Insulin Resistance, The Metabolic Syndrome And Renal Failure – Is There A Special Problem For Patients Treated With Peritoneal Dialysis?
Beddhu S, Kimmel P L, Ramkumar N, Cheung A K, “Associations of metabolic syndrome with inflammation in CKD: Results from the Thirst National Health and Nutrition Examination Survey (NHANES III)”, Am. J. Kidney Dis. (2005);46: pp. 577–586. Kramer H, Luke A, Bidani A et al., “Obesity and prevalent and incident CKD: the Hypertension Detection and Followup Program”, Am. J. Kidney Dis. (2005);46: pp. 587–584. Kobayashi S, Maesato K, Moriya H, Ohtake T, Ikeda T, “Insulin resistance in patients with chronic kidney disease”, Am. J. Kidney Dis. (2005);45; pp. 275–280. Kurella M, Lo J C, Chertow G M, “Metabolic syndrome and the risk for chronic kidney disease among non-diabetic adults”, J. Am. Soc. Nephrol. (2005);16: pp. 2,134–2,140. El-Atat F A, Stas S N, McFarlane S I, Sower J R, “The relationship between hyperinsulinemia, hypertension and progressive renal disease”, J. Am. Soc. Nephrol. (2004);15: pp. 2,816–2,828. Shinohara K, Shoji T, Emoto M et al., “Insulin resistance as an independent predictor of cardiovascular mortalilty in patients with end-stage renal disease”, J. Am. Soc. Nephrol. (2002);13: pp. 1,894–1,900. Becker B, Krönenberg F, Kielstein J T, “Renal insulin resistance syndrome, adiponectin and cardiovascular events in patients with kidney disease: The Mild and Moderate Kidney Disease Study”, J. Am. Soc. Nephrol. (2005);16: pp. 1,091–1,098. Dekker J M, Girman C, Rhodes T, “Metabolic syndrome and 10-year cardiovascular disease risk in the Hoorn Study”, Circulation (2005);112: pp. 666–673. Mak R H K, “Insulin resistance in uremia: effect of dialysis modality”, Pediatr. Res. (1995);40: pp. 304–308. Kobayashi S, Maejima S, Ikeda T, Nagase M, “Impact of dialysis therapy on insulin resistance in end-stage renal di Continue reading >>
Insulin Is Key To Kidney Disease
A form of kidney disease may result from defective insulin signaling, challenging conventional wisdom Diabetic kidney disease likely results from defective insulin signaling in the kidneys, contradicting long-standing suspicions, according to findings appearing online today (October 5) in Cell Metabolism. Scientists have long attributed this type of kidney disease -- the leading cause of renal failure -- to high glucose levels in the blood and defects in the kidney microvasculature. The study "suggests there's a direct effect of insulin" on epithelial cells in the kidney, "which is really a new idea," said nephrologist linkurl:Thomas Coffman;of Duke University School of Medicine, who was not involved in the research. "I'm sure it will be a highly cited paper." Diabetes causes numerous health problems, including a form of kidney disease known as diabetic nephropathy (DN). DN is characterized by protein in the urine, enlarged kidneys, and abnormalities in the glomeruli, specialized capillaries where the urine filtration process begins, and other parts of the kidney. Researchers most often attribute the disease to defects in the microvasculature of the kidneys as a result of high blood glucose levels, which are known to be toxic to a variety of cell types. But growing evidence suggests that another cell type may be involved -- epithelial cells known as podocytes. Furthermore, some people with insulin resistance accumulate protein in their urine, even when glucose is normal. To investigate the role of podocytes and insulin signaling in the development of DN, a team led by molecular biologist and pediatrician linkurl:Richard Coward;of the University of Bristol in the UK examined two knockout mice models whose podocytes lacked the insulin receptor. Within 5 weeks of birth, th Continue reading >>
Insulin Therapy And Acute Kidney Injury In Critically Ill Patientsa Systematic Review
Insulin therapy and acute kidney injury in critically ill patientsa systematic review Division of Nephrology, Department of Medicine, Caritas St Elizabeth's Medical Center, 2Division of Pulmonary and Critical Care Medicine, Caritas St Elizabeth's Medical Center and 3Institute for Clinical Research and Health Policy Studies, Tufts-New England Medical Center, Boston, MA, USA Search for other works by this author on: Division of Nephrology, Department of Medicine, Caritas St Elizabeth's Medical Center, 2Division of Pulmonary and Critical Care Medicine, Caritas St Elizabeth's Medical Center and 3Institute for Clinical Research and Health Policy Studies, Tufts-New England Medical Center, Boston, MA, USA Search for other works by this author on: Division of Nephrology, Department of Medicine, Caritas St Elizabeth's Medical Center, 2Division of Pulmonary and Critical Care Medicine, Caritas St Elizabeth's Medical Center and 3Institute for Clinical Research and Health Policy Studies, Tufts-New England Medical Center, Boston, MA, USA Search for other works by this author on: Division of Nephrology, Department of Medicine, Caritas St Elizabeth's Medical Center, 2Division of Pulmonary and Critical Care Medicine, Caritas St Elizabeth's Medical Center and 3Institute for Clinical Research and Health Policy Studies, Tufts-New England Medical Center, Boston, MA, USA Search for other works by this author on: Division of Nephrology, Department of Medicine, Caritas St Elizabeth's Medical Center, 2Division of Pulmonary and Critical Care Medicine, Caritas St Elizabeth's Medical Center and 3Institute for Clinical Research and Health Policy Studies, Tufts-New England Medical Center, Boston, MA, USA Search for other works by this author on: Division of Nephrology, Department of Medicine, Carit Continue reading >>
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Insulin Resistance In Patients With Chronic Kidney Disease
Journal of Biomedicine and Biotechnology Volume 2012 (2012), Article ID 691369, 12 pages 1Department of Pediatrics, Taoyuan Armed Forces General Hospital, Taoyuan 325, Taiwan 2Department of Pediatrics, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan 3Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan 4Division of Nephrology, Department of Medicine, Cardinal Tien Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan Academic Editor: Sandro Massao Hirabara Copyright © 2012 Min-Tser Liao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Metabolic syndrome and its components are associated with chronic kidney disease (CKD) development. Insulin resistance (IR) plays a central role in the metabolic syndrome and is associated with increased risk for CKD in nondiabetic patients. IR is common in patients with mild-to-moderate stage CKD, even when the glomerular filtration rate is within the normal range. IR, along with oxidative stress and inflammation, also promotes kidney disease. In patients with end stage renal disease, IR is an independent predictor of cardiovascular disease and is linked to protein energy wasting and malnutrition. Systemic inflammation, oxidative stress, elevated serum adipokines and fetuin-A, metabolic acidosis, vitamin D deficiency, depressed serum erythropoietin, endoplasmic reticulum stress, and suppressors of cytokine signaling all cause IR by suppressing insulin receptor-PI3K-Akt pathways in CKD. In addition to adequate renal Continue reading >>
Low Blood Sugar And Chronic Kidney Disease
Disclaimer: This article is for informational purposes only and is not intended to be a substitute for medical advice or diagnosis from a physician. The most common cause of kidney disease is diabetes. The bodies of people with diabetes do not use the hormone insulin properly or does not make insulin at all, so insulin injections or other diabetes medications are required. Because insulin helps keep the amount of sugar in the blood at a normal level, people with diabetes are at risk for both low blood sugar (hypoglycemia) and high blood sugar (hyperglycemia), especially when there are changes in diet, activity or medications. Blood sugar below 70 mg/dL is considered low. Kidney disease and the risk for low blood sugar The greatest risk of low blood sugar occurs in someone who has both chronic kidney disease (CKD) and diabetes. Whether or not someone has diabetes, a person with CKD is at risk for low blood sugar because of changes in appetite and meal routine. When kidney function declines insulin and other diabetes medications remain in the system longer because of decreased kidney clearance. For a person with diabetes, insulin and other diabetes medications that lower blood sugar may require an adjustment to prevent low blood sugar. Causes of low blood sugar Common causes of low blood sugar include: Skipping meals or waiting too long to eat A decrease in usual food intake because of poor appetite Taking too much insulin or diabetes medicine Receiving insulin or diabetes medicine at the wrong time Increasing physical activity Drinking alcoholic beverages People with chronic kidney disease sometimes experience a loss of appetite that can lead to skipping meals or not eating enough. This often causes a drop in blood sugar. Symptoms of low blood sugar Some of the symptoms Continue reading >>
Effect Of Insulin Resistance In Chronic Kidney Disease
1Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK 2Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran *Corresponding Author: Andrew H Frankel Imperial College Kidney and Transplant Institute Hammersmith Hospital Imperial College London London, UK Tel: +98 912 188 1096 E-mail: [email protected] Citation: Frankel AH, Kazempour-Ardebili S (2016) Effect of Insulin Resistance in Chronic Kidney Disease. Endocrinol Metab Syndr 5:255. doi:10.4172/2161-1017.1000255 Copyright: © 2016 Frankel AH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Endocrinology & Metabolic Syndrome Abstract Insulin resistance accompanies many well-established cardiovascular risk factors, such as obesity, hypertension, dyslipidaemia and type 2 diabetes. Since cardiovascular disease (CVD) is the leading cause of death in patients with end stage renal disease (ESRD), insulin resistance is thought to play a role in the morbidity and mortality associated with ESRD. This paper reviews the available information on insulin resistance in patients with impaired kidney function as well as those on renal replacement therapy in the form of maintenance hemodialysis. Potential mechanisms for the dynamic changes in insulin resistance, which occur through the different stages of kidney disease, are also discussed. We hypothesize that stabilizing insulin sensitivity may have a positive effect on improving outcome in ESRD subjects Continue reading >>
Carbohydrate And Insulin Metabolism In Chronic Kidney Disease
INTRODUCTION Uremia is typically associated with impaired glucose metabolism. Some patients have hyperglycemia in response to oral and intravenous glucose loads, while others are able to maintain normoglycemia by raising plasma insulin levels. Studies utilizing the euglycemic and hyperglycemic clamp techniques suggest that several disturbances in carbohydrate handling may be present. Tissue insensitivity to insulin is of primary importance, but alterations in insulin degradation and insulin secretion also may contribute [1-3]. The variable severity of these changes in individual patients explains the variable plasma levels of insulin and glucose that may be seen both fasting and following a glucose load. This topic will review the changes in carbohydrate and insulin metabolism that occur in chronic kidney disease (CKD) and the clinical implications of these abnormalities in nondiabetics. The impact of these changes on the management of hyperglycemia in diabetic patients with end-stage renal disease (ESRD) is discussed separately. (See "Management of hyperglycemia in patients with type 2 diabetes and pre-dialysis chronic kidney disease or end-stage renal disease".) NORMAL RENAL HANDLING OF INSULIN The kidney plays a central role in the metabolism of insulin in normal subjects [1,2,4]. Insulin has a molecular weight of 6000 and is therefore freely filtered. Of the total renal insulin clearance, approximately 60 percent occurs by glomerular filtration and 40 percent by extraction from the peritubular vessels. Insulin in the tubular lumen enters proximal tubular cells by carrier-mediated endocytosis and is then transported into lysosomes, where it is metabolized to amino acids [5]. The net effect is that <1 percent of filtered insulin appears in the final urine. The renal c Continue reading >>
Insulin Therapy In Renal Disease.
Department of Endocrinology, Hospital General, Segovia, Spain. [email protected] Diabetes Obes Metab. 2008 Sep;10(10):811-23. doi: 10.1111/j.1463-1326.2007.00802.x. Epub 2008 Feb 1. Diabetes mellitus (DM) is the main cause of end-stage renal disease (ESRD). Conversely, chronic renal failure (CRF) is also associated with diverse alterations in carbohydrate and insulin metabolism. CRF-induced metabolic disorders should be borne in mind when treating diabetic patients, to ensure the introduction of adequate therapy adjustments that are in line with the onset of renal function decline. Moreover, several specific therapies employed in CRF may also influence pharmacological therapy of DM in uraemic patients. Adequate glycaemic control has also been associated with a reduction in the onset and progression of diabetic nephropathy as well as in the morbidity and mortality in uraemic diabetic patients during dialysis. Intensive insulin therapy can notably improve glycemic control and it should be considered part of the management of insulin-treated CRF diabetic patients. Insulin analogues have been recently evaluated in CRF diabetic patients, with encouraging results. In this study, we review the more relevant aspects related to insulin therapy in diabetic patients with different degrees of renal failure and in patients with ESRD, both in conservative therapy and dialysis. Continue reading >>
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Diabetes - A Major Risk Factor For Kidney Disease
Diabetes mellitus, usually called diabetes, is a disease in which your body does not make enough insulin or cannot use normal amounts of insulin properly. Insulin is a hormone that regulates the amount of sugar in your blood. A high blood sugar level can cause problems in many parts of your body. The most common ones are Type 1 and Type 2. Type 1 diabetes usually occurs in children. It is also called juvenile onset diabetes mellitus or insulin-dependent diabetes mellitus. In this type, your pancreas does not make enough insulin and you have to take insulin injections for the rest of your life. Type 2 diabetes, which is more common, usually occurs in people over 40 and is called adult onset diabetes mellitus. It is also called non insulin-dependent diabetes mellitus. In Type 2, your pancreas makes insulin, but your body does not use it properly. The high blood sugar level often can be controlled by following a diet and/or taking medication, although some patients must take insulin. Type 2 diabetes is particularly prevalent among African Americans, American Indians, Latin Americans and Asian Americans. With diabetes, the small blood vessels in the body are injured. When the blood vessels in the kidneys are injured, your kidneys cannot clean your blood properly. Your body will retain more water and salt than it should, which can result in weight gain and ankle swelling. You may have protein in your urine. Also, waste materials will build up in your blood. Diabetes also may cause damage to nerves in your body. This can cause difficulty in emptying your bladder. The pressure resulting from your full bladder can back up and injure the kidneys. Also, if urine remains in your bladder for a long time, you can develop an infection from the rapid growth of bacteria in urine that h Continue reading >>
Glycemic Control And Critical Illness: Is The Kidney Involved?
Glycemic Control and Critical Illness: Is the Kidney Involved? Department of Medicine, University of California San Diego, San Diego, California Dr. Ravindra L. Mehta, UCSD Medical Center 8342, 200 W. Arbor Drive, San Diego, CA 92103. Phone: 619-543-7310; Fax: 619-543-7420; E-mail: rmehta{at}ucsd.edu The pathophysiology, consequences, and management of hyperglycemia during critical illness is an important clinical issue. Uncontrolled hyperglycemia in this setting is associated with a variety of adverse events, including mortality. The kidneys have a major role in glucose and insulin metabolism, and emerging evidence suggests that they both are actively involved in the development, maintenance, and resolution of hyperglycemia. The development of acute kidney injury is also a risk in this setting. This article discusses potential approaches for efficient and effective management of hyperglycemia. Effective management of hyperglycemia in critically ill patients has been a major topic of discussion since a landmark study demonstrated a significant reduction in mortality and morbidity in surgical patients who were treated with an intensive regimen to control blood glucose. 1 Subsequent studies have highlighted the importance of hyperglycemia for adverse outcomes in various populations and proposed algorithms for glycemic control. 2 4 However, achieving glycemic control is not easy, and additional questions have emerged. 5 , 6 These include identifying potential mechanisms for the deleterious effects of hyperglycemia and the protective role of insulin in glycemic control. 7 , 8 The risk for hypoglycemia has also prompted concerns that one must identify patients who are most likely to benefit from insulin therapy. 9 Emerging evidence raises intriguing questions on the role of Continue reading >>
- The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus
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- Early-onset and classical forms of type 2 diabetes show impaired expression of genes involved in muscle branched-chain amino acids metabolism
Insulin Is Key To Kidney Disease
A form of kidney disease may result from defective insulin signaling, challenging conventional wisdom Diabetic kidney disease likely results from defective insulin signaling in the kidneys, contradicting long-standing suspicions, according to findings appearing online today (October 5) in Cell Metabolism. Scientists have long attributed this type of kidney disease -- the leading cause of renal failure -- to high glucose levels in the blood and defects in the kidney microvasculature. The study "suggests there's a direct effect of insulin" on epithelial cells in the kidney, "which is really a new idea," said nephrologist linkurl:Thomas Coffman;of Duke University School of Medicine, who was not involved in the research. "I'm sure it will be a highly cited paper." Diabetes causes numerous health problems, including a form of kidney disease known as diabetic nephropathy (DN). DN is characterized by protein in the urine, enlarged kidneys, and abnormalities in the glomeruli, specialized capillaries where the urine filtration process begins, and other parts of the kidney. Researchers most often attribute the disease to defects in the microvasculature of the kidneys as a result of high blood glucose levels, which are known to be toxic to a variety of cell types. But growing evidence suggests that another cell type may be involved -- epithelial cells known as podocytes. Furthermore, some people with insulin resistance accumulate protein in their urine, even when glucose is normal. To investigate the role of podocytes and insulin signaling in the development of DN, a team led by molecular biologist and pediatrician linkurl:Richard Coward;of the University of Bristol in the UK examined two knockout mice models whose podocytes lacked the insulin receptor. Within 5 weeks of birth, th Continue reading >>
Chronic Kidney Disease
Chronic kidney disease (CKD) is defined as kidney damage or glomerular filtration rate (GFR) below 60 ml/min per 1.73 m2 for 3 months or more irrespective of the cause. Melissa Gregory, in Comprehensive Pediatric Hospital Medicine , 2007 Chronic renal failure (CRF) is an irreversible reduction in renal function, or glomerular filtration rate (GFR), with accompanying derangements in biochemical homeostasis. End-stage renal disease (ESRD) is defined as CRF so severe that a form of renal replacement therapy is required. The incidence of CRF in children is low, and the incidence of ESRD is 3 to 6 children per 1 million total population.1 Unlike adults with CRF, in whom the primary causes are diabetes and hypertension, the overwhelming majority of children with CRF have primary renal disease, usually of congenital origin.2 This means that the care of children with CRF can deviate dramatically from that of adults. William E. Mitch, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 Chronic kidney disease (CKD) refers to the many clinical abnormalities that progressively worsen as kidney function declines. CKD results from a large number of systemic diseases that damage the kidney or from disorders that are intrinsic to the kidney (Table 132-1). A glomerular filtration rate (GFR) persistently below 60mL/minute/1.73m2, which is below the level of kidney function expected to occur with aging, defines clinically significant CKD. In CKD, the damage is rarely repaired, so loss of function persists. This distinguishes CKD from acute kidney damage (Chapter 122), which can be repaired to permit the return of kidney function. The chronic loss of kidney function generates even more kidney damage and more severe clinical abnormalities. As a result, CKD progressively worsens even Continue reading >>
Management Of Diabetes Mellitus In Patients With Chronic Kidney Disease
Abstract Glycemic control is essential to delay or prevent the onset of diabetic kidney disease. There are a number of glucose-lowering medications available but only a fraction of them can be used safely in chronic kidney disease and many of them need an adjustment in dosing. The ideal target hemoglobin A1c is approximately 7 % but this target is adjusted based on the needs of the patient. Diabetes control should be optimized for each individual patient, with measures to reduce diabetes-related complications and minimize adverse events. Overall care of diabetes necessitates attention to multiple aspects, including reducing the risk of cardiovascular disease, and often, multidisciplinary care is needed. Introduction Diabetes mellitus is a growing epidemic and is the most common cause of chronic kidney disease (CKD) and kidney failure. Diabetic nephropathy affects approximately 20–40 % of individuals who have diabetes [1], making it one of the most common complications related to diabetes. Screening for diabetic nephropathy along with early intervention is fundamental to delaying its progression in conjunction with providing proper glycemic control. Given the growing population that is now affected by diabetes and thus, nephropathy, knowledge regarding the safe use of various anti-hyperglycemic agents in those with nephropathy is of importance. In addition, attention to modification of cardiovascular disease (CVD) risk factors is essential. Altogether, knowledge regarding the prevention and management of diabetic nephropathy, along with other aspects of diabetes care, is part of the comprehensive care of any patient with diabetes. Review Recommendations for nephropathy screening in diabetes Patients with diabetes should be screened on an annual basis for nephropathy. I Continue reading >>
Insulin Resistance, The Metabolic Syndrome And Renal Failure – Is There A Special Problem For Patients Treated With Peritoneal Dialysis?
Beddhu S, Kimmel P L, Ramkumar N, Cheung A K, “Associations of metabolic syndrome with inflammation in CKD: Results from the Thirst National Health and Nutrition Examination Survey (NHANES III)”, Am. J. Kidney Dis. (2005);46: pp. 577–586. Kramer H, Luke A, Bidani A et al., “Obesity and prevalent and incident CKD: the Hypertension Detection and Followup Program”, Am. J. Kidney Dis. (2005);46: pp. 587–584. Kobayashi S, Maesato K, Moriya H, Ohtake T, Ikeda T, “Insulin resistance in patients with chronic kidney disease”, Am. J. Kidney Dis. (2005);45; pp. 275–280. Kurella M, Lo J C, Chertow G M, “Metabolic syndrome and the risk for chronic kidney disease among non-diabetic adults”, J. Am. Soc. Nephrol. (2005);16: pp. 2,134–2,140. El-Atat F A, Stas S N, McFarlane S I, Sower J R, “The relationship between hyperinsulinemia, hypertension and progressive renal disease”, J. Am. Soc. Nephrol. (2004);15: pp. 2,816–2,828. Shinohara K, Shoji T, Emoto M et al., “Insulin resistance as an independent predictor of cardiovascular mortalilty in patients with end-stage renal disease”, J. Am. Soc. Nephrol. (2002);13: pp. 1,894–1,900. Becker B, Krönenberg F, Kielstein J T, “Renal insulin resistance syndrome, adiponectin and cardiovascular events in patients with kidney disease: The Mild and Moderate Kidney Disease Study”, J. Am. Soc. Nephrol. (2005);16: pp. 1,091–1,098. Dekker J M, Girman C, Rhodes T, “Metabolic syndrome and 10-year cardiovascular disease risk in the Hoorn Study”, Circulation (2005);112: pp. 666–673. Mak R H K, “Insulin resistance in uremia: effect of dialysis modality”, Pediatr. Res. (1995);40: pp. 304–308. Kobayashi S, Maejima S, Ikeda T, Nagase M, “Impact of dialysis therapy on insulin resistance in end-stage renal di Continue reading >>
Effect Of Insulin Resistance In Chronic Kidney Disease
1Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK 2Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran *Corresponding Author: Andrew H Frankel Imperial College Kidney and Transplant Institute Hammersmith Hospital Imperial College London London, UK Tel: +98 912 188 1096 E-mail: [email protected] Citation: Frankel AH, Kazempour-Ardebili S (2016) Effect of Insulin Resistance in Chronic Kidney Disease. Endocrinol Metab Syndr 5:255. doi:10.4172/2161-1017.1000255 Copyright: © 2016 Frankel AH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Endocrinology & Metabolic Syndrome Abstract Insulin resistance accompanies many well-established cardiovascular risk factors, such as obesity, hypertension, dyslipidaemia and type 2 diabetes. Since cardiovascular disease (CVD) is the leading cause of death in patients with end stage renal disease (ESRD), insulin resistance is thought to play a role in the morbidity and mortality associated with ESRD. This paper reviews the available information on insulin resistance in patients with impaired kidney function as well as those on renal replacement therapy in the form of maintenance hemodialysis. Potential mechanisms for the dynamic changes in insulin resistance, which occur through the different stages of kidney disease, are also discussed. We hypothesize that stabilizing insulin sensitivity may have a positive effect on improving outcome in ESRD subjects Continue reading >>
