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The natural course of extracapillary glomerulonephritis is severe leading to End-Stage Renal Disease (ESRD) or death in most cases. Despite immunosuppressive treatment, long-term renal outcome remains poor since active crescents usually progress to fibrotic scars with glomerular occlusion and disruption.In experimental models Angiotensin Converting Enzyme (ACE)-inhibitor therapy targeting the over-expression of angiotensin type 1 (AT1) receptors, that are responsible for dysregulated proliferation of parietal cell progenitors, blocks the formation of crescents and their fibrotic evolution. Should these drugs have similar effects in humans, ACE-inhibitor therapy on top of standard immunosuppression might be instrumental to prevent ESRD and promote renal function recovery in clinical practice.
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Inclusion criteria
Rapidly progressive renal failure associated with acute nephritic syndrome and/or nephrotic syndrome;
Histology evidence of extracapillary proliferation with less than 50% of sclerotic glomeruli and associated with:
Clinical indication to immunosuppressive therapy;
No specific indication to treatment with Renin Angiotensin System (RAS) inhibitors such as heart failure or coronary ischemic disease;
Written informed consent.
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Primary purpose
Allocation
Interventional model
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22 participants in 2 patient groups
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Central trial contact
Ettore Sabadini, MD; Barbara Ruggiero, MD
Data sourced from clinicaltrials.gov
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