Drug-Induced Kidney Injury — MCQs
Which of the following contrast agents is PREFERRED in a patient with renal dysfunction for the prevention of contrast-induced nephropathy?
Which of the following drugs is associated with an untoward side effect of renal tubular damage?
The most common form of acute kidney injury is:
A 52-year-old man was referred to the clinic due to increased abdominal girth. He is diagnosed with ascites by the presence of a fluid thrill and shifting dullness on percussion. After administering diuretic therapy, which nursing action would be most effective in ensuring safe care for this patient?
Drug causing oliguria through prostaglandin inhibition is:
Which of the following drugs shows nephrotoxicity during administration?
Which of the following drugs is associated with untoward side effect of renal tubular damage?
Which drug is least likely to cause exanthematous skin eruptions?
Ulipristal acetate (progesterone receptor modulator) should not be prescribed as emergency contraceptive in women with
Most common cause of postoperative renal failure:
Drug-Induced Kidney Injury Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following contrast agents is PREFERRED in a patient with renal dysfunction for the prevention of contrast-induced nephropathy?
- A. Iso-osmolar contrast (Correct Answer)
- B. High osmolar contrast
- C. Ionic contrast
- D. Low osmolar contrast
Explanation: ***Iso-osmolar contrast*** - **Iso-osmolar contrast agents** (e.g., iodixanol) have an osmolality of ~290 mOsm/kg, which is identical to that of plasma. - **This is the PREFERRED choice** in patients with renal dysfunction as multiple studies demonstrate the lowest risk of contrast-induced nephropathy (CIN). - The iso-osmolar formulation minimizes osmotic stress on renal tubules and reduces the risk of acute kidney injury. - **Current guidelines recommend iso-osmolar agents as first-line** in high-risk patients with pre-existing renal impairment. *Low osmolar contrast* - **Low osmolar contrast agents** have osmolality of 600-900 mOsm/kg, which is significantly lower than high osmolar agents but still 2-3 times higher than plasma. - While **acceptable and safer than high osmolar agents**, they are not as optimal as iso-osmolar contrast for patients with renal dysfunction. - These agents are widely used and represent a reasonable alternative when iso-osmolar agents are not available. *High osmolar contrast* - **High osmolar contrast agents** have osmolality >1400 mOsm/kg (about 5 times that of plasma). - They carry the **highest risk of contrast-induced nephropathy** due to severe osmotic load and direct tubular toxicity. - **Contraindicated or strongly avoided** in patients with pre-existing renal dysfunction. *Ionic contrast* - **Ionic contrast** refers to the chemical structure (dissociates into ions) rather than osmolality. - Can be either high or low osmolar—the ionic nature alone does not determine renal safety. - The critical factor for nephrotoxicity prevention is osmolality, not ionic charge.
Question 2: Which of the following drugs is associated with an untoward side effect of renal tubular damage?
- A. Cisplatin (Correct Answer)
- B. Streptozocin
- C. Methysergide
- D. Cyclophosphamide
Explanation: ***Cisplatin*** - **Cisplatin** is the **classic and most prominent example** of a drug causing **direct renal tubular damage**, specifically **acute tubular necrosis (ATN)** - Nephrotoxicity is **dose-limiting** and occurs in up to 30% of patients, making it the hallmark side effect - Mechanism: Direct toxic injury to proximal and distal tubular epithelial cells with mitochondrial dysfunction - Results in reduced GFR, electrolyte disturbances (hypomagnesemia, hypokalemia), and potentially irreversible renal impairment - **Most closely associated** with the term "renal tubular damage" in medical education *Streptozocin* - Streptozocin is also nephrotoxic and can cause proximal tubular dysfunction - However, it manifests more specifically as **Fanconi syndrome** (glycosuria, phosphaturia, aminoaciduria) rather than the classic acute tubular necrosis pattern - Its toxicity profile is more complex, affecting both pancreatic beta cells and renal tubules - While it causes tubular dysfunction, it is **not the primary drug** associated with direct tubular damage in standard teaching *Methysergide* - Methysergide causes **retroperitoneal fibrosis**, not direct renal tubular damage - Kidney injury occurs **indirectly** through ureteral obstruction and compression - Does not cause intrinsic tubular cell injury *Cyclophosphamide* - Primary toxicity is **hemorrhagic cystitis** due to acrolein metabolite affecting the bladder - Does not cause significant direct renal tubular damage - Renal effects are minimal compared to bladder toxicity, which can be prevented with hydration and mesna
Question 3: 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 4: A 52-year-old man was referred to the clinic due to increased abdominal girth. He is diagnosed with ascites by the presence of a fluid thrill and shifting dullness on percussion. After administering diuretic therapy, which nursing action would be most effective in ensuring safe care for this patient?
- A. Measuring serum potassium for hypokalemia
- B. Assessing the client for hypovolemia
- C. Measuring the client’s weight weekly
- D. Documenting precise intake and output (Correct Answer)
Explanation: ***Documenting precise intake and output*** - **Accurate intake and output (I&O)** monitoring helps track fluid balance and the effectiveness of diuretic therapy in reducing ascites [1]. - This data is crucial for adjusting diuretic dosages and preventing complications like **dehydration** or **fluid overload** [2]. *Measuring serum potassium for hypokalemia* - While monitoring electrolytes is important, **hypokalemia** is a potential side effect of some diuretics, but not the *most effective* immediate nursing action for *safe care* post-diuretic administration for ascites [3]. - This is an important monitoring parameter, but not the primary action for overall safe care in this context. *Assessing the client for hypovolemia* - **Hypovolemia** is a risk with aggressive diuretic therapy, but frequently reassessing **I&O** provides more concrete data to *prevent* this complication rather than just *assessing* for it after it may have started [1]. - While important, focusing on the *outcome* rather than the *preventative measure* makes it less effective as a primary safe care action. *Measuring the client’s weight weekly* - **Weekly weight measurement** is a useful tool for tracking fluid shifts over time but is not immediate enough to ensure *safe care* after diuretic administration [3]. - **Daily weight measurements** or even more frequent monitoring might be warranted, but precise **I&O** provides real-time data for fluid balance decisions.
Question 5: Drug causing oliguria through prostaglandin inhibition is:
- A. Aspirin (Correct Answer)
- B. Montelukast
- C. Diazepam
- D. Acyclovir
Explanation: ***Aspirin*** - **Aspirin** and other **NSAIDs** cause oliguria by **inhibiting cyclooxygenase (COX)**, which reduces prostaglandin synthesis - Prostaglandins (especially PGE2 and PGI2) normally maintain renal vasodilation and adequate glomerular filtration - **Inhibition leads to**: Afferent arteriolar vasoconstriction → ↓ Renal blood flow → ↓ GFR → **Oliguria** - **High-risk patients**: Pre-existing renal disease, heart failure, volume depletion, elderly - This is a **hemodynamic/functional** renal impairment *Montelukast* - **Leukotriene receptor antagonist** used for asthma and allergic rhinitis - Acts on airways, not kidneys - No significant association with oliguria or renal dysfunction *Diazepam* - **Benzodiazepine** acting on CNS GABA receptors - Used for anxiety, seizures, muscle relaxation - No direct renal effects or oliguria association *Acyclovir* - **Antiviral drug** that can cause nephrotoxicity via **crystal formation** in renal tubules (crystal nephropathy) - Can lead to acute kidney injury and oliguria, especially with rapid IV infusion or dehydration - However, mechanism is **direct tubular toxicity**, NOT prostaglandin inhibition - The question specifically asks for prostaglandin-mediated oliguria, making **Aspirin** the correct answer
Question 6: Which of the following drugs shows nephrotoxicity during administration?
- A. Azathioprine
- B. Tacrolimus (Correct Answer)
- C. Mycophenolate mofetil
- D. Leflunomide
Explanation: ***Tacrolimus*** - **Tacrolimus** is a calcineurin inhibitor and a well-known cause of **nephrotoxicity**, which can manifest as acute kidney injury or chronic renal dysfunction [1], [4]. - Its mechanism involves vasoconstriction of afferent arterioles and direct tubular toxicity, leading to reduced glomerular filtration. *Azathioprine* - **Azathioprine** is an immunosuppressant primarily associated with **bone marrow suppression** (leukopenia, thrombocytopenia) and **hepatotoxicity**, not typically nephrotoxicity [2]. - While it can cause renal impairment in rare cases, it is not a primary mechanism of action. *Mycophenolate mofetil* - **Mycophenolate mofetil (MMF)** is an immunosuppressant that primarily causes **gastrointestinal side effects** (diarrhea, nausea) and **myelosuppression**. - It is generally considered **renal-sparing** and is often used in situations where calcineurin inhibitors are contraindicated due to nephrotoxicity. *Leflunomide* - **Leflunomide** is an immunosuppressant used in rheumatoid arthritis, known for causing **hepatotoxicity**, **hypertension**, and **teratogenicity** [3]. - While it can affect various organ systems, direct and significant nephrotoxicity is not a prominent adverse effect.
Question 7: Which of the following drugs is associated with untoward side effect of renal tubular damage?
- A. Streptozotocin
- B. Methysergide
- C. Cyclophosphamide
- D. Cisplatin (Correct Answer)
Explanation: ***Cisplatin*** - **Cisplatin** is a platinum-based chemotherapy drug well-known for its dose-limiting nephrotoxicity, primarily causing **renal tubular damage**. - Its mechanism involves direct DNA damage within renal tubular cells, leading to **acute tubular necrosis** if not managed with aggressive hydration and other protective measures. *Streptozotocin* - **Streptozotocin** is an alkylating agent primarily used in treating **pancreatic neuroendocrine tumors**; its main toxicity is typically to pancreatic beta cells (leading to hypoglycemia) and to the liver. - While it can be nephrotoxic, its predominant and most recognized untoward side effect is not renal tubular damage, but rather **pancreatic beta-cell destruction**. *Methysergide* - **Methysergide** is an ergot alkaloid used for **migraine prophylaxis** but is largely discontinued due to severe side effects like **retroperitoneal fibrosis**. - Renal damage in the context of methysergide is typically due to this fibrosis compressing the ureters, rather than direct tubular toxicity. *Cyclophosphamide* - **Cyclophosphamide** is an alkylating agent known for its immunosuppressive and chemotherapeutic effects; its major side effects include **hemorrhagic cystitis** and myelosuppression. - While high doses can cause nephrotoxicity, its primary and most feared renal-related toxicity is hemorrhagic cystitis, not direct tubular damage as seen with cisplatin.
Question 8: Which drug is least likely to cause exanthematous skin eruptions?
- A. Phenytoin
- B. Ampicillin
- C. Phenylbutazone
- D. Hydrocortisone (Correct Answer)
Explanation: ***Hydrocortisone*** - **Corticosteroids** like hydrocortisone are **anti-inflammatory** and immunosuppressive agents. - They are commonly used to **treat allergic reactions** and skin eruptions, making them highly unlikely to cause exanthematous eruptions themselves. *Phenytoin* - **Anticonvulsant** medications like phenytoin are frequently associated with various **drug-induced skin reactions**, including exanthematous eruptions. - It is a common cause of **drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome**, which manifests with a widespread rash. *Ampicillin* - **Antibiotics**, particularly **aminopenicillins** like ampicillin, are well-known triggers for **maculopapular rashes** and other exanthematous eruptions. - The incidence of ampicillin-induced rash is notably higher, especially in patients with **viral infections** like infectious mononucleosis. *Phenylbutazone* - This **non-steroidal anti-inflammatory drug (NSAID)** has a documented history of causing severe cutaneous adverse reactions, including **exanthematous eruptions**. - Due to its potential for serious side effects, such as **aplastic anemia** and severe skin reactions, its use is now highly restricted.
Question 9: Ulipristal acetate (progesterone receptor modulator) should not be prescribed as emergency contraceptive in women with
- A. liver dysfunction (Correct Answer)
- B. glaucoma
- C. coagulopathy
- D. kidney failure
Explanation: ***Correct: liver dysfunction*** - **Ulipristal acetate** is extensively metabolized in the **liver** by the CYP450 enzyme system, predominantly CYP3A4. - In individuals with **severe hepatic impairment**, the metabolism of ulipristal acetate can be impaired, leading to increased plasma concentrations and potential adverse effects. - **Severe liver dysfunction** is a documented contraindication in product labeling. *Incorrect: glaucoma* - There is **no known contraindication** for ulipristal acetate use in individuals with **glaucoma**. - Its mechanism of action primarily involves progesterone receptors and does not directly impact intraocular pressure. *Incorrect: coagulopathy* - Ulipristal acetate does **not significantly affect blood coagulation** parameters or platelet function. - It is not contraindicated in individuals with **coagulopathy**, unlike some estrogen-containing contraceptives. *Incorrect: kidney failure* - While urinary excretion of ulipristal acetate metabolites occurs, the **primary elimination pathway is fecal** (approximately 90%). - **Kidney failure** is not considered a contraindication, and dose adjustments are generally not required.
Question 10: Most common cause of postoperative renal failure:
- A. Decreased renal perfusion (Correct Answer)
- B. Toxicity of anesthetic drugs
- C. Toxicity of antibiotics
- D. None of the options
Explanation: **Decreased renal perfusion** - **Hypovolemia** and **hypotension** during or after surgery are frequent causes of reduced blood flow to the kidneys, leading to **ischemic injury**. - This inadequate perfusion results in **acute tubular necrosis (ATN)**, which is the most common intrinsic cause of postoperative acute renal failure. - Accounts for the majority (50-80%) of postoperative acute kidney injury cases. *Toxicity of anesthetic drugs* - While some anesthetic agents, particularly older ones, could be nephrotoxic, modern anesthetics are generally **well-tolerated** by the kidneys and rarely cause direct renal failure. - **Nephrotoxicity** from anesthetic drugs is an uncommon cause compared to the widespread issue of inadequate renal perfusion during surgical stress. *Toxicity of antibiotics* - Certain antibiotics, such as **aminoglycosides** (e.g., gentamicin) and **vancomycin**, are known to be nephrotoxic. However, their use is often monitored, and renal failure due to antibiotic toxicity is less common and often preventable compared to hypovolemia. - **Antibiotic-induced nephrotoxicity** typically presents with ATN but is not the most frequent cause in the general postoperative population. *None of the options* - This option is incorrect because **decreased renal perfusion** is, in fact, a widely recognized and leading cause of postoperative renal failure.
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