Osteopontin is upregulated in damaged non‐clipped kidney cortex from rats with renal hypertension

Separating the causes from the effects of hypertension is a recurring problem in nephrology. The present investigation addresses this question using Illumina beadarray microarrays. The non‐clipped kidney from 2k1c rats with was compared with control kidneys. Rats were sacrificed either four weeks after inducing hypertension, or after 24 weeks. Renal damage was graded in PAS stained kidney sections, and the 2K1C rats showed significantly more damage after 24 weeks compared to controls (0.019±0.013 vs. 0.51±0.21 P<0.01). In order to isolate the changes brought by renal damage from those of aging or hypertension per se, the microarray expression data was analysed by contrasting non‐clipped kidney cortex after 24 weeks of 2k1c against all other groups. Osteopontin is increased almost four‐fold in damaged kidney cortex. Trefoilfactor‐3 is lower in after 24 weeks in controls, and further decreased in kidneys with hypertensive renal damage (P<0.01). Five genes are reduced to half the expression in the pooled controls, and only two genes are upregulated more than two‐fold. In conclusion, hypertensive kidney damage in the non‐clipped kidney of 2k1c rats is associated with an upregulation of osteopontine not seen in short time renal hypertension or in age‐matched controls.