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IntroductionThe burden on the cardiovascular system is the main cause of mortality in chronic renal patients, and bone disease, which also may cause disability, is one of the most important complications in those patients. The aim of this study was to determine the link between cardiovascular and bone disease, which frequently occur together.MethodsIn this matched case-control study, 70 subjects were subjected for full laboratory assessment as well as estimation of parathyroid hormone (PTH) level, vitamin D level, complete echocardiography, and dual energy absorptiometry. Of the 70 patients, 50 were on regular hemodialysis, and there were 20 normal controls matched with the patients with respect to age and gender.ResultsThere was a significant decrease in the mean value of serum vitamin D in the hemodialysis patients, i.e., their mean value was 20.47 ± 9.60 whereas the controls had a mean value of 37.15 ± 7.67. Thus, there was a highly-significant, negative correlation between vitamin D and left ventricular mass (LVM) in the patients. We found that there was a highly-significant increase in the mean PTH levels of the patients (820.22 ± 393.51), whereas it was 57.60 ± 13.72 for the controls. The statistical significance was less than 0.001, a highly-significant increase in the mean of the T score levels in the patients (−2.15 ± 2.56), whereas it was −0.47 ± 0.71 for the controls with a statistical significance of less than 0.001. There also was a highly-significant correlation between the T score and LVM.ConclusionA significant correlation was found between bone disease and the occurrence of a left ventricular mass. We recommend early strict correction of the serum levels of vitamin D, PTH, calcium, and phosphorus.

IntroductionGlomerulonephritis is a major determinant of the course and prognosis of systemic lupus erythematosus (SLE) and is evident in 40%–85% of patients. IL10, a cytokine produced by monocytes and-to a lesser extent-lymphocytes, has pleiotropic effects in immune regulation and inflammation. It enhances B cell survival, proliferation, differentiation, and antibody production; these effects play a role in autoimmune diseases. Among identified polymorphisms in the IL10 promoter, three linked single nucleotide polymorphisms (SNPs) of −1082 G/A, 819 T/C, and −592 A/C have been shown to influence the IL10 gene expression. Compared with the −592 C allele, the 592 A is associated with lower IL10 production in vitro. The objectives of this study were to investigate the −592 A/C polymorphism in patients with and without lupus nephritis and to assess its influence on IL10 secretion in vivo and its role in pathogenesis and clinicopathological characteristics of lupus nephritis.MethodsThis case control study was conducted on 40 SLE patients recruited for the study from those attending the nephrology department of the Theodor Bilharz Research Institute (outpatient clinic and inpatient ward) in 2013. Patients were divided into two groups, group I (SLE patients without evidence of nephritis) and group II (SLE patients with lupus nephritis). Data were analyzed using SPSS (version 12), a t-test, Chi square, ANOVA, and the Pearson product–moment correlation coefficient.ResultsOur study found an increase in IL10 serum in lupus nephritis patients compared to those without renal involvement (without statistical significance). No significant differences emerged in the level of IL10 serum among different pathological classes.ConclusionThe IL10 gene (−592 A/C) polymorphism, though not associated with lupus nephritis’s susceptibility in the present study, does play a role.