Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.
Renal parenchymal disease can be a cause or consequence of hypertension. Progressive renal damage is caused by the mechanical and humoral effects of glomerular hypertension. The renal damage decreases the kidneys' ability to excrete salt and excess fluid (resulting in a low renin state, as opposed to the high renin state found in renovascular hypertension), and the hypertension worsens. As renal damage progresses, hyperparathyroidism develops and erythropoietin production increases, exacerbating the hypertension. 5 , 18 Thus, a vicious cycle of worsening renal function and hypertension begins.