Profibrotic gene transcription in renal tissues from cats with ischemia-induced chronic kidney disease.

OBJECTIVE

To characterize transcription of profibrotic mediators in renal tissues of cats with ischemia-induced chronic kidney disease (CKD).

SAMPLE

Banked renal tissues from 6 cats with experimentally induced CKD (RI group) and 8 healthy control cats.

PROCEDURES

For cats of the RI group, both kidneys were harvested 6 months after ischemia was induced for 90 minutes in 1 kidney. For control cats, the right kidney was evaluated. All kidney specimens were histologically examined for fibrosis, inflammation, and tubular atrophy. Renal tissue homogenates underwent reverse transcription quantitative PCR assay evaluation to characterize gene transcription of hypoxia-inducible factor-1α (), matrix metalloproteinase ()-, tissue inhibitor of metalloproteinase-1 (), transforming growth factor-β1, and vascular endothelial growth factor A. Gene transcription and histologic lesions were compared among ischemic and contralateral kidneys of the RI group and control kidneys.

RESULTS

Ischemic kidneys had greater transcript levels of , and transforming growth factor-β1 relative to control kidneys and of relative to contralateral kidneys. Transcription of was upregulated and that of vascular endothelial growth factor A was downregulated in ischemic and contralateral kidneys relative to control kidneys. Transcription of did not differ among kidney groups. For ischemic kidneys, there were strong positive correlations between transcription of , and and severity of fibrosis.

CONCLUSIONS AND CLINICAL RELEVANCE

Transcription of genes involved in profibrotic pathways remained altered in both kidneys 6 months after transient renal ischemia. This suggested that a single unilateral renal insult can have lasting effects on both kidneys.