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In ESRD, both uremia and dialysis

can complicate blood glucose control
by affecting the secretion,
clearance, and peripheral tissue
sensitivity of insulin.
The abnormal glucose homeostasis
in patients with dialysis is postulated
to be multifactorial issues as Figure

Hyperglycemia: Increased insulin resistance

and decrease insulin production in dialysis

ESRD can show mild fasting

hyperglycemia and abnormal glucose
tolerance, suggesting that the uremic
state alters glucose homeostasis
Insulin resistance is also frequently
recognized in uremic patients and is
a predictor of cardiovascular
mortality in ESRD patients

Uremic toxins insulin resistance in ESRD

blunted ability to suppress hepatic
gluconeogenesis and regulate peripheral
glucose utilization.
Change of total body fat and BMI occurs in
ESRD because of concomitant metabolic
acidosis, deficiency of 1,25 dihydroxy-vitamin
D, and secondary hyperparathyroidism.
Treatment with hemodialysis, active vitamin D,
erythropoietin and angiotensin receptor blocker
can improve insulin insensitivity

The dextrose concentration in the dialysate

can also affect glucose control.
Dialysates with lower dextrose concentrations
are used and may be associated with
Dialysates with higher dextrose concentrations
are occasionally used in hypoglycemic patients
on hemodialysis and low ultrafiltration patients
on peritoneal dialysis (PD), but this can lead to
hyperglycemia and insulin resistance

Hypoglycemia: Decreased insulin clearance

and renal gluconeogenesis in dialysis
Decreasing insulin requirements and frequent
hypoglycemia also occur in diabetic patients on
Renal insulin clearance decreases as glomerular
filtration rate decreases to less than 15 to 20
mL/min/1.73 m2.
Hepatic clearance of insulin is also decreased in
patients with uremia.
Deficient gluconeogenesis along with malnutrition,
deficient catecholamine release, and impaired renal
insulin degradation and clearance, can contribute to
frequent hypoglycemia in patients with CKD

Advanced CKD and ESRD on dialysis exert opposing forces on insulin
secretion, action, and metabolism, often creating unpredictable
serum glucose values.
Some patients who have insulin resistance would need more
supplemental insulin.
In contrast, the reduced renal gluconeogenesis and insulin clearance
seen in ESRD may result in less requirement for insulin treatment.
Together, all of these factors contribute to wide fluctuations in
plasma glucose levels and increase the risk of both hyperglycemic
and hypoglycemic events.
Both of these abnormalities are at least partially reversed with the
institution of dialysis.
As a result, the insulin requirement in any given patient will depend
upon the net balance between improving insulin secretion and insulin
sensitivity, and restoring normal hepatic insulin metabolism.