POTASSIUM HOMEOSTASIS AND ITS DISTURBANCES IN CHILDREN

被引:19
作者
RODRIGUEZSORIANO, J
机构
[1] Department of Paediatrics, Hospital de Cruces and Basque University School of Medicine, Bilbao
关键词
POTASSIUM; RENAL POTASSIUM EXCRETION; EXTRARENAL POTASSIUM HOMEOSTASIS; HYPOKALEMIA; HYPERKALEMIA; RENAL FAILURE;
D O I
10.1007/BF02254217
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Although only 2% of the body potassium is present in the extracellular space, its concentration is finely regulated by the internal balance, or distribution of potassium between the intracellular and extracellular compartments, and by the external balance, or difference between intake and output of potassium. Internal balance is modulated by a host of factors, including insulin, epinephrine, extracellular pH and plasma tonicity. Potassium output from the body is mainly determined by renal excretion. Renal secretion of potassium takes place predominantly in the principal cells of late distal and cortical collecting tubules, by a process involving the accumulation of potassium in the cell by the activity of the basolateral Na+,K+-ATPase and its exit through luminal conductive channels. The factors regulating renal potassium secretion are potassium intake, rate of tubular fluid flow, distal sodium delivery, acid-base status and aldosterone. Hypokalaemia may result from a low potassium intake, excessive gastrointestinal, cutaneous or renal losses and altered body distribution. Aetiological diagnosis and therapy are best accomplished when the acid-base status is assessed at the same time. Before establishing the diagnosis of hyperkalaemia, spurious hyperkalaemia due to haemolysis or release of potassium from cells during clot retraction (pseudohyperkalaemia) should be ruled out. Hyperkalaemia may result from exogenous or endogenous loading, decreased renal output and altered body distribution. Acute hyperkalaemia represents an emergency situation which requires immediate therapy.
引用
收藏
页码:364 / 374
页数:11
相关论文
共 104 条
[81]  
Bushinsky D.A., Coe F.L., Hyperkalemia during acute ammonium chloride acidosis in man, Nephron, 40, pp. 38-40, (1985)
[82]  
Fontaine B., Khurana T.S., Hoffman E.P., Bruns G., Haines J.L., Troffater J.L., Et al., Hyperkalemic periodic paralysis and the adult muscle sodium channel alpha-subunit gene, Science, 250, pp. 1000-1002, (1990)
[83]  
Rojas C.V., Wang J., Schwartz L.S., Hoffman E.P., Powell B.R., Brown R.H., Met-to-val mutation in the skeletal muscle Na+ channel α-subunit in hyperkalemic periodic paralysis, Nature, 354, pp. 387-389, (1991)
[84]  
Shortland D., Trounce J.Q., Levene M.I., Hyperkalaemic, cardiac arrhythmias, and cerebral lesions in high risk neonates, Arch Dis Child, 62, pp. 1139-1143, (1987)
[85]  
DuBose T.D., Good D.W., Effects of chronic hyperkalemia on renal production and proximal tubule transport of ammonium in rats, Am J Physiol, 260, pp. F680-F687, (1991)
[86]  
DuBose T.D., Good D.W., Chronic hyperkalemia impairs ammonium transport and accumulation in the inner medulla of the rat, J Clin Invest, 90, pp. 1443-1449, (1992)
[87]  
Montoliu J., Lens X.M., Revert L., Potassium-lowering effect of albuterol for hyperkalemia of renal failure, Arch Intern Med, 147, pp. 713-717, (1987)
[88]  
Lens X.M., Montoliu J., Cases A., Campistol J.M., Revert L., Treatment of hyperkalaemia of renal failure: salbutamol v. insulin, Nephrol Dial Transplant, 4, pp. 228-232, (1989)
[89]  
Allon M., Dunlay R., Copkney C., Nebulized albuterol for acute hyperkalemia in patients on hemodialysis, Ann Intern Med, 110, pp. 426-429, (1989)
[90]  
Allon M., Copkney C., Albuterol and insulin for treatment of hyperkalemia in hemodialyzed patients, Kidney Int, 38, pp. 869-872, (1990)