PubMed · 7406708
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M H Gardenswartz, R W Schrier. 1980. Hyponatremia a pathophysiologic approach.. https://pubmed.ncbi.nlm.nih.gov/7406708/
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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.
Studies in humans have shown that cortisol administration (200 mg/day) increases cardiac output, renal vascular resistance, glomerular filtration rate, plasma volume, extracellular fluid volume, exchangeable sodium, plasma glucose, insulin, renin substrate and atrial natriuretic peptide concentrations as well as urinary kallikrein excretion. Cortisol treatment decreases renin and angiotensin II concentrations while catecholamines and vasopressin are decreased or unchanged. We have clear evidence from a number of studies that cortisol-induced hypertension is modulated by, but not dependent on, exogenous sodium. The increase in cardiac output normally seen with cortisol administration is not essential for the blood pressure rise. The role of the increase in renal vascular resistance in the genesis of the hypertension is unclear. Studies using measurements of noradrenaline spillover and assessment of reflex function have not shown any increase in sympathetic nervous system activity but changes in vascular responsiveness, particularly to phenylnephrine and noradrenaline are marked. Cortisol is known to have a variety of effects on brain, heart, kidneys, blood vessels and body fluid volumes. To what extent the observed changes are epiphenomena, amplifiers or modulators, or are causal is unclear. Cortisol hypertension may reflect a complex interplay of these factors varying with the steroid concentrations achieved, underlying genetic factors and the particular experimental circumstances.