Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 15405024

Clinical potassium problems.

H E MARTIN·M WERTMAN
View original source ↗Export metadata ↓

Abstract

Alterations in serum potassium are common in many diseases. In a series of 390 determinations of serum potassium, the levels found were low in 24 per cent and high in 2.6 per cent. The major causes of low serum potassium are (1) decreased potassium intake due to intravenous feedings which do not contain potassium; (2) increased loss of potassium in the urine due to accelerated tissue breakdown, or renal lesions; (3) loss from the gastrointestinal tract due to diarrhea, or fistulae, and (4) shift between serum and cells, due to metabolic causes, drugs or changes in pH. The major cause of high serum potassium is uremia with renal retention.Clinical symptoms and signs of low body potassium include muscle weakness and paralysis, which may lead to death in respiratory failure if not corrected, tachycardia, gallop rhythm, dilatation of the heart. The electrocardiogram shows inverted, low amplitude, or isoelectric T waves and a prolonged QT interval. Potassium chloride orally, subcutaneously or intravenously is recommended for use in the treatment of potassium deficits. It should not be used in the presence of oliguria or anuria or dehydration. The amounts of potassium necessary to correct deficits vary widely and cannot be predicted from the serum level. Special reference is made to the prevention and therapy of potassium deficits in diabetic acidosis. High serum potassium levels are difficult to correct. Suggested measures are administration of glucose, insulin or calcium, gastric or peritoneal lavage or use of the artificial kidney.

Explore related subjects

AnuriaDehydrationDiarrheaElectrocardiographyHumansHypokalemiaOliguriaPotassiumUremiaPOTASSIUMJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H E MARTIN, M WERTMAN. 1950. Clinical potassium problems.. https://pubmed.ncbi.nlm.nih.gov/15405024/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

An integrative description of dialysis adequacy indices for different treatment modalities and schedules of dialysis.

Dialysis adequacy indices that are applied for the evaluation of the efficiency of urea removal include fractional water volume cleared from urea during dialysis (KT T/V), fractional solute removal (FSR), and equivalent urea clearance (EKR). Using a constant-volume, one-compartment urea kinetic model for an anuric patient, the FSR and EKR are shown to depend on only three nondimensional parameters: (i) KT/V, where K is the dialyzer clearance for hemodialysis (HD) or peritoneal mass transport coefficient for peritoneal dialysis (PD), T is the time period of dialysis, and V is urea distribution volume; (ii) T/Tc, where Tc is the length of treatment cycle; and (iii) VD/V, where VD is the volume of dialysis fluid applied. In particular, analytical formulas for FSR and EKR, valid for HD as well as for PD, were derived as functions of these three parameters. Numerical simulations, performed using a two-compartment urea kinetic model, showed that the analytical formulas are valid also for the two-compartment model, except for short, highly effective HD, where the overestimation of FSR and EKR using the analytical formulas is however, not higher than 20 and 16%, respectively. KT T/V is equal to KT/V for HD and FSR for PD. Thus, our formulas provide an integrative description of the relationships between dialysis efficiency indices and operational dialysis parameters that is valid for all modalities and schedules of dialysis. They may be applied not only for standard HD and continuous ambulatory PD, but also for HD with circulating dialysis fluid or intermittent forms of PD.

Anuria↗
PubMed2006

Renal tubular dysgenesis, a not uncommon autosomal recessive disorder leading to oligohydramnios: Role of the Renin-Angiotensin system.

Renal tubular dysgenesis is a clinical disorder that is observed in fetuses and characterized by the absence or poor development of proximal tubules, early onset and persistent oligohydramnios that leads to the Potter sequence, and skull ossification defects. It may be acquired during fetal development or inherited as an autosomal recessive disease. It was shown recently that autosomal recessive renal tubular dysgenesis is genetically heterogeneous and linked to mutations in the genes that encode components of the renin-angiotensin system. This study analyzed the clinical expression of the disease in 29 fetus/neonates from 18 unrelated families and evaluated changes in renal morphology and expression of the renin-angiotensin system. The disease was uniformly severe, with perinatal death in all cases as a result of persistent anuria and hypoxia related to pulmonary hypoplasia. Severe defects in proximal tubules were observed in all fetuses from 18 gestational weeks onward, and lesions also involved other tubular segments. They were associated with thickening of the renal arterial vasculature, from the arcuate to the afferent arteries. Renal renin expression was strikingly increased in 19 of 24 patients studied, from 13 families, whereas no renal renin was detected in four patients from three families. Angiotensinogen and angiotensin-converting enzyme were absent or present in only small amounts in the proximal tubule, in correlation with the severity of tubular abnormalities. No specific changes were detected in angiotensin II receptor expression. The severity and the early onset of the clinical and pathologic expression of the disease underline the major importance of this system in fetal kidney function and development in humans. The identification of the disease on the basis of precise histologic analysis and the research of the genetic defect now allow genetic counseling and early prenatal diagnosis.

Anuria↗