Loading search results
Sponsor study identifier
observational
120
1 country
1
Study Start
April 2010
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
January 2013
Actual (reported)Study Completion
July 2014
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
Henoch Schonlein Purpura (HSP), vasculitis of small vessels with deposits of IgA, is considered by many authors as the systemic form of Berger's disease (IgA-N). IgA-N is characterized by IgA1 deposits in mesangial areas associated with mesangial proliferation. These two diseases remain the leading cause of ESRD by primitive glomerulopathy in Western countries. In recent years, considerable progress has been made in understanding the pathophysiological mechanisms of IgA-N. However, only a high rate of proteinuria at one year or the presence of severe glomerular inflammation on renal biopsy remain predictors of long term renal function. Moreover, the high variability of HSP clinical expression, from few purpura skin lesions that evolve favourably spontaneously, to rapidly progressive renal failure, remains so far unexplained but suggests the existence of individual genetic susceptibility. In the first part of the study, we will study key factors based on physiopathological data obtained by our laboratory as well as by other groups. The second part of the study concerns genetic factors. Although the candidate genes that may confer a particular susceptibility to the disease, to progress to ESRD or respond to treatment are many, the genes involved in inflammation or controlling renin-angiotensin system are of particular interest. We will apply these results by studying patients with HSP showing three distinct phenotypes (HSP with isolated cutaneous purpura or associated with minimal or severe renal disease) at diagnosis and after clinical remission. The purpose of this study is to assess whether the phenotype at diagnosis is associated with the physiological markers and if one of them predicts a pejorative evolution of renal disease at 1 year. Meanwhile, study of polymorphism of selected genes of interest could allow identification of patients with specific genetic susceptibility or with bad prognosis factors who would be thus eligible for specific treatment.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
July 2014
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
Click on a node to explore related trials.
Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
April 2010
Date type not reportedThis date has not been verified as actual or estimated.
May 31, 2012
Actual (reported)June 4, 2012
Actual (reported)January 2013
Actual (reported)July 2014
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
Renal prognosis
one time measure after a four hour writing session
have skin involvement +/- an extra renal disease (arthritis, digestive and/or HSP without renal disease. The absence of renal disease is defined by the absence of hypertension (BP \<95th percentile for height in children, BP \<140/90 mmHg in adults with no known history of hypertension), the absence of hematuria (\<5 RBCs per mm3), the absence of proteinuria (proteinuria \<0.1 g/24h) and the absence of renal dysfunction (MDRD\> 80 ml / min).
HSP with renal impairment, defined by the presence of renal dysfunction (calculated clearance \<60 ml/min) and/or proteinuria (daily proteinuria greater than 0.3 g) and/or hematuria (more than 5000 RBC per ml or 5 RBC per mm3). We distinguish: * Group B1 patients with moderate renal disease if renal biopsy was not indicated or no evidence of histologic severity in renal biopsy (histological classification class 1 or 25) * Group B2 patients with severe renal impairment, with signs of histological severity in renal biopsy (class 3, 4 or 5).
Children or adults, suffering from biopsy-proven HSP.2 groups: 1. Skin involvement +/- an extra renal disease (arthritis, digestive and/or other), without renal disease. Absence of renal disease is defined by: absence of hypertension (BP \<95th percentile for height in children, BP \<140/90 mmHg in adults), absence of hematuria (\<5 RBCs /mm3 or \< 5000 RBCs/ ml), absence of proteinuria (proteinuria \<0.1 g/d) and absence of renal dysfunction (MDRD\> 80 ml / min) 2. Renal impairment, defined by the presence of renal dysfunction (calculated clearance \<60 ml/min) and/or proteinuria (daily proteinuria greater than 0.3 g) and/or hematuria.
Nephrology Unit - Hôpital St Louis
Paris, 75010, France
Blood and urine analysis - Skin and kidney biopsies
Evangeline Pillebout, Md PhD
APHP - Hôpital St Louis - Paris 10 - France
First Submitted
May 31, 2012
First Posted
June 4, 2012
Study Start
April 2010
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
January 2013
Actual (reported)Contact the study team to confirm eligibility.
Study Completion
July 2014
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
Last Updated
April 23, 2014
Record last verified: 2012-07
Download the complete ClinicalTrials.gov record imported by Syfrah, including fields not shown in this page. The registry may contain a newer revision.
Source: ClinicalTrials.gov.
JSON downloads include source attribution and retrieval details alongside the unchanged original record or the separately normalized values.
Source retrieved: