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SummaryBackground and objectives Insulin resistance is a complication of advanced CKD. Insulin resistance is less well characterized in earlier stages of CKD. The response of the pancreatic b cell, effects on glucose tolerance, and risk of diabetes are not clear.Design, setting, participants, & measurements The Cardiovascular Health Study included 4680 adults without baseline diabetes. The Chronic Kidney Disease Epidemiology Collaboration creatinine equation was used to obtain the estimated GFR (eGFR). Insulin resistance was evaluated as fasting insulin concentration. The insulin sensitivity index, b cell function, and glucose tolerance were assessed by oral glucose tolerance testing. Incident diabetes was defined as fasting glucose $126 mg/dl, nonfasting glucose $200 mg/dl, or use of glucose-lowering medications.Results Mean age was 72.5 years (range, 65-98 years). Mean eGFR was 72.2 (SD 17.1) ml/min per 1.73 m 2 . After adjustment, each 10 ml/min per 1.73 m 2 lower eGFR was associated with a 2.2% higher fasting insulin concentration (95% confidence interval [CI], 1.4%, 2.9%; P,0.001) and a 1.1% lower insulin sensitivity index (95% CI, 0.03%, 2.2%; P=0.04). Surprisingly, eGFR was associated with an augmented b cell function index (P,0.001), lower 2-hour glucose concentration (P=0.002), and decreased risk of glucose intolerance (P=0.006). Over a median 12 years' follow-up, 437 participants (9.3%) developed diabetes. eGFR was not associated with the risk of incident diabetes.Conclusions Among older adults, lower eGFR was associated with insulin resistance. However, with lower eGFR, b cell function was appropriately augmented and risks of impaired glucose tolerance and incident diabetes were not increased.

IntroductionComplications associated with insulin treatment for hyperkalemia are serious and common. We hypothesize that, in chronic kidney disease (CKD) and end-stage renal disease (ESRD), giving 5 units instead of 10 units of i.v. regular insulin may reduce the risk of causing hypoglycemia when treating hyperkalemia.MethodsA retrospective quality improvement study on hyperkalemia management (K+ ≥ 6 mEq/l) from June 2013 through December 2013 was conducted at an urban emergency department center. Electronic medical records were reviewed, and data were extracted on presentation, management of hyperkalemia, incidence and timing of hypoglycemia, and whether treatment was ordered as a protocol through computerized physician order entry (CPOE). We evaluated whether an educational effort to encourage the use of a protocol through CPOE that suggests the use of 5 units might be beneficial for CKD/ESRD patients. A second audit of hyperkalemia management from July 2015 through January 2016 was conducted to assess the effects of intervention on hypoglycemia incidence.ResultsTreatments ordered using a protocol for hyperkalemia increased following the educational intervention (58 of 78 patients [74%] vs. 62 of 99 patients [62%]), and the number of CKD/ESRD patients prescribed 5 units of insulin as per protocol increased (30 of 32 patients [93%] vs. 32 of 43 [75%], P = .03). Associated with this, the incidence of hypoglycemia associated with insulin treatment was lower (7 of 63 patients [11%] vs. 22 of 76 patients [28%], P = .03), and there were no cases of severe hypoglycemia compared to the 3 cases before the intervention.ConclusionEducation on the use of a protocol for hyperkalemia resulted in a reduction in the number of patients with severe hypoglycemia associated with insulin treatment.

Purpose of review Insulin resistance is a known complication of end-stage renal disease that also appears to be present in earlier stages of chronic kidney disease (CKD). It is a risk factor for cardiovascular disease and an important potential therapeutic target in this population. Measurement of insulin resistance is reviewed in the context of known pathophysiologic abnormalities in CKD. Recent findings Insulin resistance in CKD is due to a high prevalence of known risk factors (e.g. obesity) and to unique metabolic abnormalities. The site of insulin resistance in CKD is localized to skeletal muscle. Estimates based on fasting insulin concentration may not adequately capture insulin resistance in CKD because they largely reflect hepatic defects and because CKD impairs insulin catabolism. A variety of dynamic tests are available to directly measure insulin-mediated glucose uptake. Summary Insulin resistance may be an important therapeutic target in CKD. Complementary methods are available to assess insulin resistance, and each method has unique advantages, disadvantages, and levels of complexity. These characteristics, and the likelihood that CKD alters the performance of some insulin resistance measurements, must be considered when designing and interpreting clinical studies.

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