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Focal segmental glomerulosclerosis (FSGS) represents the most common primary
glomerular disease responsible for the development of end-stage renal disease
(ESRD) in the United States (US). The disease progresses from podocyte injury to
chronic kidney disease (CKD), ultimately leading to total nephron degeneration.
Extensive basic science research has been conducted to unwind the mechanisms of
FSGS and, with those insights, understand major contributors of CKD in general.
As a result, several putative molecules and pathways have been studied, all
implicated in the disease; some serve, in addition, as early biomarkers. The
ongoing research is currently focusing on understanding how these molecules and
pathways can interplay and be utilized as potential diagnostic and therapeutic
targets. Among these molecules, the soluble urokinase plasminogen activating
receptor (suPAR) has been studied in detail, both clinically and from a basic
science perspective. By now, it has emerged as the earliest and most robust
marker of future CKD. Other circulating factors harming podocytes include
anti-CD40 auto-antibody and possibly cardiotrophin-like cytokine factor-1.
Understanding these factors will aid our efforts to ultimately cure FSGS and
possibly treat a larger portion of CKD patients much more effectively.
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