Risk factors for progression in children and young adults with IgA nephropathy: an analysis of 261 cases from the VALIGA European cohort
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
27557557
DOI
10.1007/s00467-016-3469-3
PII: 10.1007/s00467-016-3469-3
Knihovny.cz E-zdroje
- Klíčová slova
- IgA nephropathy, Pathology classification, Progression, Proteinuria, Risk factors,
- MeSH
- analýza přežití MeSH
- biopsie MeSH
- chronické selhání ledvin epidemiologie patologie MeSH
- dítě MeSH
- hodnoty glomerulární filtrace MeSH
- hormony kůry nadledvin terapeutické užití MeSH
- IgA nefropatie farmakoterapie epidemiologie patologie MeSH
- imunosupresiva MeSH
- kohortové studie MeSH
- kojenec MeSH
- ledviny patologie MeSH
- lidé MeSH
- předškolní dítě MeSH
- progrese nemoci MeSH
- proteinurie epidemiologie patologie MeSH
- retrospektivní studie MeSH
- rizikové faktory MeSH
- sexuální faktory MeSH
- stanovení cílového parametru MeSH
- věkové faktory MeSH
- Check Tag
- dítě MeSH
- kojenec MeSH
- lidé MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Evropa epidemiologie MeSH
- Názvy látek
- hormony kůry nadledvin MeSH
- imunosupresiva MeSH
BACKGROUND: There is a need for early identification of children with immunoglobulin A nephropathy (IgAN) at risk of progression of kidney disease. METHODS: Data on 261 young patients [age <23 years; mean follow-up of 4.9 (range 2.5-8.1) years] enrolled in VALIGA, a study designed to validate the Oxford Classification of IgAN, were assessed. Renal biopsies were scored for the presence of mesangial hypercellularity (M1), endocapillary hypercellularity (E1), segmental glomerulosclerosis (S1), tubular atrophy/interstitial fibrosis (T1-2) (MEST score) and crescents (C1). Progression was assessed as end stage renal disease and/or a 50 % loss of estimated glomerular filtration rate (eGFR) (combined endpoint) as well as the rate of renal function decline (slope of eGFR). Cox regression and tree classification binary models were used and compared. RESULTS: In this cohort of 261 subjects aged <23 years, Cox analysis validated the MEST M, S and T scores for predicting survival to the combined endpoint but failed to prove that these scores had predictive value in the sub-group of 174 children aged <18 years. The regression tree classification indicated that patients with M1 were at risk of developing higher time-averaged proteinuria (p < 0.0001) and the combined endpoint (p < 0.001). An initial proteinuria of ≥0.4 g/day/1.73 m2 and an eGFR of <90 ml/min/1.73 m2 were determined to be risk factors in subjects with M0. Children aged <16 years with M0 and well-preserved eGFR (>90 ml/min/1.73 m2) at presentation had a significantly high probability of proteinuria remission during follow-up and a higher remission rate following treatment with corticosteroid and/or immunosuppressive therapy. CONCLUSION: This new statistical approach has identified clinical and histological risk factors associated with outcome in children and young adults with IgAN.
Annunziata Hospital Cosenza Italy
Bambino Gesù Hospital Rome Italy
Belcolle Hospital Viterbo Italy
Borgomanero Hospital Borgomanero Italy
General University Hospital Prague Czech Republic
Hacettepe University Ankara Turkey
Hospital 12 de Octubre Madrid Spain
Hospital Maggiore di Lodi Lodi Italy
Imperial College Hammersmith Hospital London UK
Karolinska Institutet Stockholm Sweden
Karolinska University Hospital Huddinge Sweden
Leicester General Hospital Leicester UK
Oxford University Hospitals Oxford UK
Radboud University Nijmegen The Netherlands
San Giovanni Bosco Hospital Turin Italy
Silesian University Katowice Poland
Spedali Civili University Hospital Brescia Italy
Toronto General Hospital University Health Network Toronto Canada
University of Bari and Foggia Bari Italy
University of Istanbul Istanbul Turkey
University of Turin Turin Italy
University of Uppsala Uppsala Sweden
University of Warsaw Warsaw Poland
Zobrazit více v PubMed
Clin Exp Nephrol. 2008 Feb;12(1):1-8 PubMed
BMC Nephrol. 2012 Nov 27;13:158 PubMed
Kidney Int. 2016 Jan;89(1):167-75 PubMed
Kidney Int. 2009 Sep;76(5):546-56 PubMed
J Am Soc Nephrol. 2007 Dec;18(12):3177-83 PubMed
Pediatr Nephrol. 2013 Jan;28(1):71-6 PubMed
Ann Intern Med. 1999 Mar 16;130(6):461-70 PubMed
Pediatr Nephrol. 2007 Feb;22(2):317-8 PubMed
Int J Surg. 2014 Dec;12(12):1500-24 PubMed
Pediatr Nephrol. 2012 May;27(5):783-92 PubMed
J Hypertens. 2002 Oct;20(10):1995-2007 PubMed
Curr Opin Nephrol Hypertens. 2008 May;17(3):320-5 PubMed
Kidney Int. 2009 Sep;76(5):534-45 PubMed
N Engl J Med. 2013 Jun 20;368(25):2402-14 PubMed
Nephrol Dial Transplant. 2012 Apr;27(4):1485-91 PubMed
Nephrol Dial Transplant. 1991;6 Suppl 1:5-35 PubMed
J Nephrol. 2005 Sep-Oct;18(5):503-12 PubMed
Stat Med. 2007 Aug 30;26(19):3550-65 PubMed
Semin Nephrol. 2008 Jan;28(1):18-26 PubMed
Kidney Int. 2014 Oct;86(4):828-36 PubMed
Kidney Int. 2010 May;77(10):921-7 PubMed
Nephrol Dial Transplant. 2008 Aug;23(8):2537-45 PubMed
Nephrol Dial Transplant. 2016 Feb;31(2):317-24 PubMed
Clin Exp Nephrol. 2015 Dec;19(6):1149-56 PubMed
Pediatr Nephrol. 2015 Dec;30(12):2121-7 PubMed
Pediatr Nephrol. 2006 Sep;21(9):1266-73 PubMed
Nephrol Dial Transplant. 2012 Feb;27(2):715-22 PubMed
J Nephrol. 2005 Nov-Dec;18(6):690-5 PubMed