The extent of tubulointerstitial inflammation is an independent predictor of renal survival in lupus nephritis.

Interstitial fibrosis Interstitial inflammation Lupus nephritis Renal biopsy Tubular atrophy

Journal

Journal of nephrology
ISSN: 1724-6059
Titre abrégé: J Nephrol
Pays: Italy
ID NLM: 9012268

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 28 11 2020
accepted: 17 02 2021
pubmed: 16 3 2021
medline: 29 1 2022
entrez: 15 3 2021
Statut: ppublish

Résumé

Lupus nephritis (LN) is a major complication in patients with systemic lupus erythematosus (SLE). Tubulointerstitial injury is an inflammatory process that, if not attenuated, can promote renal damage. Despite this, the current 2003 ISN/RPS "glomerulocentric" classification does not include a score for tubulointerstitial injury. We sought to establish predictors for tubulointerstitial injury and to determine their influence on renal outcomes. This is a retrospective study of a cohort of 166 patients with biopsy-proven LN diagnosed in a Spanish referral center, with a median follow-up of 86 months. Chronic tubulointerstitial lesions were defined as interstitial fibrosis and tubular atrophy (IF/TA), whereas tubulointerstitial inflammation (TII) was defined as an acute interstitial lesion. Activity (0-24) and chronicity (0-12) indices were assigned. Composite outcome, defined as advanced CKD or development of kidney failure. The prevalence of tubulointerstitial lesions was 69.3%. Eighty-one of the biopsies had features of tubulointerstitial inflammation and only 6 of these 81 (7%) patients had moderate/severe tubulointerstitial inflammation. The incidence of interstitial fibrosis and tubular atrophy was 56.6%. Renal survival was shorter in patients with moderate/severe as compared with absent/mild interstitial fibrosis and tubular atrophy (median: 15-19 years, p = 0.009). In the Cox regression model, the grade of interstitial fibrosis and tubular atrophy was independently associated with shorter renal survival (hazard ratio: 3.9, 95% CI 1.4-10.5; p = 0.008) after adjusting for degree of IF/TA and hypertension or diabetes. The extent of tubulointerstitial inflammation emerged as an independent predictor of renal survival after adjusting for the grade of interstitial fibrosis and tubular atrophy and co-morbid conditions including hypertension or diabetes. Regarding disease duration at the time of renal biopsy, no significant association was found between the interstitial fibrosis and tubular atrophy groups. The results reported herein need to be validated in future studies to include also groups of patients who usually have a worse prognosis. Consensus on histological classification is needed to aid in defining prognosis.

Sections du résumé

BACKGROUND AND OBJECTIVE OBJECTIVE
Lupus nephritis (LN) is a major complication in patients with systemic lupus erythematosus (SLE). Tubulointerstitial injury is an inflammatory process that, if not attenuated, can promote renal damage. Despite this, the current 2003 ISN/RPS "glomerulocentric" classification does not include a score for tubulointerstitial injury. We sought to establish predictors for tubulointerstitial injury and to determine their influence on renal outcomes.
METHODS METHODS
This is a retrospective study of a cohort of 166 patients with biopsy-proven LN diagnosed in a Spanish referral center, with a median follow-up of 86 months. Chronic tubulointerstitial lesions were defined as interstitial fibrosis and tubular atrophy (IF/TA), whereas tubulointerstitial inflammation (TII) was defined as an acute interstitial lesion. Activity (0-24) and chronicity (0-12) indices were assigned.
OUTCOME RESULTS
Composite outcome, defined as advanced CKD or development of kidney failure.
RESULTS RESULTS
The prevalence of tubulointerstitial lesions was 69.3%. Eighty-one of the biopsies had features of tubulointerstitial inflammation and only 6 of these 81 (7%) patients had moderate/severe tubulointerstitial inflammation. The incidence of interstitial fibrosis and tubular atrophy was 56.6%. Renal survival was shorter in patients with moderate/severe as compared with absent/mild interstitial fibrosis and tubular atrophy (median: 15-19 years, p = 0.009). In the Cox regression model, the grade of interstitial fibrosis and tubular atrophy was independently associated with shorter renal survival (hazard ratio: 3.9, 95% CI 1.4-10.5; p = 0.008) after adjusting for degree of IF/TA and hypertension or diabetes.
CONCLUSIONS CONCLUSIONS
The extent of tubulointerstitial inflammation emerged as an independent predictor of renal survival after adjusting for the grade of interstitial fibrosis and tubular atrophy and co-morbid conditions including hypertension or diabetes. Regarding disease duration at the time of renal biopsy, no significant association was found between the interstitial fibrosis and tubular atrophy groups. The results reported herein need to be validated in future studies to include also groups of patients who usually have a worse prognosis. Consensus on histological classification is needed to aid in defining prognosis.

Identifiants

pubmed: 33721269
doi: 10.1007/s40620-021-01007-z
pii: 10.1007/s40620-021-01007-z
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1897-1905

Subventions

Organisme : Instituto de Salud Carlos III
ID : PI17/00080

Informations de copyright

© 2021. Italian Society of Nephrology.

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Auteurs

Manuel Ferreira Gomes (MF)

Department of Autoimmune Diseases, Hospital Clínic, Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, Barcelona, Catalonia, Spain.

Claudia Mardones (C)

Department of Autoimmune Diseases, Hospital Clínic, Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, Barcelona, Catalonia, Spain.

Marc Xipell (M)

Department of Nephrology and Renal Transplantation, Hospital Clínic, Barcelona, Spain.
Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.
Centro de Referencia en Enfermedad Glomerular Compleja del Sistema Nacional de Salud de España (CSUR), Barcelona, Spain.

Miquel Blasco (M)

Department of Nephrology and Renal Transplantation, Hospital Clínic, Barcelona, Spain.
Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.
Centro de Referencia en Enfermedad Glomerular Compleja del Sistema Nacional de Salud de España (CSUR), Barcelona, Spain.

Manel Solé (M)

Centro de Referencia en Enfermedad Glomerular Compleja del Sistema Nacional de Salud de España (CSUR), Barcelona, Spain.
Department of Pathology, Hospital Clínic, Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.

Gerard Espinosa (G)

Department of Autoimmune Diseases, Hospital Clínic, Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, Barcelona, Catalonia, Spain.
Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.

Adriana García-Herrera (A)

Centro de Referencia en Enfermedad Glomerular Compleja del Sistema Nacional de Salud de España (CSUR), Barcelona, Spain.
Department of Pathology, Hospital Clínic, Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.

Ricard Cervera (R)

Department of Autoimmune Diseases, Hospital Clínic, Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, Barcelona, Catalonia, Spain.
Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.

Luis F Quintana (LF)

Department of Nephrology and Renal Transplantation, Hospital Clínic, Barcelona, Spain. lfquinta@clinic.cat.
Department of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain. lfquinta@clinic.cat.
Centro de Referencia en Enfermedad Glomerular Compleja del Sistema Nacional de Salud de España (CSUR), Barcelona, Spain. lfquinta@clinic.cat.

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