Chronic Kidney Disease and Renal Transplantation by M. Sahay

By M. Sahay

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Laboratory of Renal Physiology and Experimental Nephrology, Department of Physiology Spain 1. Introduction End-stage renal disease (ESRD) is a public health problem worldwide, with an increasing incidence and prevalence, poor prognosis and high cost (Ministerio de Salud, 2005). In 2005 the prevalence of ESRD in the USA was 1,131 patients per million inhabitants, with an incidence of 296 new patients per year per million inhabitants. In 2008, the adjusted incident rate for patients age 45–64 fell to the same level seen in 1998 -605 per million population.

Collectively, all the available data demonstrate a major role for PTHrP in renal fibrogenesis due to its capacity to induce the expression of extracellular matrix proteins as well as by modulating EMT in renal tubuloepithelial cells. 8. Conclusion The upregulation of the renal PTHrP/PTH1R system represents a common event in several experimental nephropathies. Current data support the notion that AngII is a major factor Parathyroid Hormone-Related Protein as a Mediator of Renal Damage: New Evidence from Experimental as well as Human Nephropathies 39 responsible for PTHrP overexpression in both ARI and diabetic nephropathy.

2010) expanded these studies and show that PTHrP is capable of inducing a variety of phenotypic changes related to EMT in tubuloephithelial cells. Hence, this peptide induced snail overexpression and its nuclear translocation, associated with the loss of ZO-1 and E-cadherin, key proteins in the maintenance of basolateral polarity and intercellular junction in renal tubuloepithelial cells. PTHrP also induced the phenotypic conversion to a fibroblast-like morphology, related to α-SMA and ILK upregulation.

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