Abstract
DOI of original article: 10.1016/j.jss.2012.0 * Corresponding author. Department of Sur Tel.: þ1 212 844 8570; fax: þ1 212 844 8440. E-mail address: mleitman@chpnet.org (I. 0022-4804/$ e see front matter a 2013 Elsev http://dx.doi.org/10.1016/j.jss.2012.08.056 End-stage renal disease affects over 500,000 patients each year in the United States. Currently, over 92,000 people wait on the kidney transplant list in the United States alone, where approximately 16,000 transplants occur annually [1]. With such a discrepancy between supply and demand, graft survival is critical. Yet, even with advances in transplantation technique and immunosuppression, year one acute rejection rates remain between 10% and 20% [2]. Acute rejection begins subclinically and progression may lead to irreversible organ damage or graft loss. Research has been focused on finding early markers of rejection. Traditionally, renal allografts have been monitored using urinalysis, serum creatinine levels, and renal biopsies. Urinalysis provides a basic substrate to monitor renal function and graft rejection. Proteinuria has long correlated with chronic kidney disease and is also positively associated with rejection. However, proteinuria is indicative of an inflammatory process that has already advanced to irreversible kidney injury. Evidence has emerged that shows a relationship between microproteinuria and rejection, which may prove beneficial in
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