A nurse is caring for a 58-year-old patient with ovarian cancer receiving cisplatin as part of combination chemotherapy. The patient's baseline creatinine is 0.9 mg/dL and BUN is 18 mg/dL, and this is the third cycle of treatment. Which nursing intervention is the MOST important to prevent nephrotoxicity?

Adequate hydration with normal saline before and after cisplatin infusion is critical to prevent nephrotoxicity by diluting drug concentration and maintaining urine output. Other interventions like CBC monitoring, antiemetics, or vital signs checks do not directly prevent kidney damage.

Clinical Context and Pathophysiology of Cisplatin Nephrotoxicity

Cisplatin is a highly effective alkylating agent used in the treatment of solid tumors, including ovarian cancer, but its clinical utility is significantly limited by dose-dependent nephrotoxicity. Cisplatin-induced acute kidney injury (AKI) occurs in approximately 30% to 45% of treated patients [2,4]. The drug is actively taken up by renal tubular epithelial cells, where it becomes concentrated. Once inside the cell, cisplatin undergoes metabolic activation, forming highly reactive thiol-cisplatin conjugates, a process catalyzed by the enzyme cysteine conjugate β-lyase 1 ^[3]. These toxic metabolites directly damage the mitochondria and cellular proteins of the proximal tubules, leading to tubular cell necrosis and apoptosis [3,4]. The resulting clinical picture is one of impaired renal concentrating ability, reduced glomerular filtration rate, and a rise in serum creatinine and BUN. For a patient on their third cycle, the cumulative tubular injury from prior cycles increases the risk of clinically significant nephrotoxicity, even when baseline renal function appears normal, as with a creatinine of 0.9 mg/dL and BUN of 18 mg/dL.

Analysis of the Correct Intervention: Aggressive Hydration

The most critical and evidence-based nursing intervention to prevent cisplatin-induced nephrotoxicity is ensuring adequate hydration with normal saline before and after the infusion. The primary mechanism of protection is straightforward and mechanical: aggressive volume expansion with isotonic saline increases renal plasma flow and glomerular filtration rate, thereby increasing urine flow. This high urine output dilutes the concentration of cisplatin and its toxic metabolites in the renal tubular lumen, reducing their contact time with and uptake by the vulnerable proximal tubular cells. This intervention directly counteracts the pathophysiological process of tubular concentration and cellular uptake described in the foundational research on cisplatin kidney injury [3,4]. The systematic review and meta-analysis of randomized controlled trials confirms that hydration-based protocols are the cornerstone of nephroprotection, against which other adjunctive strategies like forced diuresis with mannitol are compared ^[2]. The multicenter retrospective study also operates within this standard-of-care framework, where all patients received hydration as a baseline protective measure before the addition of mannitol or furosemide was evaluated . Without this foundational hydration, the risk of acute tubular necrosis escalates dramatically. The nurse’s role is to administer the prescribed intravenous fluids meticulously, often beginning hours before the cisplatin infusion, monitoring the patient’s fluid balance, and ensuring a high urine output is achieved and maintained for at least 24 hours post-infusion.

Analysis of Incorrect Options

Option 1: Monitor complete blood count every 8 hours. While cisplatin is myelosuppressive and can cause anemia, neutropenia, and thrombocytopenia, monitoring a complete blood count is a secondary safety measure, not a primary preventive one for nephrotoxicity. The nadir for chemotherapy-induced blood count changes typically occurs 7-14 days post-treatment, making frequent monitoring during the infusion irrelevant for preventing acute kidney injury. This action addresses hematologic toxicity, not the renal toxicity that is the immediate threat during and after the infusion of a known nephrotoxin.

Option 3: Administer antiemetics 30 minutes before chemotherapy. Cisplatin is classified as a highly emetogenic chemotherapy agent, and premedication with antiemetics is a standard nursing intervention to prevent acute and delayed nausea and vomiting. This intervention is essential for patient comfort and quality of life but has no direct physiological impact on the mechanisms of nephrotoxicity. While vomiting can lead to volume depletion, which would exacerbate renal injury, the primary protective strategy is the proactive administration of intravenous fluids, not simply controlling emesis. The antiemetic protocol is a parallel, supportive care measure, not the most important intervention for kidney protection.

Option 4: Check vital signs every 15 minutes during infusion. Frequent vital sign monitoring is a standard safety procedure during the administration of any intravenous medication, particularly a high-alert drug like chemotherapy, to detect acute infusion reactions or hypersensitivity. However, this is a general monitoring task for immediate adverse events, not a targeted intervention to prevent the specific, delayed pathophysiological process of cisplatin-induced nephrotoxicity. Normal vital signs during the infusion do not indicate that the kidneys are being adequately protected from the toxic insult that will develop over the subsequent days. The nephroprotective action that must be prioritized is the simultaneous delivery of high-volume intravenous fluids.