Page 42 - 51 the significance--29.2_opt

nephropathy and, along with hypertensive therapy, to slow the pro-
gression of established kidney disease. For example, further analyses of
5
the ADVANCE trial data published in 2009 showed that tight glycaemic
control reduces the risk of new or worsening nephropathy (Figure 1). 6
These effects are additive to those of blood pressure levels, without
evidence of interaction.

Figure 1. Tight glycaemic control reduces new or worsening nephropathy (Adapted
from Zoungas et al 2009). 6

In addition, data suggests that achieving and maintaining target HbA
1c
levels may improve survival and slow and/or prevent complications in
people with T2DM and kidney failure who are on dialysis. In a study
by Kalantar-Zadeh et al., higher HbA values were associated with a
1c
higher risk of mortality after adjusting for potential confounders.
7
The take home message is that tight glycaemic control is imperative for
people with T2DM, including those who also have concomitant renal
impairment. These recommendations leave the management of T2DM
in something of a quandary because the first and second line therapies,
namely metformin and SUs, are either contraindicated in renal impair-
ment or have to be used with caution due to the risk of complications
(e.g. hypoglycaemia). So, in view of this paradox, what can clinicians
on the ground do? Should they go on using the established therapies
and put the patient at risk of complications, or look at the emerging
anti-diabetic therapies that can be used safely in T2DM patients with
renal impairment thanks to their non-renal route of elimination?

Chapter 4 looks at these emerging therapies in greater detail, while the
remainder of this chapter reviews the impact of kidney disease on gly-
caemic control as well as a brief overview of the current T2DM thera-
pies and their limitations, specifically in patients with renal impairment.

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