Serum creatinine urinary biomarkers

Cystatin C is nearly completely metabolized by proximal renal tubular cells. As a consequence, under ordinary circumstances there is little to no detectable cystatin C present in the urine. Thus, a true clearance of cystatin C cannot be determined. However, in the presence of tubular damage, cystatin C may be detected in the urine [147,148] and may be more sensitive to early and mild changes of kidney function compared with creatinine [149,150]. In this regard, elevation in serum cystatin C consistent with AKI, defined by at least a 50% increase from baseline, was evident 1-2 days prior to changes in SCr [151]. Finally, in patients with AKI, elevated urinary cystatin C was highly predictive of subsequent need for acute renal replacement therapy and outperformed several other urinary biomarkers in some studies [152]., but not in others [152a]... 

In humans, there seems to be a dose-dependent association between compound A exposure and the appearance of urinary biomarkers such as albumin, glucose, and the enzymes NAG or a-GST. These findings appear in studies when the compound A exposure exceeds 160 ppm/ hour [71-74], while they are absent in studies with lower compound A exposure [75-77]. In all studies associated with higher exposure of compound A, the urinary markers are transient, lasting 3-5 days with total normalization within one week. There is no correlation between serum creatinine and the urinary markers. 

Biomarkers for decreased function include increases in urinary proteins and elevation of serum creatinine or 2-microglobulin. Biomarkers for renal cytotoxicity include increases in urinary excretion of antigens and enzymes located within renal tissues. Biomarkers for biochemical changes occurring within the kidneys include eicosanoids, fibronectin, kallikrein activity, and glycosaminoglycans in urine. 

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