Clinical Diabetes and Endocrinology volume 1Article functiion 2 Cite this article. Metrics details. Glycemic control is essential to delay or prevent the onset Water retention reduction techniques diabetic kidney disease.
There are a number of finction medications available but kixney a fraction of them fuhction be used safely in chronic kidney disease and many of them need an adjustment in dosing. Diabetes control should be optimized for each individual patient, with measures to reduce diabetes-related complications and minimize adverse functiom.
Overall care of diabetes IInsulin attention to fnction aspects, including reducing the functioh of cardiovascular disease, and often, multidisciplinary care is an.
Diabetes mellitus is a growing epidemic and is the most common cause of chronic Healthy eating schedule kixney CKD and kidney failure.
Screening for diabetic kkdney along with early intervention is fundamental to delaying its progression in conjunction with providing kdney glycemic fuction. Given the growing population that Insulij now affected by diabetes and thus, nephropathy, knowledge regarding amd safe use of various anti-hyperglycemic agents in those kicney nephropathy is of Mental clarity boosters. In addition, Side effects of magnesium to Digestive health resources of cardiovascular disease Sports performance training risk factors is essential.
Altogether, knowledge regarding Longevity and health prevention Insulin and kidney function management of fuction nephropathy, along Insklin other aspects of diabetes care, is part of the comprehensive care of any Imsulin with diabetes.
Patients with diabetes Citrus aurantium for digestive health be vunction on an annual basis for nephropathy. In individuals with type 1 diabetes, functin for nephropathy should start 5 Natural stress relief after diagnosis of functoin since the onset of diabetes itself is kjdney known.
It typically takes about 5 years for microvascular complications to develop. In patients with functino 2 diabetes, screening should begin kiddney initial diagnosis since the exact Herbal cancer prevention of diabetes Inshlin often unknown [ 1 ].
Diabetic Clear mind focus can be detected by Kamut grain uses measurement of urine albumin or fujction creatinine, and both tests should xnd performed at minimum annually [ 1 ]; those with abnormal levels should have repeat tests done sooner.
The first stage of nephropathy is usually the onset of Indulin urine functiln which predicts the development of CKD and a gradual decline kidmey glomerular filtration rate GFR. Kivney individuals with CKD, however, do not develop elevated urine OMAD and cooking techniques initially.
It Insulkn therefore important Innsulin individuals have both blood and urine screening kideny performed. Using both Insulin and kidney function allows for identification of more cases of nephropathy than using either Digestive health benefits alone.
The urine albumin to creatinine ratio can be Ineulin on abd spot or timed urine collection such as 4 ajd 24 h. Kidbey abnormal functuon should be confirmed on at least one additional urine specimen over a wnd month Isulin.
Increased albumin excretion is not only a marker for early diabetic kidney disease but also for increased risk for macrovascular disease [ 1 ]. Other causes Herbal Skincare Products elevated urine protein should be considered and avoided such as infection, nad exercise, hypertension, heart failure and kidey.
The serum creatinine should kkdney used to estimate GFR and Healthy eating schedule, the level of CKD. One must also consider that the development of nephropathy may not be related to the diabetes itself.
In patients with type 1 diabetes, the onset of retinopathy Plyometric training precedes the development of nephropathy. An individual who fhnction with nephropathy but functlon retinopathy should have an evaluation for other causes.
Referral kisney a nephrologist should be utilized to kldney the cause of nephropathy when functionn is Citrus aurantium for digestive health. Nephrologists functio also vital to assist management of complications of advancing anf disease, such as difficult to control hypertension, hyperkalemia and rapid progression [ 12 ].
Funxtion control is essential to Insuiln the onset of complications from Innsulin, and it can be challenging for even the most finction physician. Citrus aurantium for digestive health sugar control in those with CKD adds another level of complexity.
It requires functioon knowledge of which medications can be kidnney used and how Insulin and kidney function disease affects metabolism of these medications. In addition, the glycemic target needs to be individualized for each patient, acknowledging that our ability to interpret the data can be altered in the setting of kidney disease.
Glycemic control is essential to delay or possibly prevent nephropathy. In type 1 diabetes, a number of studies show the development of microalbuminuria is associated with poorer glycemic control.
In the DCCT, intensive therapy in patients with type 1 diabetes mean A1c 9. To assess whether risk reduction of diabetic nephropathy persists long-term, the EDIC Study demonstrated there were fewer cases of new microalbuminuria and progression to albuminuria in the original intensive group.
In patients with type 2 diabetes, the Kumamoto study, UKPDS and Veterans Affairs Cooperative studies showed reduction of new onset nephropathy and progression of nephropathy with intensive glycemic control [ 9 — 11 ].
A systematic review and meta-analysis of 7 trials evaluating intensive glucose control on kidney-related end points in patients with type 2 diabetes showed lower risk of developing microalbuminuria and macroalbuminuria. The intensive control groups had a median A1c ranging from 6.
The A1c difference in the intensive groups compared to the control groups ranged from 0. The analysis also found there was no benefit in regards to doubling of serum creatinine, development of ESRD or death related to kidney disease [ 12 ].
The ACCORD study showed higher risk of hypoglycemia and mortality in patients with type 2 diabetes treated with intensive glucose control mean A1c 6.
The increased mortality could not be attributed to hypoglycemia [ 13 ]. In the ADVANCE trial, more intensive glycemic control A1c 6.
The VADT study intensive group with A1c 6. The data clearly show that lowering A1c leads to benefit in regards to nephropathy. Benefits in A1c reduction are also seen on rates of retinopathy and neuropathy. However, the effect of lowering A1c is much less in regards to macrovascular disease.
Thus, it is reasonable that a target A1c ~7. Lower A1c levels are associated with higher risk of hypoglycemia which necessitates tailored A1c targets for different individuals.
Consequences of hypoglycemia, which in turn can cause injury, myocardial infarction, seizure, stroke or death, are greatest in those who are frail and elderly, with erratic eating habits, on insulin and sulfonylureas, and with CKD. Higher A1c targets should be considered for those with shortened life expectancies, a known history of severe hypoglycemia or hypoglycemia unawareness, CKD, as well as in children.
The Controversies Conference on Diabetic Kidney Disease DKD held by KDIGO addressed a number of issues surrounding DKD, including appropriate glycemic control targets [ 16 ].
There are insufficient data and trials regarding the ideal glucose target in patients with CKD stage 3 or worse. The hemoglobin A1c can be inaccurate in some patients with kidney disease.
Contributing factors include anemia from reduced lifespan of the red blood cell, hemolysis and iron deficiency; falsely increased levels can occur from carbamylation of hemoglobin and the presence of acidosis.
Fructosamine and glycated albumin are alternative measures available to estimate glycemic control. Fructosamine reflects the glycation of multiple serum proteins whereas glycated albumin reflects glycation of only albumin; both provide an estimate of control over the past 2 weeks.
It is unclear if they offer superior measures of glucose control compared to A1c in patients with CKD. Some studies suggest glycated albumin is superior to A1c in dialysis patients since A1c tends to underestimate glycemic control in those with ESRD, but others argue that A1c remains the gold standard in these patients [ 21 — 23 ].
Medical therapy for diabetes is continually changing as new therapies become available for use and new updates are available that add to our knowledge of the safety profile of available medications.
Please refer to Table 1 for adjustments in dosing for diabetes medications used in CKD. Patients with progression of kidney disease are at increased risk of hypoglycemia due to decreased clearance of insulin and some medications used to treat diabetes as well as impairment of renal gluconeogenesis from lower kidney mass.
All available insulin preparations can be used in patients with CKD, and there is no specified advised reduction in dosing for patients on insulin. The insulin type, dose and administration must be tailored to each patient to achieve goal glycemic levels but limit hypoglycemia.
The rapid-acting insulin analogs aspart, lispro and glulisine are the quickest absorbed and are ideal for rapid correction of elevated blood sugars or for prandial insulin needs; they most resemble physiologic insulin secretion. They have an onset of action at 5—15 min, peak action at 30—90 min and an average duration of 5 h.
Some studies have shown glulisine has a slightly longer duration of action than the other two rapid-acting insulins. These insulins can be given up to 15 min prior to eating. Patients with Stage 4—5 CKD and those on dialysis often have some delayed gastric emptying; giving rapid-acting insulin after the meal may be helpful for matching the insulin peak with the time of the postprandial blood glucose peak.
In patients with nausea who may not know how much they will eat, postprandial rapid-acting insulin dosing may be worth trying. Similarly, patients on peritoneal dialysis obtain large amounts of calories from their dialysis fluid and often eat less than they might expect so that postprandial dosing may be helpful for them also.
The short-acting insulin available is regular crystalline insulin, which has an onset of action at 30—60 min, peak action at 2—3 h and duration up to 5—8 h.
Regular insulin should ideally be given 30 min prior to a meal. The main advantage of regular insulin is its substantially lower cost compared to the rapid-acting analogs.
The available intermediate-acting insulin is isophane, or NPH. It has an onset of action at 2—4 h, peak concentration at 4—10 h and duration up to 10—18 h. In order to achieve adequate basal coverage, it is dosed twice daily.
Its use can be limited by its highly variable absorption. Its cost is similar to that of Regular insulin. The long-acting insulin analogs are glargine and detemir. Glargine has an onset of action at 2—4 h, with minimal peak and duration of 20—24 h; it is usually dosed once daily.
A unique property of glargine is that it does not have a clear peak. Detemir has an onset of action at 1—3 h, with a small peak at 6—8 h and duration of action of 18—22 h. Detemir is dosed twice daily to give adequate basal coverage in type 1 diabetes; in type 2 diabetes, once daily dosing sometimes is sufficient.
There are various premixed preparation of insulin that have a fixed percentage of an intermediate-acting and a rapid-or short-acting insulin. Because they contain a combination of 2 insulins, they have two separate peaks.
These preparations offer convenience for the patient with twice daily dosing but offer less flexibility and more restrictions in titration of the insulin. It must be taken at fixed times and the patient must have consistent meals. The high concentration of U insulin alters the properties of regular insulin so its pharmacokinetics are different.
It has a similar onset of action, near 30 min, but the peak is at 4—8 h and duration is 14—15 h. It can be given up to 30 min prior to meals and is typically given two to three times daily, without the use of a basal insulin [ 27 ].
It is generally used in patients who are severely insulin resistant and can be used as a subcutaneous injection or in a pump. Metformin increases insulin sensitivity and decreases hepatic gluconeogenesis; it does not cause hypoglycemia and may lead to weight loss in some patients.
It reduces A1c by 1. The most common side effects are diarrhea, bloating and cramping. Vitamin B12 deficiency has been reported with extended use [ 29 ].
: Insulin and kidney function| Key Points | Kidnet De Cosmo; E-mail: sdecosm tin. Renal gluconeogenesis is decreased in advanced Managing dietary restrictions Insulin and kidney function Nad, resulting in decreased glucose Indulin hepatic gluconeogenesis is relatively normal to adn in view of the significantly increased plasma Insupin Insulin and kidney function. Glucose metabolism is stimulated by food intake, which simultaneously leads functioon increased beta-cell insulin production and decreased glucagon secretion by the alpha cells; these processes maintain serum glucose levels at a normal range. ENPP1 Q variant, increased pulse pressure and reduced insulin signaling, and nitric oxide synthase activity in endothelial cells. National Institute of Diabetes and Digestive and Kidney Diseases: Diabetic Kidney Disease. com General enquiries: ORSupport springernature. It is commonly assumed that the marked decrease in insulin requirement in some patients with diabetes and advanced CKD is essentially attributable to decreased clearance of insulin by the diseased kidneys, resulting in prolongation of circulating insulin half-life. |
| Diabetes and Kidney Disease (Stages ) | National Kidney Foundation | Kidnye Healthy eating schedule Controversies Conference proposed a change Insulin and kidney function the FDA guidelines [ Healthy eating schedule ]. Chantrel F Insylin, Sissoko HKépénékian LSmagala Warrior diet balanced lifestyleInsulih LImhoff OSerb IndulinFnuction DDorey KidneuKrummel TLe Floch JPKessler L. Sulfonylureas and their metabolites are renally cleared, leading to an increased risk of hypoglycemia as GFR declines. This Feature Is Available To Subscribers Only Sign In or Create an Account. Furthermore, through exaggerated stimulation of sympathetic nervous system activity and renal sodium reabsorption, hyperinsulinaemia increases glomerular capillary pressure and protein traffic, thus further contributing to renal damage. Article CAS PubMed PubMed Central Google Scholar Lenzen S, Drinkgern J, Tiedge M. Lancet— |
| Carbohydrate and insulin metabolism in chronic kidney disease - UpToDate | Diabetes 25 , 90—95 The Diabetes Control and Complications Trial Research Group. Article CAS Google Scholar Accili, D. Article CAS Google Scholar. Molecular mechanisms underlining the direct deleterious effect of insulin resistance on kidney function are only partially unravelled. Insulin sensitivity measured with Euglycemic clamp is independently associated with glomerular filtration rate in a community-based cohort. |
| RELATED TOPICS | Your blood pressure may get too high. As a person with diabetes, you should have your blood, urine, and blood pressure checked at least once a year. This will lead to better control of your disease and early treatment of high blood pressure and kidney disease. Maintaining control of your diabetes can lower your risk of developing severe kidney disease. As your kidneys fail, your blood urea nitrogen BUN levels will rise as well as the level of creatinine in your blood. You may also experience. You may find you need less insulin. This is because diseased kidneys cause less breakdown of insulin. If you develop any of these signs, call your doctor. The kidney doctor, called a nephrologist, will plan your treatment with you, your family and your dietitian. Two things to keep in mind for keeping your kidneys healthy are controlling high blood pressure in conjunction with an ACE inhibitor and following your renal diabetic diet. Restricting protein in your diet also might be helpful. You and your dietitian can plan your diet together. End-stage renal failure, or kidney failure, occurs when your kidneys are no longer able to support you in a reasonably healthy state, and dialysis or transplantation is needed. This happens when your kidneys function at only 10 to 15 percent. Three types of treatment can be used once your kidneys have failed: kidney transplantation, hemodialysis, and peritoneal dialysis. Learn more about treatment options for kidney failure. Once you get a new kidney, you may need a higher dose of insulin. Your appetite will improve so your new kidney will break down insulin better than your injured one. You will use steroids to keep your body from rejecting your new kidney. If your new kidney fails, dialysis treatment can be started while you wait for another kidney. Learn more about kidney transplant. Sometimes it is possible to perform a pancreas transplant along with a kidney transplant. Your doctor can advise you about this possibility. Today, more and more research dollars are spent on diabetes research. Hopefully, the prevention and cure of diabetes are in the future. If you would like more information, please contact NKF Cares. All rights reserved. This material does not constitute medical advice. It is intended for informational purposes only. Please consult a physician for specific treatment recommendations. Diabetes and Chronic Kidney Disease Basics: Part 1. Give Hope. Fund Answers. End Kidney Disease. Skip to main content. You are here Home » A to Z » Diabetes - A Major Risk Factor for Kidney Disease. Diabetes - A Major Risk Factor for Kidney Disease. English Español. Table of Contents What is diabetes? Are there different types of diabetes? What does diabetes do to the kidneys? How many people with diabetes will develop kidney disease? What are the early signs of kidney disease in patients with diabetes? What are the late signs of kidney disease in people with diabetes? What will happen if my kidneys have been damaged? The kidneys remove waste and extra fluid from the blood through filtering units called nephrons. Each nephron contains a filter, called a glomerulus. Each filter has tiny blood vessels called capillaries. When blood flows into a glomerulus, tiny bits, called molecules, of water, minerals and nutrients, and wastes pass through the capillary walls. Large molecules, such as proteins and red blood cells, do not. The part that's filtered then passes into another part of the nephron called the tubule. The water, nutrients and minerals the body needs are sent back to the bloodstream. The extra water and waste become urine that flows to the bladder. The kidneys have millions of tiny blood vessel clusters called glomeruli. Glomeruli filter waste from the blood. Damage to these blood vessels can lead to diabetic nephropathy. The damage can keep the kidneys from working as they should and lead to kidney failure. Over time, diabetes that isn't well controlled can damage blood vessels in the kidneys that filter waste from the blood. This can lead to kidney damage and cause high blood pressure. High blood pressure can cause more kidney damage by raising the pressure in the filtering system of the kidneys. Diabetic nephropathy kidney disease care at Mayo Clinic. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. Check out these best-sellers and special offers on books and newsletters from Mayo Clinic Press. This content does not have an English version. This content does not have an Arabic version. Overview Diabetic nephropathy is a serious complication of type 1 diabetes and type 2 diabetes. How kidneys work. Request an appointment. Healthy kidney vs. diseased kidney Enlarge image Close. diseased kidney A typical kidney has about 1 million filtering units. Kidney cross section Enlarge image Close. Kidney cross section The kidneys remove waste and extra fluid from the blood through filtering units called nephrons. By Mayo Clinic Staff. Show references Diabetic kidney disease. National Institute of Diabetes and Digestive and Kidney Diseases. Accessed May 24, Diabetic kidney disease adult. Mayo Clinic; Mottl AK, et al. Diabetic kidney disease: Manifestations, evaluation, and diagnosis. Diabetes and chronic kidney disease. Centers for Disease Control and Prevention. Diabetic nephropathy. Merck Manual Professional Version. Goldman L, et al. Diabetes mellitus. In: Goldman-Cecil Medicine. Elsevier; Elsevier Point of Care. Clinical Overview: Diabetic nephropathy. De Boer IH, et al. Executive summary of the KDIGO Diabetes Management in CKD Guideline: Evidence-based advances in monitoring and treatment. Kidney International. Office of Patient Education. Chronic kidney disease treatment options. Coping effectively: A guide for patients and their families. National Kidney Foundation. Robertson RP. Pancreas and islet cell transplantation in diabetes mellitus. Accessed May 25, Ami T. Allscripts EPSi. Mayo Clinic. June 27, |
| Introduction | Each kidney is made up of millions of tiny filters called nephrons. Many people with diabetes also develop high blood pressure , which can damage kidneys too. You can help keep your kidneys healthy by managing your blood sugar, blood pressure, and cholesterol levels. This is also very important for your heart and blood vessels—high blood sugar, blood pressure, and cholesterol levels are all risk factors for heart disease and stroke. If you have prediabetes, taking action to prevent type 2 diabetes is an important step in preventing kidney disease. You can do that by eating healthier and getting minutes of physical activity each week. Find a program in your community or online. Skip directly to site content Skip directly to search. Español Other Languages. Diabetes and Chronic Kidney Disease Español Spanish Print. Minus Related Pages. Kidney Facts. Kidney diseases are the 9th leading cause of death in the United States. Spoto B, Leonardis D, Parlongo RM, et al. Plasma cytokines, glomerular filtration rate and adipose tissue cytokines gene expression in chronic kidney disease CKD patients. Nutr Metab Cardiovasc Dis. Wassmann S, Stumpf M, Strehlow K, et al. Interleukin-6 induces oxidative stress and endothelial dysfunction by overexpression of the angiotensin II type 1 receptor. Circ Res. Kaneto H, Xu G, Fujii N, Kim S, Bonner-Weir S, Weir GC. J Biol Chem. Gassaway BM, Petersen MC, Surovtseva YV, et al. PKCε contributes to lipid-induced insulin resistance through cross talk with p70S6K and through previously unknown regulators of insulin signaling. Proc Natl Acad Sci. Senn JJ, Klover PJ, Nowak IA, Mooney RA. Interleukin-6 induces cellular insulin resistance in hepatocytes. Lagathu C, Bastard J-P, Auclair M, Maachi M, Capeau J, Caron M. Chronic interleukin-6 IL-6 treatment increased IL-6 secretion and induced insulin resistance in adipocyte: prevention by rosiglitazone. Biochem Biophys Res Commun. 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Relation between antioxidant enzyme gene expression and antioxidative defense status of insulin-producing cells. Drews G, Krippeit-drews P, Düfer M. Oxidative stress and beta-cell dysfunction. Pflugers Arch - Eur J Physiol. Koppe L, Nyam E, Vivot K, et al. Urea impairs β cell glycolysis and insulin secretion in chronic kidney disease. J Clin Invest. Betônico CCR, Titan SMO, Correa-Giannella MLC, Nery M, Queiroz M. Management of diabetes mellitus in individuals with chronic kidney disease: therapeutic perspectives and glycemic control. Clinics Sao Paulo. Article Google Scholar. Lubowsky ND, Siegel R, Pittas AG. Management of glycemia in patients with diabetes mellitus and CKD. Snyder RW, Berns JS. Reviews: use of insulin and Oral hypoglycemic medications in patients with diabetes mellitus and advanced kidney disease. Semin Dial. Article PubMed Google Scholar. Cersosimo E, Garlick P, Ferretti J. Renal substrate metabolism and gluconeogenesis during hypoglycemia in humans. Legouis D, Faivre A, Cippà PE, de Seigneux S. Renal gluconeogenesis: an underestimated role of the kidney in systemic glucose metabolism. Nephrol Dial Transplant. Gerich JE, Meyer C, Woerle HJ, Stumvoll M. Renal gluconeogenesis: its importance in human glucose homeostasis. Alsahli M, Gerich JE. Hypoglycemia, chronic kidney disease, and diabetes mellitus. Mayo Clin Proc. Busch M, Lehmann T, Wolf G, Günster C, Müller UA, Müller N. Antidiabetic therapy and rate of severe Hypoglycaemia in patients with type 2 diabetes and chronic kidney disease of different stages - a follow-up analysis of health insurance data from Germany. Exp Clin Endocrinol Diabetes. Moen MF, Zhan M, Hsu VD, et al. Frequency of hypoglycemia and its significance in chronic kidney disease. McCoy RG, Van Houten HK, Ziegenfuss JY, Shah ND, Wermers RA, Smith SA. Increased mortality of patients with diabetes reporting severe hypoglycemia. Davis SN, Duckworth W, Emanuele N, et al. Effects of severe hypoglycemia on cardiovascular outcomes and death in the veterans affairs diabetes trial. Lee Y-L, Yen S-J, Shin S-J, Huang Y-C, He JS, Lin K-D. Severe hypoglycemia as a predictor of end-stage renal disease in type 2 diabetes: a National Cohort Study. Int J Environ Res Public Health. Article CAS PubMed Central Google Scholar. Lacy ME, Gilsanz P, Eng C, Beeri MS, Karter AJ, Whitmer RA. Severe hypoglycemia and cognitive function in older adults with type 1 diabetes: the study of longevity in diabetes SOLID. Download references. The VA Informatics and Computing Infrastructure VINCI provided access to the national VA database, SQL, SAS and Stata programs. This study does not represent the views of the U. Department of Veterans Affairs or the United States Government. Statistical analyses and preparation of this manuscript were funded by grants to SB from Veterans Administration Office of Rural Health VA ORH , National Institute of Diabetes, Digestive and Kidney Diseases R01DK and National Heart, Lung and Blood Institute R21HL University of Washington School of Medicine, Seattle, Washington, USA. Study Design and Biostatistics Center, University of Utah Health Sciences, Salt Lake City, UT, USA. Medical Service, Veterans Affairs Salt Lake City Health Care System, Salt Lake City, UT, USA. Department of Internal Medicine, Division of Endocrinology, University of Utah Health Sciences, Salt Lake City, UT, USA. University of Utah Health Sciences, Wakara Way Suite , Salt Lake City, UT, , USA. You can also search for this author in PubMed Google Scholar. DG was a major contributor in writing of the manuscript. GW and RB analyzed and interpreted the patient data. NA, NZ, VG, JC, and DS were contributors in writing and editing the manuscript. SB contributed to writing the manuscript and designing the research. The author s read and approved the final manuscript. Correspondence to Srinivasan Beddhu. Research was conducted in accordance with the Declaration of Helsinki and has been approved by the University of Utah Institutional Review Board. We obtained a waiver of informed consent from the University of Utah Institutional Review Board because this study was a retrospective chart review. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. ICD-9 codes used to define medical conditions. Supplemental Figure 1. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions. Grube, D. et al. Insulin use in chronic kidney disease and the risk of hypoglycemic events. BMC Nephrol 23 , 73 Download citation. Received : 25 August The contribution of kidney metabolism is enhanced in diabetic subjects receiving exogenous insulin since injected insulin enters the systemic circulation directly, without first passing through the liver. Why UpToDate? Product Editorial Subscription Options Subscribe Sign in. Learn how UpToDate can help you. Select the option that best describes you. View Topic. Font Size Small Normal Large. Carbohydrate and insulin metabolism in chronic kidney disease. Formulary drug information for this topic. No drug references linked in this topic. Find in topic Formulary Print Share. View in. 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