Treatment of chronic kidney disease

Abstract

Treatment of chronic kidney disease (CKD) can slow its progression to end-stage renal disease (ESRD). However, the therapies remain limited. Blood pressure control using angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) has the greatest weight of evidence. Glycemic control in diabetes seems likely to retard progression. Several metabolic disturbances of CKD may prove to be useful therapeutic targets but have been insufficiently tested. These include acidosis, hyperphosphatemia, and vitamin D deficiency. Drugs aimed at other potentially damaging systems and processes, including endothelin, fibrosis, oxidation, and advanced glycation end products, are at various stages of development. In addition to the paucity of proven effective therapies, the incomplete application of existing treatments, the education of patients about their disease, and the transition to ESRD care remain major practical barriers to better outcomes.

Mechanisms and Treatment of CKD

“…Data on the renoprotective effect of uric acid reduction by allopurinol therapy are encouraging (see Turner et al 118 for review), but need confirmation in adequately powered trials, whereas the renoprotective effect of anemia correction by erythropoietin congeners has been definitely challenged, at least in overt nephropathy of type 2 diabetes, by results of the Trial to Reduce Cardiovascular Events with Aranesp Therapy. 119 …”

Rostafuroxin Protects from Podocyte Injury and Proteinuria Induced by Adducin Genetic Variants and Ouabain

“…Therefore, in clinical practice, it is crucial to find a drug which can block the initial triggering events but also delay, or prevent, the progression to end-stage renal disease. Although not completely understood, the molecular mechanisms that operate in chronic renal failure causing glomerular damage, loss of active nephrons, proliferation of mesangial cells, and thickening of basal lamina are frequently associated with tubule-interstitial fibrosis, renal tissue inflammation, and matrix deposition that may ultimately induce a compensatory hypertrophy of the remaining nephrons and of the whole kidney (Turner et al, 2012). Peptides, such as angiotensin II, or the increased hydrostatic pressure, responsible for mechanical stress, and the rearrangement of actin cytoskeleton mediated by Rho family GTPases and reactive oxygen species (Babelova et al, 2013) have been considered the most likely cause of podocyte injury.…”

Self-Management Program for People with Chronic Kidney Disease in Vietnam: A Pragmatic Randomised Controlled Trial

“…Non-pharmacological therapy is used for managing the early stages of CKD, and includes dietary changes and lifestyle modifications (Johnson et al, 2013;Turner, Bauer, Abramowitz, Melamed, & Hostetter, 2012). Dietary changes include adopting a healthy eating plan that involves sodium and fat reduction.…”