Higher urinary albumin excretion is associated with abnormal erythrocyte Na(+)/Li(+) countertransport (SLC) in non-modulating essential hypertensives and offspring of hypertensive parents.

Non-modulating is a highly reproducible type of sodium-sensitive hypertension. The aim of this study was to evaluate in non-modulating individuals the erythrocyte sodium-lithium countertransport (SLC) abnormalities, which have been mentioned as a marker of non-modulation, and the association with increased microalbuminuria, as a marker of an early kidney impairment. We measured erythrocyte SLC in 10 normotensives (NT, 28 +/- 4 years), 20 offspring of hypertensive parents being 10 modulating (MHO, 25 +/- 6 years) and 10 non-modulating (NMHO, 26 +/- 5 years), and 23 essential hypertensives being 12 modulating (MHT, 34 +/- 5 years) and 11 non-modulating (NMHT, 32 +/- 4 years). In all the subjects studied, microalbuminuria was determined by duplicate 24-h urine collection by radioimmunoassay. In non-modulating offspring of hypertensive parents and essential hypertensives. SLC was significantly elevated when compared either with normotensives without family history of hypertension, modulating offspring of hypertensive parents or essential hypertensives (P < 0.025). Likewise, 24-h urinary albumin excretion was found higher in non-modulating individuals (essential hypertensives and offspring of hypertensive parents) than in modulating individuals (P < 0.01). In conclusion, non-modulators with higher SLC countertransport sodium transport abnormalities showed higher elimination of microalbuminuria suggesting that non-modulators may have an increased risk for developing cardiovascular morbidity and kidney impairment even in normotensive subjects with familiarity history of hypertension.