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.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
22
Centro di Ricerche Cliniche per le Malattie Rare Aldo e Cele Daccò
Ranica, Bergamo, Italy
RECRUITINGASST Papa Giovanni XXIII
Bergamo, Italy
RECRUITINGThe extent of extracapillary proliferation on light microscopy, measured as % of total glomeruli with proliferative lesions at post-treatment repeat biopsy.
Time frame: Changes from baseline and 6 and 18 month.
Expression of parietal cell proliferation markers at glomerular level, graded on a scale of 0 to 3 (0: no staining, 1: mild, 2: moderate, 3: strong diffuse
Time frame: Changes from baseline and 6 and 18 month.
Number of fibrosclerotic crescents
Time frame: Changes from baseline and 6 and 18 month.
Glomerular Filtration Rate (GFR) measured by iohexol plasma clearance
Time frame: Changes from baseline and 6, 12 and 18 month.
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