There were unacceptable differences related to S-Cr results between clinical laboratories.
S-Cys C, a low-molecular weight (13.3 kDa) protein that is a cysteine protease inhibitor, is produced at a constant rate by all nucleated cells.3 It does not have the same relationship with muscle mass, age and gender as serum creatinine is almost completely filtered by glomeruli and completely reabsorbed and degraded within renal proximal tubular cells.4 S-Cys C therefore appeared to be a better marker of GFR than S-Cr. Further studies have shown that S-Cys C is upregulated by certain tumours, is raised in thyroid disorders and during corticosteroid therapy.
The use of S-Cys C has been hampered by its relatively greater cost (than S-Cr) and by analytical issues related to standardisation.
A decline in GFR in these patients is often not reflected by the level of S-Cr. Only 40% of patients with a reduced GFR have normal S-Cr levels.5
Most of the equations available are based on S-Cr levels because it is routinely measured in laboratories.
Because the S-Cr results were traceable to IDMS, we used the reexpressed 4-v MDRD equation (14).
 Nonstandard abbreviations: CKD, chronic kidney disease; GFR, glomerular filtration rate; [sup.51]Cr-EDTA, chromium-51-EDTA; eGFR, estimated GFR; S-Cr, serum creatinine; 4-v MDRD, 4-variable Modification of Diet in Renal Disease; CG, Cockcroft-Gault; IDMS, isotope dilution mass spectrometry; CrCl, creatinine clearance; BSA, body surface area; mGFR, measured GFR; IQR, interquartile range.