum potassium levels. - It works by stimulating beta-2 adrenergic receptors, which activate the **Na+/K+-ATPase pump**.

Question 8: All are used for management of hyperkalemia except?

A. Insulin plus dextrose
B. Beta 2 agonist
C. Calcium gluconate
D. ACE inhibitors (Correct Answer)

Explanation: ***ACE inhibitors*** - **ACE inhibitors** (Angiotensin-Converting Enzyme inhibitors) are a common cause of **hyperkalemia** because they block the production of aldosterone, which normally promotes potassium excretion [1]. - Therefore, ACE inhibitors would worsen hyperkalemia rather than treat it. *Insulin plus dextrose* - **Insulin** drives potassium into cells, thereby lowering serum potassium levels; **dextrose** is given concurrently to prevent hypoglycemia [1]. - This is a rapid and effective treatment for acute hyperkalemia, especially in emergent situations [1]. *Beta 2 agonist* - **Beta-2 adrenergic agonists** (e.g., albuterol) stimulate the sodium-potassium pump, promoting the intracellular shift of potassium. - This effect helps to decrease extracellular potassium levels, making it a viable treatment option for hyperkalemia. *Calcium gluconate* - **Calcium gluconate** does not lower serum potassium levels but stabilizes the cardiac cell membrane potential, reducing the risk of arrhythmias caused by hyperkalemia [1]. - It is often the first-line treatment in hyperkalemic emergencies with ECG changes [1].

Question 9: Oliguria is defined as:-

A. More than 900 ml of urine excreted in a day
B. Absence of urine production
C. 600 ml to 700 ml of urine excreted in a day
D. Less than 400 ml of urine excreted in a day (Correct Answer)

Explanation: ***Less than 400 ml of urine excreted in a day*** - Oliguria is clinically defined as **urine production** of less than **400-500 mL per 24 hours** in adults. - This reduction in urine output is often a critical sign of acute kidney injury or other underlying medical conditions impacting **renal function**. *More than 900 ml of urine excreted in a day* - This volume is within the normal range of **daily urine output** for an adult, which is typically between **800 mL and 2000 mL**. - It does not represent oliguria, which indicates a significantly **decreased urine production**. *Absence of urine production* - The complete absence of urine production is known as **anuria**, which is a more severe condition than oliguria. - Anuria is typically defined as less than **50 mL of urine per 24 hours**. *600 ml to 700 ml of urine excreted in a day* - While this volume is below the typical average, it does not meet the strict clinical definition of oliguria, which is typically set at **less than 400-500 mL/day**. - This range might be considered **borderline decreased** but is not severe enough to be classified as oliguric by most standards.

Question 10: A 75-year-old man with chronic kidney disease presents with worsening dyspnea and lower extremity edema. Which class of drugs should be used cautiously in this patient?

A. NSAIDs (Correct Answer)
B. Beta-blockers
C. Diuretics
D. ACE inhibitors

Explanation: ***NSAIDs*** - **NSAIDs** can cause **acute kidney injury** by inhibiting prostaglandin synthesis, which leads to **afferent arteriolar vasoconstriction** and reduced renal blood flow. This effect is exaggerated in patients with **pre-existing chronic kidney disease**. - They also can exacerbate **fluid retention** and worsen **edema** and symptoms of **heart failure**, which is particularly problematic in a patient with dyspnea and lower extremity edema. *ACE inhibitors* - While generally beneficial in CKD to slow progression, **ACE inhibitors** can cause **acute kidney injury** in patients with **renal artery stenosis** or severe volume depletion due to efferent arteriolar vasodilation. - They can also lead to **hyperkalemia**, which requires monitoring, but they are not contraindicated in this patient's presentation per se. *Beta-blockers* - **Beta-blockers** are often prescribed for cardiovascular conditions common in CKD patients, such as **hypertension** and **heart failure**, and are generally safe in CKD with appropriate dosing. - While some beta-blockers are renally excreted, their primary mechanism does not directly worsen kidney function or fluid retention in the same way NSAIDs do. *Diuretics* - **Diuretics** are essential in managing fluid overload, dyspnea, and edema in patients with **chronic kidney disease** and heart failure. - Although loop diuretics may be less effective with reduced kidney function and higher doses might be needed, they are not typically used cautiously; rather, they are a cornerstone of treatment for these symptoms.

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