Role of podocytes in lupus nephritis.

analysis: effect of monotherapy and combination therapy with inhibitors of the renin angiotensin system on proteinuria in renal disease. A, Morita H et al. Combination treatment of angiotensin-II receptor blocker and angiotensin-converting-enzyme inhibitor in non-diabetic renal disease (COOPERATE): a randomised controlled trial. Coleman CI et al. Combination therapy with an ACE inhibitor and an angiotensin receptor blocker for diabetic nephropathy: a meta-analysis. Treatment of microalbumin-uria in hypertensive subjects with elevated cardiovascular risk: results of the IMPROVE trial. McQueen M et al. Renal outcomes with telmisartan, ramipril, or both, in people at high vascular risk (the ONTARGET study): a multicentre, randomised, double-blind, controlled trial. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern? Clarke WR et al. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropa-thy due to type 2 diabetes. N Engl J Med 2001; 345: 851–860 36. Berns JS. Is Angiotensin-converting enzyme inhibitor and angiotensin receptor blocker combination therapy better than monotherapy and safe in patients with CKD? Design of combination angiotensin receptor blocker and angiotensin-converting enzyme in-hibitor for treatment of diabetic nephropathy (VA NEPHRON-D). Clin L et al. Double-blind, placebo-controlled study on the effect of the aldosterone receptor antagonist spironolactone in patients who have persistent pro-teinuria and are on long-term angiotensin-converting enzyme in-hibitor therapy, with or without an angiotensin ii receptor blocker 10. Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency. Studi Epidemiologici in Ne-frologia). Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, non-diabetic nephropathy. Much attention has been focused on the complex pathology of lupus nephritis (LN) in an attempt to develop specific therapies targeted to this serious manifestation of systemic lupus erythematosus (SLE). The classification of LN depends on the findings at histology according to the International Society of Nephrology (INS) and Renal Pathology Section (RPS) classification criteria [1] and involves deposition of immunoglobulin in glomerular and tubular basement membrane-enhanced inflammatory response and renal fibrosis [2]. Clinically, proteinuria and haematuria are characteristic features in patients with LN and have traditionally been thought to be the result of immune complex deposition and endocapillary proliferation causing a disruption to the filtration barrier. However, in a subset of protein-uric lupus patients, there is no evidence of the typical immune complexes and instead there appears to be extensive podocyte effacement [3]. The effacement of the foot …