Blog entry by Meguid El Nahas
PROFESSOR RICHARD GLASSOCK WROTE:
New NICE CKD Guidelines
On July 23, 2014 the National Institute for Health and Care Excellence (NICE) of the United Kingdom released its new 2014 guidance for Chronic Kidney Disease (CKD). This new version updates and revises guidance distributed in 2008.
NICE was one of the first to subdivide CKD Category 3 (eGFR 30-59ml/min/1.73m2) into Categories 3A (eGFR 45-59ml/min/1.73m2) and 3B (eGFR 30-44ml/min/1.73m2) and to add proteinuria (defined as a urinary albumin to creatinine ratio >30mg/mmol) using the KDOQI 2002 classification schema as its base. This new iteration is based extensively upon the 2013 KDIGO CKD classification system.
Many changes have been made and in the interest of space I will comment on only a few. It is worth reading the original at http://www.nice.org.uk/Guidance/CG182.
First, like KDIGO they have reduced the UACR threshold for CKD from 30mg/mmol to 3mg/mmol, embracing the controversial issue of isolated “microalbuminuria” as CKD. I do not happen to agree with this step; but it is generated from the KDIGO 2013 CKD classification system, without a well-reasoned rationale. Prospective studies demonstrating benefits compared to risk for using this threshold is currently lacking.
Second, they have adopted the CKD-EPI creatinine equation (using IDMS standardized serum creatinine values and after adjustments for black vs non-black race and gender) as the standard way of determining eGFR and suggest that all clinical laboratories (including those that are hospital-based based) utilize this equation when reporting eGFR. I have concerns in that the CKD-EPI equation was developed by epidemiologic studies primarily in clinically stable outpatients. The instability of hospital inpatients and the impact of acute and chronic illness on endogenous creatinine generation may make the CKD-EPI equation a less reliable and accurate tool in hospitalized patients, especially those in an ICU environment.
Third, like KDIGO the NICE guidance suggests that eGFR- cystatin C be used as a “confirmatory” test in the subset of subjects with an eGFR-creatinine of 45-59ml/min/1.73m2 who have an UACR of <3mg/mmol and that CKD NOT BE DIAGNOSED in such patients who have an eGFR-cystatin C of >60ml/min/1.73m2. Since eGFR- cystatin C is no more accurate a tool than eGFR- creatinine in providing an accurate estimate of true or measured GFR, any improved identification of CKD (based on prognosis rather than a departure from normality of GFR) is likely to be due to the non-GFR determinants of eGFR-creatinine and/or cystatin C bearing on adverse events, such as CV disease.
Fouth, the guidance suggests that “opportunistic screening” for CKD (presumably during encounters with the health care system), be offered to those at increased risk of CKD, regardless of age (such as diabetes, hypertension, CV disease, multisystem disease or a family history of CKD). Importantly, older age per se is not regarded as a sufficient reason for such testing. This differs dramatically form recommendation for US organization, such as the National Kidney Foundation. Wisely, NICE took no position on population-based screening for CKD--- a position generally agreed upon by other agencies such as the US Preventative Services Task Force.
Finally, and most disappointingly from my perspective, NICE did not suggest that the eGFR thresholds for defining CKD be age calibrated. This position is identical to that of KDIGO 2013 and both systems ignore the normal decay of renal function with organ senescence. This mistake, in my view, will lead to an ever-increasing prevalence of falsely defined CKD as the population ages, and will lead to unnecessary referrals and testing in the older adult without abnormal albuminuria. As stated previously and until more prospective interventional information is available, I prefer to define abnormal albuminuria as >30mg/mmol persisting for 3 months or more, but I fully recognize that this is a minority position at present.
Notwithstanding these criticism of the NICE 2014 guidance, the overall document is well-written in clear and easily understandable language. I agree with many things in the document, such as when to employ an accurate and precise measured GFR, use of reagent strips to define haematuria instead of urinary sediment, how to identify progression of CKD based on repeated eGFR determinations and not recommending low-protein diets (<0.6-0.8gg/kg/d) in patients with CKD, and scrupulously avoiding the use of combinations of RAS antagonists in people with CKD.
I am confident that these new guidance statements from the highly-regarded NICE organization will elicit an interesting and informative debate in the months ahead. I look forward to reading the comments of others in this BLOG space.
Richard J. Glassock, MD
Laguna Niguel, CA
July 29, 2014