ABSTRACT
Serum creatinine is ubiquitously used as an indicator for GFR despite the knowledge that the usefulness of serum creatinine as a marker for GFR is limited by, inter alia, the influence of an individual's muscle mass on the production rate of creatinine, by the tubular secretion and reabsorption of creatinine, by the dietary intake of creatine and creatinine, and by analytical difficulties. Several recent studies have compared the use of serum cystatin C and creatinine as markers for GFR as determined by 'golden standard' procedures. In patients with reduced renal function, the plasma level of cystatin C increases reciprocally with the reduction of GFR, suggesting that cystatin C is formed at a constant rate and removed largely by glomerular filtration. Several studies in patients with manifest or subclinical reductions in GFR due to type-2 diabetes mellitus, essential hypertension, non diabetic nephropathies, renal transplant patients and coronary artery disease patients have shown a better correlation of cystatin C and GFR than creatinine and GFR