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Kidney disease and implications for monitoring glycaemic
control

HbA is the gold standard for determining glycaemic control in people
1c
with T2DM. However, there is concern that this measure may be affect-
ed by the degree of kidney dysfunction or the haematological compli-
cations of kidney disease (e.g. iron deficiency, haemolysis, shorter red
blood cell lifespan, or acidosis). 8

One small study compared correlations between HbA measurements
1c
and blood glucose in patients with moderate to severe kidney disease
who did not require dialysis to those of patients without kidney disease.
The study found no difference in the magnitude of the correlations
between HbA and blood glucose between these patient groups.
9
1c
Therefore, HbA is as effective as an indicator of glycaemic control in
1c
patients with and without kidney disease. These data are strongly sup-
portive of applying a target HbA level of <7.0% to patients not requir-
1c
ing dialysis but who have kidney disease. 5 10
The correlation between HbA and blood glucose in haemodialysis
1c
patients is unclear and results from relevant studies are conflicting.
Consequently, T2DM patients receiving dialysis are worthy of special
consideration. One study concluded that HbA was an underestimate
1c
of glycaemic control in dialysis patients. On the other hand, a second
9
study concluded that HbA measures >7.5% were likely to be an over-
1c
estimate of glycaemic control. There is no evidence that haemo-
11
dialysis treatment acutely changes the HbA measure. Further studies
12
1c
are needed to clarify the interpretation of HbA in patients receiving
1c
dialysis. Lower HbA has been associated with lower mortality risk in
1c
patients receiving haemodialysis. 7 13 In view of these data, the current
recommendations are also to aim for an HbA <7.0% in T2DM patients
1c
who are on dialysis. 5 10
Current T2DM treatments and how they should be used in
patients with declining renal function
In this section, we briefly review the mode of action and the key clinical
characteristics of the various medications used in the management
of T2DM. In particular, we consider how declining renal function in pa-
tients with T2DM influences the use of each of these medications (sum-
marised in Table 1). Insulin therapy will not be discussed, although it is
well known that the insulin dose needs to be reduced in patients with
CKD, given that insulin is metabolised by the kidney. Thus, patients with
CKD on insulin are at higher risk of hypoglycaemia and frequent blood
glucose monitoring is necessary.

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