Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 47: 2055-2059, 2001;
This Article
Right arrow Extract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (79)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Risch, L.
Right arrow Articles by Huber, A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Risch, L.
Right arrow Articles by Huber, A. R.
Related Collections
Right arrow General Clinical Chemistry
Right arrow Proteomics and Protein Markers
Right arrow Drug Monitoring and Toxicology
(Clinical Chemistry. 2001;47:2055-2059.)
© 2001 American Association for Clinical Chemistry, Inc.

Technical Briefs

Effects of Glucocorticoid Immunosuppression on Serum Cystatin C Concentrations in Renal Transplant Patients

Lorenz Risch1, Roberto Herklotz1, Alfred Blumberg2 and Andreas R. Huber1a

Departments of
1 Laboratory Medicine and
2 Nephrology, Kantonsspital Aarau, 5001 Aarau, Switzerland

aauthor for correspondence: fax 41-62-838-5399, e-mail andreas.huber{at}ksa.ch

Cystatin C is a nonglycosylated basic protein (13.36 kDa) and can be found in a variety of biologic fluids (1). Cystatin C serum concentration is not influenced by gender, inflammation, or lean tissue mass and is regarded to be mainly determined by glomerular filtration rate (GFR) (2)(3)(4)(5). Cystatin C has been described as meeting many of the characteristics of an ideal GFR marker (e.g., endogenously produced at a constant rate, freely filtered in the glomerulus, neither reabsorbed nor secreted in the renal tubule, not extrarenally eliminated) and has been reported to be at least as accurate as the commonly used serum creatinine to detect impaired renal function in various patient groups, including renal transplant patients (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24).

Despite this, Bokenkamp et al. (25) reported that cystatin C is higher in children with renal transplants than in children with other renal pathologies but comparable GFRs, suggesting an underestimation of GFRs by cystatin C in renal transplant patients. This finding suggested immunosuppression as a major influencing factor because all patients had received prednisolone and cyclosporin A medication. Interestingly, neither prednisolone nor cyclosporin A was believed to change cystatin C concentrations because no dose-dependent increase of cystatin C was found. In contrast, an in vitro study by Bjarnadottir et al. (26) described a dose-dependent increase of cystatin C production in HeLa cells exposed to dexamethasone. To further clarify these findings, we conducted a nested case-control study in a cohort of renal transplant patients who were prospectively monitored during a 1-year period (20). The present study aimed to elucidate the influence of glucorticoid immunosuppression on cystatin C concentrations in serum from renal transplant patients.

The patients were seen for routine follow-up, which included assessment of clinical data and laboratory results. To evaluate the influence of immunosuppressive regimens, especially glucocorticoids, on serum cystatin C, 20 clinically stable patients on immunosuppression therapy with low-dose glucocorticoids were matched with 20 clinically stable patients receiving cyclosporin A alone and 20 clinically stable patients receiving cyclosporin A together with azathioprine (Table 1 ).


View this table:
[in this window]
[in a new window]
  		Table 1. Characteristics of renal transplant patients with different immunosuppression.

Clinical stability was defined as the absence of acute rejection, febrile infection, and cyclosporin A toxicity, as well as stability of creatinine clearance as estimated by the formula of Cockroft and Gault (27). The three groups were matched for estimated creatinine clearance (CrCl) and had comparable gender, age, and time since transplantation. To reduce the influence of the known biologic variation of cystatin C (20)(28), all patients had six measurements during subsequent visits that demonstrated stable clinical condition. Means from cystatin C reciprocals, as well as from CrCl estimates, were calculated and used for data analysis.

Furthermore, 13 patients receiving a short course of high-dose methylprednisolone (500 mg intravenously per day for 3 days) for deteriorating renal function were analyzed to observe a possible dose-dependent effect of glucocorticoid administration. None of the 73 patients was receiving additional glucocorticoid or mineralocorticoid medication.

The group receiving short-course, high-dose methylprednisolone had results from four time points available: (a) the visit before methylprednisolone commencement (median, 17 days; range, 2–67 days; 2 patients with missing values); (b) the day methylprednisolone was started (before medication); (c) after 3 days of methylprednisolone therapy; and (d) on a follow-up visit (median, 8 days after last dose; range, 6–11 days).

Serum cystatin C was measured by a particle-enhanced turbidimetric immunoassay (PETIA; Dako) on a Cobas Mira (Roche) (9). Serum creatinine was measured with a modified kinetic Jaffe method (Dimension RXL; Dade-Behring) (29). Creatinine clearance was estimated by the formula of Cockroft and Gault (27), which in renal transplant patients has been validated against Iohexol clearance with creatinine measurements by a kinetic Jaffe method (30)(31).

Data are presented as mean ± SD or as median and interquartile range (IQR) where appropriate after testing for gaussian distribution. For linearization of the hyperbolic relationship between cystatin C and GFR, reciprocals of cystatin C concentrations were calculated. Multiple comparisons were done by Kruskal–Wallis one-way ANOVA. Linear regression lines were compared by analysis of covariance. For comparison of serial measurements in the same group, the Friedman repeated-measure ANOVA on ranks followed by the Dunn test was used. The study was approved by the Institutional Review Board and is in accordance with the Helsinki Declaration of 1975, as revised in 1983. All patients gave informed consent.

Reciprocals of cystatin C and CrCl estimates showed a linear relationship in all four groups. Equations of the linear regression lines between cystatin C reciprocals and CrCl estimates were as follows: 1/cystatin C = 0.3413 + [0.00685 x CrCl] (r = 0.65) in the cyclosporin A alone group; 1/cystatin C = 0.173 + [0.00850 x CrCl] (r = 0.76) in the cyclosporin A-azathioprine group; 1/cystatin C = 0.0860 + [0.00838 x CrCl] (r = 0.86) in the low-dose glucocorticoid group; and 1/cystatin C = 0.1318 + [0.00534 x CrCl] (r = 0.69) in the high-dose glucocorticoid group. Whereas correlation coefficients and slopes among the different groups did not differ significantly, significant differences of elevations in the regression lines could be observed: cystatin C reciprocals in the low-dose glucorticoid group were significantly lower than in the cyclosporin A-azathioprine group (P = 0.016) and the cyclosporin A alone group (P <0.001), but significantly higher than in the high-dose glucocorticoid group (P = 0.008). No significant difference of increase was seen between the groups with cyclosporin A alone and cyclosporin A-azathioprine (P = 0.15). Together, glucocorticoid administration was associated in a dose-dependent fashion with increased cystatin C values, leading to systematic underestimation of GFR in renal transplant patients.

To estimate the magnitude of cystatin C increases among the different groups, hyperbolic relationships between cystatin C and CrCl estimates, as derived from linear regression equations, are shown in Fig. 1A . In comparison with the group receiving cyclosporin A alone, the group receiving low-dose glucocorticoids had cystatin C concentrations that differed by the following: 0.20 mg/L at 80 mL · min-1 · 1.73 m-2; 0.27 mg/L at 70 mL · min-1 · 1.73-2; by 0.37 mg/L at 60 mL · min-1 · 1.73 m-2; by 0.52 mg/L at 50 mL · min-1 · 1.73 m-2; by 0.75 mg/L at 40 mL · min-1 · 1.73 m-2; by 1.13 mg/L at 30 mL · min-1 · 1.73 m-2; and by 1.85 mg/L at 20 mL · min-1 · 1.73 m-2.



View larger version (19K):
[in this window]
[in a new window]
  		Figure 1. Serum cystatin C concentrations in renal transplant patients receiving different immunosuppressive medication.

(A), glucocorticoid medication is associated in a dose-dependent fashion with significantly increased cystatin C. Hyperbolic relationships derived from linear regression equations are shown. The low-dose glucocorticoid group received <=10 mg prednisone daily combined with cyclosporin A and azathioprine, and the high-dose glucocorticoid group received three doses of 0.5 g of methylprednisolone in combination with cyclosporin A and azathioprine. The groups without glucocorticoids had no significant difference in cystatin C concentrations. - - - - -, high-dose glucocorticoid; — - - —, low-dose glucocorticoid; —- —-, cyclosporin A plus azathioprine; ———, cyclosporin A alone. (B), time course of cystatin C concentrations after administration of a high-dose methylprednisolone therapy. Each line represents the course of a patient. Point A, determinations 17 days before methylprednisolone course was started (median range, 2–67 days; 2 patients with missing values); point B, before first dose; point C, after three daily doses of 500 mg of methylprednisolone; point D, follow-up 8 days after cessation of methylprednisolone (range, 6–11 days). Increases from points B to C and decreases from points C to D are both significant (P <0.05). Serum creatinine and CrCl estimates underwent no significant changes.

Because patients receiving long-term, low-dose glucocorticoid therapy demonstrated higher cystatin C concentrations than controls, cystatin C kinetics after glucocorticoid administration and withdrawal were investigated. High-dose methylprednisolone given intravenously led to significant differences in cystatin C values at different time points (before administration, after three doses, and 8 days after discontinuation; P <0.001). After three daily doses of 500 mg, cystatin C concentrations increased from 2.13 mg/L (IQR, 1.72–2.80) to 2.69 mg/L (IQR, 2.34–3.5; P <0.05). Eight days after discontinuation, cystatin C concentrations significantly decreased to 1.96 mg/L (IQR, 1.63–2.4; P <0.05; Fig. 1BUp ) At these time points, neither the CrCl estimate (45 ± 13 mL · min-1 · 1.73 m-2, 43 ± 12 mL · min-1 · 1.73 m-2, and 46 ± 14 mL · min-1 · 1.73 m-2; P = 0.08) nor the serum creatinine concentrations (175 µmol/L, IQR, 156–202; 178 µmol/L, IQR 161–203; and 158 µmol/L, IQR 144–199; P = 0.17) underwent significant changes.

By ROC analysis of all four groups, cystatin C had higher diagnostic accuracy than serum creatinine in detecting a creatinine clearance estimate <=60 mL · min-1 · 1.73 m-2 (data not shown). This finding was significant in the low-dose glucocorticoid group (P = 0.005). Furthermore, in vitro interference of the administered immunosuppressive drugs (cyclosporin A, azathioprine, and methylprednisolone) on the cystatin C and creatinine assays used was tested and excluded as a cause of the false increase of cystatin C (data not shown).

This study demonstrates that renal transplant patients receiving glucocorticoid medication have higher cystatin C than two comparable groups with glucocorticoid-free immunosuppression. Because patients receiving 500 mg of methylprednisolone had significantly higher cystatin C values than patients receiving <=10 mg of prednisone, a dose-dependent influence of the administered glucocorticoid dose is suggested. Thus, glucocorticoid medication leads to systematic underestimation of GFR in renal transplant patients. The hyperbolic relationships deriving from linear regression lines allow for an estimate of cystatin C increase at specific levels of CrCl.

Similar to our findings, Bjarnadottir et al. (26) observed that dexamethasone caused a dose-dependent increase in the cystatin C secretion of cultivated HeLa cells. Furthermore, when an expression system was transfected in HeLa cells by chimeric plasmid constructs of the cystatin C promoter coupled to the structural gene coding for human growth hormone, a statistically significant increase of human growth hormone secretion after dexamethasone administration could be detected. These findings suggest that the glucocorticoid-induced increase of cystatin C production reflects a promoter-mediated increase in transcription of the cystatin C gene. Despite these in vitro results, cystatin C serum concentration in vivo is thought to be mainly determined by GFR, although some exceptions have been reported (25)(32).

Bokenkamp et al. (25) reported that serum cystatin C in pediatric renal transplant patients is higher than in nonrenal transplant children with comparable GFR. It was not stated, however, how many participants in the control group had received a glucocorticoid-free medication. Furthermore, the control group was matched only for GFR, age, and gender, but not for kidney transplantation. With this, it was not possible to determine whether glucocorticoid medication or renal transplantation led to the difference in cystatin C concentrations. In contrast to our observations, a dose-dependent influence of glucocorticoid medication on cystatin C could not be demonstrated, probably because the differences in individual prednisolone doses were too small to be reflected in cystatin C concentrations.

A similar effect of glucocorticoid medication has been reported in asthmatics by Cimerman et al. (32). Comparable to our observations in renal transplant patients receiving a 3-day course of 500 mg of methylprednisolone per day, they found a highly significant increase of cystatin C after 1 week of 40 mg of methylprednisolone daily. The present study demonstrates that the increase is a transitory phenomenon, because after a median of 8 days after cessation of methylprednisolone, cystatin C concentrations decreased to values observed before high-dose glucocorticoid administration.

Our finding that glucocorticoid medication is associated with increased cystatin C could explain observations in another study by Newman et al. (7), who found three outliers exhibiting increased cystatin C, when comparing cystatin C concentrations and GFR measurements by 51Cr- EDTA clearance in 209 patients. One of these outliers originated from a renal transplant patient after several rejection episodes that were treated with steroids and full immunosuppression therapy. Although not stated in the report, the other two patients may also have been on glucocorticoids because one suffered from systemic sclerosis and the other patient had severe rheumatoid arthritis.

In summary, glucocorticoid medication in adult renal transplant patients is associated in a dose-dependent manner with increased cystatin C, leading to systematic underestimation of GFR. This does not preclude the use of cystatin C in detecting impaired renal function in renal transplant patients with glucocorticoids, because this study and others (19)(20)(21)(22) showed cystatin C to be significantly more accurate in detecting impaired renal function in this patient group. Moreover, our data illustrate the need for specific reference intervals in patients on glucocorticoid therapy. Depending on steroid dose and CrCl impairment, the cystatin C increase can be estimated to be 0.20–1.85 mg/L in patients receiving low-dose glucocorticoids and is even higher in patients receiving high-dose glucocorticoids. However, a more detailed study evaluating dose effects is needed. In conclusion, in clinical routine settings, as well as in future clinical studies, it is important to take glucocorticoid medication into account when interpreting serum cystatin C concentrations in renal transplant patients and, presumably, in other patient groups.


References

  1. Grubb AO. Cystatin C—properties and use as diagnostic marker. Adv Clin Chem 2000;35:63-99.[Web of Science][Medline] [Order article via Infotrieve]
  2. Randers E, Kornerup K, Erlandsen EJ, Hasling C, Danielsen H. Cystatin C levels in sera of patients with acute infectious diseases with high C-reactive protein levels. Scand J Clin Lab Invest 2001;61:333-335.[Web of Science][Medline] [Order article via Infotrieve]
  3. Randers E, Krue S, Erlandsen EJ, Danielsen H, Hansen LG. Reference intervals for serum cystatin C in children. Clin Chem 1999;45:1856-1857.[Free Full Text]
  4. Vinge E, Lindergard B, Nilsson-Ehle P, Grubb A. Relationships among serum cystatin C, serum creatinine, lean tissue mass and glomerular filtration rate in healthy adults. Scand J Clin Lab Invest 1999;59:587-592.[Web of Science][Medline] [Order article via Infotrieve]
  5. Finney H, Newman DJ, Price CP. Adult reference ranges for serum cystatin C, creatinine and predicted creatinine clearance. Ann Clin Biochem 2000;37:49-59.
  6. Swan SK. The search continues—an ideal marker of GFR [Editorial]. Clin Chem 1997;43:913-914.[Free Full Text]
  7. Newman DJ, Thakkar H, Edwards RG, Wilkie M, White T, Grubb AO, et al. Serum cystatin C measured by automated immunoassay: a more sensitive marker of changes in GFR than serum creatinine. Kidney Int 1995;47:312-318.[Web of Science][Medline] [Order article via Infotrieve]
  8. Coll E, Botey A, Alvarez L, Poch E, Quinto L, Saurina A, et al. Serum cystatin C as a new marker for noninvasive estimation of glomerular filtration rate and as a marker for early renal impairment. Am J Kidney Dis 2000;36:29-34.[Web of Science][Medline] [Order article via Infotrieve]
  9. Kyhse-Andersen J, Schmidt C, Nordin G, Andersson B, Nilsson-Ehle P, Lindström V, et al. Serum cystatin C, determined by a rapid, automated particle-enhanced turbidimetric method, is a better marker than serum creatinine for glomerular filtration rate. Clin Chem 1994;40:1921-1926.[Abstract/Free Full Text]
  10. Randers E, Erlandsen EJ, Pedersen OL, Hasling C, Danielsen H. Serum cystatin C as an endogenous parameter of the renal function in patients with normal to moderately impaired kidney function. Clin Nephrol 2000;54:203-209.[Web of Science][Medline] [Order article via Infotrieve]
  11. Chantrel F, Agin A, Offner M, Koehl C, Moulin B, Hannedouche T. Comparison of cystatin C versus creatinine for detection of mild renal failure. Clin Nephrol 2000;54:374-381.[Web of Science][Medline] [Order article via Infotrieve]
  12. Bokenkamp A, Domanetzki M, Zinck R, Schumann G, Byrd D, Brodehl J. Cystatin C—a new marker of glomerular filtration rate in children independent of age and height. Pediatrics 1998;101:875-881.[Abstract/Free Full Text]
  13. Helin I, Axenram M, Grubb A. Serum cystatin C as a determinant of glomerular filtration rate in children. Clin Nephrol 1998;49:221-225.[Web of Science][Medline] [Order article via Infotrieve]
  14. Stickle D, Cole B, Hock K, Hruska KA, Scott MG. Correlation of plasma concentrations of cystatin C and creatinine to inulin clearance in a pediatric population. Clin Chem 1998;44:1334-1338.[Abstract/Free Full Text]
  15. Fliser D, Ritz E. Serum cystatin C concentration as a marker of renal dysfunction in elderly. Am J Kidney Dis 2001;37:79-83.[Web of Science][Medline] [Order article via Infotrieve]
  16. Stabuc B, Vrhovec L, Stabuc-Silih M, Cizej TE. Improved prediction of decreased creatinine clearance by serum cystatin C: use in cancer patients before and during chemotherapy. Clin Chem 2000;46:193-197.[Abstract/Free Full Text]
  17. Woitas RP, Stoffel-Wagner B, Flommersfeld S, Poege U, Schiedermaier P, Klehr HU, et al. Correlation of serum concentrations of cystatin C and creatinine to inulin clearance in liver cirrhosis. Clin Chem 2000;46:712-715.[Free Full Text]
  18. Harmoinen AP, Kouri TT, Wirta OR, Lehtimaki TJ, Rantalaiho V, Turjanmaa VM, Pasternack AI. Evaluation of plasma cystatin C as a marker for glomerular filtration rate in patients with type 2 diabetes. Clin Nephrol 1999;52:363-370.[Web of Science][Medline] [Order article via Infotrieve]
  19. Plebani M, Dall’Amico R, Mussap M, Montini G, Ruzzante N, Marsilio R, et al. Is serum cystatin C a sensitive marker of glomerular filtration rate (GFR)? A preliminary study on renal transplant patients. Ren Fail 1998;20:303-309.[Web of Science][Medline] [Order article via Infotrieve]
  20. Risch L, Blumberg A, Huber A. Rapid and accurate assessment of glomerular filtration rate in patients with renal transplants using serum cystatin C. Nephrol Dial Transplant 1999;14:1991-1996.[Abstract/Free Full Text]
  21. Le Bricon T, Thervet E, Benlakehal M, Bousquet B, Legendre C, Erlich D. Changes in plasma cystatin C after renal transplantation and acute rejection in adults. Clin Chem 1999;45:2243-2249.[Abstract/Free Full Text]
  22. Le Bricon T, Thervet E, Froissart M, Benlakehal M, Bousquet B, Legendre C, Erlich D. Plasma cystatin C is superior to 24-h creatinine clearance and plasma creatinine for estimation of glomerular filtration rate 3 months after kidney transplantation [Letter]. Clin Chem 2000;46:1206-1207.[Free Full Text]
  23. Herget-Rosenthal S, Trabold S, Huesing J, Heemann U, Philipp T, Kribben A. Cystatin C—an accurate marker of glomerular filtration rate after renal transplantation?. Transpl Int 2000;13:285-289.[Web of Science][Medline] [Order article via Infotrieve]
  24. Bokenkamp A, Ozden N, Dieterich C, Schumann G, Ehrich JH, Brodehl J. Cystatin C and creatinine after successful kidney transplantation in children. Clin Nephrol 1999;52:371-376.[Web of Science][Medline] [Order article via Infotrieve]
  25. Bokenkamp A, Domanetzki M, Zinck R, Schumann G, Byrd D, Brodehl J. Cystatin C serum concentrations underestimate glomerular filtration rate in renal transplant recipients. Clin Chem 1999;45:1866-1868.[Free Full Text]
  26. Bjarnadottir M, Grubb A, Olafsson I. Promoter-mediated, dexamethasone-induced increase in cystatin C production by HeLa cells. Scand J Clin Lab Invest 1995;55:617-623.[Web of Science][Medline] [Order article via Infotrieve]
  27. Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal function: new insights into old concepts. Clin Chem 1992;38:1933-1953.[Abstract]
  28. Keevil BG, Kilpatrick ES, Nichols SP, Maylor PW. Biological variation of cystatin C: implications for the assessment of glomerular filtration rate. Clin Chem 1998;44:1535-1539.[Abstract/Free Full Text]
  29. Knapp ML, Mayne PD. Development of an automated kinetic Jaffé method designed to minimise bilirubin interference in plasma creatinine assays. Clin Chim Acta 1987;168:239-246.[Web of Science][Medline] [Order article via Infotrieve]
  30. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999;130:461-470.[Abstract/Free Full Text]
  31. Bedros F, Kasiske BL. Estimating GFR from serum creatinine in renal transplant recipients [Abstract]. J Am Soc Nephrol 1998;9:666A.
  32. Cimerman N, Brguljan PM, Krasovec M, Suskovic S, Kos J. Serum cystatin C, a potent inhibitor of cysteine proteinases, is increased in asthmatic patients. Clin Chim Acta 2000;300:83-95.[Web of Science][Medline] [Order article via Infotrieve]



The following articles in journals at HighWire Press have cited this article:


Home page
 CJASNHome page
G. J. Schwartz and D. F. Work
Measurement and Estimation of GFR in Children and Adolescents
Clin. J. Am. Soc. Nephrol., November 1, 2009; 4(11): 1832 - 1843.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Chem.Home page
N. Taglieri, W. Koenig, and J. C. Kaski
Cystatin C and Cardiovascular Risk
Clin. Chem., November 1, 2009; 55(11): 1932 - 1943.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
M. Madero, C. L. Wassel, C. A. Peralta, S. S. Najjar, K. Sutton-Tyrrell, L. Fried, R. Canada, A. Newman, M. G. Shlipak, M. J. Sarnak, et al.
Cystatin C Associates with Arterial Stiffness in Older Adults
J. Am. Soc. Nephrol., May 1, 2009; 20(5): 1086 - 1093.
[Abstract] [Full Text] [PDF]

Home page
 haematolHome page
E. Terpos, E. Katodritou, E. Tsiftsakis, E. Kastritis, D. Christoulas, A. Pouli, E. Michalis, E. Verrou, K. Anargyrou, K. Tsionos, et al.
Cystatin-C is an independent prognostic factor for survival in multiple myeloma and is reduced by bortezomib administration
Haematologica, March 1, 2009; 94(3): 372 - 379.
[Abstract] [Full Text] [PDF]

Home page
 CJASNHome page
H. Kramer, W. Palmas, B. Kestenbaum, M. Cushman, M. Allison, B. Astor, and M. Shlipak
Chronic Kidney Disease Prevalence Estimates among Racial/Ethnic Groups: The Multi-Ethnic Study of Atherosclerosis
Clin. J. Am. Soc. Nephrol., September 1, 2008; 3(5): 1391 - 1397.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Chem.Home page
A. Bokenkamp, C. A.R.C. Laarman, K. I. Braam, J. A.E. van Wijk, W. A. Kors, M. Kool, J. de Valk, A. A. Bouman, M. D. Spreeuwenberg, and B. Stoffel-Wagner
Effect of Corticosteroid Therapy on Low-Molecular Weight Protein Markers of Kidney Function
Clin. Chem., December 1, 2007; 53(12): 2219 - 2221.
[Full Text] [PDF]

Home page
 Clin. Chem.Home page
C. A. White, A. Akbari, S. Doucette, D. Fergusson, N. Hussain, L. Dinh, G. Filler, N. Lepage, and G. A. Knoll
A Novel Equation to Estimate Glomerular Filtration Rate Using Beta-Trace Protein
Clin. Chem., November 1, 2007; 53(11): 1965 - 1968.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
A. Zahran, M. Qureshi, and A. Shoker
Comparison between creatinine and cystatin C-based GFR equations in renal transplantation
Nephrol. Dial. Transplant., September 1, 2007; 22(9): 2659 - 2668.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
F. J. Hoek, J. C. Korevaar, F. W. Dekker, E. W. Boeschoten, and R. T. Krediet
Estimation of residual glomerular filtration rate in dialysis patients from the plasma cystatin C level
Nephrol. Dial. Transplant., June 1, 2007; 22(6): 1633 - 1638.
[Abstract] [Full Text] [PDF]

Home page
 ANN INTERN MEDHome page
M. G. Shlipak, R. Katz, M. J. Sarnak, L. F. Fried, A. B. Newman, C. Stehman-Breen, S. L. Seliger, B. Kestenbaum, B. Psaty, R. P. Tracy, et al.
Cystatin C and Prognosis for Cardiovascular and Kidney Outcomes in Elderly Persons without Chronic Kidney Disease
Ann Intern Med, August 15, 2006; 145(4): 237 - 246.
[Abstract] [Full Text] [PDF]

Home page
 Annals of Clinical & Laboratory ScienceHome page
J. Westhuyzen
Cystatin C: a Promising Marker and Predictor of Impaired Renal Function
Ann. Clin. Lab. Sci., January 1, 2006; 36(4): 387 - 394.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
C. White, A. Akbari, N. Hussain, L. Dinh, G. Filler, N. Lepage, and G. A. Knoll
Estimating Glomerular Filtration Rate in Kidney Transplantation: A Comparison between Serum Creatinine and Cystatin C-Based Methods
J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3763 - 3770.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
A. Berghout, R. W. Wulkan, J. G. den Hollander, L. Risch, H. Drexel, A. R. Huber, B. A. Perkins, R. G. Nelson, A. S. Krolewski, M. G. Shlipak, et al.
Cystatin C and the risk of death.
N. Engl. J. Med., August 25, 2005; 353(8): 842 - 844.
[Full Text] [PDF]

Home page
 Clin. Chem.Home page
A. R. Huber and L. Risch
Recent Developments in the Evaluation of Glomerular Filtration Rate: Is There a Place for {beta}-Trace?
Clin. Chem., August 1, 2005; 51(8): 1329 - 1330.
[Full Text] [PDF]

Home page
 Clin. Chem.Home page
U. Poge, T. M. Gerhardt, B. Stoffel-Wagner, H. Palmedo, H.-U. Klehr, T. Sauerbruch, and R. P. Woitas
{beta}-Trace Protein Is an Alternative Marker for Glomerular Filtration Rate in Renal Transplantation Patients
Clin. Chem., August 1, 2005; 51(8): 1531 - 1533.
[Full Text] [PDF]

Home page
 Clin. Chem.Home page
A. Grubb, U. Nyman, J. Bjork, V. Lindstrom, B. Rippe, G. Sterner, and A. Christensson
Simple Cystatin C-Based Prediction Equations for Glomerular Filtration Rate Compared with the Modification of Diet in Renal Disease Prediction Equation for Adults and the Schwartz and the Counahan-Barratt Prediction Equations for Children
Clin. Chem., August 1, 2005; 51(8): 1420 - 1431.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
U. Poge, T. Gerhardt, A. Bokenkamp, B. Stoffel-Wagner, H.-U. Klehr, T. Sauerbruch, and R. P. Woitas
Time course of low molecular weight proteins in the early kidney transplantation period--influence of corticosteroids
Nephrol. Dial. Transplant., November 1, 2004; 19(11): 2858 - 2863.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
F. J. Hoek, F. A. W. Kemperman, and R. T. Krediet
A comparison between cystatin C, plasma creatinine and the Cockcroft and Gault formula for the estimation of glomerular filtration rate
Nephrol. Dial. Transplant., October 1, 2003; 18(10): 2024 - 2031.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Chem.Home page
A. Bokenkamp, J. A.E. van Wijk, M. J. Lentze, and B. Stoffel-Wagner
Effect of Corticosteroid Therapy on Serum Cystatin C and {beta}2-Microglobulin Concentrations
Clin. Chem., July 1, 2002; 48(7): 1123 - 1126.
[Full Text] [PDF]

This Article
Right arrow Extract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (79)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Risch, L.
Right arrow Articles by Huber, A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Risch, L.
Right arrow Articles by Huber, A. R.
Related Collections
Right arrow General Clinical Chemistry
Right arrow Proteomics and Protein Markers
Right arrow Drug Monitoring and Toxicology

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS