2008 Clinical Practice Guidelines - Canadian Diabetes Association

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2008 CLINICAL PRACTICE GUIDELINES S130 RECOMMENDATIONS 1.The best possible glycemic control and, if necessary, intensive diabetes management should be instituted in people with type 1 or type 2 diabetes for the prevention of onset and delay in progression to CKD [Grade A, Level 1A (34,71,72)]. 2. In adults, screening for CKD in diabetes should be conducted using a random ACR and a serum creatinine converted into an eGFR [Grade D, Consensus]. Screening should be performed annually in adults with type 1 diabetes of >5 years’ duration. Individuals with type 2 diabetes should be screened at diagnosis of diabetes and yearly thereafter. Screening should be delayed when causes of transient albuminuria or low eGFR are present [Grade D, Consensus]. 3. People with diabetes and CKD should have a random urine ACR and a serum creatinine converted into an eGFR performed at least every 6 months [Grade D, Consensus]. 4.Adults with diabetes and persistent albuminuria (ACR >2.0 mg/mmol in males, >2.8 mg/mmol in females) should receive an ACE inhibitor or an ARB to delay progression of CKD, even in the absence of hypertension [Grade A, Level 1A (37,39-42,47,48,50,51,73), for ACE inhibitor use in type 1 and type 2 diabetes, and for ARB use in type 2 diabetes; Grade D, Consensus, for ARB use in type 1 diabetes]. 5. People with diabetes on an ACE inhibitor or an ARB should have their serum creatinine and potassium levels checked within 1 to 2 weeks of initiation or titration of ney or severe bilateral disease (62,63). However, serum creatinine and potassium levels should be monitored carefully if these medications are used when renovascular disease is suspected (64). Individuals who develop mild to moderate hyperkalemia should receive nutritional counselling regarding a potassiumrestricted diet, and consideration should be given to the use of nonpotassium-sparing diuretics (such as thiazides or furosemide). If an ACE inhibitor or ARB is not tolerated due to severe hyperkalemia, or >30% increase in serum creatinine or allergic reactions, the drug should be withdrawn and other ACE inhibitors or ARBs should not be substituted. To avoid acute renal failure, ACE inhibitors, ARBs and diuretics should be stopped during acute illnesses associated with intravascular volume contraction. There is no upper limit of the serum creatinine level for initiation of ACE inhibitor or ARB therapy, but if the creatinine clearance is 30% increase in serum creatinine within 3 months of starting an ACE inhibitor or ARB [Grade D, Consensus]. should be given to stopping these drugs prior to conception. Individuals started on a non-DHP CCB should be monitored clinically for development of bradycardia. As all nephroprotective drugs are also antihypertensives, individuals should be monitored for development of hypotension. The role of proteinuria reduction The amount of proteinuria correlates with the likelihood of progression of many kidney diseases, including diabetic nephropathy (66-69). Individuals with an antiproteinuric response to an ACE inhibitor or an ARB are less likely to progress to renal failure (66).These findings, in combination with basic science evidence (70), suggest that proteinuria may contribute to kidney damage, and many clinicians now target proteinuria for reduction independent of BP level. However, no large-scale hard-endpoint trials in which proteinuria reduction was the primary intervention have been completed, and the role of proteinuria as a causative factor in renal damage remains controversial. Which populations should be targeted for reduction of proteinuria, the thresholds and targets for antiproteinuric therapies, and the optimal antiproteinuric drug regimens remain topics of active research. While reduction of proteinuria in diabetic nephropathy may be desirable, it is not possible to generate a clinical practice guideline in this area at this time.
Referral Most people with CKD and diabetes will not require referral to a specialist in renal disease. However, specialist care may be necessary when renal dysfunction is severe, when there are difficulties implementing renal-protective strategies or when there are problems managing the sequelae of renal disease (see Recommendation #8). OTHER RELEVANT GUIDELINES Targets for Glycemic Control, p. S29 Identification of Individuals at High Risk of Coronary Events, p. S95 Vascular Protection in People With Diabetes, p. S102 Treatment of Hypertension, p. S115 Type 1 Diabetes in Children and Adolescents, p. S150 Diabetes and Pregnancy, p. S168 RELATED WEBSITES Canadian Hypertension Society. Available at http://www. hypertension.ca/chs. Accessed September 1, 2008. Canadian Society of Nephrology. Available at http://www. csnscn.ca. Accessed September 1, 2008. Nephron Information Center. Available at: http://www. nephron.com. Accessed September 1, 2008. REFERENCES 1. Canadian Institute for Health Information (CIHI). Canadian Organ Replacement Registry (CORR): 2001 Annual Report. Ottawa, ON: CIHI; 2001. 2. Warram JH, Gearin G, Laffel L, et al. Effect of duration of type I diabetes on the prevalence of stages of diabetic nephropathy defined by urinary albumin/creatinine ratio. J Am Soc Nephrol. 1996;7:930-937. 3. Reenders K, de Nobel E, van den Hoogen HJ, et al. Diabetes and its long-term complications in general practice: a survey in a well-defined population. Fam Pract. 1993;10:169-172. 4. Weir MR. Albuminuria predicting outcome in diabetes: incidence of microalbuminuria in Asia-Pacific Rim. Kidney Int. 2004;66(suppl 92):S38-S39. 5. Mathiesen ER, Ronn B, Storm B, et al. The natural course of microalbuminuria in insulin-dependent diabetes: a 10-year prospective study. Diabet Med. 1995;12:482-487. 6. Lemley KV,Abdullah I, Myers BD, et al. Evolution of incipient nephropathy in type 2 diabetes mellitus. Kidney Int. 2000;58: 1228-1237. 7. Gall MA, Nielsen FS, Smidt UM, et al. The course of kidney function in type 2 (non-insulin-dependent) diabetic patients with diabetic nephropathy. Diabetologia. 1993;36:1071-1078. 8. Jacobsen P, Rossing K,Tarnow L, et al. Progression of diabetic nephropathy in normotensive type 1 diabetic patients. Kidney Int. 1999;71(suppl):S101-S105. 9. Hasslacher C, Ritz E,Wahl P, et al. Similar risks of nephropathy in patients with type I or type II diabetes mellitus. Nephrol Dial Transplant. 1989;4:859-863. 10. Ballard DJ, Humphrey LL, Melton LJ, et al. Epidemiology of persistent proteinuria in type II diabetes mellitus. Populationbased study in Rochester, Minnesota. Diabetes. 1988;37:405- 412. 11. Winaver J,Teredesai P, Feldman HA, et al. Diabetic nephropathy as the mode of presentation of diabetes mellitus. Metabolism. 1979;28:1023-1030. 12. Middleton RJ, Foley RN, Hegarty J, et al. The unrecognized prevalence of chronic kidney disease in diabetes. Nephrol Dial Transplant. 2006;21:88-92. 13. Ruggenenti P, Gambara V, Perna A, et al. The nephropathy of non-insulin-dependent diabetes: predictors of outcome relative to diverse patterns of renal injury. J Am Soc Nephrol. 1998;9:2336-2343. 14. Gerstein HC, Mann JF,Yi Q, et al.Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286:421-426. 15. Gaede P, Vedel P, Parving HH, et al. Intensified multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: the Steno type 2 randomised study. Lancet. 1999;353:617-622. 16. VenkataRaman TV, Knickerbocker F, Sheldon CV. Unusual causes of renal failure in diabetics: two case studies. J Okla State Med Assoc. 1990;83:164-168. 17. Clinical path conference. Unusual renal complications in diabetes mellitus. Minn Med. 1967;50:387-393. 18. Amoah E, Glickman JL, Malchoff CD, et al. Clinical identification of nondiabetic renal disease in diabetic patients with type I and type II disease presenting with renal dysfunction. Am J Nephrol. 1988;8:204-211. 19. El-Asrar AM,Al-Rubeaan KA,Al-Amro SA, et al. Retinopathy as a predictor of other diabetic complications. Int Ophthalmol. 2001;24:1-11. 20. Ahn CW, Song YD, Kim JH, et al.The validity of random urine specimen albumin measurement as a screening test for diabetic nephropathy. Yonsei Med J. 1999;40:40-45. 21. Kouri TT, Viikari JS, Mattila KS, et al. Microalbuminuria. Invalidity of simple concentration-based screening tests for early nephropathy due to urinary volumes of diabetic patients. Diabetes Care. 1991;14:591-593. 22. Rodby RA, Rohde RD, Sharon Z, et al. The urine protein to creatinine ratio as a predictor of 24-hour urine protein excretion in type 1 diabetic patients with nephropathy. The Collaborative Study Group. Am J Kidney Dis. 1995;26:904-909. 23. Chaiken RL, Khawaja R, Bard M, et al. Utility of untimed urinary albumin measurements in assessing albuminuria in black NIDDM subjects. Diabetes Care. 1997;20:709-713. 24. Bakker AJ. Detection of microalbuminuria. Receiver operating characteristic curve analysis favors albumin-to-creatinine ratio over albumin concentration. Diabetes Care. 1999;22:307-313. 25. Gault MH, Longerich LL, Harnett JD, et al. Predicting glomerular function from adjusted serum creatinine. Nephron. 1992;62:249-256. 26. Bending JJ, Keen H, Viberti GC. Creatinine is a poor marker S131 COMPLICATIONS AND COMORBIDITIES
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2008 Clinical Practice Guidelines - Canadian Diabetes Association

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