[Clinical investigation of cis-platinum nephrotoxicity in 244 cases of primary lung cancer]

Abstract

Cisplatin (CDDP) is used widely in the treatment of a large number of carcinomas. The clinical use of cisplatin, however, can be complicated by myelotoxicity, intestinal toxicity and nephrotoxicity. We reviewed CDDP nephrotoxicity in 244 cases with primary lung cancer retrospectively. The enzyme histochemically localized in proximal tubular cells, N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (BMG), a low molecular weight peptide normally reabsorbed by the renal tubular cells that has been used as an indicator for renal proximal tubular damage, were measured. And fractional excretion of Na (FENa%) and serum magnesium (Mg) levels were also measured before and after CDDP administration serially. The following results were obtained; 1) Over 45% of patients with lung cancer showed transient hyperexcretion of urinary NAG and BMG after CDDP administration. And peak excretion of NAG and BMG appeared to occur within 36 hours after administration of CDDP. 2) Almost all cases with persistent azotemia after CDDP administration showed high values of FENa (%), in spite of gradual normalization of urinary NAG and BMG excretion. 3) Hypomagnesemia was a common complication of CDDP nephrotoxicity that might be caused by a defect in renal Mg reabsorption. CDDP-induced nephrotoxicity seemed to be initiated by an acute, mainly proximal tubular impairment that reflects alterations in excretion of urinary enzymes and low molecular weight protein. In cases with persistent azotemia after CDDP administration depressed renal function might be attributed to the impairment of proximal as well as distal tubular reabsorptive functions.