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risk remains to be determined. However, given the short survival of pa-
tients with diabetes on haemodialysis, such short-term gains appear to
have primacy.

ESRD is associated with an increased prevalence of protein-calorie
malnutrition, reflected in reduced serum albumin concentrations and
diminished hepatic glycogen stores. Institution of dialysis can have ad-
ditional effects on protein and energy balance, including the loss of
free amino acids, peptides and small proteins in the dialysate, espe-
cially with high flux dialysers. The net result of this can be to attenuate
the counter-regulatory response to hypoglycaemia. Adding glucose to
the dialysate can also reduce this effect by suppressing gluconeogen-
esis and catabolism.

Another technique widely used to avoid hypoglycaemia on dialysis is to
provide a meal to patients during the dialysis procedure. In theory, this
can provide the glucose reserve to balance losses during and subse-
quent to dialysis. However, in practice, patients with advanced diabe-
tes have significant gastroparesis , meaning that the effect of the meal
31
is often manifested after dialysis. Moreover, dilation of the splanchnic
bed following a meal can drop the blood pressure during dialysis. This
32
has led some units to deliberately not feed during dialysis. However,
feeding afterwards may also be problematic when plasma volumes are
at their lowest and patients are attempting to mobilise to get home or
return to their ward. Moreover, glucose control during dialysis (achieved
by a glucose-containing dialysate that stimulates insulin release),
if unmatched by food intake, subsequently and in the setting of an im-
paired counter-regulatory response, leads to a significant risk of hypo-
glycaemia that is greatest 2-6 hours after dialysis. Indeed, this post-dialysis
period may be the most dangerous for patients with diabetes on dialysis.

Finally, changes in the cytoplasmic pH of erythrocytes when using high
bicarbonate dialysate, can result in the increased uptake of glucose
into red cells, as intracellular acidosis stimulates the consumption of glu-
cose by anaerobic metabolism. 33

One of the major difficulties of hypoglycaemia on dialysis is that few pa-
tients are aware of low glucose levels, due to blunting of the counter-
regulator response in advanced disease (detailed above) and/or the
use of sympathetic blockade. Symptoms are often attributed to dialysis
disequilibrium or co-morbid disease. While hypoglycaemia should be
suspected in any diabetic patient with CKD who exhibits any change
in mental status, its prevention ultimately relies on frequent and careful
glucose determinations. It is also important to remember that testing
from an extracorporeal line is problematic because of recirculation.

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