# A nurse is caring for a client receiving cisplatin chemotherapy. Which nursing intervention is the most important priority to prevent nephrotoxicity?

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## 문제

A nurse is caring for a client receiving cisplatin chemotherapy. Which nursing intervention is the most important priority to prevent nephrotoxicity?

A 58-year-old client with ovarian cancer is receiving cisplatin as part of combination chemotherapy. The client's baseline creatinine is 0.9 mg/dL and BUN is 18 mg/dL. This is the client's third cycle of treatment.

## 보기

1. Monitor serum creatinine and blood urea nitrogen levels every 8 hours
2. Administer prescribed antiemetics 30 minutes before chemotherapy
3. Assess for signs of peripheral neuropathy daily
4. Ensure adequate hydration with normal saline before and after infusion **✔ 정답**

**정답: 4**

## 해설

Cisplatin is highly nephrotoxic; pre- and post-hydration with normal saline is critical to maintain urine output and dilute drug concentration, preventing acute kidney injury. Other options are important but not the highest priority for nephrotoxicity prevention.

## 심화 해설

Clinical Context

Cisplatin is a highly effective platinum-based antineoplastic agent used for solid tumors such as ovarian cancer, but its clinical utility is significantly limited by dose-dependent nephrotoxicity. The client in this scenario has a baseline serum creatinine of 0.9 mg/dL and BUN of 18 mg/dL, which are within normal limits, but the risk of acute kidney injury (AKI) escalates with cumulative cycles. Cisplatin-induced nephrotoxicity (CIN) occurs in approximately 30% of patients and is primarily driven by the accumulation of cisplatin within renal proximal tubular cells, where it forms toxic thiol-cisplatin conjugates via the enzyme cysteine conjugate β-lyase 1 [1][4]. This process leads to tubular cell apoptosis, oxidative stress, and a decline in glomerular filtration rate.

Answer Rationale

The most important priority nursing intervention to prevent CIN is **ensuring adequate hydration with normal saline before and after infusion** (Option 4). Aggressive intravenous volume expansion with isotonic saline remains the cornerstone of nephroprotection because it increases renal plasma flow, dilutes the concentration of cisplatin in the renal tubules, and accelerates its urinary excretion, thereby reducing the contact time between the drug and tubular epithelial cells. Current evidence underscores that beyond hydration and magnesium supplementation, no pharmacologic agent has definitively proven effective for preventing CIN in clinical practice [4]. While mannitol has historically been used as a forced diuresis adjunct, a recent meta-analysis of randomized controlled trials found that the clinical evidence for its nephroprotective benefit remains inconclusive, and its use does not replace the fundamental need for robust saline hydration [3]. A large multicenter retrospective study comparing mannitol and furosemide for forced diuresis similarly highlighted that the choice of diuretic is secondary to the primary strategy of maintaining high urine output through volume loading [2].

Distractor Analysis

- **Option 1:** Monitoring serum creatinine and BUN is essential for detecting nephrotoxicity early, but it is a surveillance measure, not a preventive one. By the time creatinine rises, significant tubular damage has already occurred. Prevention through hydration takes precedence over monitoring.

- **Option 2:** Administering antiemetics is a critical component of cisplatin care due to its high emetogenic potential, but this intervention targets gastrointestinal toxicity, not the pathophysiologic mechanism of renal tubular injury.

- **Option 3:** Assessing for peripheral neuropathy addresses cisplatin's dose-limiting neurotoxicity. While important for safety and quality of life, it does not mitigate the risk of AKI, which is the immediate threat to organ function during this third cycle of treatment.

Pathophysiology and Clinical Integration

The mechanism of CIN involves cisplatin entering renal proximal tubular cells via the organic cation transporter 2 (OCT2). Once intracellular, the drug undergoes enzymatic activation by cysteine conjugate β-lyase 1 to form a highly reactive thiol-cisplatin conjugate, which directly damages mitochondrial DNA and proteins, triggering cell death [1]. Adequate saline hydration works upstream of this pathway by reducing the luminal concentration of cisplatin in the proximal tubule, thus limiting its cellular uptake. This mechanistic understanding explains why hydration is the single most effective and evidence-based nursing intervention. Investigational agents such as flopropione, which inhibits the β-lyase enzyme, and SGLT2 inhibitors are being explored in preclinical and early-phase trials to directly block the intracellular toxicity cascade, but they are not yet standard of care [1][4].

References (research sources)

- [1]Flopropione, a Cysteine Conjugate β-Lyase 1 Inhibitor, for Prevention of Cisplatin-Induced Nephrotoxicity: Protocol for a Randomized, Open-Label, Proof-of-Concept Phase 1 and 2a Trial.RCT/clinical trialKoseki T, Kondo M, Fujigaki H, Kikuchi K, Oya Y, Kato H, Mizuno T, Tsuboi N, Kawada K, Goto Y, Hashimoto N, Imaizumi K, Kada A, Yabuuchi H, Saito K, Saya H. (2026) · DOI: 10.2196/87907

- [2]Mannitol versus furosemide for prevention of cisplatin-induced nephrotoxicity in a multicenter retrospective cohort study.Research articleHarimitsu Y, Hayashi T, Shimokawa M, Miyoshi T, Yamashita A, Uchiyama M, Ushio S, Shiraishi C, Matsuo K, Egawa T. (2025) · DOI: 10.1038/s41598-025-25510-6

- [3]Mannitol for prevention of cisplatin-induced nephrotoxicity: a systematic review and meta-analysis of randomized controlled trials.Meta-analysis/systematic reviewKao CC, Tai HY, Sio YC, Lin YC, Tran TT, Huang TW. (2025) · DOI: 10.1007/s00520-025-10171-y

- [4]Beneficial Effects of Sodium-Glucose Cotransporter 2 Inhibitors in Cisplatin Nephrotoxicity: A Mechanistic Review.Research articleMathavan A, Mathavan A, Shah CV. (2026) · DOI: 10.34067/kid.0000001194

## 임상 시나리오

Preventing Cisplatin NephrotoxicityHydration is the Cornerstone of Renal Protection
The primary strategy to prevent cisplatin-induced nephrotoxicity (CIN) is aggressive IV hydration with isotonic normal saline. This dilutes the drug concentration in renal tubules and accelerates excretion.

A standard prophylactic regimen involves infusing 1 to 2 liters of normal saline before and after cisplatin administration. Adequate hydration is evidenced by a urine output of at least 100 mL/hour.

CautionWhile monitoring serum creatinine and BUN is essential for early detection, it is not a preventive measure. Do not substitute assessment for the critical intervention of ensuring adequate hydration to protect kidney function.

## 핵심 개념

- **Cisplatin-induced nephrotoxicity (CIN)** — Dose-dependent kidney injury occurring in ~30% of patients, caused by cisplatin accumulation in renal proximal tubular cells leading to oxidative stress and apoptosis.
- **Aggressive hydration** — Intravenous volume expansion with isotonic saline (e.g., 0.9% NaCl) before and after cisplatin infusion to increase renal plasma flow, dilute urinary drug concentration, and accelerate excretion.
- **Cysteine conjugate β-lyase 1** — A renal enzyme that converts cisplatin into toxic thiol-cisplatin conjugates within proximal tubular cells, a key mechanism in the pathogenesis of CIN.

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