Clinical and experimental nephrology
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Clin. Exp. Nephrol. · Feb 2013
ReviewNew strategy for the treatment of type 2 diabetes mellitus with incretin-based therapy.
Incretin-based therapy was first made available for the treatment of type 2 diabetes mellitus (T2DM) in the US in 2006 and in Japan in 2009. Four DPP-4 inhibitors and two GLP-1 analog/receptor agonists are currently available. ⋯ The protective effects of this therapy on vulnerable pancreatic β-cells and against micro/macroangiopathy in T2DM are also most welcome. Indications and/or contraindications for incretin-based therapy should be clarified by prospectively studying the experiences of Japanese T2DM patients undergoing this therapy in the clinical setting.
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Clin. Exp. Nephrol. · Aug 2011
ReviewLung injury following acute kidney injury: kidney-lung crosstalk.
The mortality of acute kidney injury (AKI) remains unacceptably high, especially associated with acute respiratory failure. Lung injury complicated with AKI was previously considered as "uremic lung", which is characterized by volume overload and increased vascular permeability. ⋯ In this review, we outline the history of uremic lung and acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), the epidemiological data on the synergistic effect of AKI and lung injury on mortality, and recent basic research which has identified possible pathways in AKI-induced lung injury. These findings will enable us to develop new therapeutic strategies against lung injury associated with AKI and improve the outcomes of critically ill patients in intensive care units.
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The prevalence of end-stage renal disease (ESRD) is rising throughout the developed and developing world, although the rate of increase may be attenuating in some regions. Type 2 diabetes mellitus, often a consequence of obesity and accompanied by the metabolic syndrome, is a major cause of progressive renal disease and the increasing global burden of ESRD. ⋯ Primary and secondary prevention measures, involving screening and interventions, have demonstrated beneficial effects when appropriately designed and targeted to "high-risk" groups. If these strategies can be implemented at the societal level and compliance with the interventions is robust, it is entirely possible that the rising tide of ESRD can be converted into a receding tide of ESRD in the future.
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There have been significant advances recently in the understanding of the molecular causes of nephrogenic diabetes insipidus. The resistance of the collecting duct to the action of vasopressin in this disorder results from abnormalities in several of the intricate steps that mediate the increase in principal cell hydraulic conductivity in response to the hormone. In this article, we review the current understanding of the known genetic causes of nephrogenic diabetes insipidus that affect the binding of vasopressin to the V2 receptor and subsequent intracellular signaling events, as well as the translocation of aquaporin-2 water channels to the apical membrane. In addition, genetic diseases, which decrease collecting-duct water absorption by diminishing the interstitial medullary osmolarity, are discussed.