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in diabetic patients with advanced CKD and those on dialysis. How-
36
ever, such observational data cannot be used to prove that attempts
to improve glycaemic control through anti-diabetic agents or other
interventions will therefore result in better clinical outcomes. Indeed,
recent studies in diabetic patients without CKD have failed to dem-
onstrate mortality and cardiovascular benefits from better glycaemic
control, even though HbA remains closely correlated with adverse
1c
outcomes in these cohorts. This does not mean that there is no point
5
in any glucose control. Rather, that the utility for aggressive glycaemic
control has probably passed and that other targets may be more ap-
propriate for intensification. Poor glycaemic control remains a potent
risk marker for those at increased absolute risk, in whom the absolute
gain from intervention may therefore also be enhanced. Nonetheless,
a modest degree of glucose control is probably still effective in reduc-
ing the risk of infection and cataracts, while choosing an individual tar-
get that reduces the risk of hypoglycaemia, especially in those with
advanced age, irregular compliance or lifestyles. Patients that hope to
maintain a driving license offer an additional challenge in balancing
risk and mobility. Ultimately, careful individualisation of glucose man-
agement is the best recourse, which can never be reflected in guide-
lines or performance indices aimed at generic utility. As Sir William Osler
once said, “If it were not for the great variability among individuals,
medicine might as well be a science and not an art!”

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