Increased Sodium-Lithium Countertransport in Erythrocytes of Pregnant Women

Worley, R. J.; Hentschel, Wayne M.; Cormier, Cynthia; Nutting, Suzanne; Pead, Gene; Zelenkov, Kristine; Smith, Jean B.; Ash, K O; Williams, Roger R.

doi:10.1097/00006254-198302000-00003

Cited by 6 publications

(6 citation statements)

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“…Less obvious to explain is the increase in blood lithium concentrations in late gestation. We speculate that it is related to the previously demonstrated increase in the sodium-lithium counter-transport activity in erythrocytes near term (Worley et al, 1982), possibly also an increase in lithium transport in the small intestine (Diamond et al, 1983).…”

Section: Fetal Measurementsmentioning

confidence: 63%

Environmental exposure to lithium during pregnancy and fetal size: A longitudinal study in the Argentinean Andes

Harari

Langeén

Casimiro³

et al. 2015

Environment International

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Section: Fetal Measurementsmentioning

confidence: 63%

Environmental exposure to lithium during pregnancy and fetal size: A longitudinal study in the Argentinean Andes

Harari

Langeén

Casimiro³

et al. 2015

Environment International

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“…From references [8][9][10][11] it appeared that these populations were associated with significantly higher mean flux values compared with populations of non-pregnant women or non-pill users.…”

Section: Pooling Of Data For Statistical Analysismentioning

confidence: 99%

“…For COT studies this number amounted to three. The data in those reports were used for statistical analyses and are from references [2,3,8,9,. Figure 1 illustrates the time course of appearance of these publications during the period 1980-1996.…”

Section: Studies Available For Statistical Analysismentioning

confidence: 99%

Erythrocyte Na+/Li+ countertransport and Na+/K+–2Cl− co-transport measurement in essential hypertension: useful diagnostic tools or failure? A meta-analysis of 17 years of literature

Tepper¹,

Sluiter

Huisman³

et al. 1998

Clinical Science

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1.A meta-analysis of 17 years of literature on erythrocyte Na+/Li+ countertransport (NLCT) and Na+/K+ co-transport (COT) measurements in relation to essential hypertension is presented. The analysis aimed to answer two questions: (i) Which clinical or laboratory variables influence NLCT and COT flux values? (ii) How useful are NLCT and COT measurements as a diagnostic aid in essential hypertension?2. Regression analysis was performed on the mean flux values and relevant clinical and laboratory values. Studies in both normotensive and hypertensive subjects were stratified for variables which showed a significant association with the measured flux. For hypertensive subjects the studies were also stratified for medication. Means of strata were calculated after weighing the mean of a study by the inverse of its own variance and were compared in normotensive as well as hypertensive subjects using a t-test.3.The analysis did not demonstrate systematic effects of laboratory variables for either NLCT or COT. It was found that essential hypertension, family history of hypertension, gender and antihypertensive medication are main determinants for the flux values of both transport systems. After stratification for these determinants, significant differences in weighed mean flux values between normotensive and hypertensive subjects were demonstrated. However, these differences are much smaller than the variance in the weighed mean flux values, suggesting the existence of other unknown variables that strongly affect the flux rates.4.In conclusion, NLCT and COT measurements cannot be of diagnostic use in essential hypertension.

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“…Although SLC activity can be affected by several environmental factors [19][20], family and genetic epidemiology studies have shown that of polygenic inheritance and/or recessive major gene represent the major determinants in the interindividual variability of SLC [15][16][17].…”

Section: Sodium-lithium Countertransportmentioning

confidence: 99%

Dysfunction of Cellular Transporters and Predisposition to Diabetic Nephropathy

Zerbini¹,

Gabellini

Ruggieri

et al. 2006

CDR

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Diabetic nephropathy is presently the first reason of end stage renal failure in Europe and the USA and its worldwide prevalence is rapidly increasing. Several studies have demonstrated that diabetes per se is not sufficient to induce nephropathy and a genetic predisposition has to be present as well. Looking for genetic markers, investigators have been helped by the finding that a predisposition to hypertension facilitates the development of nephropathy in diabetic patients. Prompted by the evidence that essential hypertension is characterized by a number of defects at cellular level, similar dysfunctions have been searched also in cells obtained from diabetic patients with nephropathy. Increased Na-Li countertransport and Na-H exchange activities, slower Ca pump and faster cell proliferation rate have been found in cells obtained from patients affected by diabetic nephropathy. The definition of these intermediate phenotypes represents a necessary step toward the identification of the molecular dysfunction(s) underlying the development of diabetic nephropathy. The present review will focus on the description of the different cell dysfunctions identified in patients affected by diabetic nephropathy, their pathophysiologic meaning and will try to define an unifying hypothesis that, by linking together the different dysfunctions, will highlight a few areas "at risk", candidate to home the primitive genetic abnormality.

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Increased Sodium-Lithium Countertransport in Erythrocytes of Pregnant Women

Cited by 6 publications

References 0 publications

Environmental exposure to lithium during pregnancy and fetal size: A longitudinal study in the Argentinean Andes

Environmental exposure to lithium during pregnancy and fetal size: A longitudinal study in the Argentinean Andes

Erythrocyte Na+/Li+ countertransport and Na+/K+–2Cl− co-transport measurement in essential hypertension: useful diagnostic tools or failure? A meta-analysis of 17 years of literature

Dysfunction of Cellular Transporters and Predisposition to Diabetic Nephropathy

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