Browsing by Subject "kidney disease"
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Item Acknowledging Socioecological Systems to Address the Systemic Racial Disparities in Children with Kidney Disease(Wolters Kluwer, 2022-10) Dawson, Anne E.; LaMotte, Julia E.; Bignall, O. N. Ray, II; Pediatrics, School of MedicineItem Biosimilars—Emerging Role in Nephrology(American Society of Nephrology, 2019-09-01) Wish, Jay B.; Medicine, School of MedicineThe Food and Drug Administration (FDA) defines a “biosimilar” agent as a biologic that is highly similar to the reference or originator biologic product notwithstanding minor differences in clinically inactive components with no clinically meaningful differences in terms of the safety, purity, and potency. The advantage of biosimilars is that they are usually about 15%–30% less expensive than the reference product, which results in system-wide cost savings and increased patient access. Because biologic drugs are produced by living organisms, they are by nature heterogeneous and identical copies cannot be made, unlike generic versions of small-molecule drugs. Proposed biosimilars must undergo a rigorous evaluation process to demonstrate a high degree of structural and functional similarity with the reference biologic. Once that is confirmed, a stepwise process of comparison with the reference agent with regard to animal trials, pharmacokinetics/pharmacodynamics, immunogenicity, and human efficacy/safety is conducted. The experience with biosimilars in other highly regulated markets where patent protection for originator biologics is not as robust as in the United States has been favorable in terms of safety, efficacy, and cost savings. An FDA approval pathway was created in 2009 to expedite the approval of biosimilars; as of early 2018 nine agents had been approved through that pathway, none in nephrology. The first United States biosimilar epoetin was approved on May 15, 2018, but does not have an interchangeability designation, meaning that prescribers must specifically write for the biosimilar product for patients to receive it. Given the unfamiliarity of biosimilars within the nephrology community it is recommended that educational programs be developed to address this unmet need and for research to be conducted addressing the perceptual, clinical, and economic effect of biosimilars on our patients.Item A comparison of calcium to zoledronic acid for improvement of cortical bone in an animal model of CKD(Published article can be found at: http://onlinelibrary.wiley.com/doi/10.1002/jbmr.2089/abstract doi: 10.1002/jbmr.2089, 2013-09-03) Moe, Sharon M.; Chen, Neal X.; Newman, Christopher L.; Gattone II, Vincent H.; Organ, Jason M.; Chen, Xianming; Allen, Matthew R.Patients with chronic kidney disease (CKD) have increased risk of fractures, yet the optimal treatment is unknown. In secondary analyses of large randomized trials, bisphosphonates have been shown to improve bone mineral density and reduce fractures. However, bisphosphonates are currently not recommended in patients with advanced kidney disease due to concern about over-suppressing bone remodeling, which may increase the risk of developing arterial calcification. In the present study we used a naturally occurring rat model of CKD with secondary hyperparathyroidism, the Cy/+ rat, and compared the efficacy of treatment with zoledronic acid, calcium given in water to simulate a phosphate binder, and the combination of calcium and zoledronic acid. Animals were treated beginning at 25 weeks of age (approximately 30% of normal renal function) and followed for ten weeks. The results demonstrate that both zoledronic acid and calcium improved bone volume by microCT and both equally suppressed mineral apposition rate, bone formation rate, and mineralizing surface of trabecular bone. In contrast, only calcium treatment with or without zoledronic acid improved cortical porosity and cortical biomechanical properties (ultimate load and stiffness) and lowered parathyroid hormone (PTH). However, only calcium treatment led to the adverse effects of increased arterial calcification and fibroblast growth factor 23 (FGF23). These results suggest zoledronic acid may improve trabecular bone volume in CKD in the presence of secondary hyperparathyroidism, but does not benefit extraskeletal calcification or cortical biomechanical properties. Calcium effectively reduces PTH and benefits both cortical and trabecular bone yet increases the degree of extra skeletal calcification.Item Empagliflozin and incidence of events consistent with acute kidney injury: Pooled safety analysis in >15 000 individuals(Wiley, 2022) Agarwal, Rajiv; Hauske, Sibylle Jenny; Wheeler, David C.; Doi, Kent; Elsaesser, Amelie; Ritter, Ivana; Steubl, Dominik; Wanner, Christoph; Medicine, School of MedicineItem Erythropoietin stimulates murine and human fibroblast growth factor-23, revealing novel roles for bone and bone marrow(Ferrata Storti Foundation, 2017-11) Clinkenbeard, Erica L.; Hanudel, Mark R.; Stayrook, Keith R.; Appaiah, Hitesh Nidumanda; Farrow, Emily G.; Cass, Taryn A.; Summers, Lelia J.; Ip, Colin S.; Hum, Julia M.; Thomas, Joseph C.; Ivan, Mircea; Richine, Briana M.; Chan, Rebecca J.; Clemens, Thomas L.; Schipani, Ernestina; Sabbagh, Yves; Xu, Linlin; Srour, Edward F.; Alvarez, Marta B.; Kacena, Melissa A.; Salusky, Isidro B.; Ganz, Tomas; Nemeth, Elizabeta; White, Kenneth E.; Medical and Molecular Genetics, School of MedicineItem Novel roles for mucin 1 in the kidney(Wolters Kluwer, 2017-09) Al-bataineh, Mohammad; Sutton, Timothy A.; Hughey, Rebecca P.; Medicine, School of MedicinePurpose of review Recent studies in the kidney have revealed that the well characterized tumor antigen mucin 1 (MUC1/Muc1) also has numerous functions in the normal and injured kidney. Recent findings Mucin 1 is a transmembrane mucin with a robust glycan-dependent apical targeting signal and efficient recycling from endosomes. It was recently reported that the TRPV5 calcium channel is stabilized on the cell surface by galectin-dependent cross-linking to mucin 1, providing a novel mechanism for regulation of ion channels and normal electrolyte balance. Our recent studies in mice show that Muc 1 is induced after ischemia, stabilizing hypoxia-inducible factor 1 (HIF-1)α and β-catenin levels, and transactivating the HIF-1 and β-catenin protective pathways. However, prolonged induction of either pathway in the injured kidney can proceed from apparent full recovery to chronic kidney disease. A very recent report indicates that aberrant activation of mucin 1 signaling after ischemic injury in mice and humans is associated with development of chronic kidney disease and fibrosis. A frameshift mutation in MUC1 was recently identified as the genetic lesion causing medullary cystic kidney disease type 1, now appropriately renamed MUC1 Kidney Disease. Summary Studies of mucin 1 in the kidney now reveal significant functions for the extracellular mucin-like domain and signaling through the cytoplasmic tail.Item Proteinuria(StatPearls, 2022) Haider, Mobeen Z.; Aslam, Ahsan; Medicine, School of MedicineItem Research Center for Quantitative Renal Imaging(Office of the Vice Chancellor for Research, 2015-04-17) Research Center for Quantitative Renal ImagingMission: The overall mission of the Research Center for Quantitative Renal Imaging is to provide a focused research environment and resource for the development, implementation, and dissemination of innovative, quantitative imaging methods designed to assess the status of and mechanisms associated with acute and chronic kidney disease and evaluate efficacy of therapeutic interventions. Nature of the Center: IUPUI has several established research programs focused on understanding the fundamental mechanisms associated with kidney diseases along with established groups of investigators dedicated to the development of advanced imaging methods and quantitative analyses. This Research Center provides a formal mechanism to link these independently successful research efforts into a focused effort dedicated toward the development and implementation of quantitative renal imaging methods. The goals of the IUPUI Research Center for Quantitative Renal Imaging are to: Identify, develop, and implement innovative imaging methods that provide quantitative imaging biomarkers for assessing and inter-relating renal structure, function, hemodynamics and underlying tissue micro-environmental factors contributing to kidney disease. Establish an environment that facilitates and encourages interdisciplinary collaborations among investigators and offers research support to investigators focused on developing and utilizing innovative quantitative imaging methods in support of kidney disease research. Provide a resource to inform the greater research and healthcare communities of advances in quantitative renal imaging and its potential for enhanced patient management and care. Offer an imaging research resource to companies engaged in product development associated with the diagnosis and treatment of kidney diseases. Further Information: For further information regarding the IUPUI Research Center for Quantitative Renal Imaging and its funding programs please visit http://www.renalimaging.iupui.edu/ or contact the Center at renalimg@iupui.edu. Acknowledgments: The IUPUI Research Center for Quantitative Renal Imaging is supported by contributions from the IUPUI Signature Center Initiative, the Department of Radiology & Imaging Sciences; the Division of Nephrology, the IUPUI School of Science, the IUPUI School of Engineering & Technology, and the Indiana Clinical and Translational Sciences Institute (CTSI).