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Copyright of Néphrologie & Thérapeutique is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Néphrologie & Thérapeutique is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this work was to evaluate the intracellular Na concentration, the passive Na permeability and the activity of Na, K pump, Na, K cotransport, Na, Li countertransport in the red cells of patients with autosomal dominant polycystic kidney disease (ADPKD) in relationship with their blood pressure status. Sixteen patients with ADPKD and normal renal function (6 males, 10 females, median age 31.5 years, range 20-42 years) and twenty healthy controls (10 males, 10 females, median age 30 years, range 23-47 years) were studied. Eight ADPKD were hypertensive. The rate constant of ouabain-sensitive Na efflux was lower in hypertensive than in normotensive ADPKD patients. The activity of Na,Li countertransport was significantly higher in hypertensive ADPKD patients than in both normotensive patients and control subjects. A significant inverse correlation was found between Na,Li countertransport activity and the rate constant of ouabain-sensitive Na efflux in fresh red cells (rho = 0.62; p = 0.016). Hypertension in patients with ADPKD and normal renal function is associated with abnormalities of red cell sodium transport: an increase of Na,Li countertransport, possibly primitive, and a reduction of Na,K pump in fresh cells, possibly secondary to a circulating inhibitor.

It has been suggested that an increased erythrocyte Na-Li countertransport (Na-Li CNT) rate in patients with IDDM is associated to the risk of developing diabetic nephropathy. Little is known, however, about the possible influence of metabolic control on Na-Li activity. Aims of the study were to evaluate Na-Li CNT at the onset of IDDM and during the remission phase and its relationship with some clinical and metabolic parameters. Twelve insulin-dependent diabetic children (6 males, 6 females; mean age 10 +/- 0.6 years) were studied at the onset and 1, 4, 12 months after the diagnosis; 6 of them had a family history of hypertension. Twelve healthy children (6 males, 6 females; mean age 12 +/- 0.3 years) served as controls. As compared to control subjects (212 +/- 24 mumol/l RBC/h), red cell Na-Li countertransport activity of diabetic children was significantly higher at the onset (354 +/- 31 mumol/l RBC/h) of IDDM and at the first month (348 +/- 36 mumol/l RBC/h). Red cell Na-Li countertransport activity returned toward normal range at the fourth (239 +/- 33 mumol/l RBC/h) and twelfth month (162 +/- 34 mumol/l RBC/h). No correlation was found between the values of red cell Na-Li countertransport activity and those of clinical and biochemical parameters at any time. Patients with hypertensive relatives showed at baseline evaluation a significantly higher red cell Na-Li countertransport activity than those without (436 +/- 28 vs 273 +/- 34 mumol/l RBC/h; p < 0.002). This difference, although not statistically significant, was still evident at the late follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Aim of this study is to evaluate whether among type I diabetic adolescents (IDDM) the erythrocyte Na-Li countertransport (CNT Na-Li) is correlated with arterial pressure and tubular sodium reabsorption. We have studied 16 IDDM adolescents (age 15 +/- 0.5 year) et 15 normal subjects (age 14.5 +/- 1 year). CNT Na-Li, creatinine and lithium clearances (as markers of glomerular filtration rate and proximal tubular sodium reabsorption) have been measured in all subjects and nocturnal urinary albumin excretion rate (UAER) was measured in IDDM adolescents. CNT Na-Li was 308 +/- 26 mumol Li/l RBC/h in IDDM adolescents and 211 +/- 74 mumol Li/l RBC/h in controls (p less than 0.01). The fractional excretion of lithium (FELi) was significantly reduced in IDDM adolescents compared to normal subjects (12 +/- 2 vs 19 +/- 2%; p less than 0.01). Among the IDDM adolescents, 5 had the CNT Na-Li higher than the 95th percentile of controls (greater than 360 mumol Li/l GR/h); their systolic arterial pressure was significantly higher than in diabetics with normal CNT Na-Li (126 +/- 2 vs 116 +/- 2; p = 0.03), while there were no differences for diabetes duration, glycemic control, serum potassium, creatinine clearance, FELi and UAER. The relationship between CNT Na-Li and arterial pressure in IDDM adolescents deserves further studies.