The incidence of chronic kidney disease (CKD) is increasing worldwide; however, the association between CKD and anemia and hyperuricemia has yet to be clarified. In addition, whether anemia and hyperuricemia only influence renal damage in combination with other comorbidities or whether they are direct causative factors is also controversial. Therefore, the aim of this longitudinal study was to investigate these issues in a large Taiwanese cohort. We enrolled 26,631 participants from the Taiwan Biobank (TWB) after excluding those with CKD at the baseline, all of whom had follow-up data for a median of 4 years. In this study, CKD was defined as an estimated glomerular filtration rate < 60 mL/min/1.73 m2, incident new-onset CKD was defined as the development of CKD during follow-up, anemia was defined as a hemoglobin level <13 mg/dL in males and <12 mg/dL in females, and hyperuricemia was defined as a serum uric acid (UA) level >7 mg/dL in males and >6 mg/dL in females. The participants were divided into four groups according to whether or not they had anemia and hyperuricemia. Multivariable analysis showed that low hemoglobin (per 1 g/dL; odds ratio [OR], 0.760; p < 0.001) and high serum UA (per 1 mg/dL; OR, 1.444; p < 0.001) in model 1 and anemia (OR, 2.367; p < 0.001) and hyperuricemia (OR, 2.516; p < 0.001) in model 2 were significantly associated with new-onset CKD. Furthermore, compared to the group without anemia or hyperuricemia, the groups with anemia without hyperuricemia (OR, 2.502; p < 0.001), without anemia with hyperuricemia (OR, 2.559; p < 0.001), and with anemia and hyperuricemia (OR, 5.505; p < 0.001) were significantly associated with new-onset CKD. There was a significant interaction between hemoglobin and serum UA and new-onset CKD (p < 0.001). In conclusion, we found that anemia and hyperuricemia were associated with new-onset CKD, respectively, and also had a synergetic effect on new-onset CKD.
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http://dx.doi.org/10.3390/ijerph20021421 | DOI Listing |
J Health Econ Outcomes Res
January 2025
Ultragenyx Pharmaceutical Inc., Novato, CA, USA.
Glycogen storage disease type Ia (GSDIa) is a rare inherited disorder resulting in potentially life-threatening hypoglycemia, metabolic abnormalities, and complications often requiring hospitalization. This retrospective database analysis assessed the complications, resource utilization, and costs in a large cohort of patients with GSDIa. We conducted a retrospective cohort study of GSDIa patients and matched non-GSDIa comparators utilizing the PharMetrics® Plus database.
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December 2024
Department of Internal Medicine, North China University of Science and Technology, Tangshan, China.
Background: Autosomal dominant tubulointerstitial kidney disease (ADTKD) caused by -causing pathogenic variants (ADTKD-) is a rare group of heritable diseases. ADTKD- often manifests in childhood with symptoms such as mild hypotension, chronic kidney disease, hyperkalemia, anemia, and acidosis. The diagnosis of ADTKD- remains challenging.
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November 2024
Hematology and Medical Oncology, University of Kentucky College of Medicine, Lexington, USA.
Tumor lysis syndrome (TLS) is a critical oncologic emergency characterized by metabolic disturbances resulting from rapid cancer cell lysis. Rasburicase, a recombinant urate oxidase, is the primary treatment for hyperuricemia in TLS but poses a risk for methemoglobinemia in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency. We present the case of a 59-year-old male with diffuse large B-cell lymphoma (DLBCL) who developed spontaneous TLS.
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October 2024
Hematology and Medical Oncology, Northwell Health, New Hyde Park, USA.
Rasburicase is a recombinant form of urate oxidase, a medication used to treat hyperuricemia by metabolizing uric acid into an inactive and more soluble metabolite, allantoin. An oxidizing agent, hydrogen peroxide, is produced during the conversion of uric acid to allantoin. We present here a case of hemolytic anemia secondary to rasburicase treatment which was later confirmed to have glucose-6-phosphate dehydrogenase deficiency (G6PDD).
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