Tubular Na+ handling in type I insulin-dependent diabetics during saline and ketone body infusion.

It has been reported that patients with type I insulin dependent diabetes mellitus (IDDM) are characterized by reduced Na+ excretion during water immersion and saline infusion and abnormal glomerulo-tubular balance. Aims of the present study were therefore to investigate firstly the fractional tubular Na+ reabsorption during saline infusion to clarify the altered tubular site and secondly the glomerulo-tubular balance during acute increase of glomerular filtration rate induced by sodium acetoacetate infusion in IDDM. During saline and euglycaemic glucose clamp, after an overnight fast, glomerular filtration rate, renal plasma flow, filtration fraction and plasma sodium were 99 +/- 15 ml min-1 1.73 m-2, 452 +/- 109 ml min-1 1.73 m-2, 0.23 +/- 0.04 and 142 +/- 8 mmol l-1 (Mean +/- SD) in 10 type I insulin dependent diabetic patients and 96 +/- 18, 452 +/- 87, 0.21 +/- 0.02, 143 +/- 2 in five matched normal subjects, respectively. The lithium and sodium clearances were significantly lower in diabetic patients than in normal subjects (23 +/- 5 ml min-1 1.73 m-2 vs 28 +/- 6, p less than 0.05 and 1.1 +/- 0.4 vs 1.6 +/- 0.3, p less than 0.01 respectively). The fractional lithium reabsorption was greater (0.77 +/- 0.04 vs 0.72 +/- 0.03, p less than 0.05) and the distal fractional sodium reabsorption smaller (0.22 +/- 0.04 vs 0.27 +/- 0.03, p less than 0.01) in the diabetic patients compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Red blood cell sodium and potassium fluxes in psoriatic patients.

Psoriasis might be a widespread membrane disorder. Therefore, the red blood cell sodium, potassium and lithium outward fluxes (through Na-K-ATPase, Na-K-Cl co-transport, Li-Na countertransport and passive permeability), as well as the Na and K content, were studied in 31 psoriatic patients and 23 normal controls. A significant increase in intracellular potassium content, in the maximal velocity of the Na-K ATPase and of Na-K-Cl co-transport as well as in the outward passive permeability for Na were found in the psoriatic patients compared with controls. On the contrary, no differences were observed in sodium content, Li-Na countertransport and passive potassium permeability between the two groups. These results are compatible with a selective increase in inward, as well as outward, membrane permeability to sodium, which is compensated for by increased activity of the Na-K pump, and of the outward Na-K-Cl cotransport with a secondarily increased erythrocyte potassium content. They indicate that the red blood cell might be a useful model for the study of membrane transport in psoriatics.

Intra-erythrocytic sodium content in normotensive offspring of normotensive and hypertensive subjects: an epidemiological study.

An increase in intra-erythrocytic sodium (IENa) content has been proposed as a genetic marker of essential hypertension. Intra-erythrocytic sodium was studied using hypotonic lysis and flame photometry after four washings with isotonic MgCl2 in 240 normotensive subjects (aged 10-45 years) on a free diet with (F+, 121 patients) or without (F-, 119 patients) hypertensive parents, recruited from a random sample of the general population. Systolic blood pressure was significantly higher in males F+ than in males F- (130 +/- 2 versus 125 +/- 2 mmHg, mean +/- s.e.m., P < 0.05), while IENa did not differ. In contrast, intra-erythrocytic potassium content (IEK) was significantly lower and red cell sodium potassium (Na:K) ratio significantly higher in F+ than F-. This might reflect decreased NaK pump activity, or increased membrane permeability to cations which causes increased K leakage. No differences in blood pressure, IENa or IEK showed in female F+ versus F-. It is concluded that IENa is not a genetic marker of hypertension, and that it is probably influenced by exogenous factors. Being associated with differences in blood pressure, the abnormalities of IEK and Na:K ratio might be pathogenetically linked to an early increase in blood pressure.