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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. The rate for those aged 75 and older declined 0.9 percent between 2007 and 2008. However, racial and ethnic discrepancies persist with 2008 incident rates in the African American and Native American populations 3.6 and 1.8 times greater, respectively, than the rate among whites, and the rate in the Hispanic population 1.5 times higher than that of non-Hispanics (U. S. Renal Data System, 2010). Diabetic nephropathy (DN) is one of the major causes of ESRD in the Western world. The incidence of nephropathy owing to type 1 diabetes is declining; however, diabetes mellitus type 2 is now the most common single cause of renal insufficiency in the USA, Japan and Europe (Tisher & Hostetter, 1994). It has been estimated that 4% of the world’s current population is diabetic, and that in Europe there will be more than 32 million patients with diabetes in 2010, causing an increase in related complications, such as DN. This pathology has been recognized as a worldwide medical catastrophe (Ziyadeh & Sharma, 2003). DN appears clinically in 10-50% of diabetic patients after 10-20 years of evolution of the disease. These patients show a progressive increase in urinary excretion of protein, starting from an initial microalbuminuria to clear nephrotic syndrome with progressive decline of renal function (Cooper et al., 1999; Katoh et al., 2000; Tisher & Hostetter, 1994; Yotsumoto et al., 1997).

Parathyroid Hormone-Related Protein as a Mediator of Renal Damage: New Evidence from Experimental as well as Human Nephropathies