Background. Glomerular lesions in lupus nephritis have been extensively studied in recent decades, but much less attention has been paid to the tubulo-interstitial compartment. To evaluate the presence and phenotype of the interstitial inflammatory infiltrate in renal tissue of SLE nephritis patients and possible relationships with clinical, histological parameters and treatment response. Patients and Methods. 31 consecutive patients with newly diagnosed lupus nephritis were evaluated for demographic, clinical, immunological, renal evolution data and with renal biopsy. Tissues were stained also with cellular markers CD3 (T lymphocytes), CD20 (B lymphocytes) and CD68 (macrophages) and cell count was expressed as number of positive cells per square millimeter. Patients were divided in responder (R) and non responder (NR) subgroups at sixth month of therapy. Results. Characteristics of the 31 patients are: 27 women, age at renal biopsy 35.6±11.6, number of class IV WHO=31, AI 9.1±4.3 and CI 2.1±1.9. In our series, macrophages were the main class of immune cells infiltrating the kidney (CD68+: 9.1±9.6/mm2), followed by T (CD3+: 3.0±4.0/mm2) and B lymphocytes (CD20+: 2.2±3.4/mm2). Chronicity index directly correlated with CD3+ cells presence (r=0.5, p=0.004). 17/31 (54.8%) renal biopsies had a significant interstitial infiltrate and 14 had a poor or none infiltrate. 13/14 patients without infiltrate were responder with respect to 10/17 with infiltrate (93% vs 59%, p=0.04). Responder patients (n=23) differ from non responder only for the presence of inflammatory infiltrate (43.5%vs87.5%, p=0.04) and the number of CD3+ cells (p=0.03). On the multivariate analysis, the interstitial infiltrate resulted the independent predictive parameter of response (p=0.05, OR 9.1 95%IC 1.0-86.1). Conclusion. These data supported the hypothesis that the cell-mediated immunity play a central role in the SLE nephritis pathogenesis and that interstitial infiltrate may have a role in the nephritis progression up to chronic damage.
Renal inflammatory infiltrate in lupus nephritis patients
Gremese E;
2011-01-01
Abstract
Background. Glomerular lesions in lupus nephritis have been extensively studied in recent decades, but much less attention has been paid to the tubulo-interstitial compartment. To evaluate the presence and phenotype of the interstitial inflammatory infiltrate in renal tissue of SLE nephritis patients and possible relationships with clinical, histological parameters and treatment response. Patients and Methods. 31 consecutive patients with newly diagnosed lupus nephritis were evaluated for demographic, clinical, immunological, renal evolution data and with renal biopsy. Tissues were stained also with cellular markers CD3 (T lymphocytes), CD20 (B lymphocytes) and CD68 (macrophages) and cell count was expressed as number of positive cells per square millimeter. Patients were divided in responder (R) and non responder (NR) subgroups at sixth month of therapy. Results. Characteristics of the 31 patients are: 27 women, age at renal biopsy 35.6±11.6, number of class IV WHO=31, AI 9.1±4.3 and CI 2.1±1.9. In our series, macrophages were the main class of immune cells infiltrating the kidney (CD68+: 9.1±9.6/mm2), followed by T (CD3+: 3.0±4.0/mm2) and B lymphocytes (CD20+: 2.2±3.4/mm2). Chronicity index directly correlated with CD3+ cells presence (r=0.5, p=0.004). 17/31 (54.8%) renal biopsies had a significant interstitial infiltrate and 14 had a poor or none infiltrate. 13/14 patients without infiltrate were responder with respect to 10/17 with infiltrate (93% vs 59%, p=0.04). Responder patients (n=23) differ from non responder only for the presence of inflammatory infiltrate (43.5%vs87.5%, p=0.04) and the number of CD3+ cells (p=0.03). On the multivariate analysis, the interstitial infiltrate resulted the independent predictive parameter of response (p=0.05, OR 9.1 95%IC 1.0-86.1). Conclusion. These data supported the hypothesis that the cell-mediated immunity play a central role in the SLE nephritis pathogenesis and that interstitial infiltrate may have a role in the nephritis progression up to chronic damage.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
