Calcineurin upregulation was also found in the podocytes of FSGS patients, in which miR-30s were downregulated. Finally, luciferase reporter

assays confirmed that TRPC6, PPP3ca, PPP3cb, PPP3r1 and NFATc3 are the direct targets of miR-30s inpodocytes. Conclusion: miR-30s inhibit calcineurin signaling in podocytes by directly targeting calcineurin signaling components. Downregulation of miR-30s and the consequent upregulation of calcineurin signaling may be an alternative mechanism by which TGF-beta, LPS or PAN damages podocytes. FUKUDA AKIHIRO1, SATO YUJI1, IWAKIRI TAKASHI1, KOMATSU HIROYUKI1, KIKUCHI MASAO1, KITAMURA KAZUO1, FUJIMOTO SHOUICHI1,2 1First Department of Internal Medicine, University of Miyazaki; 2Department of Hemovascular Medicine and Artificial Organs, University of Miyazaki Introduction: Proteinuria and/or albuminuria are widely used selleck compound for noninvasive

assessment of kidney diseases. Proteinuria is a nonspecific marker of diverse forms of kidney injury, therefore, more glomerular disease specific biomarkers are required. Podocyte depletion is a major mechanism driving glomerulosclerosis, and that persistent podocyte loss check details is the likely driver for most forms of glomerular disease progression. Podocyte cell lineage specific mRNAs can be recovered from urine pellets of model systems and man. We have previously reported that urine podocyte mRNAs could serve as useful glomerular disease biomarker in model system (Sato Y et al. J Am Soc Nephrol 2009, Fukuda A et al. Kidney Int 2012). The purpose of this study was to test whether the urine podocyte mRNAs could Nutlin-3 solubility dmso be useful biomarker in human glomerular diseases. Methods: From January 2008 to October 2013, early morning voided urine samples were obtained from 121 patients with histology-proven glomerular diseases (minimal change nephrotic syndrome (MCNS, n = 16), crescentic glomerulonephritis (Crescentic GN, n = 14), membranous nephropathy (MN, n = 21), IgA nephropathy (IgAN, n = 60) and lupus nephritis (LN, n = 10)). A total of 29 urine samples were collected

from healthy volunteer who had no known kidney disease or hypertension. We examined urine podocyte mRNAs (urine podocin/AQP2 mRNA ratio, urine podocin/nephrin mRNA ratio and urine podocin/creatinine ratio) and urine protein/creatinine ratio (U-PCR)), also examined the relationships between urine podocyte mRNAs and U-PCR, or renal histological findings. Results: Compared with controls, urine podocyte mRNAs significantly increased in patients with glomerular diseases except MCNS. Compared with no proteinuria (U-PCR < 0.3), urine podocyte mRNAs were significantly increased in with proteinuria (U-PCR ≥ 0.3), however, urine podocyte mRNAs did not reveal linear correlation with U-PCR in any glomerular diseases.