Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: a unique clinical/physiologic exercise in internal potassium balance

Abstract

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.

Hyperkalemia in two patients with diabetes mallitus and chronic kidney disease. Role of disrupted internal potassium balance

“…Uremia also causes peripheral tissue resistance to the hypoglycemic effect of insulin [30], while the effect of insulin on cellular uptake of potassium is unchanged [31] or enhanced [32] Tables 4-5). These findings are consistent with previous findings supporting an added hyperkalemic effect of ketoacidosis in CKD patients [19,21].…”

“…Urinary potassium losses are also limited, and hyperkalemia is frequent in hyperglycemic episodes occurring in this setting [19][20]. The degree of hyperglycemic hyperkalemia in dialysis patients is higher when ketoacidosis is present [19,21]. Ketoacidosis contributes to the development of hyperglycemic hyperkalemia by affecting the function of several transport pathways in the cell membrane [22].…”

Вплив Альтерації Гомеостазу Глюкози На Водно-Електролітний Баланс Та Кислотно-Основний Стан У Пацієнтів Із Цукровим Діабетом

“…Гіперкаліємія може бути спричинена збільшенням тонічності (осмолярнос-ті) плазми, що є результатом перерозподілу калію з внутрішньоклітинного простору в позаклітин-ний [42]. Вихід калію з клітини відбувається через внутрішньоклітинну дегідратацію, що є наслідком осмотично індукованого трансцелюлярного руху води, і власне він створює сприятливий градієнт для відтоку калію [58]. Введення розчину глюкози як короткострокової терапії при гіперкаліємії без супутнього введення інсуліну може погіршити гі-перкаліємію в пацієнтів із ЦД, оскільки ендогенна секреція інсуліну може бути недостатньою чи непе-редбачуваною і тим самим призвести до збільшення тонічності плазми.…”

Principles of Quantitative Fluid and Cation Replacement in Extreme Hyperglycemia

“…Hyperglycemia disrupts both the internal and the external potassium balance. Transfers of potassium outside the cells are caused by insulin deficits and hypertonicity [48]. Whether ketoacidosis or lactic acidosis also affect these transfers has been disputed because the transfer of monocarboxylic acids (e.g.…”

“…Whether ketoacidosis or lactic acidosis also affect these transfers has been disputed because the transfer of monocarboxylic acids (e.g. ketoacids, lactic acid) through transporters in cell membranes has no direct effects on potassium transport [48]. However, changes in intracellular pH that accompany organic acidosis have indirect effects on potassium transport through other membrane transporters and exchangers [49].…”