The aim of the present study was to assess the fetal and maternal outcome in a cohort of patients with lupus nephritis. Twenty-four pregnancies in 22 women with lupus nephritis occurring between 1991 and 2000 were analysed retrospectively. Lupus nephritis was biopsy proven before pregnancy in all cases. Women were followed from the beginning of pregnancy up to 6 months postpartum. Close fetal-maternal monitoring and frequent laboratory investigations were applied routinely to all patients. All women were prescribed steroid therapy from the beginning of the pregnancy. There were 18 live births, four spontaneous abortions and two stillbirths. Of the 18 live births, 14 were premature and four were term deliveries, representing a 25% fetal loss rate and 58% prematurity rate. There were two fetuses with congenital heart block. We recorded hypertension in 42%, proteinuria in 50% and pre-eclampsia in 25% of our patients. Proteinuria was irreversible in four cases. No maternal deaths or postpartum exacerbation of the disease were recorded in the study period. All renal flares were reversed postpartum. Patients positive for antiphospholipid antibodies had a worse perinatal outcome. Hypertension, proteinuria and antiphospholipid antibodies appear to be associated with adverse perinatal outcome and pregnancy complications. Pregnancy is not contraindicated in women with lupus nephritis, but is associated with significant fetal and maternal risks.
Coronary heart disease incidence in elderly HD patients increases with age, male sex, diabetes, SHP, hypertension, increased CRP levels, HOC, smoking, time on HD and inadequacy of HD.
It has been reported recently that a number of cytokines, mainly tumor necrosis factor alpha (TNFalpha), interleukin (IL)-1beta, and IL-6, can alter lipid metabolism and produce hyperlipidemia. Studies in hemodialysis (HD) patients have demonstrated increased production of these cytokines during HD. In order to investigate any possible relationship between changes of cytokines and lipid concentrations during HD in the serum of 25 uremic patients on chronic HD using modified cellulose membranes, TNFalpha, IL-1beta, IL-6, total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), lipoprotein a (Lp[a]), and total proteins were measured immediately before (pre-HD) and after HD (post-HD), in one session. The post-HD values were corrected according to the hemoconcentration based on the changes in serum total proteins. Serum TNFalpha and IL-1beta levels were significantly increased from 38.24 +/- 17.85 pg/ml and 2. 60 +/- 3.64 pg/ml pre-HD to 48.86 +/- 25.21 and 3.49 +/- 4.08 pg/ml post-HD, p < 0.001 and p < 0.05 respectively. Also Lp(a) levels presented a statistically significant increase post-HD and were almost doubled (pre-HD: 15.41 mg/dl, to post-HD: 27.39 mg/dl, p < 0. 05). Serum IL-6 as well as serum TC, TG, HDL-C, and LDL-C did not show any statistically significant alterations during HD. A significant positive correlation was detected between TNFalpha and Lp(a) values post-HD (r: 0.413, p: 0.04), but not between pre-HD values. No further relationship between serum cytokines and the other estimated lipid parameters was observed, either between pre- or post-HD values. Our results indicate that release of TNFalpha and IL-1beta during HD have no effect on serum lipids concentration, except on Lp(a). It seems that the acute rise of this lipoprotein during hemodialysis may be related with the TNFalpha overproduction.
Aim of the study was to estimate the incidence of coronary heart disease (CAD) in patients (pts) with end stage renal disease (ESRD) maintained on chronic hemodialysis (HD) and its association with the presence of predisposing factors. The study included 171 dialysis pts (107 male (M) and 64 female (F)). Mean age of pts was 67±13 years, mean time on dialysis 52.7±44 months and Body Mass Index (BMI) 25.9±3.7 kg/m2. Fifty pts (29.2%) were clinically diagnosed with CAD. The diagnosis was established by coronary angiography in 24 (48%) and in 26 by combined dipyridamole - exercise thallium imaging (52%). Pts’ data in association with the development of CAD that were recorded included age, sex, smoking habits, hypertension, obesity, the presence of diabetes mellitus (DM), hyperlipidemia, anemia, low albumin levels, secondary hyperparathyroidism (SHP), the presence of chronic inflammation, as evidenced by the presence of elevated levels of CRP and hyperhomocystinemia. There was a statistically significant association of increasing age and CAD (p<0.0001). Relative risk (RR) was significantly increased i) in male pts compared to female pts (RR: 8.56, p<0.001), ii) in anemic pts compared to pts with hemoglobin levels ≤11 g/dL (RR: 8.26, p<0.0001), iii) in obese pts compared to pts with BMI ≤ 30 (RR: 5.09, p<0.005) and iv) in pts with increased levels of homocysteine compared to pts with levels of homocysteine <15 μM (RR: 4.14, p<0.0001). Using linear regression analysis, CAD was associated with the inadequacy of HD (r =-0.05, p<0.0001), time on HD (r =0.04, p =0.012) and increasing age (r =0.24, p<0.001). There was no statistically significant association between CAD and the presence of the other traditional risk factors. The incidence of CAD in dialysis pts is significantly increased with age, male sex, obesity, time on dialysis, the presence of anemia, hyperhomocysteinemia and inadequacy of HD.
In 18 uremic patients under regular hemodialysis (HD) with bicarbonate dialysate, the echinocytes and erythrocyte sedimentation rates (ESR) were determined in 4 blood samples collected from the arterial line at 0,45, 120, and 240 rnin (end-HD) in one HD session by a bioincompatible dialyzer and in another by a biocompatible one. In the H D session by a bioincompatible dialyzer, the mean values (-+SEM) of echinocytes (YO) at 0.45, 120, and 240 min were 8.
SummaryBackground: Evidence suggests that distensibility of the aorta is decreased in patients with end-stage renal failure, while the underlying mechanisms are unclear.Hypothesis: The purpose of the study was to evaluate the distensibility of the aorta in patients at the end stage of chronic renal failure before and after hemodialysis (HD).Methods: The diameter of the ascending aorta and distensibility were assessed in 48 patients on HD (31 men, 17 women, aged 45 ± 14 years) and in 27 normal subjects (17 men, 10 women, aged 44 ± 14 years). The diameter of the aorta was evaluated by M-mode in the parasternal long-axis view.Results: Aortic distensibility was significantly lower in patients on HD before HD (1.9 ± 0.7 cm 2 ·dyn Ϫ1 ·10 Ϫ6 ) than in normal control subjects (3.8 ± 1.0 cm 2 ·dyn Ϫ1 ·10 Ϫ6 , p < 0.0001). After dialysis, it increased to 2.6 ± 1.2 (p < 0.05 compared with baseline, p < 0.001 compared with controls). The change of aortic distensibility correlated with age (R 2 = 0.629 p < 0.001) and ultrafiltration volume (R 2 = 0.168, p < 0.01).Conclusions: Aortic distensibility in patients with endstage renal disease is significantly lower than in normal subjects, and it is significantly improved after HD.
Background. Lipoprotein(a), Lp(a), has been recognized as an atherogenic and thrombogenic lipoprotein in the general population and in hemodialysis (HD) patients. In addition, fibrinogen and fibronectin may promote atherothrombosis. The aim of this study was to investigate any possible relationship between Lp(a) and thrombogenic coagulation proteins in non-diabetic HD patients. Patients and Methods. Serum Lp(a) and plasma fibrinogen, plasminogen, and fibronectin levels were measured pre-HD in 60 uremic patients (30 male, 30 female) aged 58.6 AE 8.0 years who had been receiving HD treatment for 61.3 AE 50.7 months. The control group comprised 20 age-and sex-matched healthy subjects. All patients were receiving erythropoietin treatment. Results. The mean serum Lp(a) (33.88 AE 34.12 mg/dL) and plasma fibrinogen (329.45 AE 80.62 mg/dL) levels were significantly higher in the HD patients compared with those in the controls (16.70 AE 10.36 and 254.00 AE 43.34 mg/dL, respectively; p < .05 and p < .001, respectively). Plasminogen levels did not differ between the HD patients (11.64 AE 3.22 mg/dL) and the control group (10.67 AE 1.41 mg/dL, p>.05). Fibronectin levels were slightly increased in the HD patients (33.96 AE 5.49 mg/dL) versus in the control group (30.9 AE 5.80 mg/dL, p < .05). There was a significant positive correlation between Lp(a) and fibrinogen levels (r ¼ 0.305, p < .02), as well as between Lp(a) and fibronectin levels (r ¼ 0.360, p < .01). Moreover, there was a significant positive correlation between fibrinogen and fibronectin levels (r ¼ 0.587, p < .0001). Conclusions. According to our results, in non-diabetic HD patients, abnormal serum Lp(a) levels significantly correlated with abnormal levels of fibrinogen and fibronectin. There is a concern that the relationship between these atherogenic and thrombogenic acute-phase proteins may contribute to the increased incidence of atherosclerotic cardiovascular disease in this patient population.
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