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      The role of an out-patient renal clinic in renal disease management

      review-article
      ,
      Journal of Translational Internal Medicine
      De Gruyter Open
      ESRD, out-patient clinic, renal diseases, renal failure

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          Abstract

          The out-patient renal clinic (ORC) represents an important part of the nephrology service in general hospitals. The majority of renal diseases are chronic and patients need a systematic follow-up according to the severity and progression of kidney failure. The most important clinical manifestation is chronic renal failure (CRF) or chronic renal disease (CKD) The management of CKD, apart from medical and nursing services, also involves a number of community structures and financial resources. CRF treatment is costly and is a serious problem for the health systems in the western world. Effective treatment in the early stages aims to decrease the progression of kidney damage and, therefore, to prolong kidney function. Patients with renal failure can be managed as out-patients. The increased number of patients and the complexity of kidney diseases demand the collaboration of other out-patient clinics. The ORC may play an important role in this process. In this article. we present a literature review of the role of ORCs in the management of renal diseases around the world and we also present data based on our experience in our ORC.

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          Chronic kidney disease and the risk for cardiovascular disease, renal replacement, and death in the United States Medicare population, 1998 to 1999.

          Knowledge of the excess risk posed by specific cardiovascular syndromes could help in the development of strategies to reduce premature mortality among patients with chronic kidney disease (CKD). The rates of atherosclerotic vascular disease, congestive heart failure, renal replacement therapy, and death were compared in a 5% sample of the United States Medicare population in 1998 and 1999 (n = 1,091,201). Patients were divided into the following groups: 1, no diabetes, no CKD (79.7%); 2, diabetes, no CKD (16.5%); 3, CKD, no diabetes (2.2%); and 4, both CKD and diabetes (1.6%). During the 2 yr of follow-up, the rates (per 100 patient-years) in the four groups were as follows: atherosclerotic vascular disease, 14.1, 25.3, 35.7, and 49.1; congestive heart failure, 8.6, 18.5, 30.7, and 52.3; renal replacement therapy, 0.04, 0.2, 1.6, and 3.4; and death, 5.5, 8.1, 17.7, and 19.9, respectively (P < 0.0001). With use of Cox regression, the corresponding adjusted hazards ratios were as follows: atherosclerotic vascular disease, 1, 1.30, 1.16, and 1.41 (P < 0.0001); congestive heart failure, 1, 1.44, 1.28, and 1.79 (P < 0.0001); renal replacement therapy, 1, 2.52, 23.1, and 38.9 (P < 0.0001); and death, 1, 1.21, 1.38, and 1.56 (P < 0.0001). On a relative basis, patients with CKD were at a much greater risk for the least frequent study outcome, renal replacement therapy. On an absolute basis, however, the high death rates of patients with CKD may reflect accelerated rates of atherosclerotic vascular disease and congestive heart failure.
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            Polycystic kidney disease.

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              Leptin and renal disease.

              Leptin is a small peptide hormone that is mainly, but not exclusively, produced in adipose tissue. The circulating leptin concentration therefore directly reflects the amount of body fat. Leptin was identified through positional cloning of the obese (ob) gene, which is mutated in the massively obese ob/ob mouse, and it has a pivotal role in regulating food intake and energy expenditure. It binds to the so-called long receptor (Ob-Rb) in the hypothalamus and regulates food intake through the release of other neurotransmitters. Moreover, leptin exerts several other important metabolic effects on peripheral tissue, including modification of insulin action, induction of angiogenesis, and modulation of the immune system. As a small peptide, leptin is cleared principally by the kidney. Not surprisingly, serum leptin concentrations are increased in patients with chronic renal failure and those undergoing maintenance dialysis. Whether the hyperleptinemia of chronic renal failure contributes to some uremic manifestations, such as anorexia and weight loss, requires additional investigation. The kidney expresses abundant concentrations of the truncated isoform of the leptin receptor Ob-Ra, but only a small amount of the full-length receptor Ob-Rb. We recently discovered that leptin has direct effects on renal pathophysiological characteristics. Both cultured glomerular endothelial cells and mesangial cells obtained from the diabetic db/db mouse possess the Ob-Ra receptor, but whether biological effects of leptin are transduced through this receptor remains unknown. In glomerular endothelial cells, leptin stimulates cellular proliferation, transforming growth factor-beta1 (TGF-beta1) synthesis, and type IV collagen production. Conversely, in mesangial cells, leptin upregulates synthesis of the TGF-beta type II receptor, but not TGF-beta1, and stimulates glucose transport and type I collagen production through signal transduction pathways involving phosphatidylinositol-3-kinase. These data suggest that leptin triggers a paracrine interaction in which glomerular endothelial cells secrete TGF-beta, to which sensitized mesangial cells may respond. Both cell types increase their expression of extracellular matrix in response to leptin. Infusion of leptin into normal rats for 3 weeks fosters the development of focal glomerulosclerosis and proteinuria. Additional previously described direct and indirect effects of leptin on the kidney include natriuresis, increased sympathetic nervous activity, and stimulation of reactive oxygen species. These findings collectively suggest that the kidney is not only a site of leptin metabolism, but also a target organ for leptin action in pathophysiological states. Copyright 2002 by the National Kidney Foundation, Inc.
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                Author and article information

                Journal
                J Transl Int Med
                J Transl Int Med
                Journal of Translational Internal Medicine
                De Gruyter Open
                2450-131X
                2224-4018
                Jan-Mar 2015
                30 March 2015
                : 3
                : 1
                : 3-7
                Affiliations
                Nephrology Department, Aretaieio University Hospital University of Athens, Athens, Greece
                Author notes
                Address for Correspondence: Dr. Grapsa Eirini, Kousidou 97 Zografou, Athens 15772, Greece. E-mail: grapse@ 123456otenet.gr
                Article
                2224-4018.154287
                10.4103/2224-4018.154287
                4936470
                cf2a2ff5-bef6-4c9b-add4-ef035c4cb109
                Copyright © International Society of Translational Sciences

                This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License (CC BY-NC-ND 3.0)

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                Categories
                Review Article

                esrd,out-patient clinic,renal diseases,renal failure
                esrd, out-patient clinic, renal diseases, renal failure

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