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Pathophysiology of proteinuria and its value as an outcome measure in chronic kidney disease
Author(s) -
Cravedi Paolo,
Remuzzi Giuseppe
Publication year - 2013
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/bcp.12104
Subject(s) - proteinuria , medicine , renal function , kidney disease , glomerular hyperfiltration , kidney , urology , endocrinology , diabetic nephropathy
Chronic kidney diseases share common pathogenic mechanisms that, independently from the initial injury, lead to glomerular hyperfiltration, proteinuria, and progressive renal scarring and function loss. Consistent experimental evidence supports the crucial role of proteinuria in accelerating kidney disease progression to end‐stage renal failure through multiple pathways, including induction of tubular chemokine expression and complement activation. These events, in turn, lead to inflammatory cell infiltration in the interstitium and sustained fibrogenesis. The extent of proteinuria is widely recognized as a marker of the severity of chronic kidney disease and as a predictor of future decline in glomerular filtration rate. More importantly, a reduction in proteinuria invariably translates into a protection from renal function decline in patients with diabetic and non‐diabetic renal disease. Recent evidence also showed the existence of a relatioship between proteinuria levels and cardiovascular risk, which extends to the range of urinary albumin excretion that was previously thought ‘normal’. Thus, proteinuria should be considered a valuable surrogate end point for clinical trials in patients with chronic renal diseases and a target for reno‐ and cardioprotecive strategies.