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The prevalence of chronic kidney diseases is increasing worldwide, and many of these nephropathies progress to renal failure. Our understanding of the pathophysiology of deteriorating renal function is still limited, and the choices for therapy are confined to a few general interventions. The degree of proteinuria correlates with the rate of progression to ESRD, suggesting that proteinuria itself could be one of the mechanisms for progression. Finding that upon therapeutic intervention the rate of decline of GFR correlates negatively with reduction in proteinuria and positively with persistent proteinuria provides further evidence for a pathogenic role of proteinuria in renal progression.1Albumin is the major protein present in nephrotic urine, and a variety of studies have examined the toxic effect of filtered albumin in the kidney. Special attention has been paid to proximal tubule cells (PTCs), because the majority of the albumin in the glomerular filtrate is absorbed by phosphatidylinositol-3-kinase–mediated endocytosis after the binding to the multiligand receptors megalin and cubulin2 for tubular degradation by lysosomes. Gene expression profiling of PTCs from mice overloaded with BSA identified 2000 genes that are regulated differentially.1 In vitro and in vivo models of albumin overload also describe increased production of proinflammatory molecules, matrix genes, and profibrogenic cytokines such as monocyte chemoattractant protein 1, TGF-β, IL-8, endothelin 1, transcriptional factor NF-κB, and RANTES. Most of these mediators are responsible for tubulointerstitial inflammation and fibrosis through recruitment and activation of lymphocytes, macrophages, and fibroblasts. In addition, numerous studies have reported that high concentrations of albumin in vitro and in vivo induce apoptosis in PTCs, although some issues on the effect of albumin on tubular cell apoptosis are still misunderstood or controversial. First, it has been argued that tubular cell apoptosis is induced by high molecular weight proteins …

Is PKC-δ a New Killer Molecule in Kidney?