Supporting the early detection of chronic kidney disease
Kidney disease has a major effect on global health, both as a direct cause of global morbidity and mortality and as an important risk factor for cardiovascular disease.
Globally, in 2017, 1·2 million people died from CKD. The global all-age mortality rate from CKD increased 41·5% between 1990 and 2017, although there was no significant change in the age-standardised mortality rate.1
Cystatin C, has been shown to be subject to less biological interference and more sensitive to early declines in kidney function, than endogenous serum biomarkers such as albumin and creatinine.2
Serum creatinine levels only begin to rise in CKD stage 3 when approximately 50 % of renal function is already lost (“creatinine-blind area”). Subtle changes in the GFR in
CKD stages 1 and 2 – not detectable by creatinine-based measurements – can be determined by cystatin C due to its higher sensitivity and specificity.
Figure 1: Stages of chronic kidney disease according to NKF KDOQI4
Cystatin C is not affected by any physical factors such as muscle mass, age, gender or ethnicity. As a result, cystatin C shows a relatively high diagnostic sensitivity and specificity compared with creatinine, making it a reliable early marker of renal dysfunction. In a study of 93,000 patients, cystatin C-based estimation of GFR, correctly reclassified 42 % of patients with a creatinine-based estimation of GFR of 45 - 59 mL/min/1.73 to a “normal” risk group concerning end-stage renal disease and cardiovascular death.5
Figure 2: ROC analysis of cystatin C and creatinine3
Figure 3: Correlation between cobas c 501 and Siemens BN II cystatin C application. Highly developed turbidimetric detection technology delivers accurate results comparable to nephelometric measurement methods.6
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