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The increasing global prevalence of chronic kidney disease (CKD) and end-stage renal disease (ESRD) has significant public health and economic implications. The recently published UK National Institute for Health and Clinical Excellence (NICE) clinical guidelines for the early identification and management of CKD provide a framework of disease management for both primary and secondary care with the stated aim of reducing the progression of CKD and the associated risk of cardiovascular death. Identification of at-risk individuals with proteinuria and inhibition of the renin-angiotensin system are the cornerstones of this strategy. However, the vast majority of patients with CKD will not develop ESRD and it is far from clear whether the NICE recommendations will reduce either ESRD or cardiovascular death associated with CKD., (Copyright 2009 S. Karger AG, Basel.)

Metabolic acidosis causes renal growth and proteinuria, and may contribute to the progression of CRF. This study assessed the effects of HCI-induced acidosis on the structure and function of normal kidneys. Acidosis was induced in 12 rats by dietary HCl. After 2 weeks, acidotic animals had higher kidney/body weight ratios (0.47 +/- 0.10 vs. 0.35 +/- 0.10 g%, p < 0.001) and higher kidney protein content (123 +/- 3 vs. 111 +/- 4 mg/kidney, p < 0.05) than controls, but tubular nuclear densities were lower, suggesting tubular hypertrophy. Acidotic animals developed tubular proteinuria (16.4 +/- 2.6 mg/day after 2 weeks of acidosis vs. 2.9 +/- 0.3 mg/day at baseline; p < 0.001), and the pattern of immunohistochemical staining for Tamm-Horsfall protein suggested tubular injury. These data suggest that a tubulotoxic effect of metabolic acidosis may contribute to the progression of CRF.