Red cell sodium-lithium countertransport and blood pressure in children with insulin-dependent diabetes mellitus

Dobos, M.; Madácsy, László; Yaşar, Semih; Breckner, M.; Körner, Anna; Szücs, L; Nagy, I.; Tulassay, Tivadar

doi:10.1016/0168-8227(94)90134-1

Cited by 5 publications

(5 citation statements)

References 26 publications

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“…Higher SLC was found during the acute phase of NS when edema and sodium retention developed. Sodium transporter activity was elevated to levels found in insulin-dependent diabetic children and adults [8][9][10][11], and in idiopathic hypertension [13][14][15]. Our findings suggest that in edema-forming NS the altered body sodium homeostasis is coupled to enhanced erythrocyte SLC, and that this is a transitory phenomenon, since values decreased when sodium metabolism returned towards normal.…”

Section: Discussionmentioning

confidence: 54%

“…SLC was measured in vitro on RBC according to the method of Trevisan et al [7] modified as described previously [8]. SLC activity was expressed as µmols per hour per liter RBC and measured at 60 min.…”

Section: Methodsmentioning

confidence: 99%

“…Erythrocytes express type-1 NHE, while renal tubular cells express type-2 NHE. SLC has been studied extensively in erythrocytes and it has been suggested that enhanced SLC indicates altered Na + /H + exchange activity [6][7][8][9][10][11][12]. Despite the different isoforms of NHE expressed on erythrocytes and renal tubular cells, SLC has been shown to be a sensitive marker for diseases with altered vascular reactivity and/or disturbances in sodium metabolism [9][10][11]13].…”

Section: Introductionmentioning

confidence: 99%

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Sodium-lithium countertransport in children with nephrotic syndrome

Tulassay¹,

Dobos²,

Luczay³

et al. 1999

Pediatric Nephrology

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The mechanisms of sodium retention in edema-forming minimal change nephrotic syndrome (MCNS) have not been completely evaluated. The aim of this study was to characterize the transmembrane sodium transport in nephrotic syndrome by measuring the erythrocyte sodium-lithium countertransport (SLC) in vitro. Eighteen children with MCNS were studied in the edema-forming state, and subsequently at the beginning of remission. Nephrotic children with edema retained sodium (10+/-12 micromol/day) and had a higher SLC [426+/-118 vs. 281+/-60 micromol/l red blood cells (RBC) per hour, P=0.003). The intracellular sodium concentration of nephrotics was 6.1+/-2.1 mmol/l RBC, which did not differ from that of controls (6.42+/-2.24, n=13). In remission sodium balance became negative (-30+/-21 mmol/day), and the SLC decreased but still differed significantly from control values (P=0.009). The intracellular sodium content decreased to 4.4+/-0.9 mmol/l RBC (P=0.002). There was a negative correlation between erythrocyte SLC and plasma albumin concentration (r=0.48, P=0.003), and urinary sodium excretion rate (r=0.66, P=0.001). In conclusion, erythrocyte SLC is high in the edema-forming state of childhood nephrotic syndrome and decreases with the onset of remission. A role for the SLC in the altered sodium homeostasis of nephrotic syndrome is suggested.

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Section: Discussionmentioning

confidence: 54%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sodium-lithium countertransport in children with nephrotic syndrome

Tulassay¹,

Dobos²,

Luczay³

et al. 1999

Pediatric Nephrology

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“…The Na + /Li + countertransport was measured by the modified method of Canessa et al [25], as described previously [26]. Li was measured on an atomic absorption spectrophotometer (GBCAA 932) at 670.8 nm.…”

Section: Methodsmentioning

confidence: 99%

Sodium transport and bone mineral density in hypercalciuria with thiazide treatment

et al. 1998

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Erythrocyte sodium-potassium (Na+/K+)-ATPase and sodium-lithium (Na+/Li+) countertransport activities were measured in 18 children (aged 9.6 years, range 6-16 years) with idiopathic hypercalciuria (IHU) to evaluate cellular Na handling. The effect of chronic thiazide administration on these parameters and on bone mineral density was also evaluated. Patients with IHU had significantly lower erythrocyte Na+/K+-ATPase activity than 23 age-matched healthy controls (mean +/- SEM 2,156 +/- 110 micromol P/l erythrocyte per hour vs. 3,165 +/- 175, P < 0.01). Thiazide treatment significantly lowered urinary calcium excretion; this was followed by a slight suppression of intact parathyroid hormone (iPTH). The urinary calcium/creatinine ratio before and during treatment was 0.90 +/- 0.07 mmol/mmol versus 0.51 +/- 0.06 respectively, P < 0.01. The corresponding iPTH levels were 5.9 +/- 0.6 pmol/l and 5.1 +/- 0.7, P < 0.05. The Na+/K+-ATPase activity increased significantly (2,769 +/- 169 micromol P/l erythrocyte per hour vs. 2,156 +/- 110 in the control period, P < 0.01) and the Na+/Li+ countertransport decreased (268 +/- 28 micromol Li/l erythrocyte per hour vs. 328+26 in the control period, P < 0.03). The bone mineral density Z score rose from -1.3 +/- 0.26 to -0.8 +/- 0.22 (P < 0.03). We conclude that IHU is accompanied by abnormalities of erythrocyte Na+/K+-ATPase and Na+/Li+ countertransport which are corrected by chronic hydrochlorothiazide administration. These changes could model alterations in renal tubular transport mechanisms still to be elucidated. Chronic thiazide treatment also has a positive effect on bone mineral density.

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“…Measurement of eiythrocyte SLC activity SLC activity was measured on red blood cells in vitro according to Trevisan (8). modified as described previously (9). Activity of the transporter was expressed as ,umoVh/l RBCs and measured at 60 min.…”

Section: Preparation Of Erythrocyte Membrunesmentioning

confidence: 99%

Altered erythrocyte sodium‐lithium counter‐transport and Na+/K+‐ATPase activity in cystic fibrosis

Luczay¹,

Vásárhelyi²,

Dobos³

et al. 1997

Acta Paediatrica

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Patients with cystic fibrosis (CF) exhibit normal concentrations of sodium and chloride in spite of the disturbance of Cl- and Na+ transport in epithelial cells. To characterize compensatory mechanisms in the regulation of sodium homeostasis, erythrocytes of 13 CF patients were analysed for sodium-lithium counter-transport (SLC), Na+/K(+)-ATPase activity and intracellular sodium content. Values were compared to those of healthy controls. Patients with CF had normal serum sodium and chloride concentrations and renal excretions of these ions were within the physiological range. Intracellular sodium concentration was similar in the CF and the control group (6.8 +/- 2.2 vs 5.7 +/- 1.0 mmol/l RBCs). Red blood cells' SLC and Na+/ K(+)-ATPase activity were elevated in CF patients (381 +/- 106 mumol/h/l RBCs vs 281 +/- 64; p < 0.01) and (445 +/- 129 mumol ATP mg prot/h vs 322 +/- 84, p < 0.01). Our study demonstrates that transmembrane cation transport systems are highly activated in CF. The increased sodium transport may be part of a compensatory mechanism of sodium homeostasis in children with CF.

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Red cell sodium-lithium countertransport and blood pressure in children with insulin-dependent diabetes mellitus

Cited by 5 publications

References 26 publications

Sodium-lithium countertransport in children with nephrotic syndrome

Sodium-lithium countertransport in children with nephrotic syndrome

Sodium transport and bone mineral density in hypercalciuria with thiazide treatment

Altered erythrocyte sodium‐lithium counter‐transport and Na+/K+‐ATPase activity in cystic fibrosis

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