Diabetic nephropathy is more common in patients with a positive family history of hypertension and with elevated red blood cell sodium-lithium countertransport, a marker of risk for essential hypertension. To evaluate whether there is a relationship between this cation transport system and indicators of risk of renal and cardiovascular complications in diabetic patients before the development of clinical proteinuria, we studied 31 type 1 (insulin-dependent) diabetic patients with arterial hypertension, without clinical proteinuria and 12 normotensive normoalbuminuric diabetic patients. Sodium-lithium countertransport activity was significantly higher in hypertensive patients (0.43 +/- 0.03 mmol/l RBC x hr) than in normotensive patients (0.23 +/- 0.03; P less than 0.001). To better explore the nature of the association between this transport system and arterial hypertension, hypertensive patients were divided in two groups, with high (greater than 0.41 mmol/l RBC x hr) or normal (less than 0.41) sodium-lithium countertransport activity. The two groups of hypertensive diabetics were similar in age, sex, body mass index and blood pressure levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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http://dx.doi.org/10.1038/ki.1992.131 | DOI Listing |
Case Rep Nephrol Dial
September 2021
Department of Nephrology and Hypertension, Glickman Urological & Kidney Institute, Cleveland Clinic, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA.
Lithium is one of the first-line agents for treating bipolar disorder. Although this agent is highly effective in treating mood disorders, renal toxicity is a frequent side effect. Lithium metabolism is affected by sodium-lithium counter-transporter (SLC-T) in erythrocytes.
View Article and Find Full Text PDFJ Am Soc Hypertens
March 2017
Department of Genetics, Texas Biomedical Research Institute, San Antonio, TX, USA; Southwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA.
An increased level of sodium-lithium countertransport (SLC) activity has been associated with salt-sensitive hypertension. Previous findings have suggested that dysregulation of the renin-angiotensin-aldosterone system (RAAS) may be involved in the mechanism linking elevated SLC activity and hypertension. Therefore, baboons with different levels of SLC activity were given two diets differing in sodium content, with and without an angiotensin II (ANG II) infusion, to investigate the relationship between SLC activity, the RAAS, and physiological regulation by sodium.
View Article and Find Full Text PDFJ Physiol Biochem
May 2017
Department of Physiology, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD, 21205, USA.
Increased renal reabsorption of sodium is a significant risk factor in hypertension. An established clinical marker for essential hypertension is elevated sodium lithium countertransport (SLC) activity. NHA2 is a newly identified Na(Li)/H antiporter with potential genetic links to hypertension, which has been shown to mediate SLC activity and H-coupled Na(Li) efflux in kidney-derived MDCK cells.
View Article and Find Full Text PDFClin Endocrinol (Oxf)
September 2014
Department of Endocrinology and Metabolism, Odense University Hospital, Odense, UK.
Objective: Antibodies against thyroglobulin, thyroid peroxidase and the TSH receptor are accepted as pathophysiological and diagnostic biomarkers in autoimmune thyroid disease (AITD). In contrast, the prevalence, aetiology and clinical relevance of autoantibodies against the human sodium-iodine symporter (NISAb) and pendrin (PenAb) remain unclear. The objectives of the study were to investigate the presence of NISAb and PenAb in Danish twins, with and without AITD, to study whether the published variations in NISAb and PenAb frequencies were related to differences in methodology or study populations, and to evaluate whether the presence of NISAb or PenAb most likely results from genetic or nongenetic factors.
View Article and Find Full Text PDFClin Chim Acta
March 2014
Department of Biochemical Genetics, National Center of Medical Genetics, 146 Street No. 3102, Havana, Cuba.
Background: Mucopolysaccharidosis I (MPS I) is a genetic disorder caused by deficiency of L-iduronidase (IDUA) activity. Heterozygote screening is a highly requested service by risk families; however, determination of IDUA activity alone is not sufficient to discriminate between heterozygotes and normal individuals because a significant overlap occurs between them. The aim of this study was to characterize the enzyme eluted from heterozygote's dried blood samples and determine if there are differences with that of normal individuals.
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