By Joel D. Kopple, Shaul G Massry, Kamyar Kalantar-Zadeh
This translational text offers in-depth stories of the metabolic and dietary problems which are favourite in sufferers with renal disorder. bankruptcy themes handle the turning out to be epidemic of weight problems and metabolic syndrome. every one chapter integrates uncomplicated and scientific techniques, from cellphone biology and genetics to analysis, sufferer administration and remedy. Chapters in sections 4-7 include new illustrative case experiences, and all chapters emphasize key options with chapter-ending summaries. New features also comprise the most recent nationwide Kidney beginning scientific perform directions on food in power Renal Failure, the latest clinical discoveries and the newest innovations for assessing dietary prestige in renal disorder, and literature studies on sufferers who obtain non-stop veno-venous hemofiltration without or with dialysis.
- Provides a standard language for nephrologists, nutritionists, endocrinologists, and different physicians to debate the underlying study and translation of top practices for the dietary administration and prevention of renal disease
- Saves clinicians and researchers time in quick gaining access to the very most up-to-date info on dietary perform in place of looking through hundreds of thousands of magazine articles.
- Correct analysis (and for that reason right therapy) of renal, metabolic, and dietary issues will depend on a robust realizing of the molecular foundation for the illness - either nephrologists and nutritionists will benefit
- Nephrologists and nutritionists will achieve perception into which remedies, drugs, and diets to exploit in accordance with the heritage, development, and genetic makeup of a sufferer
- Case reviews will supply an further source for fellows, nutritionists, and dieticians who desire a refresher course
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Additional resources for Nutritional Management of Renal Disease
Thiazolidinediones The currently available TZDs, rosiglitazone and pioglitazone, are selective agonists of the peroxisomal proliferator-activated receptor-g (PPAR-g) [117,119]. The ligands for these receptors are normally free fatty acids and eicosanoids. By activating PPARg they inhibit angiogenesis, decrease leptin levels and certain interleukins, while adiponectin levels increase . TZDs act as prandial glucose regulators and improve insulin sensitivity. TZDs are predominantly metabolized and eliminated by the liver [117,119].
A minor amount of netaglinide, together with its active metabolite, is excreted in the urine . Therefore in advanced CKD netaglinide treatment still increases the risk of hypoglycemia. Glucagon-Like Peptide 1 (GLP-1) Agonists The two main incretins secreted by K cells in the upper small intestine are GLP-1 and glucose-dependent insulinotropic peptide (GIP) . Gut hormones have been shown to play an important role in whole-body glucose homeostasis by suppressing meal-related glucagon secretion, delaying gastric emptying and inducing satiety .
Consequently, no dose adjustments are necessary in patients with renal dysfunction [160,161]. A major side effect is sodium retention, particularly in patients with CKD, causing weight gain with reduction of hematocrit, edema and even pulmonary edema, particularly in patients with CV disease . Further side effects include higher fracture rates of distal extremities in women and gastrointestinal side effects . Therefore great caution is advised with PPARg agonist use in patients with an eGFR less than 30 mL/min [117,119].