Abstract
To investigate the roles of SLC22A2 gene polymorphism 808 G/T and cimetidine on cisplatin-induced nephrotoxicity, a total of 123 Chinese cancer patients treated with cisplatin alone (n=55) or in combination with cimetidine (n=68) were genotyped. The changes of serum creatinine (SCr), blood urea nitrogen (BUN) and cystatin C levels were used as biomarkers for the evaluation of cisplatin-induced nephrotoxicity. The changes of BUN and SCr levels showed no significant difference between groups divided by genotypes and treatments (P>0.05). However, patients with mutant genotype (GT/TT) or with cimetidine treatment had smaller increase of the cystatin C levels compared to those with wild genotype (GG) or without cimetidine treatment (P<0.05). In the non-cimetidine-treated group, the changes of cystatin C level in patients with mutant genotype (GT/TT) was significantly smaller than those with wild genotype (GG) (P=0.043). In the wild type group, the cystatin C level change of patients without cimetidine treatment was significantly larger than those with cimetidine treatment (P=0.007). These results suggested that SLC22A2 gene polymorphism 808 G/T and cimetidine could attenuate cisplatin nephrotoxicity in Chinese cancer patients. But the renoprotection mechanism of cimetidine might be damaged by the mutation.
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