Recommendation 2: The ACP recommends against testing for proteinuria in adults with or without diabetes who are currently taking an angiotensin-converting enzyme inhibitor or an angiotensin II-receptor blocker. (Grade: weak recommendation, low quality evidence)
This is an interesting recommendation and from a nephrologist's perspective, at first glance, it appears inappropriate but it should be remembered that these guidelines are not aimed at nephrologists but at primary care doctors and internists who are not dealing with patients who have frank nephrotic syndrome. This is similar in a way to the new guidelines for managing LDL cholesterol - there is no longer a specific target and regular monitoring of LDL is recommended only to demonstrate an appropriate response to therapy and compliance with treatment.
What is the evidence for UACR monitoring in patients with CKD. First of all, all patients with macroalbuminuria and all diabetics with microalbuminuria should unequivocally be on RAAS blockade unless there are contraindications. However, there are no trials demonstrating that targeting a specific level of proteinuria or that regularly monitoring proteinuria improves outcomes. With the recent demise of double RAAS blockade, it could be argued that once an individual is maximized on a single drug, regular checks of UACR are not going to alter therapy anyway.
That said, I do feel that there is value in rechecking UACR levels in patients on therapy. The ONTARGET Study showed very nicely that response to therapy was an excellent predictor of long term outcomes. A greater than twofold increase in albuminuria from baseline to 2 years despite therapy was associated with a 50% increase risk of mortality and a 40% increased risk of ESRD or doubling of creatinine. In contrast, a twofold decrease in UACR was associated with a 15% decrease in mortality and a 25% decrease in renal outcomes. Thus, periodic measurement of the UACR, despite its faults, provides important prognostic information.
The UACR is a surrogate marker and as a result it is suboptimal but if we learned anything from the Bardoxolone saga, it was that we should not ignore increasing albuminuria as a signal of adverse outcomes. As I said, this guideline was aimed at PCPs and it can certainly be argued that checking the UACR at every visit will not be enormously beneficial in that setting, particularly in patients with minimal albuminuria and early stage CKD. However, I don't think nephrologists will stop checking the UACR anytime soon, or stop seeing its value. However, I would agree that we do not know for certain what to do with an increasing UACR in a patient on maximal ACE/ARB therapy or what level we should be targeting. I would score this one 0.5/1 (total so far, 1.5/2)
This is an interesting recommendation and from a nephrologist's perspective, at first glance, it appears inappropriate but it should be remembered that these guidelines are not aimed at nephrologists but at primary care doctors and internists who are not dealing with patients who have frank nephrotic syndrome. This is similar in a way to the new guidelines for managing LDL cholesterol - there is no longer a specific target and regular monitoring of LDL is recommended only to demonstrate an appropriate response to therapy and compliance with treatment.
What is the evidence for UACR monitoring in patients with CKD. First of all, all patients with macroalbuminuria and all diabetics with microalbuminuria should unequivocally be on RAAS blockade unless there are contraindications. However, there are no trials demonstrating that targeting a specific level of proteinuria or that regularly monitoring proteinuria improves outcomes. With the recent demise of double RAAS blockade, it could be argued that once an individual is maximized on a single drug, regular checks of UACR are not going to alter therapy anyway.
That said, I do feel that there is value in rechecking UACR levels in patients on therapy. The ONTARGET Study showed very nicely that response to therapy was an excellent predictor of long term outcomes. A greater than twofold increase in albuminuria from baseline to 2 years despite therapy was associated with a 50% increase risk of mortality and a 40% increased risk of ESRD or doubling of creatinine. In contrast, a twofold decrease in UACR was associated with a 15% decrease in mortality and a 25% decrease in renal outcomes. Thus, periodic measurement of the UACR, despite its faults, provides important prognostic information.
The UACR is a surrogate marker and as a result it is suboptimal but if we learned anything from the Bardoxolone saga, it was that we should not ignore increasing albuminuria as a signal of adverse outcomes. As I said, this guideline was aimed at PCPs and it can certainly be argued that checking the UACR at every visit will not be enormously beneficial in that setting, particularly in patients with minimal albuminuria and early stage CKD. However, I don't think nephrologists will stop checking the UACR anytime soon, or stop seeing its value. However, I would agree that we do not know for certain what to do with an increasing UACR in a patient on maximal ACE/ARB therapy or what level we should be targeting. I would score this one 0.5/1 (total so far, 1.5/2)
I think what we should be doing in the face of increasing albuminuria is preparing the patient for the possibility of ESRD. The biggest problem in CKD 3 care is selecting the patients that will have a bad outcome from those who will have no meaningful renal outcome (i.e. die of cardiovascular disease). Increasing albuminuria is one powerful clue to the patients that will have this meaningful outcome.
ReplyDeleteAgree completely. It is an important marker of outcome that should not be ignored. This is missed completely in the guideline.
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