Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: a unique clinical/physiologic exercise in internal potassium balance.
The absence of significant losses of potassium in the urine makes dialysis-associated hyperglycemia (DH) a model for the study of the internal potassium balance. Studies of DH have revealed that hyperkalemia is frequent at presentation, insulin infusion is usually the only treatment required, and the magnitude of the decrease in serum potassium concentration (K(+)) during treatment of DH with insulin depends on the starting serum K(+) level, the decreases in serum glucose concentration and tonicity, and the increase in serum total carbon dioxide level. We present an analysis of these findings based on previously studied actions of insulin. Calculations of transcellular potassium shifts based on the combined effects of insulin-the increase in the electrical potential differences (hyperpolarization) of the cell membranes and the correction of the hyperglycemic intracellular dehydration through decrease in serum glucose concentration-produced quantitative predictions of the decrease in serum K(+) similar to the reported changes in serum K(+) during treatment of DH with insulin. The lessons from analyzing serum K(+) changes during treatment of DH with insulin are applicable to other conditions where internal potassium balance is called upon to protect serum K(+), such as the postprandial state. The main questions related to internal potassium balance in DH that await clarification include the structure and function of cell membrane potassium channels, the effect of insulin on these channels, and the mechanisms of feedforward potassium regulation.
Tzamaloukas
Antonios H
AH
Medicine Service, New Mexico Veterans Affairs Health Care System, Albuquerque, NM, USA. antonios.tzamaloukas@med.va.gov
Ing
Todd S
TS
Elisaf
Moses S
MS
Raj
Dominic S C
DS
Siamopoulos
Kostas C
KC
Rohrscheib
Mark
M
Murata
Glen H
GH
D006801:Humans; D006943:Hyperglycemia / Q000097:blood* / Q000188:drug therapy* / Q000209:etiology; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D011188:Potassium / Q000097:blood* / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects*
D007004:Hypoglycemic Agents; D007328:Insulin; D011188:Potassium