Reducing proteinuria is often a target of treatment because of the close correlation between improvement of proteinuria and better renal outcomes in human studies involving angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB).Conventional explanations for the protective effects of ACEI and ARB centre on their haemodynamic effects, suggesting that reducing glomerular filtration pressure is the key to their protective action. The fact that blood pressure reduction by any means protects renal function in proteinuric renal disease (the Modification of Diet in Renal Disease Study) suggests that this can explain at least some of the effect. Others have added that ACEI/ ARB may also modulate the toxicity of filtered proteins by effects on non-glomerular cells [1]. The close correlation between long-term outcomes and proteinuria has triggered a large body of work documenting potential mechanisms by which excessive filtered protein may damage renal tubular cells and promote interstitial fibro-sis [2].
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