# A hospitalized client develops early acute kidney injury after several days of vomiting and exposure to nephrotoxic medications. For each finding or intervention, select the best classification.

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=396180&lang=en  
> language: en  
> subject: Potential for Alterations in Body Systems  
> category: ROR

## Question

A hospitalized client develops early acute kidney injury after several days of vomiting and exposure to nephrotoxic medications. For each finding or intervention, select the best classification.

|  | Evidence of AKI or kidney hypoperfusion | Kidney-protective assessment or response | Unsafe or unsupported action |
| --- | --- | --- | --- |
| Serum creatinine rises from 0.9 to 1.4 mg/dL with urine output below 0.5 mL/kg/hr for 7 hours |  |  |  |
| Review nephrotoxic and renally cleared drugs with the prescriber and adjust monitoring or dosing |  |  |  |
| Administer prescribed isotonic crystalloid for assessed intravascular depletion and reassess hemodynamics, urine output, and lungs |  |  |  |
| Trend intake and output, creatinine, potassium, bicarbonate, daily weight, and fluid balance |  |  |  |
| Give prophylactic furosemide solely to prevent AKI in a client without volume overload |  |  |  |
| Continue the NSAID without review despite rising creatinine and sustained oliguria |  |  |  |

## Explanation

The creatinine increase and sustained oliguria meet AKI criteria and require prompt cause assessment. Review and question nephrotoxic or renally cleared medications, trend creatinine, urine output, electrolytes, weight, and fluid balance, and correct true intravascular depletion with prescribed isotonic crystalloid while reassessing response. Do not use prophylactic furosemide solely to prevent AKI or continue NSAIDs during rising creatinine without review.

## In-depth explanation

Quick answer
Recognize AKI from the creatinine rise and oliguria, look for reversible causes, stop or adjust harmful exposures through the prescriber, restore true volume deficits, and monitor trends closely.

Why this is correct
AKI is identified by changes in serum creatinine and urine output. Volume depletion and nephrotoxic drugs can be reversible contributors, but treatment must be individualized because both under-resuscitation and fluid overload can cause harm.

Easy analogy or mental picture
The kidneys need adequate flow and a low toxin burden. Restore the supply line, remove avoidable stressors, and watch the output gauge.

Memory hook
Trend creatinine and urine, review toxins, correct volume, reassess.

NCLEX decision rule
Use trends rather than a single value. Measure urine output, creatinine, electrolytes, and fluid balance; promptly evaluate reversible causes; adjust renally cleared drugs; and use prescribed isotonic crystalloid for true intravascular depletion. Diuretics do not prevent AKI and are reserved for specific indications such as volume overload.

Why the other choices are wrong
Continuing an NSAID during a rising creatinine ignores a modifiable exposure. Prophylactic furosemide does not prevent AKI, and forcing fluid without assessing volume status can worsen pulmonary edema or other complications.

Source
1KDIGO Clinical Practice Guideline for Acute Kidney Injury
2KDIGO AKI/AKD Guideline Resource Page
32026 NCLEX-RN Test Plan

## Clinical scenario

Serum creatinine has increased from 0.9 to 1.4 mg/dL and urine output has remained below 0.5 mL/kg/hr for 7 hours. The client has dry mucous membranes and orthostatic hypotension. The medication list includes an NSAID and a renally cleared antibiotic. Prescribed isotonic crystalloid and laboratory monitoring are available.

## Key concepts

- **Acute kidney injury** — An abrupt decline in kidney function identified through changes in serum creatinine, urine output, or both.
- **Oliguria** — Urine output below the expected rate; sustained output below 0.5 mL/kg/hr is part of AKI staging criteria.
- **Nephrotoxin stewardship** — Systematic review, avoidance, monitoring, and dose adjustment of drugs or exposures that can injure the kidneys.

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