Internal potassium shift in premature infants: cause of nonoliguric hyperkalemia.

To study the pathophysiology of nonoliguric hyperkalemia, we measured serum potassium concentration and external K balance (intake and excretion), and estimated internal K balance (a shift from intracellular space to extracellular space) in 24 nonoliguric premature infants during the first 72 hours after birth. Data were analyzed from two aspects: gestational age (group 1, 24 to 28 weeks, n = 9; group 2, 29 to 32 weeks, n = 9; group 3, 33 to 36 weeks, n = 6) and postnatal age (0 to 72 hours). Serum K concentration rose from baseline (0 hour) to 24 hours in groups 1 and 2 (p < 0.01) but did not rise in group 3. The external K balance was negative in all groups during the study period, and was more negative in the more premature infants (group 1 > group 2 > group 3) during the second 24 hours. There was a significant difference (p < 0.01) between the internal K balance of the three groups during the first 24 hours (group 1 > group 2 > group 3), and the K shift decreased significantly (p < 0.05) during the study period in groups 1 and 2. The more premature the infants, the larger the K shift and the larger the rise in serum K concentration during the first 24 hours, and the more negative the external K balance after 24 hours. These data indicate that K loading caused by the K shift associated with prematurity produces a rapid rise in serum K concentration, resulting in an increase in urinary K excretion. We conclude that an internal K shift inversely proportional to gestational and postnatal age is the primary cause of nonoliguric hyperkalemia in very premature infants.