ABSTRACT
Background: lupus nephritis [LN] is an inflammation of the kidney caused by systemic lupus erythematosus [SLE], a disease by the immune system. Anti-C1q antibodies have been found in many different systemic autoimmune diseases, they are strongly linked to immune complex disorder most prominently SLE and severe rheumatoid arthritis and have been suggested to be closely associated with lupus nephritis [LN]. Generally anti-dsDNA antibodies have been acknowledged as an important tool in the diagnosis of SLE, however their predictive value as to the activity of the disease remains controversial, on the contrary anti-C1q antibodies appear to have a clear-cut relationship with renal complications of SLE not only have they been shown to play a pathogenic role in the development of lupus nephritis but also their serum levels correlate with the presence of active proliferation lupus nephritis
Aim of the study: this study aimed to investigate association between serum titer of anti-C1q antibody and disease manifestation of SLE
Methodology: the study was carried out in three different groups: healthy group, rheumatoid arthritis group and lupus nephritis group. All groups were subjected to determination of anti-C1q antibody, blood urea nitrogen [BUN] and serum creatinine
Results: there was no significant difference in BUN levels between the normal and rheumatoid arthritis groups in contrast there was a highly significant difference in BUN between the normal and lupus groups also, between the rheumatoid arthritis and lupus nephritis groups [p<0.001]. No significant difference was detected in serum creatinine levels between the normal and rheumatoid arthritis groups in there was a highly significant difference in serum creatinine between the normal and lupus groups and also between the rheumatoid arthritis and lupus nephritis groups [p<0.001]. No significant difference was realized in serum anti-C1q antibodies levels between the normal and rheumatoid arthritis groups in contrast there was a highly significant difference in serum anti-C1q antibodies between the normal and lupus groups and also between rheumatoid arthritis and lupus nephritis groups [p<0.001]. In the control group and rheumatoid arthritis groups, only BUN showed a highly significant positive correlation with serum creatinine concentration [r=0.906, r=0.404] and [P<0.001, P<0.05] respectively, while in lupus nephritis group, BUN showed a highly positive correlation with serum creatinine concentration [r=0.773, P<0.001] also serum creatinine concentration showed a positive concentration with serum anti-C1q antibody [r=0.513, P<0.05]
Conclusion: the present study suggested that anti-C1q antibody might be a new parameter for the development of lupus nephritis since the increased of anti-ds DNA antibody and hypocomplementemia [C3 and C4] are serological markers of SLE activity, but they are not enough to identify which organ may be affected, while anti-C1q antibody either alone or in combination with other serological markers could give information of the diagnosis of a renal flare with 100% sensitivity and specificity
ABSTRACT
Chronic renal insufficiency [CRI] is a predictor of stroke, cardiovascular, and all-cause mortality, but the mechanisms responsible for these associations are unclear. Whether CRI was associated with severity of coronary artery disease [CAD]. 230 patients with CRI were subjected to stress echocardiography to evaluate stable CAD. The correlations of various parameters with the prevalence of CAD were also examined. Atherosclerotic surrogate markers, including intima-media thickness of carotid artery and ankle-brachial BP index [ABI], were also evaluated. Renal function was assessed by 24-h urine collection, and CRI was defined as measured creatinine clearance 60 ml/min. Stress echocardiography was used to identify inducible ischemia, defined as any wall motion abnormality seen at stress but not at rest. Logistic regression was used to evaluate the association of CRI with exercise-induced ischemia after adjustment for cardiovascular risk factors. Among the 230 participants, 55 [23.9%] had CAD, and were characterized by older age, lower ejection fraction, greater left ventricular mass and higher C-reactive protein values. The prevalence of exercise-induced ischemia was also substantially greater in the participants with CRI distributed in such way that 20.1% in group I compared with 44.4% group II [odds ratio [OR], 2.3; 95% confidence interval [CI], 1.4 to 3.8; p < 0.01]. After multivariate adjustment, CRI remained strongly associated with exercise-induced ischemia [OR, 2.0; 95% CI, 1.2 to 3.3; p = 0.01]. After further adjustment for CRP, the adjusted association was essentially unchanged [OR, 2.3; 95% CI, 1.0 to 5.1; p <0.05]. Univariate analysis showed that diabetes [p <0.01], left ventricular mass index [p<0.05], hyperlipidemia [p <0.01], total cholesterol [p <0.01], LDL cholesterol [p <0.01], and intima-media thickness [p < 0.01], were positively correlated with the presence of CAD, whereas ABI [p <0.01] showed a negative correlation with CAD. Stepwise logistic regression analysis revealed that diabetes was significant and independent risk factor for CAD in asymptomatic CRI patients. CRI is strongly associated with exercise-induced ischemia in patients with CAD. The greater severity of atherosclerotic disease observed in patients with CRI may in part explain the association of CRI with increased cardiovascular risk among individuals with CAD