How to assess the risk of Cisplatin related renal injury?

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Cisplatin is a type of chemotherapy drug, called an alkylating agent. It contains the metal platinum. It damages the DNA (deoxyribonucleic acid) of dividing cells in a way that cannot be repaired. This stops or slows the growth of cancer cells and other rapidly dividing cells and causes them to die. Cisplatin may also induce injury in renal vasculature and result in decreased blood flow and ischemic injury of the kidneys, contributing to a decline in the glomerular filtration rate. These events, together, culminate in the loss of renal function during cisplatin nephrotoxicity, triggering acute renal failure. Prevention and treatment- to minimize the risk of Cisplatin-induced kidney adverse events, adequate preventive and supportive care measures (as per local institutional policies) are advised for all patients receiving Cisplatin. This includes appropriate antiemetics, maintaining adequate euvolemia (fluid balance), monitoring urine output throughout hydration pre and post-infusion, and preventing salt wasting with magnesium and potassium supplementation. However, given the differences in cancer types, Cisplatin doses, study types, hydration regimens, and definitions of nephrotoxicity across studies, no definitive conclusions can be made regarding optimal hydration regimens.

Diuresis induction with intravenous sodium chloride 0.9 %:

The administration of intravenous isotonic sodium chloride 0.9 % to induce diuresis continues to be the primary approach for preventing CIN (Cisplatin-induced nephrotoxicity) and is recommended for all patients receiving Cisplatin-containing regimens. However, the optimal hydration solution and regimen to prevent nephrotoxicity associated with Cisplatin administration remain unclear. The use of hypertonic sodium chloride or dextrose sodium chloride is not recommended.

Supplementation in hydration regimens:

The main objective of hydration during cisplatin therapy is to maintain sufficient urine flow, thereby facilitating the drug's elimination from the kidneys and minimizing the risk of kidney damage. The rationale for adding potassium and magnesium to sodium chloride 0.9 % is to avoid the development of hypokalemia (low potassium in the blood) and hypomagnesemia that may occur with forced diuresis; in addition, magnesium supplementation may help to limit CIN.

Magnesium: Cisplatin and magnesium affect the same sodium and water channels in the outer medulla, leading to magnesium depletion induced by Cisplatin. This depletion can enhance Cisplatin nephrotoxicity. To minimize the risk of CIN, it is important to manage hypomagnesemia following local policy before and during cisplatin treatment. There is robust evidence supporting the effectiveness of this approach. In alignment with these considerations, the default pre-hydration regimen includes magnesium sulfate supplementation. This regimen incorporates 10 mmol of magnesium sulfate (MgSO4) in 1000 mL of sodium chloride 0.9 %, regardless of the administered cisplatin dose.

Potassium: Cisplatin does not result in significant potassium loss, and the administration of intravenous sodium chloride 0.9 % helps maintain fluid balance, promoting urine production, without requiring additional potassium supplementation. It has been shown that cisplatin (at doses 60 to 80 mg/m2) can be safely administered to patients with nephrotoxicity or low potassium levels using a short hydration method, even in the absence of potassium chloride (KCL) supplementation

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