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      Creatinine and cystatin C. There is a lack of studies that compare endogenous and exogenous GFR markers in ICU patients

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      Upsala Journal of Medical Sciences
      Informa Healthcare

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          Abstract

          Dear Sir, We appreciate the letter to the Editor by Dr Chia-Ter Chao regarding our article entitled ‘Significant differences when using creatinine, modification of diet in renal disease, or cystatin C for estimating glomerular filtration rate in ICU patients’ (1). Kidney function is a very important variable in intensive care patients, and we believe that this variable has not gained sufficient attention. We certainly agree with the statement that ‘both formulae will not suffice as good estimators of renal function in critically ill patients with acute kidney injury’. The problem is that these two markers are widely analyzed in intensive care patients and that the results are often used indiscriminately. We agree that both markers are subject to interference. However, we would like to question the comment that serum cystatin C level is confounded by inflammation status. Several studies have shown an association between inflammation and serum cystatin C levels, but this may be mediated by kidney damage induced by inflammation. We have in a recently published study shown that inflammation per se had no effect on cystatin C levels (2). We thank Dr Chia-Ter Chao for bringing up the effect of sampling time on creatinine and cystatin C results (3). This is an important aspect that we failed to mention in our original study. The sampling time may contribute to the differences, but we find the same differences between creatinine and cystatin C-estimated glomerular filtration rate (GFR) also in patients who have spent several days in the intensive care unit (ICU). The combination of creatinine-based and cystatin C-based results for estimation of GFR is an interesting approach. However, this strategy is probably most effective if there is a fair agreement between the two markers and the mean of the two estimates can be used. The problem in intensive care patients is that the differences between the two estimates are profound and that we do not know which of the markers is correct. We have tried to find comparisons in the literature between creatinine or cystatin C and iohexol or other exogenous GFR markers in intensive care patients. To our surprise, we were not able to find any such studies. We hope that UJMS readers will continue the discussion on the use of endogenous GFR markers. Hopefully, this discussion could also lead to the initiation of studies that compare creatinine/cystatin C with exogenous GFR markers in intensive care patients so that in the future we will know how we should interpret GFR results based on endogenous GFR markers.

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          Significant differences when using creatinine, modification of diet in renal disease, or cystatin C for estimating glomerular filtration rate in ICU patients

          Background Renal dysfunction is associated with increased morbidity and mortality in intensive care patients. In most cases the glomerular filtration rate (GFR) is estimated based on serum creatinine and the Modification of Diet in Renal Disease (MDRD) formula, but cystatin C-estimated GFR is being used increasingly. The aim of this study was to compare creatinine and MDRD and cystatin C-estimated GFR in intensive care patients. Methods Retrospective observational study was performed, on patients treated within the general intensive care unit (ICU) during 2004–2006, in a Swedish university hospital. Results GFR markers are frequently ordered in the ICU; 92% of the patient test results had cystatin C-estimated GFR (eGFRcystatinC) ≤ 80 mL/min/1.73 m2, 75% had eGFR ≤ 50 mL/min/1.73 m2, and 30% had eGFR ≤ 20 mL/min/1.73 m2. In contrast, only 46% of the patients had reduced renal function assessed by plasma creatinine alone, and only 47% had eGFRMDRD ≤ 80 mL/min/1.73 m2. The mean difference between eGFRMDRD and eGFRcystatinC was 39 mL/min/1.73 m2 for eGFRcystatinC values ≤ 60 mL/min/1.73 m2. Conclusions GFR is commonly assessed in the ICU. Cystatin C-estimated GFR yields markedly lower GFR results than plasma creatinine and eGFRMDRD. Many pharmaceuticals are eliminated by the kidney, and their dosage is adjusted for kidney function. Thus, the differences in GFR estimates by the methods used indicate that the GFR method used in the intensive care unit may influence the treatment.
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            Postsurgical inflammatory response is not associated with increased serum cystatin C values.

            Cystatin C is used both as a glomerular filtration (GFR) marker and a cardiovascular risk marker. There are several studies showing an association between cystatin C and inflammatory markers and it has been suggested that the inflammatory response in itself could result in elevated cystatin C levels. The aim of this study was to evaluate if an induced inflammatory response has an effect on cystatin C levels in humans. CRP and cystatin C were analyzed in serum samples from orthopedic surgery patients (n=29). The patients were sampled prior to surgery and four and thirty days after surgery. The surgery induced a pronounced CRP elevation on day four, median 137.3 (interquartile range 104.1-178.2) mg/L compared to 1.94 (1.20-8.70) mg/L before surgery, P<0.001, but no significant difference in cystatin C levels before and four and thirty days after surgery could be seen. The orthopedic surgery-induced inflammatory response does not cause changes in cystatin C levels. Copyright (c) 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
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              Creatinine and cystatin C: Shooting at a flying target

              Dear Sir, I read with great interest the article entitled ‘Significant differences when using creatinine, modification of diet in renal disease, or cystatin C for estimating glomerular filtration rate in ICU patients’ by Lipcsey et al. (1) in the March 2011 issue of the Upsala Journal of Medical Sciences. This article provides an interesting analysis of estimating renal function in critically ill patients, but I believe there are several aspects that may warrant further discussion: First of all, the equations estimating glomerular filtration rate (GFR) are all notoriously flawed in the setting of rapidly changing renal function, that is, acute kidney injury. The creatinine-based formula for creatinine clearance is shown to over-estimate renal function when actual GFR is low, due to its multiple interfering factors and tubular secretion nature, but the cystatin C-based formula is also affected by muscle mass and adiposity (2). To complicate things further, serum cystatin C level is confounded by inflammation status and corticosteroid use, both of which are frequently found in patients under critical care (3). With this in mind, we can presume that both formulae will not suffice as good estimators of renal function in critically ill patients with acute kidney injury, especially when patients are admitted with relative adrenal insufficiency or septic shock status. Second, the duration of illnesses and timing of tests are also not taken into consideration in Lipcsey's article. Nejat et al. in their multicenter observation study have indicated that cystatin C rises earlier than creatinine in patients with acute kidney injury by 4–5 hours from a general ICU population (4). Herget-Rosenthal et al. also demonstrated a lag time, on average one-and-a-half days, between cystatin C elevation and creatinine to the same level (5). In this sense, the significant difference between cystatin C and creatinine-estimated GFR in Lipcsey's results will be prominently influenced by the timing of blood tests. If intensivists elect to check renal markers earlier in the course of disease by hours or days, they will undoubtedly discover a sharp difference between actual and estimated renal function, while later tests will not. This is also reflected in the study by Endre et al., in which a biomarker for acute kidney injury achieves better predictability of outcome when it is tested earlier (6). Finally, is there any better way of determining renal function in the critically ill with convenient point-of-care feasibility? Tidman et al. in their study of GFR determination in chronic kidney disease patients have provided a new thought: combining creatinine-based and cystatin C-based results for estimation (7). Though this study focuses on patients with stable renal function, it may be worthwhile to extrapolate this finding to the critically ill ones. To target flying objects, we need to trace more accurately their path and take it with one shot.
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                Author and article information

                Journal
                Ups J Med Sci
                UPS
                Upsala Journal of Medical Sciences
                Informa Healthcare
                0300-9734
                2000-1967
                August 2011
                29 June 2011
                : 116
                : 3
                : 223
                Affiliations
                simpleDepartment of Medical Sciences, Clinical Chemistry , Uppsala University, Uppsala, Sweden
                Author notes
                Correspondence: Anders Larsson, simpleDepartment of Medical Sciences, Clinical Chemistry , Uppsala University, S-751 85 Uppsala, Sweden. +46-18-552562. anders.larsson@ 123456akademiska.se
                Article
                UPS_A_578763_O
                10.3109/03009734.2011.578763
                3128730
                5d9b0126-44aa-4092-bb53-66986d55e9f9
                © Upsala Medical Society

                This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited.

                History
                : 01 April 2011
                : 01 April 2011
                Categories
                Letter to the Editor

                Medicine
                Medicine

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