Increase in Renal and Urinary Low and High Molecular Weight Kininogens during Chromate-Induced Acute Renal Failure in the Rat: Evidence for Renal Kininogen Production

Abstract

In the present study, we investigated the plasma, urinary and intrarenal concentrations of low and high molecular weight kininogens during sodium chromate (25 mg/kg body weight)-induced acute renal failure (ARF) in the rat. Urinary kininogen underwent a transient increase with a maximum on day 7 (78 ± 22 versus 4.2 ± 1.6 ng bradykinin/mg creatinine) whereas plasma kininogen did not and glomerular filtration rate decreased (92 ± 8 versus 895 ± 70 μl/min). The tissue level of kininogen was enhanced both in the cortex (1,319 ± 123 versus 86 ± 8 pg bradykinin Eq/mg protein) and in the medulla (1,673 ± 138 versus 44 ± 9 pg bradykinin Eq/mg protein) but more in the medulla (36 ± 4- versus 15 ± 3-fold). As plasma kininogen level was unchanged and glomerular filtration rate decreased, the increase in both renal concentration and urinary excretion of kininogen probably reflects stimulated renal production of kininogen in this model of ARF. Whether the evoked renal production of kininogen results from a local inflammatory response only or may subserve another physiological purpose remains to be elucidated.

Urinary proteome profile of renal papillary necrosis in experimental model rats

“…Alpha-2-HS-glycoprotein, also known as fetuin-A, was identified in the urinary exosome of a cisplatin-induced acute kidney injury rat model (Zhou et al, 2006). Fibrinogen gamma chain, hemopexin, and kininogen 2 are also associated with kidney injury (Krishnamoorthy et al, 2011;Kaushal and Shah, 2012;Zager et al, 2012;Bompart et al, 1993). However, most of the other identified proteins have not been linked to kidney injury to date, and could therefore represent novel biomarkers.…”