Abstract

Objective Renal vascular injury, especially thrombotic microangiopathy (TMA), is an im-portant prognostic factors in patients with lupus nephritis. TMA is most likely to be associated with proliferative lupus nephritis. This single-center retrospective study was conducted in order to explore the characteristics and prognosis of patients with TMA associated with proliferative lupus nephritis. Methods From January 2013 to June 2016, 146 hospitalized patients with lupus nephritis underwent renal biopsy in the Department of Rheumatology, South Campus, Ren Ji Hospital, of which 108 were proliferative nephritis including 32 with TMA and 76 without TMA. All the clinical records were collected. All data were analyzed by Graphpad 5.0 or SPSS 22.0 statistical software analysis. Nonparametric test, t test and Fisher test were used for comparison between the two groups. Predictors were analyzed by multiple factors regression analysis, survival curve was analyzed by Kaplan-Meire method. Results Patients with TMA were found to have higher levels of creatinine (Cr) [93.5(69.0, 179.8) μmol/L vs 73.0(56.3, 116.3) μmol/L, U=833, P=0.010 1], B-type brain natriuretic peptide (BNP) [177(93.2, 619) pg/ml vs 87.5(28.5, 255) pg/ml, U=765, P=0.004 6], 24-hour urinary protein [4.98(1.99, 7.62) g vs 2.83(1.71,4.38) g, U=875, P=0.022] and highersystemic lupus erythematosus disease activity index (SLEDAI) [16(13.25, 18) vs 12(10.25, 14), U=559, P<0.000 1], as well as lower complement [C3:(0.37±0.15) g/L vs (0.52±0.20) g/L, t=3.713, P=0.000 3; C4: 0.056(0.035, 0.140) g/L vs 0.088(0.053, 0.167) g/L, U=912, P=0.047 9], albumin (Alb) [(24±6) g/L vs (28±6) g/L, t=3.416, P=0.000 9] and hemoglobin (Hb) [(88±19) g/L vs (99±21) g/L, t=2.627, P=0.015 7]. They were more prone to hypertension [(24/32,75%) vs (35/76, 46%), χ2=7.613, P=0.006 4], had less glomerular sclerosis [0(0, 0.038)% vs 7(0, 17)%, U=848, P=0.007 7] and higher acute score [16(14.25, 19.75) vs 13(10, 15), U=612, P<0.000 1]; while these patients received higher doses of corticosteroid therapy, and more patients were treated with cyclophosphamide for induction therapy. Multivariate regression analysis showed that Cr (OR=1.008, P=0.033) and SLEDAI (OR=1.272, P=0.003) scores might be predictors of TMA in patients with proliferative lupus nephritis. During follow up, 6 and 2 patientsin two groups progressed to end-stage renal disease (ESRD), respectively (P=0.010 4). Univariate analysisfound that patients progressed to ESRD were more likely to have TMA[(6/8, 75%) vs (23/85, 27%), χ2=7.831, P=0.010 4], and had more crescents[54.5(12, 83.5)% vs 20(6, 41)%, U=183, P=0.032]. Higher activity indices (AI) [(20±6) vs (14±4), t=3.489, P=0.000 7], Cr [286(214.5, 395) μmol/L vs 76(59, 115.5) μmol/L, U=19, P<0.000 1] and BNP [456(192.3, 1 060) vs 110(45.38, 275.5), U=116.5, P=0.002 4], as well as lower Hb [(71±12) vs (97±19), t=3.776, P=0.000 3] and platelets (PLT) [(130±71)×109/L vs (196±76)×109/L, t=2.399, P=0.018 5] were observed in these patients. Conclusion This study has shown that patients with proliferative lupus nephritis with renal TMA have a higher level of Cr and more active disease state, requiring more aggressive immunosuppressive therapy and more likely to progress to ESRD. So renal TMA may be one of the risk factors of renal survival in these patients. Key words: Lupus erythematosus, systemic; Lupus nephritis; Thrombotic microangiopathy

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