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2008 Clinical Practice Guidelines - Canadian Diabetes Association

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<strong>2008</strong> CLINICAL PRACTICE GUIDELINES<br />

S130<br />

RECOMMENDATIONS<br />

1.The best possible glycemic control and, if necessary, intensive<br />

diabetes management should be instituted in people<br />

with type 1 or type 2 diabetes for the prevention of onset<br />

and delay in progression to CKD [Grade A, Level 1A<br />

(34,71,72)].<br />

2. In adults, screening for CKD in diabetes should be conducted<br />

using a random ACR and a serum creatinine converted<br />

into an eGFR [Grade D, Consensus]. Screening<br />

should be performed annually in adults with type 1 diabetes<br />

of >5 years’ duration. Individuals with type 2 diabetes<br />

should be screened at diagnosis of diabetes and<br />

yearly thereafter. Screening should be delayed when causes<br />

of transient albuminuria or low eGFR are present<br />

[Grade D, Consensus].<br />

3. People with diabetes and CKD should have a random<br />

urine ACR and a serum creatinine converted into an eGFR<br />

performed at least every 6 months [Grade D, Consensus].<br />

4.Adults with diabetes and persistent albuminuria (ACR<br />

>2.0 mg/mmol in males, >2.8 mg/mmol in females) should<br />

receive an ACE inhibitor or an ARB to delay progression<br />

of CKD, even in the absence of hypertension [Grade A,<br />

Level 1A (37,39-42,47,48,50,51,73), for ACE inhibitor use in<br />

type 1 and type 2 diabetes, and for ARB use in type 2 diabetes;<br />

Grade D, Consensus, for ARB use in type 1 diabetes].<br />

5. People with diabetes on an ACE inhibitor or an ARB<br />

should have their serum creatinine and potassium levels<br />

checked within 1 to 2 weeks of initiation or titration of<br />

ney or severe bilateral disease (62,63). However, serum<br />

creatinine and potassium levels should be monitored carefully<br />

if these medications are used when renovascular disease<br />

is suspected (64).<br />

Individuals who develop mild to moderate hyperkalemia<br />

should receive nutritional counselling regarding a potassiumrestricted<br />

diet, and consideration should be given to the use<br />

of nonpotassium-sparing diuretics (such as thiazides or<br />

furosemide). If an ACE inhibitor or ARB is not tolerated due<br />

to severe hyperkalemia, or >30% increase in serum creatinine<br />

or allergic reactions, the drug should be withdrawn and other<br />

ACE inhibitors or ARBs should not be substituted.<br />

To avoid acute renal failure, ACE inhibitors, ARBs and<br />

diuretics should be stopped during acute illnesses associated<br />

with intravascular volume contraction. There is no upper<br />

limit of the serum creatinine level for initiation of ACE<br />

inhibitor or ARB therapy, but if the creatinine clearance is<br />

30% increase in serum<br />

creatinine within 3 months of starting an ACE inhibitor<br />

or ARB [Grade D, Consensus].<br />

should be given to stopping these drugs prior to conception.<br />

Individuals started on a non-DHP CCB should be monitored<br />

clinically for development of bradycardia. As all<br />

nephroprotective drugs are also antihypertensives, individuals<br />

should be monitored for development of hypotension.<br />

The role of proteinuria reduction<br />

The amount of proteinuria correlates with the likelihood of<br />

progression of many kidney diseases, including diabetic<br />

nephropathy (66-69). Individuals with an antiproteinuric<br />

response to an ACE inhibitor or an ARB are less likely to<br />

progress to renal failure (66).These findings, in combination<br />

with basic science evidence (70), suggest that proteinuria<br />

may contribute to kidney damage, and many clinicians now<br />

target proteinuria for reduction independent of BP level.<br />

However, no large-scale hard-endpoint trials in which proteinuria<br />

reduction was the primary intervention have been<br />

completed, and the role of proteinuria as a causative factor in<br />

renal damage remains controversial. Which populations<br />

should be targeted for reduction of proteinuria, the thresholds<br />

and targets for antiproteinuric therapies, and the optimal<br />

antiproteinuric drug regimens remain topics of active<br />

research. While reduction of proteinuria in diabetic<br />

nephropathy may be desirable, it is not possible to generate a<br />

clinical practice guideline in this area at this time.

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