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Parathyroid hormone (PTH) and glucose control
The metabolic actions of PTH extend beyond calcium homeostasis.
Parathyroid hormone-related protein is produced by the pancreatic
islet, where it acts to suppress insulin release from the beta cells. Sec-
ondary hyperparathyroidism acts to suppress insulin release in patients
with CKD. Suppression of PTH levels with vitamin D supplementation or
surgical removal of the glands, results in significant improvement in in-
sulin release, and with it, an increased risk of hypoglycaemia in patients
with CKD following such interventions. 26, 27
Specific situations: hypoglycaemia on haemodialysis
Haemodialysis is the most common modality for renal replacement
therapy in patients with type 2 diabetes and end stage renal disease
(ESRD). Haemodialysis clears the blood of toxins via diffusion across a
semi-permeable membrane and ultrafiltration, maintained by altering
the pressure in the dialysate compartment that allows free water and
some dissolved solutes to move across the membrane along a created
pressure gradient. This has the potential to alter glucose homeostasis in
a number of ways:
Firstly, insulin resistance associated with uraemic toxicity can be sub-
stantially alleviated by dialysis. This means that when starting haemo-
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dialysis in diabetic patients there can be a dramatic improvement in
peripheral insulin sensitivity, which alongside increased physical activity
and a persisting prolonged insulin half-life can lead to an increased
risk of hypoglycaemia in the days and weeks after starting dialysis. In-
sulin requirement should therefore be closely monitored after starting
dialysis in patients with type 2 diabetes, as doses will need to be rapidly
adjusted, sometimes to less than half of what was previously needed.
Secondly, haemodialysis with a sodium bicarbonate buffer can lead to
a loss of serum glucose in the dialysate effluent. In order to get around
the problem of hypoglycaemia, it is common practice to add glucose
to the dialysate, especially for diabetic patients on insulin. Certainly,
less hypoglycaemia occurs when using a dialysate containing glucose
compared to a glucose-free dialysate. Hypoglycaemia is further re-
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duced when using 11 mM as opposed to 5.5 mmol/l of glucose. Blood
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pressures may be modestly lower with glucose in the dialysate, possibly
due to suppression of counter-regulatory sympathetic drive. In addi-
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tion, inter-dialytic weight gain, hypertriglyceridaemia and increased
oxidative stress can also result from a high glucose dialysate. Some
authors also suggest that the risk of post-dialysis hypoglycaemia is in-
creased by a glucose-containing dialysate (by stimulating insulin then
withdrawing dialysate glucose). The long-term balance of benefits of
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