Mallamaci F, Leonardis D, Bellizzi V, Zoccali C
CNR Centro di Fisiologia Clinica, Reggio Cal, Italy.
J Hum Hypertens. 1996 Mar;10(3):157-61.
In animal models of salt-dependent hypertension, hyperfiltration is associated with a faster decline in renal function and there is evidence that in hypertensive man, increased creatinine clearance is a marker of early hypertensive nephropathy. We have studied the influence of salt intake on the glomerular filtration rate (GFR) (Creatinine Clearance) in 14 patients with mild hypertension. Each patient was studied in random order and according to a crossover design, at habitual salt intake, at high salt intake (ie habitual +50/100 mmol/day) and at low salt intake (habitual -50/100 mmol/day). Protein, calcium and potassium intake was fixed across the three study periods. The control group was formed by seven healthy subjects. High salt intake, caused a significant (P < 0.01) increase in 24 h mean arterial pressure (MAP) and the expected suppression in plasma renin activity (PRA) and in plasma aldosterone. Seven patients were classified as salt-sensitive. The GFR was significantly higher (P < 0.01) at high salt intake (125 +/- 10 ml/min) than at habitual (113 +/- 7 ml/min) and at low salt intake (97 +/- 6 ml/min). On aggregate urinary salt excretion was significantly related with the GFR (P < 0.01 by correlation analysis for repeated observations) and the slope of this relationship predicted that a 100 mmol/day increase in salt intake is associated with the 14.6 ml/min rise in the GFR. The relationship between GFR and 24 h urinary salt in salt sensitive patients did not differ from that in salt resistant patients. The GFR response to salt loading was largely independent of the renin-aldosterone system. No change in arterial pressure nor in GFR was observed in healthy subjects. At fixed protein intake, changes in salt intake in the physiological range are associated with important GFR variations in mild hypertensives. As long as hyperfiltration in mild hypertension is a predictor of renal function deterioration, high salt intake, independent of the effect of arterial pressure, could be a factor that contributes to nephronic obsolescence in patients with essential hypertension.
在盐依赖性高血压动物模型中，超滤与肾功能更快下降相关，并且有证据表明，在高血压患者中，肌酐清除率升高是早期高血压肾病的一个标志。我们研究了盐摄入量对14例轻度高血压患者肾小球滤过率（GFR）（肌酐清除率）的影响。每位患者按照随机顺序并根据交叉设计进行研究，分别处于习惯盐摄入量、高盐摄入量（即习惯摄入量+50/100 mmol/天）和低盐摄入量（习惯摄入量-50/100 mmol/天）状态。在三个研究阶段，蛋白质、钙和钾的摄入量保持固定。对照组由7名健康受试者组成。高盐摄入量导致24小时平均动脉压（MAP）显著升高（P<0.01），并如预期那样抑制了血浆肾素活性（PRA）和血浆醛固酮。7例患者被归类为盐敏感型。高盐摄入量时的GFR（125±10 ml/分钟）显著高于习惯盐摄入量时（113±7 ml/分钟）和低盐摄入量时（97±6 ml/分钟）（P<0.01）。总的尿盐排泄量与GFR显著相关（重复观察的相关分析P<0.01），并且这种关系的斜率预测盐摄入量每天增加100 mmol与GFR升高14.6 ml/分钟相关。盐敏感患者中GFR与24小时尿盐之间的关系与盐抵抗患者并无差异。GFR对盐负荷的反应在很大程度上独立于肾素-醛固酮系统。健康受试者未观察到动脉压或GFR的变化。在固定蛋白质摄入量时，生理范围内盐摄入量的变化与轻度高血压患者的GFR重要变化相关。只要轻度高血压中的超滤是肾功能恶化的一个预测指标，那么高盐摄入量，独立于动脉压的影响，可能是导致原发性高血压患者肾单位荒废的一个因素。
