Differential effects of peritoneal and hemodialysis on circulating regulatory T cells one month post initiation of renal replacement therapy.

Backgroundː Chronic kidney disease stage G5 (CKD G5) patients show an activated but impaired immune system. One function of the FOXP3 regulatory T (Treg) cells is to preserve tolerance to self while maintaining the ability to fight infectious agents. The aim of this pilot study is to evaluate longitudinal changes in Treg cells before and 1 month after the first dialysis treatment.

Remote Patient Management in Peritoneal Dialysis Improves Clinical Outcomes.

Chronic diseases are a global concern and a leading cause of death and disability. These conditions require intensive and ongoing medical assistance to maximize outcomes and avoid the risk of frequent flare-ups and hospitalizations, which increase the cost of healthcare. Remote patient management (RPM) is a strategy that allows for accurate home monitoring of chronic patients, enabling the team to improve care through prevention and early identification of problems, with consequent timely interventions.

Usefulness of glycated albumin as a biomarker for glucose control and prognostic factor in chronic kidney disease patients on dialysis (CKD-G5D).

In chronic kidney disease patients on dialysis (CKD-G5D) accurate assessment of glycemic control is vital to improve their outcome and survival. The best glycemic marker for glucose control in these patients is still debated because several clinical and pharmacological factors may affect the ability of the available biomarkers to reflect the patient's glycemic status properly. This review discusses the role of glycated albumin (GA) both as a biomarker for glucose control and as a prognostic factor in CKD-G5D; it also looks at the pros and cons of GA in comparison to the other markers and its usefulness in hemodialysis and peritoneal dialysis.

Brief Review and a Clinical Case of Hemolytic Uremic Syndrome Associated with Interferon β Treatment.

The hemolytic uremic syndrome (HUS) is one of the thrombotic microangiopathies and it consists of the triad of nonimmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The atypical form of HUS (aHUS) is related to causative mutations in complement genes. Some conditions act as a trigger for aHUS in individuals that have a genetic background predisposing to complement activation.