Abstract P150: Podocyte Derived Urinary Microparticles Are Elevated in Angiotensin II Induced Hypertension

Abstract

Background: Early and non-invasive biomarkers of kidney damage are needed to identify hypertensive patients at risk for kidney damage. Urinary micropaticles (UMPs) have gained significant attention as potential novel biomarkers for kidney damage, and have already been identified in pre-albuminuric diabetic glomerular injury. These vesicles are less than 1 micron in size and carry markers of the parent cell. We hypothesized that podocyte derived UMPs are elevated in angiotensin II-induced hypertension (HTN) Methods: Primary podocytes were isolated and grown in culture. Wild-type mice were treated with AII (400ng/kg/min) via mini-osmotic pumps. Untreated WT mice served as controls. 24 hour urines were collected after 5 days of AII treatment. Enumeration and phenotyping of MPs was done of podocyte culture supernatant and urine. Podocalyxin (Pcal), podoplanin (Ppla) and annexin 5 (AV) were used as surface markers. Result: Pcal and Ppla positive MPs as well as AV positive and negative MPs were detectable in supernatant from primary podocyte cultures. Compared to untreated controls (n=3), AII treated mice (n=2) had an increase in systolic blood pressure (SBP) by 33 mmHG (p=0.02). Despite similar urinary albumin/creatinine ratios between groups, there was a trend of higher levels of total numbers of Ppla and Pcal positive MPs in hypertensive mice compared to untreated (Figure 1). In addition, Annexin negative but Ppla and Pcal positive MPs were also numerically higher in hypertensive mice. In conclusion, podocyte derived UMPs are detectable in AII HTN. These findings need to be confirmed in a larger group of animals. UMPs can be potential marker for kidney end-organ damage in HTN.