Nephrosis

Studies from University of Groningen provide new data on proteinuria

"First published February 25, 2009; doi:10.1152/ajprenal.00541.2007.-Tubulointerstitial lesions are important in the progression of proteinuric renal disease. Tubular kidney injury molecule-1 (Kim-1) is induced in acute renal injury and reversible as a natural course. Kim-1 is also present in chronic renal damage; however, the dynamics of Kim-1 in chronic renal damage and effects of antiproteinuric treatment on Kim-1 are unknown. We studied Kim-1 in adriamycin nephrosis (AN) before and after reninangiotensin system blockade. A renal biopsy was taken 6 wk after adriamycin injection to study renal damage and Kim-1 expression. Subsequently, ACE inhibition (ACEi; n = 23), angiotensin II antagonist (AT(1A); n = 23), or vehicle (n = 10) was given for 6 wk; healthy rats served as controls (CON; n = 8). In AN, renal Kim-1 mRNA was induced 26-fold vs. CON at week 6, with further increase in vehicle to week 12 (40-fold) but was reduced by ACEi and AT(1A) to 10- and 12-fold vs. CON (P < 0.05 vs. week 6). Kim-1 protein was undetectable in CON; in AN, it was present in brush border of dilated tubules in areas with adjacent interstitial lesions. Renal Kim-1 protein levels increased from weeks 6-12 in vehicle and decreased in ACEi- and AT(1A)-treated groups (P < 0.05). In vehicle, urinary Kim-1 was increased (P < 0.05 vs. CON), with a reduction by ACEi and AT(1A) (P < 0.05 vs. vehicle). Renal and urinary Kim-1 correlated with proteinuria and interstitial damage cross-sectionally. Reductions in proteinuria and renal Kim- 1 correlated, which was not associated by corresponding changes in tubulointerstitial fibrosis," wrote A.B. Kramer and colleagues, University of Groningen.

The researchers concluded: "On longitudinal follow-up during antiproteinuric treatment increased renal Kim-1 expression is reversible in proportion to proteinuria reduction, likely reflecting reversibility of early tubular injury, supporting its potential as a biomarker for tubulointerstitial processes of damage and repair."

Kramer and colleagues published their study in American Journal of Physiology - Renal Physiology (Reduction of proteinuria in adriamycin-induced nephropathy is associated with reduction of renal kidney injury molecule (Kim-1) over time. American Journal of Physiology - Renal Physiology, 2009;296(5):F1136-F1145).

For additional information, contact G. Navis, University of Groningen, Dept. of Nephrology, Groningen University Medical Center, POB 30-001, NL-9700 RB Groningen, Netherlands.

The publisher's contact information for the American Journal of Physiology - Renal Physiology is: American Physiological Society, 9650 Rockville Pike, Bethesda, MD 20814, USA.

Keywords: Netherlands, ACE-Inhibitors, Adriamycin, Angiotensin, Biopsy, Fibrosis, Hepatology, Kidney Disease, Nephrology, Nephropathy, Nephrosis, Proteinuria, Renal Disease, Renal Physiology, Surgery, Therapy, Treatment, University of Groningen.

This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2009, Biotech Business Week via NewsRx.com.