The ASQ did not predict low IQ scores when children born VPT were six years.

AIM: There is a need for methods that can provide valid assessment tools in a follow-up programme without great financial costs. This study assessed the accuracy of the 60-month Ages and Stages Questionnaire as a screening tool to predict a low intelligence quotient score at 6 years in children born very preterm. METHODS: Totally, 54 children participated in a six-year follow-up study, which included an intelligence quotient test at 6 years of age and a 60-month Ages and Stages Questionnaire at four and a half or 5 years of age at respond. We used the receiver operating characteristic curve and evaluated the optimal cut-off score to predict a low intelligence quotient score. RESULTS: At four and a half years, the optimal cut-off value for predicting a low intelligence quotient score was 242, with a sensitivity of 67% and a specificity of 59%. At 5 years, only one child had a low intelligence quotient score, and the analysis was not performed. CONCLUSION: Our results did not support the use of the 60-month Ages and Stages Questionnaire as a valuable screening tool to predict a low intelligence quotient score in children born very preterm at 6 years of age.

The Effect of Magnesium Supplementation on Vascular Calcification in CKD: A Randomized Clinical Trial (MAGiCAL-CKD).

SIGNIFICANCE STATEMENT: Magnesium prevents vascular calcification in animals with CKD. In addition, lower serum magnesium is associated with higher risk of cardiovascular events in CKD. In a randomized, double-blinded, placebo-controlled trial, the authors investigated the effects of magnesium supplementation versus placebo on vascular calcification in patients with predialysis CKD. Despite significant increases in plasma magnesium among study participants who received magnesium compared with those who received placebo, magnesium supplementation did not slow the progression of vascular calcification in study participants. In addition, the findings showed a higher incidence of serious adverse events in the group treated with magnesium. Magnesium supplementation alone was not sufficient to delay progression of vascular calcification, and other therapeutic strategies might be necessary to reduce the risk of cardiovascular disease in CKD. BACKGROUND: Elevated levels of serum magnesium are associated with lower risk of cardiovascular events in patients with CKD. Magnesium also prevents vascular calcification in animal models of CKD. METHODS: To investigate whether oral magnesium supplementation would slow the progression of vascular calcification in CKD, we conducted a randomized, double-blinded, placebo-controlled, parallel-group, clinical trial. We enrolled 148 subjects with an eGFR between 15 and 45 ml/min and randomly assigned them to receive oral magnesium hydroxide 15 mmol twice daily or matching placebo for 12 months. The primary end point was the between-groups difference in coronary artery calcification (CAC) score after 12 months adjusted for baseline CAC score, age, and diabetes mellitus. RESULTS: A total of 75 subjects received magnesium and 73 received placebo. Median eGFR was 25 ml/min at baseline, and median baseline CAC scores were 413 and 274 in the magnesium and placebo groups, respectively. Despite plasma magnesium increasing significantly during the trial in the magnesium group, the baseline-adjusted CAC scores did not differ significantly between the two groups after 12 months. Prespecified subgroup analyses according to CAC>0 at baseline, diabetes mellitus, or tertiles of serum calcification propensity did not significantly alter the main results. Among subjects who experienced gastrointestinal adverse effects, 35 were in the group receiving magnesium treatment versus nine in the placebo group. Five deaths and six cardiovascular events occurred in the magnesium group compared with two deaths and no cardiovascular events in the placebo group. CONCLUSIONS: Magnesium supplementation for 12 months did not slow the progression of vascular calcification in CKD, despite a significant increase in plasma magnesium. CLINICAL TRIALS REGISTRATION: www.clinicaltrials.gov ( NCT02542319 ).

[Severe reversible penile ischaemia after terlipressin treatment of hepatorenal syndrome].

This case report presents a 70-year-old man with alcoholic liver cirrhosis, who was hospitalised due to pulmonary oedema, and who developed acute renal injury. Though the criteria were not fulfilled, hepatorenal syndrome was suspected and treated with terlipressin, after which the patient developed severe penile ischaemia. Hepatorenal syndrome is one of many potential causes of acute kidney injury in patients with acute or chronic liver disease. The syndrome is an exclusion diagnosis, and other causes of liver and renal failure should be investigated, before treatment is started. A flow chart can be used for a correct diagnosis.