October 22nd, 2013

No Support for Broad Screening of Chronic Kidney Disease

Although taught in  medical school and widely used in clinical practice, broad screening of otherwise healthy people for chronic kidney disease (CKD) is unwarranted, according to new recommendations from the American College of Physicians published in the Annals of Internal Medicine. People with early kidney disease, who are classified as having stages 1 to 3 CKD, usually do not have symptoms and are generally diagnosed with laboratory tests or imaging.

The authors of “Screening, Monitoring, and Treatment of Stage 1-3 Chronic Kidney Disease” discuss the paucity of evidence in the field and highlight the absence of randomized, controlled trials evaluating the risks and benefits of screening for CKD or evaluating the sensitivity and specificity of screening tests.

“There is no evidence that evaluated the benefits of screening for stage 1-3 chronic kidney disease,” said Molly Cooke, ACP President, in a press release. “The potential harms of all the screening tests — false positives, disease labeling, and unnecessary treatment and associated adverse effects — outweigh the benefits.”

Although people with diabetes, hypertension, and cardiovascular disease are at higher risk for CKD, there is no evidence that shows that the benefits of screening outweighs the risks in people with these conditions, according to the document. The recommendations also state that people taking ACE inhibitors or ARBs do not need to be tested for proteinuria.

People who have hypertension and early stage CKD should take either an ACE inhibitor or an ARB. People with CKD who have elevated LDL cholesterol should take a statin. The benefits of these drugs have been demonstrated in clinical trials, though there are no proven differences between ACE inhibitors and ARBs, and the combination of an ACE inhibitor and an ARB increases the risk of adverse events.

The authors also recommended against periodic laboratory monitoring tests of people with early-stage CKD. “Ordering lab tests is not going to have any impact on clinical outcomes of asymptomatic patients with CKD without risk factors but will add unnecessary costs to the health care system due to increased medical visits and unnecessary tests,” said  Cooke.


One Response to “No Support for Broad Screening of Chronic Kidney Disease”

  1. Vimal Ramjee, MD says:

    Interesting post Larry.

    I don’t think these guidelines really change much in my clinical practice and I’m curious to know what others think..

    The authors do a nice job summarizing the data – clearly pointing out the lack of any randomized control trial data assessing benefits / harms of routine screening for stage I-III CKD in adults. The lack of RCTs in this area is interesting in and of itself. Without ESRD as a “hard” direct cause of mortality – thanks to renal replacement therapies (i.e. HD) – I wonder if there is just no financial incentive for therapeutic strategies, which is what ultimately drives RCTs.

    With that said, the authors conclude their document with four summation recommendations, albeit with “weak” strength per their own assessment –

    (1) Don’t screen asymptomatic adults who have no risk factors

    They state: “There was no randomized trial evidence evaluating the effectiveness of treatment on clinical outcomes of CKD identified through screening.” I don’t really get why this matters. The treatment of CKD on outcomes is not something in my mind that needs to be objectively proven at this point. We have good evidence that patients who have CKD or ESRD for that matter, do worse than those who do not (higher rates of mortality, CV disease, infection, etc.). Whether or not treatment has been formally tested to demonstrate a tangible benefit is irrelevant since this benefit is implicit in our daily practice. We have a pathologic process (i.e. CKD or ESRD) and there is a proven therapy to curb progression (i.e. ACEi, ARB). We know that patients without CKD do better than those who have it, and that those with CKD do better than those with ESRD – we see it every day in our clinical practice, and while there is no randomized trial data that speaks to this, we have observational and registry level data that does. With that said, I would agree that their is no need to screen asymptomatic adults who do not have risk factors.

    (2) Don’t test for proteinuria in adults on an ACEi or ARB

    More controversial – whether or not a patient on standard-of-care therapy has any meaningful progression or regression of proteinuria is difficult for multiple reasons. Factors including but not limited to other drugs that may modulate actual protein filtration, other drugs that may modulate the levels of renal markers, nutritional level (i.e. albumin), muscle mass (i.e. albumin) confound the trajectory of renal markers (including protein levels) thereby making it a difficult to follow renal function. It is helpful to know whether or not a patient has proteinuria (or microalbuminuria) at baseline, but I would favor not trending this parameter for the above reasons.

    (3) Start an ACEi or ARB in adults with HTN + CKD (I-III)

    I do this as I’m sure most physicians do (contraindications aside).

    (4) Start a statin in adults with high LDL + CKD (I-III)

    I do this so long as the LDL-C level is above the target goal (generally, < 100 mg/dL) and therapeutic lifestyle adjustments have been addressed.

    I believe a dominant portion of their data shows no difference or no reduced risk of disease with a number of cornerstone therapies (in the hypertension, hyperlipidemia, CV arenas), largely because the substrate they are testing is of high variance. In other words, creatinine is a poor surrogate of dynamic renal function by a number of standards. It follows renal insult by a lag of up to 2 to 3 days, it covaries with a myriad of other high-fluctuating factors (mentioned above), and there is a growing effort to replace it with something better. Also, we bin patients with CKD into GFR ranges using a number of different equations to estimate filtration rates – each of which vary in their output. Without much more refined markers of disease and renal function, we may very well be missing a real benefit of some of these therapies in studies.

    I would argue that the benefits of therapy, although not proven in a trial, are time-tested and have gained their own track record in the practice of medicine. Importantly, the knowledge of renal insufficiency by itself modifies the manner in which we handle each patient – considering everything from potential harms that we may inflict, concurrent therapeutic strategies (i.e. use of an ACEi in hypertensive patients), less contrast for an imaging modality, to preventive interventions (i.e. fluid pre-loading) is something that all of us can attest to.

    Knowing about CKD or ESRD is very important in clinical practice, but I do believe that we need to work more on refining markers of renal injury, as well as markers of renal disease going forward.