Hypertension is caused by metabolic syndrome. The primary cause of hypertension, however, is excess salt intake and an impaired renal salt excretory mechanism of the tubuloglomerular feedback mechanism involved in macula densa. Salt-losing nephropathy such as Gitelman's syndrome (which is caused by loss of function mutation in the tyhiazide-sensitive Na-Cl transporter, NCCT gene) is lacking in hypertension and has fewer cardiovascular complications despite the presence of the stimulated rennin-angiotensin-aldosterone system. It has been reported that an NCCT gene mutation is closely associated with diabetic nephropathy, suggesting an important role of NaCl metabolism in diabetic nephropathy. Loss of function of peroxisome proliferator-activated receptor(PPAR) -gamma(one of the key molecules of insulin resistance) has been shown to lead to obesity, diabetes and hypertension, suggesting a common basic background of such diseases. High insulin levels observed in insulin resistance would stimulate salt reabsorption in renal tubules, which may result in high blood pressure. Adipocytokines such as adiponectin, leptin and angiotensinogen may play some roles in metabolic syndrome. Taken together, good understanding of salt intake and its related factors in renal salt metabolism involved in metabolic syndrome will suppress further progression of atherosclerotic changes including chronic kidney disease.
|Number of pages||5|
|Journal||Rinsho byori. The Japanese journal of clinical pathology|
|Publication status||Published - 2007 May|
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