Background: Recent studies suggest that cytokines modulate bone turnover. Idiopathic hypercalciuria (IH) seems to be associated with bone mineral loss. Therefore, the aim of this study was to assess cytokines involved in bone turnover in patients with IH.
Methods: Plasma and spot-urine levels of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor alpha (TNF-α), transforming growth factor β1 (TGF-β1), and monocyte chemoattractant protein (MCP-1) were measured in 70 children and adolescents with IH and in 37 healthy controls. Patients with IH were subdivided according to their calciuria at the time of sample collection: ≥4 mg/kg/day (persistent IH, n=27) and below 4 mg/kg/day (controlled IH, n=43). Cytokines were determined by enzyme-linked immunoassay.
Results: Plasma and urinary concentrations of IL-1β, IL-6, IL-8, and TNF-α were undetectable in all groups. No differences were found between controlled and persistent hypercalciuria for plasma and urinary levels of MCP-1 and TGF-β1. On the other hand, MCP-1 levels were significantly higher in both subgroups of IH in comparison to healthy controls. Furthermore, urinary MCP-1 levels of IH patients correlated positively with bone mineral content (p=0.013).
Conclusion: Although cytokine measurements did not allow the differentiation between persistent and controlled IH, our findings suggest that MCP-1 might play a role in patients with IH.
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http://dx.doi.org/10.1007/s00467-011-2094-4 | DOI Listing |
Nephrology (Carlton)
January 2025
Division of Nephrology, Department of Internal Medicine, Faculty of Medicine, Thammasat University, Pathumthani, Thailand.
The case report presents a male patient in his mid-60s with a history of hypertension, benign prostatic hyperplasia and chronic kidney disease (CKD). He presented with gradually increasing serum creatinine levels and hyperglobulinemia, leading to suspicion of multiple myeloma. However, subsequent testing revealed features consistent with systemic lupus erythematosus (SLE) and IgG4-related kidney disease (IgG4-RKD).
View Article and Find Full Text PDFActa Physiol (Oxf)
February 2025
Department of Medicine, Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Aim: Proteinuria is the most robust predictive factors for the progression of chronic kidney disease (CKD), and interventions targeting proteinuria reduction have shown to be the most effective nephroprotective treatments to date. While glomerular dysfunction is the primary source of proteinuria, its consequences extend beyond the glomerulus and have a profound impact on tubular epithelial cells. Indeed, proteinuria induces notable phenotypic changes in tubular epithelial cells and plays a crucial role in driving CKD progression.
View Article and Find Full Text PDFNutrients
December 2024
Departament de Nutrició, Ciències de l'Alimentació i Gastronomia, Campus de l'Alimentació de Torribera, Universitat de Barcelona (UB), 08921 Santa Coloma de Gramenet, Spain.
Background/objectives: Histamine intolerance is primarily caused by a deficiency in the diamine oxidase (DAO) enzyme at the intestinal level. The reduced histamine degradation in the gut leads to its accumulation in plasma, thereby causing multiple clinical manifestations, such as urticaria, diarrhea, headache, dyspnea, or tachycardia, among others. The dietary management of this food intolerance consists of the follow-up of a low-histamine diet, often combined with DAO supplementation.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Animal Experimentation, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Accra P.O. Box LG581, Ghana.
Cisplatin is a common and highly effective chemotherapeutic agent whose nephrotoxic side effect is well-characterized. Sodium thiosulfate (STS), an FDA-approved hydrogen sulfide (HS) donor drug, is emerging as a chemoprotective agent against cisplatin-induced nephrotoxicity (CIN). In this study, we investigated the chemoprotective mechanism of STS in a rat model of CIN.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, 28922 Alcorcón, Madrid, Spain.
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