Proc Natl Acad Sci USA 2010;107:1666–71 PubMedCrossRef 31 Segaw

Proc Natl Acad Sci USA. 2010;107:1666–71.PubMedCrossRef 31. Segawa H, Yamanaka S, Ohno Y, Onitsuka A, Shiozawa K, Aranami F, et al. Correlation between hyperphosphatemia and type II Na–Pi cotransporter activity in klotho mice. Am J Physiol Renal Physiol. 2007;292:F769–79.PubMedCrossRef”
“Introduction Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis among primary glomerular diseases [1, 2]. It has a poor long-term prognosis, and the renal survival rates are presumed to be approximately 50–80% in a long-term follow-up of more than 10 or 20 years [3, 4]. P5091 in vivo Several treatment agents including angiotensin-converting-enzyme SB-715992 chemical structure inhibitors [5], angiotensin

II blockers [6], cAMP elevating agents [7], immunosuppressive agents [8], fish oils [9], and tonsillectomy have been reported to be effective in slowing the progression to end-stage renal failure. Moreover, recent studies from Japan indicated that tonsillectomy followed by treatment with steroids introduces clinical remission if treatment begins at the early stage [10–13]. Although the early detection of IgAN is very important not only to slow the progression but also to obtain clinical remission, the chance of early detection is limited because renal biopsy, which needs hospitalization and is associated with an unavoidable risk of critical bleeding, is the only tool to give a definite diagnosis SAR302503 datasheet of IgAN. Therefore, a

non-invasive method for Monoiodotyrosine accurate diagnosis of IgAN is desirable and a must-to-have tool for the clinics. In this context, several candidates in urine such as the IgA–fibronectin complex [14], and proteomics [15] have been proposed. Recently, urinary uromodulin fragment was reported as a candidate marker by use of matrix-associated laser desorption/ionization-time of flight mass spectrometry [16]. To our knowledge, however, no practical marker with sufficient specificity and sensitivity has been developed to date. Urinary IgA and IgA–IgG complex levels are high in IgAN patients [17]. In this study we examined the urinary IgA immune complex (IC) and determined proteins that combine with IgA. We then evaluated the diagnostic value of the urinary IgA–uromodulin complex

by ELISA and showed that the IgA–uromodulin complex could be a good clinical diagnostic marker of IgAN. Method Patients and urine samples In the first study (ELISA result of disease urine samples—a widely used test among kidney diseases), urine samples were obtained from various forms of biopsy-proven kidney disease patients including IgAN (95 patients), membranous nephropathy (MN; 18 patients), lupus nephritis (SLE; 5 patients), focal segmental glomerulosclerosis (FGS; 6 patients), minimal change nephrotic syndrome (MCNS; 3 patients), diabetic nephropathy (DMN; 5 patients), other kidney diseases (including amyloidosis, Alport syndrome, rapidly progressive glomerulonephritis, kidney sclerosis, kidney tumor, urethral lithiasis, etc.; 15 patients), and healthy controls (normal; 20 patients).

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