Page 35 - 51 the significance--29.2_opt
P. 35

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-
                                       13
          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-
                                                28
          duced when using 11 mM as opposed to 5.5 mmol/l of glucose.  Blood
                                                                      29
          pressures may be modestly lower with glucose in the dialysate, possibly
          due to suppression of counter-regulatory sympathetic drive.  In addi-
                                                                    30
          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


                                          35
   30   31   32   33   34   35   36   37   38   39   40