Parvovirus B19-Induced Pure Red Cell Aplasia Several Years After Kidney Transplantation and Following a Transition From Everolimus to Tacrolimus.

A 57-year-old male patient, who underwent a preemptive living donor renal transplant from his mother 22 years earlier, was switched from everolimus to tacrolimus after 21 years because of development of proteinuria. Four months after transition of medication, the patient presented with anemia and reduced reticulocyte count, whereas leukocyte and platelet counts remained within normal limits. Investigation into the cause of anemia ruled out deficiencies in iron, folate, or vitamin B12, as well as inflammation, monoclonal gammopathy, hemolysis, and hypothyroidism.

In renal proximal tubular epithelial cells of the hibernator Syrian hamster, anoxia-reoxygenation-induced reactive oxygen species bursts do not trigger a DNA damage response and cellular senescence.

Ischemia-reperfusion (I-R) injury represents a predominant etiology of acute kidney injury (AKI), for which effective treatments remain unavailable. In contrast, hibernating mammals exhibit notable resistance to cell death induced by I-R injury. However, the impact of I-R injury on cellular senescence-an important factor in AKI-has not been extensively studied in these species.

In human CD4+ T-Cells, omeprazole suppresses proliferation, downregulates V-ATPase, and promotes differentiation toward an autoimmunity-favoring phenotype.

Background: Proton pump inhibitors (PPIs) represent a commonly prescribed class of medications. Triggered by findings indicating a correlation between PPI usage and susceptibility to infectious or autoimmune diseases, we studied the impact of a pharmacological concentration of omeprazole on human CD4+ T-cells.

Methods: In mixed lymphocyte reactions (MLRs), we analyzed the proliferation index and measured the concentration of key cytokines representative of distinct CD4+ T-cell subsets.

Malate dehydrogenase-2 inhibition shields renal tubular epithelial cells from anoxia-reoxygenation injury by reducing reactive oxygen species.

Ischemia-reperfusion (I-R) injury is the most common cause of acute kidney injury. In experiments involving primary human renal proximal tubular epithelial cells (RPTECs) exposed to anoxia-reoxygenation, we explored the hypothesis that mitochondrial malate dehydrogenase-2 (MDH-2) inhibition redirects malate metabolism from the mitochondria to the cytoplasm, towards the malate-pyruvate cycle and reversed malate-aspartate shuttle. Colorimetry, fluorometry, and western blotting showed that MDH2 inhibition accelerates the malate-pyruvate cycle enhancing cytoplasmic NADPH, thereby regenerating the potent antioxidant reduced glutathione.

The Relationship of Adherence to the Mediterranean Diet with Disease Activity and Quality of Life in Crohn's Disease Patients.

: Emerging evidence is placing the Mediterranean diet (MD) in the spotlight as a potential dietary model that could benefit inflammatory bowel disease (IBD) patients in terms of prevention and progress of the disease. The main aim of the present study is to shed some light on the relationship between the adherence to the MD and the degree of disease activity, as well as the quality of life in patients with Crohn's disease (CD). : An administered questionnaire was used to assess and record a number of parameters, including recent medical and weight history, anthropometric characteristics, disease activity (in remission or active disease), and quality of life of both male and female CD patients.

Routes of Albumin Overload Toxicity in Renal Tubular Epithelial Cells.

Besides being a marker of kidney disease severity, albuminuria exerts a toxic effect on renal proximal tubular epithelial cells (RPTECs). We evaluated whether an unfolded protein response (UPR) or DNA damage response (DDR) is elicited in RPTECs exposed to high albumin concentration. The deleterious outcomes of the above pathways, apoptosis, senescence, or epithelial-to-mesenchymal transition (EMT) were evaluated.