Disorders of potassium homeostasis

Derangements in potassium homeostasis affect the body's bioelectric processes, including muscle contraction, nerve conduction, and myocardial electric pacing. Changes in extracellular potassium concentration occur with altered routes of elimination (renal or gastrointestinal) or with pathologic shifts in potassium from one body fluid compartment to another. The therapeutic interventions may either restore a normal resting potential for excitable cells or affect the threshold potential. Thus, an understanding of the basic pathophysiology is the foundation for treatment.     

Sodium and water homeostasis in children with shigellosis

Studies in Bangladesh have shown that the mortality in shigellosis is significantly higher in hyponatraemic (HN) than in normo- (NN) or hypernatraemic children. The aim of this study was to describe the effect of shigellosis on renal haemodynamics and sodium and water homeostasis before treatment was started. Twenty-one moderately ill children infected with Shigella dysenteriae type 1 were studied. Eight of them had a serum sodium concentration below 130 mmol/L. Renal function was determined by glomerular filtration rate measured by clearances of inulin and iohexol. Effective renal plasma flow was estimated by clearance of paraaminohippuric acid. Plasma renin, aldosterone and anti-diuretic hormone were also studied. The HN children had significantly higher haemoglobin and haematocrit levels than the NN group. There was an inverse correlation between serum sodium and haemoglobin, and a direct correlation between serum sodium and urinary sodium and urinary chloride. Direct correlations were found between serum aldosterone and haemoglobin, plasma renin and systolic blood pressure and an inverse correlation between serum aldosterone and serum sodium. Clearances of inulin and iohexol were normal. Detectable levels of ADH were found in both groups, despite low serum osmolalities.

Conclusion : The HN state seems to be triggered by multiple factors. The normal glomerular filtration rate excludes a volume expansion secondary to reduced renal function. Inappropriate or a physiological increase of anti-diuretic hormone secretion may be of importance. The higher sodium losses in stools of the HN children might also be a factor contributing to the HN.     

Sodium potassium adenosine triphosphatase activity in preterm and term infants and its possible role in sodium homeostasis during maturation.

AIM: To investigate sodium (NA(+)) potassium (K(+)) adenosine triphosphatase (ATPase) activity in newborn infants at different gestational ages, to elucidate the mechanism underlying poor renal sodium conservation in preterm infants. METHODS: Fifty three healthy newborn infants, gestational age 30-42 weeks, were studied. Umbilical cord red blood cell Na(+) K(+)ATPase activity, plasma renin activity, and plasma aldosterone activities were measured in all of them. Red blood cell Na(+) K(+)ATPase activity was re-examined in eight preterm infants, one and two weeks after birth. Total and ouabain sensitive ATPase activity was measured spectrophotometrically using a method that couples ATP hydrolysis with NADH oxidation. RESULTS: Red blood cell Na(+) K(+)ATPase activity was significantly lower (p<0.01) in preterm babies with a gestational age below 35 weeks, compared with those with aged 35 weeks and above: 2.3 (0.8) and 6.7 (1.3) nmol NADH/minute/mg protein, respectively. There was no correlation between gestational age, Na(+) K(+)ATPase, plasma renin activity and aldosterone values either in the preterm or term babies. Two weeks after birth, irrespective of gestational age, the enzyme activity of the preterm babies increased to values similar to those observed in the term neonates at birth. CONCLUSION: The differences in sodium homeostasis between term and preterm babies are modulated via changes in Na(+) K(+)ATPase activity.     

Sodium and potassium levels in colostrum.

The sodium and potassium concentrations of serum, urine and breast milk from 40 healthy, lactating mothers aged 18 to 35 years were measured. Nineteen women were primiparous and 26 were delivered prematurely for various reasons. No correlation was found between colostrum and urine sodium and potassium levels, and colostrum and serum potassium levels, however, there was a correlation found between colostrum and serum sodium levels (r: 0.311, p less than 0.05).     

Sodium and potassium metabolism in infancy]

BACKGROUND: Recommendations for the concentration of most nutrients in infant formulas are based on their concentration in human milk. Industry succeeded in adapting sodium and potassium content in infant formulas to concentration found in human milk. Whether this adaptation affects on infants' mineral balances was studied in breast-fed and artificially-fed infants. METHODS: Sodium and potassium balances were performed in 16 term male infants from their 3rd until their 17th week of life. The balances were performed at home and comprised up to five periods in intervals of three to four weeks. Each balance period consisted of subsequent three 24 h collections of milk, stool and urine samples. Ten infants were breast-fed, six received an adapted infant formula supplemented with copper, zinc and iron. RESULTS: The breast-fed infants got a mean intake of 1 mmol Na/kg b w x day and a mean intake of 1.8 mmol K/kg b w x day. Man retention was 0.4 mmol Na and 0.7 mmol K/kg b w x day. The formula-fed infants received 1.9 mmol Na/kg b w x day and 2.1 mmol K/kg b w x day. Na- and K-retention in this group was 0.5 and 0.6 mmol/kg b w x day respectively. Although sodium intake in the formula-fed infants was nearly twice as much as in the breast-fed infants the difference in sodium retention was only small (0.4 vs 0.5 mmol/kg b w x day). The formula-fed infants got more potassium than the breast-fed infants, but potassium retention was the same in both groups. CONCLUSIONS: With the adapted infant formula of this study the artificially fed infant was as well supplied with sodium and potassium as the breast-fed infant. A further reduction of the sodium concentration seems not to be useful.     

Sodium homeostasis in infants with biliary drainage procedures

We studied biliary excretion of sodium and chloride in 17 infants with external bile drainage through a "biliostomy" and describe four additional children who became ill from sodium depletion following external biliary drainage procedures for biliary tract anomalies. In the 17 infants, the mean +/- SD bile sodium concentration was 122 +/- 15 mEq/L. The mean +/- SD serum sodium concentration was low (132 +/- 7 mEq/L) (normal, 138 to 145 mEq/L). The mean +/- SD bile volume was 388 +/- 317 mL/day at one year following surgery (range, 40 to 1,000 mL/day). In the four children, clinical manifestations of sodium depletion (lethargy, anorexia, dehydration, and malnutrition) necessitated hospital admission. At that time, the serum sodium concentration ranged from 109 to 129 mEq/L, and the simultaneous urinary sodium concentration ranged from 0 to 5 mEq/L. Although dietary sodium was normal, biliary losses exceeded dietary intake, resulting in salt and water depletion despite renal conservation. Children with biliary drainage procedures are at risk for sodium depletion and should be monitored closely and supplemented accordingly until biliostomy closure is performed.     

Sodium homeostasis in neonatal infection of eutrophic premature infants

In 14 premature infants suffering from bacterial sepsis during the first week of life the daily renal sodium and potassium losses as well as the concentrations in serum of both electrolytes were measured before and during the period of infection. 24 hours before appearance of first clinical symptoms of sepsis the sodium concentration in urine increases and the balance becomes negative. Hyponatraemia occurs later and is in correlation with the clinical course of the disease. Thus, the hyponatraemia is caused more by shifting of sodium from the extracellular space than by renal sodium excretion. To prevent this hyponatraemia the sodium intake has to be increased to 6 mmol/kg X 24 h as a minimum and the fluid intake has to be decreased to 80 ml/kg X 24 h as a maximum in the same time when antibiotic treatment is started. A short-term control of serum electrolytes is an important premise for a sufficient treatment. Increased sodium concentrations in urine of more than 50 mmol/l or again increasing concentrations beyond the second day of life can be appreciated as early signs of neonatal sepsis.     

Sodium, potassium and chloride needs in low-birth-weight infants

A review of the daily requirements of sodium, potassium and chloride in preterm infants with particular emphasis on very low-birth-weight (VLBW) infants is given against the background of our present knowledge of the homeostatic regulation of these electrolytes during early postnatal life. Particular attention has been given to the importance of balanced fluid and electrolyte homeostasis in the control of compartment volumes and tonicity. The risk of rapid changes of extracellular fluid osmolality for many organs, and particularly for the brain, has been stressed. In order to obtain an adequate sodium and fluid balance during the first postnatal weeks in preterm infants of varying gestational age, recommendations for sodium intake during the first 4-5 postnatal weeks are given.     

Sodium homeostasis in term and preterm neonates. II. Gastrointestinal aspects.

Eighty five 24 hour balance studies were performed on 70 healthy newborn infants of gestational age 27-40 weeks; dietary intake and stool losses of sodium were measured. There was a relation between gastrointestinal sodium absorption and conceptional age (the sum of gestational and postnatal age), whether expressed as absolute stool sodium losses or as the ratio of stool sodium to dietary sodium intake. The stool K:Na ratio rose appreciably with maturation, although stool content of potassium was not greatly increased. These findings suggest that intestinal sodium absorption is inefficient in immature babies and that the degree of malabsorption is inversely related to conceptional age.     

Sodium homeostasis in term and preterm neonates. I. Renal aspects.

Eighty five 24 hour sodium balance studies and creatinine clearance measurements were performed in 70 infants of gestational age 27-40 weeks and postnatal age 3-68 days. The kidney''s capacity to regulate sodium excretion was a function of conceptional age (the sum of gestational age and postnatal age) and an independent effect of postnatal age was also observed--extrauterine existence increased the maturation of this function. The sodium balance was negative in 100% of infants of less than 30 weeks'' gestation, in 70% at 30-32 weeks, in 46% at 33-35 weeks, and in 0% of greater than 36 weeks, and the incidence of hyponatraemia closely paralleled that of negative sodium balance. Despite a low glomerular filtration rate (GFR) urinary sodium losses were highest in the most immature babies but fractional sodium excretion (FENa) was exponentially related to gestational age. An independent effect of postnatal age could be identified on FENa but not in GFR. These findings indicate that in infants of greater than 33 weeks'' gestation sodium conservation is possible because of a favourable balance between the GFR and tubular sodium reabsorption, but that below this age GFR exceeds the limited tubular sodium reabsorption capacity. The rapid increase in sodium reabsorption in the first few postnatal days seems to be due to maturation of distal tubular function, probably mediated by aldosterone. We suggest that the glomerulotubular imbalance for sodium is a consequence of the immaturity of the tubuloglomerular feedback mechanism, and we estimate that the minimum sodium requirement during the first 2 weeks of extrauterine life is 5 mmol (mEq)/kg/day for infants of less than 30 weeks'' gestation and 4 mmol (mEq)/kg/day for those born between 30 and 35 weeks.     

Sodium homeostasis in term and preterm neonates. III. Effect of salt supplementation.

Clinical and biochemical effects of supplementing dietary sodium intake to 4 to 5 mmol(mEq)/kg/day from days 4 to 14 of life were studied in 22 infants of gestational age 27 to 34 weeks. These infants were compared with a group of 24 unsupplemented babies. Supplemented infants lost less weight postnatally and regained birthweight more quickly: their improved weight gain continued after supplementation was stopped. Sodium balance was positive at age 5 to 11 days in supplemented babies but slightly negative in controls. Potassium balance was more strongly positive in the supplemented group. Plasma sodium concentration was higher in supplemented infants during weeks 3 and 4. Hyponatraemia was significantly more common in unsupplemented (37.5%) than supplemented (13.6%) infants. No infant became oedematous, hypernatraemic, or showed evidence of circulatory overload. The incidence of patent ductus arteriosus and necrotising enterocolitis was not increased; no intracranial haemorrhages occurred. Urinary potassium:sodium ratio was lower in supplemented babies than controls suggesting responsiveness of the distal tubule to mineralocorticoids. Providing 4 to 5 mmol(mEq)/kg/day of sodium to infants born before 34 weeks'' gestation for the first two postnatal weeks improves growth and biochemical status and causes no undesirable side effects.