Angiotensin II Local Hyperreactivity in the Progression of IgA Nephropathy

Coppo, Rosanna; Amore, Alessandro; Gianoglio, Bruno; Cacace, Gianluigi; Picciotto, Giuseppe; Roccatello, Dario; Peruzzi, Licia; Piccoli, Giuseppe; Filippi, P

doi:10.1016/s0272-6386(12)80031-x

Cited by 68 publications

(32 citation statements)

References 28 publications

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“…Therefore, when ACE-I were demonstrated to be capable of reducing proteinuria after a few months of treatment in IgAN (9,23), most nephrologists thought that there was no longer any need for demonstrating the benefit, and ACE-I indeed became a first-choice treatment in proteinuric IgAN, even without hypertension or reduced renal function. Our group was one of the first to emphasize that in IgAN, particularly in proteinuric cases, there was a local hyperreactivity of the RAS (24), and a precocious activation of the RAS has recently been demonstrated (25). However, ACE-I induced a limited reduction in proteinuria (by 20 to 50% of the baseline values) in a subgroup only (40 to 60%) of IgAN (9,23), and it was not proved that this was enough for renoprotection, so leaving open the need for an RCT (19).…”

Section: Discussionmentioning

confidence: 95%

IgACE

Coppo

Peruzzi

Amore

et al. 2007

Journal of the American Society of Nephrology

222

130

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2 ) for >6 mo. Analysis was by intention to treat. A single patient (3.1%) in the ACE-I group and five (14.7%) in the placebo group showed a worsening of CrCl >30%. The composite end point of >30% decrease of CrCl or worsening of proteinuria until nephrotic range was reached by one (3.1%) of 32 patients in the ACE-I group, and nine (26.5%) of 34 in the placebo group; the difference was significant (log-rank P ‫؍‬ 0.035). A stable, partial remission of proteinuria was observed in 13 (40.6%) of 32 patients in the ACE-I group versus three (8.8%) of 34 in the placebo group (log-rank P ‫؍‬ 0.033), with total remission in 12.5% of ACE-I-treated patients and in none in the placebo group (log-rank P ‫؍‬ 0.029). The multivariate Cox analysis showed that treatment with ACE-I was the independent predictor of prognosis; no influence on the composite end point was found for gender, age, baseline CrCl, systolic or diastolic BP, mean arterial pressure, or proteinuria.

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Section: Discussionmentioning

confidence: 95%

IgACE

Coppo

Peruzzi

Amore

et al. 2007

Journal of the American Society of Nephrology

222

130

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“…The hemodynamic studies of the acute administration of ACEIs demonstrated a decrease in filtration fraction consequent to an increase in the effective renal plasma flow, suggesting local activation of the RAS in some cases of IgA nephropathy (Coppo et al, 1993). To investigate intrarenal activation of the RAS in IgA nephropathy, Kobori et al (2007) evaluated renal specimens from 39 patients with IgA nephropathy.…”

Section: Patients With Renal Injury a Chronic Kidney Diseasesmentioning

confidence: 99%

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

et al. 2007

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“…Proteinuria persisting after the acute phase might be due to two different mechanisms: either hyperfiltration due to nephronic mass reduction during the acute phase or the effect of chemokines produced by persistently stimulated MCs on podocytes (47,48,116,117). Theoretically, both mechanisms could be counteracted by ACE inhibitors, whereas corticosteroids might prevent MC proliferation and metabolic stimulation.…”

Section: Mesangial Proliferation Glomerulosclerosis and Proteinuriamentioning

confidence: 99%

Henoch-Schönlein Purpura Nephritis

Davin¹

2011

Clinical Journal of the American Society of Nephrology

146

123

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SummaryHenoch-Schö nlein purpura nephritis is a rare kidney disease leading to chronic kidney disease in a non-negligible percentage of patients. Although retrospective studies suggest beneficial effects of some therapies, prospective randomized clinical trials proving treatment efficacy are still lacking. The dilemma of spontaneous recovery even in patients with severe clinical and histologic presentation and of late evolution to chronic kidney disease in patients with mild initial symptoms renders it difficult for clinicians to expose patients to treatment protocols that are not evidence-based. A better understanding of the pathophysiology of progression to chronic kidney disease in Henoch-Schö nlein purpura patients could be achieved by designing prospective international multicenter studies looking at determinants of clinical and histopathological evolution as well as possible circulating and urinary markers of progression. Such studies should be supported by a database available on the web and a new histologic classification of kidney lesions. This paper reports clinical, pathologic, and experimental data to be used for this strategy and to assist clinicians and clinical trial designers to reach therapeutic decisions.

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Angiotensin II Local Hyperreactivity in the Progression of IgA Nephropathy

Cited by 68 publications

References 28 publications

IgACE

IgACE

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

Henoch-Schönlein Purpura Nephritis

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