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IOS Press, Incorporated
Moderately Proteinuric IgA Nephropathy in the Young
Moderately Proteinuric IgA Nephropathy in the Young
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IgA Nephropathy (IgAN) is one of the most common glomerular diseases world-wide. Its natural history is consistent with a clinical onset in the first decades of life. Clinical indicators of poor prognosis are proteinuria and hypertension. Angiotensin-converting enzyme-inhibitors (ACE-I) are a promising treatment, since Angiotensin II plays a key role in glomerular hypertension and permselectivity and modulates mesangial and tubular cell functions.
This Concerned Action was designed to evaluate the effect of ACE-I (benazepril 0.2 mg/Kg) versus placebo in young IgAN patients (<35 years, proteinuria >1g/day<3.5g/day, renal function >50 ml/min/1.73m2). Activity and chronicity indexes are evaluated on renal biopsies together with the spatial distribution of IgA and C3 deposits by confocal microscopy. Ambulatory blood pressure measurements allow the identification of medium-high pressure levels.
Enrolled patients are investigated for factors modulating the disease progression, including genetic predictors (gene polymorphism of HLA, IgA switch region, ACE, AT1 receptor, adducin, complement factors) and immunologic parameters (aberrantly glycosylated and macromolecular IgA in serum and cytokine urinary excretion)."
This Concerned Action was designed to evaluate the effect of ACE-I (benazepril 0.2 mg/Kg) versus placebo in young IgAN patients (<35 years, proteinuria >1g/day<3.5g/day, renal function >50 ml/min/1.73m2). Activity and chronicity indexes are evaluated on renal biopsies together with the spatial distribution of IgA and C3 deposits by confocal microscopy. Ambulatory blood pressure measurements allow the identification of medium-high pressure levels.
Enrolled patients are investigated for factors modulating the disease progression, including genetic predictors (gene polymorphism of HLA, IgA switch region, ACE, AT1 receptor, adducin, complement factors) and immunologic parameters (aberrantly glycosylated and macromolecular IgA in serum and cytokine urinary excretion)."