Serum Creatinine as an Index of Renal Function: New Insights into Old Concepts

Perrone, Ronald D.; Madias, Nicolaos E.; Levey, Andrew S.

doi:10.1093/clinchem/38.10.1933

Cited by 1,347 publications

(736 citation statements)

References 124 publications

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“…Any compound used as an endogenous marker of glomerular filtration rate should be generated at a constant rate and be eliminated only by glomerular filtration [11]. Cystatin C (CysC) is an endogenous protease inhibitor that is produced in all nucleated cells [12] and seems to undergo extensive glomerular filtration [13].…”

Section: Introductionmentioning

confidence: 99%

A population pharmacokinetic model for cefuroxime using cystatin C as a marker of renal function

Viberg

Lannergård

Larsson

et al. 2006

Brit J Clinical Pharma

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AimsSince cefuroxime mainly is excreted by renal filtration, dosing is currently based on serum creatinine (Scr) or creatinine clearance (CLcr). However, it has been suggested that cystatin C (CysC) is superior to Scr as a marker of renal function. The aim of this prospective study was to develop a population model that describes the pharmacokinetics of cefuroxime and to investigate the usefulness of CysC as a covariate of the model parameters. MethodsNinety-seven patients were studied (CLcr range 6.5-115 ml min − 1 ). Blood samples ( n = 407) for the determination of cefuroxime were withdrawn according to a sparse data sampling schedule and analysed by liquid chromatography mass spectrometry. The population analysis was performed in NONMEM. ResultsA two-compartment model described the data well. The biomarkers Scr, CLcr and CysC were evaluated as covariates on clearance (CL). The model that included CysC generated the best fit. In the final population model CL was a function of CysC and body weight, whereas V 1 was only a function of body weight. Final parameter estimates (relative standard errors) were 6.00 (3.2%) l h − 1 , 11.4 (5.3%) l and 5.11 (11%) l for CL, V 1 and V 2 , respectively. ConclusionsBased on the results of the present study, and because CysC is practical to use in the clinic, it is suggested that individual dosing of cefuroxime may be based on CysC rather than on Scr or CLcr. Furthermore, our final population model may be useful as a tool when designing new dosing schedules for cefuroxime.

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Section: Introductionmentioning

confidence: 99%

A population pharmacokinetic model for cefuroxime using cystatin C as a marker of renal function

Viberg

Lannergård

Larsson

et al. 2006

Brit J Clinical Pharma

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“…Over the past three decades, however, many clinical findings have accumulated, suggesting that creatinine undergoes tubular secretion in addition to the glomerular filtration, and therefore the serum creatinine clearance (CL cre ) overestimates the GFR. [3][4][5][6][7][8] Levey et al reported that the secretory component of creatinine elimination could account for 10-40% of urinary creatinine excretion in healthy individuals. 5 In addition, Kabat-Koperska et al showed that the bias in renal function data estimated on the basis of creatinine clearance could be reduced by determining the clearance after the administration of cimetidine, bringing the GFR close to the value estimated by inulin clearance (81.8 ± 23.6 ml/min) (ref.…”

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confidence: 99%

Prediction of Fluoroquinolone-Induced Elevation in Serum Creatinine Levels: A Case of Drug–Endogenous Substance Interaction Involving the Inhibition of Renal Secretion

Imamura

Murayama

Okudaira

et al. 2010

Clin Pharmacol Ther

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The aim of this study was to examine the mechanism underlying the elevation in serum creatinine levels caused by a novel des-fluoro(6)-quinolone antibacterial agent, DX-619, in healthy subjects. hOCT2 showed a prominent uptake of creatinine (K(m) = 56.4 mmol/l) among renal organic ion transporters. DX-619 is a potent inhibitor of hOCT2 (K(i) = 0.94 micromol/l), hMATE1 (0.82 µmol/l), and hMATE2-K (0.10 micromol/l). The pharmacokinetic model involving the inhibition of hOCT2 (model 1), hOCT2, and MATE1 or MATE2-K (model 2) could predict the elevation in serum creatinine levels in individual subjects receiving DX-619. This assumes that a significant contribution of tubular secretion (59, 38, and 31%) and reabsorption ranged from 3-50, 4-30, and 5-21% in model 1, -2a (hOCT2/hMATE1), and -2b (hOCT2/hMATE2-K), respectively, for creatinine. In conclusion, DX-619, at its therapeutic dose, is able to inhibit hOCT2, hMATE1, and hMATE2-K, leading to a significant inhibition of tubular secretion of creatinine and consequently to elevation of serum creatinine levels.

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“…Creatinine clearance increased more than 45% is shown with green color. detection of early renal dysfunction [24,25]. Cystatin C is a 13 kD endogenous cysteine proteinase inhibitor and is produced by nucleated cells at a constant rate.…”

Section: Discussionmentioning

confidence: 99%

N‐Acetylcysteine in Preventing Contrast‐Induced Nephropathy Assessed by Cystatin C

Alioğlu

Saygı

Türk

et al. 2011

Cardiovascular Therapeutics

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SUMMARYAims: Prophylactic oral N-acetylcysteine (NAC) has been widely used for prevention of contrast-induced nephropathy (CIN). However, clinical studies have not been demonstrating this effect consistently because of evidence that NAC can alter serum creatinine levels without affecting glomerular filtration rate (GFR). We investigated NAC for the prevention of CIN by monitoring creatinine and cystatin C. Methods: We enrolled 113 patients (49 patients in NAC group and 64 patients in control group) with normal to subnormal GFR who were scheduled for cardiovascular procedures. Patients in NAC group receive acetylcysteine 600 mg twice a day, on the day before and on the day of cardiovascular procedure. All patients received a periprocedural intravenous infusion ("volume expansion") of 1 ml/kg/h with 0.45% saline for 24 h (12 h before and 12 h after exposure to contrast medium). Serum cystatin C and creatinine levels were measured before and at 12, 24, and 48 h after procedure. Results: The incidence of cystatin C-based CIN was 28.5% (n = 14) in NAC and 23.4% (n = 15) in control group (p = 0.663) and serum creatinine-based CIN was 12.2% (n = 6) in NAC and 17.2% (n = 11) in control group (P = 0.468). In this study, oral NAC had no effect on the prevention of CIN in patients undergoing cardiovascular procedures. Conclusion: In this study, oral NAC administration does not reduce neither the incidence of cystatin C-based CIN nor serum creatinine-based CIN in patients undergoing cardiovascular procedures.

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Serum Creatinine as an Index of Renal Function: New Insights into Old Concepts

Cited by 1,347 publications

References 124 publications

A population pharmacokinetic model for cefuroxime using cystatin C as a marker of renal function

A population pharmacokinetic model for cefuroxime using cystatin C as a marker of renal function

Prediction of Fluoroquinolone-Induced Elevation in Serum Creatinine Levels: A Case of Drug–Endogenous Substance Interaction Involving the Inhibition of Renal Secretion

N‐Acetylcysteine in Preventing Contrast‐Induced Nephropathy Assessed by Cystatin C

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