In healthy humans, a normal decline in renal function begins soon after maturity and constitutes a fairly constant decrease in glomerular filtration, which averages 8 ml/min lost glomerular filtration rate (GFR) (6%) for each decade after the age of 40.¹

Prevention of the development or progression of chronic renal failure is the holy grail of nephrology. Success will depend in part on the screening and detection of underlying renal disorders but systemic diseases, namely hypertension and diabetes mellitus, remain the “big players” in the causation of endstage renal failure. Early detection of renal disease is very feasible in both settings using microalbuminuria as a marker of increased cardiovascular and renal risk. Although there are many effective interventions, organisational (health service resource allocation) and motivational (because alterations to patients’ lifestyles are often required) challenges often need to be overcome first.

The association between raised blood pressure and adverse renal outcome in hypertension² and in diabetes³ has become universally accepted, with control of blood pressure now being the cornerstone of “nephroprotection”.⁴ Angiotensin converting enzyme inhibitors and angiotensin receptor blockers have achieved pre-eminent status among antihypertensive drugs, with suggestions that their actions go further than can be explained by a reduction of blood pressure alone.⁵ However, several other important risk factors for the development of renal failure have been identified that, independently or in concert with blood pressure, can cause renal deterioration.⁶ These include sex, smoking, proteinuria, and dyslipidaemia.⁴

One of the paradoxes in renal medicine has been the enormous amount of experimental, mainly murine, evidence that dyslipidaemia leads to glomerulosclerosis (reviewed in …