| pubmed-article:2560358 | pubmed:abstractText | Various pathogenetic mechanisms are involved in IgA nephritis: immunological; platelet, coagulation and vascular injury; mesangial cell proliferation and contractility; hypertension; glomerular hyperperfusion and tubulo-interstitial injury. It is now possible to identify the subgroup of patients with IgA nephritis who have adverse prognostic features and may develop progressive glomerular scarring with renal failure. These features are proteinuria greater than 1 gm/day, non-selective proteinuria, glomerulosclerosis, hypertension, crescents and medial hyperplasia of blood vessels on renal biopsy. Controlled trials involving cyclophosphamide, anti-platelet agent (dipyridamole) and low dose warfarin; prednisolone; angiotensin converting enzyme inhibitors and eicosapentanoic acid (fish oil) appear promising. Currently, patients with bad prognostic indices in the Department are offered entry into an ongoing controlled trial of dipyridamole and low dose (anti-thrombotic dose) warfarin. Those patients with nephrotic syndrome especially with selective proteinuria are treated with a course of prednisolone and failing that, cyclophosphamide. It is important to maintain adequate blood pressure control among hypertensive patients as uncontrolled hypertension can lead to accelerated renal failure. With the onset of even mild renal impairment, dietary protein restriction should be recommended as this will help to decrease the rate of renal deterioration due to glomerular hyperfusion. | lld:pubmed |
