A prospective study about impact of renal dysfunction and morbidity and mortality on cardiovascular events after ischemic stroke

Background: The aim of our prospective study was to define the impact of renal dysfunction on future cardiovascular events and total mortality in 390 patients suffering from ischemic stroke. Methods: A quantitative measurement of neurologic deficit according to National Institutes of Health Stroke Scale (NIHSS) score was performed. Blood parameters were measured. Diabetes, hypertension and smoking habits were defined. Estimated glomerular filtration rate was calculated. Results: 153 (39.2%) patients had renal dysfunction. In the follow-up period in 36 (9.2%) patients acute coronary syndrome, in 102 (26.2%) recurrent ischemic stroke and in 44 (11.3%) peripheral arterial disease were documented. 191 (49%) patient died, 118 (30.3%) of whom died of cardiovascular events. Patients who died were older, had higher prevalence of renal dysfunction and NIHSS score. The Kaplan-Meier survival analysis showed that total mortality (p < 0.003) and cardiovascular mortality (p < 0.01) were higher in patients with renal dysfunction. According to Cox’s regression analysis, renal dysfunction was the predictor of cardiovascular events, cardiovascular and total mortality. Conclusions: Patients with ischemic stroke and renal dysfunction are at higher risk for long term cardiovascular and total mortality. The patients with ischemic stroke and renal dysfunction are also at higher risk of new cardiovascular morbidity. Renal dysfunction should be added to the other known prognostic factors in patients with ischemic stroke. Our results also emphasize the importance of identification and management of renal dysfunction in stroke patients.

Management of multiple sclerosis patients in central European countries: current needs and potential solutions

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Cardiovascular disease and chronic renal failure

Izhodišča. Srčnožilne bolezni so najpogostejši vzrok obolevnosti in umrljivosti bolnikov s kronično ledvično odpovedjo. V primerjavi s splošno populacijo je tveganje bolnikov s kronično ledvično odpovedjo za nastanek srčnožilnih bolezni 10- do 2-krat večje. Visoka prevalenca srčnožilnih bolezni med bolniki ob pričetku nadomestnega zdravljenja kronične ledvične odpovedi z dializo nakazuje domnevo, da se začne pospešen proces ateroskleroze že na začetni stopnji kronične ledvične odpovedi. Zaključki. Opisana je vloga znanih in manj znanih dejavnikov tveganja za razvoj srčnožilnih bolezni, ki so pri bolnikih s kronično ledvično odpovedjo pogosto prisotni in delujejo aditivno. Preprečevanje in zdravljenje srčnožilnih bolezni pri bolnikih s kronično ledvično odpovedjo je v prihodnosti velik izziv nefrologom.Background. Cardiovascular disease (CVD) is the main cause of morbidity and mortality in patients with chronic renal failure. CVD morbidity is approximately 10-20 times higher in patients with chronic renal failure compared with that in general population. The high prevalence of CVD among patients with chronic renal failure starting dialysis treatment suggests that CVD begins in earlier stages of chronic renal failure or disease. Conclusions.This review discusses the major and other risk factors for CVD in patients with chronic renal failure. Prevention and treatment of CVD in patients with chronic renal failure should represent a great challenge for nephrologists in the future

CARDIOVASCULAR DISEASE AND CHRONIC RENAL FAILURE

Background. Cardiovascular disease (CVD) is the main cause of morbidity and mortality in patients with chronic renal failure. CVD morbidity is approximately 10–20 times higher in patients with chronic renal failure compared with that in general population. The high prevalence of CVD among patients with chronic renal failure starting dialysis treatment suggests that CVD begins in earlier stages of chronic renal failure or disease.Conclusions. This review discusses the major and other risk factors for CVD in patients with chronic renal failure. Prevention and treatment of CVD in patients with chronic renal failure should represent a great challenge for nephrologists in the future.</p

Cholecalciferol Supplementation Induced Up-Regulation of <i>SARAF</i> Gene and Down-Regulated miR-155-5p Expression in Slovenian Patients with Multiple Sclerosis

Multiple sclerosis is a common immune-mediated inflammatory and demyelinating disease. Lower cholecalciferol levels are an established environmental risk factor in multiple sclerosis. Although cholecalciferol supplementation in multiple sclerosis is widely accepted, optimal serum levels are still debated. Moreover, how cholecalciferol affects pathogenic disease mechanisms is still unclear. In the present study, we enrolled 65 relapsing–remitting multiple sclerosis patients who were double-blindly divided into two groups with low and high cholecalciferol supplementation, respectively. In addition to clinical and environmental parameters, we obtained peripheral blood mononuclear cells to analyze DNA, RNA, and miRNA molecules. Importantly, we investigated miRNA-155-5p, a previously published pro-inflammatory miRNA in multiple sclerosis known to be correlated to cholecalciferol levels. Our results show a decrease in miR-155-5p expression after cholecalciferol supplementation in both dosage groups, consistent with previous observations. Subsequent genotyping, gene expression, and eQTL analyses reveal correlations between miR-155-5p and the SARAF gene, which plays a role in the regulation of calcium release-activated channels. As such, the present study is the first to explore and suggest that the SARAF miR-155-5p axis hypothesis might be another mechanism by which cholecalciferol supplementation might decrease miR-155 expression. This association highlights the importance of cholecalciferol supplementation in multiple sclerosis and encourages further investigation and functional cell studies

Validation of the Slovenian version of multiple sclerosis quality of life (MSQOL-54) instrument

To cross-culturally adapt and validate Multiple Sclerosis Quality of Life-54 (MSQOL-54) instrument