Drug Induced Kidney Injury Panel
The Randox Drug Induced Kidney Injury Array (DIKI) allows superior monitoring of nephrotoxicity for enhanced safety in drug development.
Poor sensitivity of serum creatinine for detecting and monitoring DIKI is well documented in academic journals. As a result for early phase trials European Medicines Agency (EMA) and Food and Drug Administration (FDA) are encouraging the use of more novel urinary biomarkers alongside conventional safety monitoring. The new panel, developed in collaboration with Pacific Biomarkers, detects early stage toxicity.
This marker is highly upregulated in kidney tubule cells following nephrotoxic injury severe enough to result in acute renal failure, acute tubular necrosis or acute tubulo-interstitial nephropathy.
Due to its small size and basic pH, Cystatin C is freely filtered by the glomerulus. It is then reabsorbed by tubular epithelial cells and subsequently metabolized. Accumulation of Cystatin C in urine is specific for tubular kidney damage and suggests reduced reabsorption at the proximal tubules as a result of
toxicant-induced kidney injury.
Expression of Clusterin is upregulated following a variety of renal injuries and is detectable in urine following acute kidney injury induced by administration of nephrotoxic agents. This occurs before the profound renal transformations that give rise to changes in creatinine and BUN.
KIM-1 is a 30kDa type 1 transmembrane glycoprotein found on actvated CD4+ T cells. It is undetectable in healthy kidney tissue but is expressed at very high levels in proximal tubule epithelial cells in the kidney after toxic injury.
Randox Biochip Array Technology
Biochip Array Technology enables multiplex immunoassay testing. The DIKI panel of 4 markers is combined on a single biochip, enabling simultaneous results from each patient sample, delivering:
- Excellent inter-assay precision and required sensitivity
- Superior specificity
- Lower sample volume
- Fast turnaround time
- Safer drug development