Diabetes and CKD Guidelines Update

Phil Vinall

doi:10.1177/155989771210012

Summary

This article discusses the 2012 revisions to the National Kidney Foundation and Kidney Disease Outcomes Quality Initiative 2007 guidelines. Revisions were made in Guideline 2 (Management of Hyperglycemia and General Diabetes Care in Chronic Kidney Disease [CKD]), Guideline 4 (Management of Dyslipidemia in Diabetes and Chronic Kidney Disease), and Guideline 6 (Management of Albuminuria in Normotensive Patients With Diabetes).

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Rudy Bilous, MD, Newcastle University, Newcastle upon Tyne, United Kingdom, discussed the 2012 revisions to the National Kidney Foundation and Kidney Disease Outcomes Quality Initiative 2007 guidelines. Revisions were made in Guideline 2 (Management of Hyperglycemia and General Diabetes Care in Chronic Kidney Disease [CKD]), Guideline 4 (Management of Dyslipidemia in Diabetes and Chronic Kidney Disease), and Guideline 6 (Management of Albuminuria in Normotensive Patients With Diabetes). The guidance is expected to be published in the September/October 2012 issue of the American Journal of Kidney Diseases and will also be available online at http://www.kidney.org/professionals/KDOQI/index.cfm.

Revisions to Guideline 2:

2.1: A target HbA1C of ∼7.0% is recommended to prevent or delay progression of the microvascular complications of diabetes, including diabetic kidney disease
2.2: Treating patients at risk of hypoglycemia to an HbA1C target of <7.0% is not recommended
2.3: Target HbA1C should be extended above 7.0% in individuals with comorbidities or limited life expectancy and risk of hypoglycemia

These revisions were based on the lack of data that suggested true efficacy for glycemic control in kidney disease in patients with type 2 diabetes. Although observational studies suggest that better glycemic control leads to less risk of death and vascular disease in patients with type 2 diabetes [Selvin E et al. Diabetes 2011; DCCT/EDIC Research Group N Engl J Med 2011], randomized clinical trials in these patients did not detect clinically significant reductions in cardiovascular disease or mortality with very intensive glycemic control [Patel A et al. N Engl J Med 2008; Duckworth W et al. N Engl J Med 2009]. In a meta-analysis (n=27,769) that compared intensive (most with HbA1C <7%) with conventional glycemic control, investigators reported no statistically significant effect of intensive glycemic control on nephropathy [Hemmingsen B et al. BMJ 2011].

Revisions to Guideline 4:

4.1: Low-density lipoprotein-cholesterol (LDL-C)-lowering medicines, such as statins or statin/ezetimibe combinations, are recommended to reduce the risk of major atherosclerotic events in patients with diabetes and CKD, including those who have received a kidney transplant
4.2: Initiation of statin therapy in patients with diabetes who are treated by dialysis is not recommended.

These changes were based on a number of studies of diabetes and CKD that showed small to no effect of lipid lowering on glomerular filtration rate. In the Study of Heart and Renal Protection [SHARP; NCT00125593], reduction of LDL-C with statins reduced the incidence of major atherosclerotic events in patients with diabetes but had no effect on mortality [Baigent C et al. Lancet 2011]. These findings were the basis for the changes regarding statin therapy in the predialysis population (4.2).

Revisions to Guideline 6:

6.1: Use of an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) for the primary prevention of diabetic kidney disease in normotensive normoalbuminuric patients with diabetes is not recommended (1A)
6.2: Use of an ACE inhibitor or an ARB in normotensive patients with diabetes and albuminuria levels ≥30 mg/g who are at high risk of diabetic kidney disease or its progression is not recommended (2C)

Clinical evidence has failed to provide evidence that ACE inhibitors or ARBs can prevent the development of microalbuminuria in normotensive normoalbuminuric patients, but there are some signs that renin-angiotensin system (RAS) blockade may be effective in preventing the development of microalbuminuria in patients with type 2 diabetes. Prof. Bilous cautioned that the majority of the patients in all of the studies were hypertensive. In addition, there were varying levels of blood pressure control among the studies, with the studies achieving the best control being neutral in terms of any preventive effect. What the studies do tell us, Prof. Bilous said, is that “we need to manage blood pressure effectively in patients with type 2 diabetes, and while RAS blockade may be an important part of that blood pressure control, it may not be the RAS blockers per se that reduce albuminuria.”

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