Mechanisms responsible for mineralocorticoid receptor-dependent renal injury

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Possible roles of aldosterone and mineralocorticoid receptor (MR) in the pathphysiology of renal injury have been indicated. We have demonstrated that MR antagonist elicits blood-pressure independent renoprotective effect in type 2 diabetic rats. We also showed that MR is expressed not only in renal distal tubular cells, but also in other renal epithelial and non-epithelial cells including proximal tubular cells, glomerular mesangial cells, podocytes and renal interstitial fibroblasts. Aldosterone induced cell injury through the activation of MAP kinases and reactive oxygen species generation. Treatment with an MR antagonist inhibits renal cell injuries induced by aldosterone. Similar cell injuries were also induced through MR activation by glucocorticoid and high glucose. These observations suggest that locally expressed MR is involved in renal injury through multiple pathways that cannot be simply explained by high aldosterone levels.