Aviv Abraham, Hollenberg Norman K, Weder Alan B
Hypertension Research Center, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey 07103, USA.
Kidney Int. 2004 Feb;65(2):361-8. doi: 10.1111/j.1523-1755.2004.00389.x.
African Americans are prone to develop not only essential hypertension but also progressive renal injury. We present a simple model to explain salt-induced renal injury (sodium glomerulopathy) in African Americans, the central features of which are the tubuloglomerular feedback and the balance/imbalance between the vascular tones of the afferent and efferent glomerular arterioles. We propose that in African Americans, habitual consumption of high salt causes chronic intermittent tubular hyperperfusion of the macula densa, resulting in a rightward and upward resetting of the operating point for the tubuloglomerular feedback. The resetting of the operating point causes an imbalance between the vascular tones of the afferent/efferent arterioles, a rise in the glomerular capillary hydraulic pressure, and consequent hyperfiltration. Increased susceptibility to glomerular hyperfiltration of African Americans on a high salt intake may explain their proclivity to progressive renal injury associated with essential hypertension.
非裔美国人不仅容易患原发性高血压，还容易出现进行性肾损伤。我们提出一个简单模型来解释非裔美国人中盐诱导的肾损伤（钠性肾小球病），其核心特征是肾小管-肾小球反馈以及肾小球入球小动脉和出球小动脉血管张力之间的平衡/失衡。我们认为，在非裔美国人中，长期高盐饮食会导致致密斑慢性间歇性肾小管高灌注，从而使肾小管-肾小球反馈的工作点向右上方重置。工作点的重置会导致入球/出球小动脉血管张力失衡、肾小球毛细血管液压升高，进而导致超滤过。高盐摄入时非裔美国人对肾小球超滤过的易感性增加，这可能解释了他们易患与原发性高血压相关的进行性肾损伤的原因。
