Lessons learned from ischemic and cisplatin-induced nephrotoxicity in animals.
Following ischemic or nephrotoxic injury, the regenerating kidney assumes an earlier developmental stage and a less mature phenotype. Recovery involves the activation of a group of genes, including protooncogenes and growth factor genes that initiate and sustain cell growth. Inflammation also plays an important role in the recovery process as several of the changes in gene expression implicate the participation of the inflammatory cascade. Many of the changes in gene expression may eventually be reflected in the urine of the damaged kidney. By exploiting these changes in urine composition as a consequence of injury it should be possible to detect evidence of biologic effects of exposure and may yield predictions of eventual risk of serious damage to kidney.
Division of Nephrology, University of Texas Medical School, Galveston 77555-0562, USA. rsafirst@utmb.edu
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D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000503:physiopathology / Q000652:urine; D000818:Animals; D000970:Antineoplastic Agents / Q000009:adverse effects*; D015415:Biomarkers / Q000652:urine; D002945:Cisplatin / Q000009:adverse effects*; D015870:Gene Expression; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects*
D000970:Antineoplastic Agents; D015415:Biomarkers; D002945:Cisplatin