Lower serum Mg level was significantly associated with an increased all-cause and cardiovascular mortality in HD patients, especially in inflamed patients.

BACKGROUND:Carnitine palmitoyltransferase II deficiency (CPT II) is an autosomal recessive disorder and the most common inherited disorder of mitochondrial long-chain fatty acid oxidation, characterised by attacks of myalgia and myoglobinuria. The most common “classic” myopathic form occurs in young adults and is characterised by recurrent episodes of rhabdomyolysis triggered by prolonged exercise, fasting or febrile illness.CASE PRESENTATION:We present a case of a 22-year-old Caucasian male admitted to our hospital with fever, dyspnea, fatigue, myalgia and dark urine (brown-coloured). The symptoms appeared after viral infection followed by fever. Acute kidney injury (AKI) developed as a complication, and there was a need for treatment with hemodialysis. At the clinical presentation, the patient had plasma creatine kinase (pCK) level of 130.383 U/L and plasma myoglobin level over 5000 µg/L. Genetic testing (molecular analysis) confirmed the diagnosis of inherited rhabdomyolysis, a metabolic disorder of carnitine palmitoyltransferase II deficiency. A previous episode with the same symptoms, the patient had four years ago but did not ask for medical treatment. The patient was discontinued from hemodialysis because of the resolution of acute kidney injury. The patient was discharged from the hospital in good condition, with a recommendation about his future lifestyle in order to prevent similar episodes.CONCLUSION:Every patient presenting with myalgia, dark urine (brown-coloured), high level of pCK and development of AKI requiring hemodialysis, should be explored for inherited rhabdomyolysis induced by CPT II deficiency.

BACKGROUND:Elderly population (≥ 65) are more prone to develop acute kidney injury (AKI) compared to younger, also elderly with AKI have an increased requirement for dialysis treatment and an elevated risk of short-term and long-term mortality.AIM:The objectives of this study were to examine the effect of treatment of short-term outcomes and mortality in elderly patients with AKI.MATERIAL AND METHODS:Seventy elderly AKI patients, that filled one of the criteria of AKI definition and had hospitalization over 24 hours, were enrolled in the study.RESULTS:The median age of patients was 74.28 ± 6.64, with mean CCI (Charlson Comorbidity Index) score of 6.94 ± 1.94. The majority of patients (70%) were classified at stage 3 of AKIN, 20% of patients were classified at stage 2 and 10% at stage 1. In the groups of patients with death outcome, the chronic cardiomyopathy was more frequently present (p = 0.034). Regarding treatment, 58.6% of the AKI patients underwent hemodialysis while 41.4% received conservative treatment. Mortality rate was 52.8%, out of which 28.6% was in-hospital mortality, while in 24.3% of patients death occurred in the follow-up period of 90 days.CONCLUSION:In our study, short- term survival is not related to different treatment options. Applied treatment in elderly patients with AKI should be assessed by measuring the long term outcome.

Background The impact of serum uric acid (UA) on morbidity and mortality in hemodialysis (HD) patients is quite controversial in relation to the general population. The aim of this study was to evaluate the association of serum UA with both mortality and left ventricular hypertrophy (LVH) in HD patients. Methods This longitudinal study enrolled 225 prevalent HD patients who were classified into three groups according to their follow-up-averaged UA (FA-UA) levels: low FA-UA (FA-UA <400 µmol/L), intermediate/reference FA-UA (FA-UA between 400 and 450 µmol/L) and high FA-UA (FA-UA >450 µmol/L). Echocardiography was performed on a nondialysis day and the presence of LVH was defined based on a left ventricular mass index (LVMI) >131 and >100 g/m2 for men and women, respectively. The patients were followed during a 60-month period. Results The mean FA-UA level was 425 ± 59 µmol/L (range 294–620). There was a consistent association of higher FA-UA with better nutritional status (higher body mass index, normalized protein catabolic rate, creatinine, albumin and phosphorus), higher hemoglobin, but lower C-reactive protein and LVMI. During the 5-year follow-up, 81 patients died (36%) and the main causes of death were cardiovascular (CV) related (70%). When compared with the reference group, the hazard ratio for all-cause mortality was 1.75 [95% confidence interval (CI) 1.02–2.98; P = 0.041] in the low FA-UA group, but there was no significant association with the high FA-UA group. In contrast, FA-UA did not show an association with CV mortality neither with the lower nor with the high FA-UA group. The unadjusted odds ratio (OR) of LVH risk in the low FA-UA compared with the reference FA-UA group was 3.11 (95% CI 1.38–7.05; P = 0.006), and after adjustment for age, gender, diabetes and CV disease, ORs for LVH persisted significantly only in the low FA-UA group [OR 2.82 (95% CI 1.16–6.88,); P = 0.002]. Conclusions Low serum UA is a mortality risk factor and is associated with LVH in HD patients. These results are in contrast with the association of UA in the general population and should be the subject of further research.

Introduction. Post-transplant diabetes (PTDM), impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are common complications of immunosuppressive therapy (IT) and are associated with increased cardiovascular morbidity and impaired graft function (GF). Methods. Fifty-nine living donor kidney transplant recipients (KTR) were included in a combined cross-sectional and 8-month-observational prospective study about the impact of impaired glucose homeostasis (IGH) on GF. All patients were on standard IT including cyclosporine A (CsA), steroids and mycophenolate mofetil (MMF). In all patients a standard oral glucose tolerans test (OGTT) was performed. Results were classified according to the criteria of the American Diabetes Association: normal-with fasting blood glucose level (FGL) <5.6, IFG with FGL of 5.6-6.9, IGT with FGL of 7.8-11.1 and DM between > 6.9 FGL and >11 mmol/l. According to the results, all patients were divaded into two groups: Group 1 with impaired and Group 2 with normal GH. GF was estimated by GFR-Cockroft Gault (CG) and by degree of proteinuria in the beginning and end of the study. Results. Twenty of 59(33.9%) patients showed overt IGH after transplantation while the remaining 39(66.1) were normal. The principal dysglycemia in KTR were PTDM (2 patients-3.3%), IGT (18 patients-30.5%) and IFG (7 patients-11.8%). In Group 1, postprandial glucose was higher (8.1±2.3 vs 5.8±0.7), more KTR were male (70% vs 33.3%), higher CsA levels were observed (160.9±81.2 vs 115.1±59.9) and time after the surgery was shorter (24.5±21.3 vs 41.4±28.). After a follow-up period of approximately 18 months in Group 1 a significant decline in GFR (62.6-52.7 ml/min) was noted, with no significant change in proteinuria. The correlation analysis was positive between CsA level and IGH and the time after transplantation and IFG. Conclusion. Post-transplant dysglycemia and associated metabolic abnormalities are a significant factor for the deterioration of GF. CsA higher levels are associated with the occurrence of IGH and they affect the GF.