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Immunoglobulin A nephropathy (IgAN), which is the most prevalent form of primary glomerulonephritis and one of the major causes of end stage renal disease (ESRD), has a variable clinical course.1–3 Poor prognostic factors for the progression of renal dysfunction in IgAN have been identified as high blood pressure, heavy proteinuria, and a severe histopathological appearance of the renal biopsy.4,5 In addition to these prognostic factors, it has been proposed that several genetic backgrounds are associated with a susceptibility to ESRD in patients with IgAN.6,7
The renin-angiotensin-aldosterone system is an important regulator of blood pressure and plays a central role in the development and progression of end organ damage. Polymorphisms in genes that encode components of this system have been reported to be associated with physiological risk factors for progressive renal dysfunction in IgAN. The most consistent of these is the angiotensinogen (AGT) gene, which is associated with essential hypertension and with an increased risk of cardiovascular diseases and renal failure.8–10 A deletion polymorphism in the angiotensin converting enzyme (ACE) gene influences the circulating ACE levels, and although it has little effect on blood pressure, it has been associated with an increased risk of cardiovascular diseases in some but not all studies.11–13
Aldosterone is one of the main effectors of the renin-angiotensin system14 and has classically been thought to act as a regulator for the absorption of Na and water, as well as the excretion of K in normal physiology, and as a mediator of oedema in numerous disease states. However, it is now well recognised that the actions of aldosterone are not limited to effects on ion transport in epithelial tissue, and its important role in cardiovascular disease involves non-epithelial tissues.15,16 Recently, it has been shown that …
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