View Immunoassay Arrays
Adhesion Molecule
Intercellular Adhesion Molecule-I – ICAM-I
Intercellular Adhesion Molecule-I – ICAM-I
Vascular Cell Adhesion Molecule-I – VCAM-I
Acute Kidney Injury
Kidney Injury Molecule – KIM-I
Neutrophil Gelatinase-Associated
Lipocalin – NGAL
Cystatin C
Apolipoprotein E4 – ApoE4
Pan Apolipoprotein E – Apo E
Cardiac Troponin I – cTnl
Creatine Kinase MB – CKMB
Heart Type Fatty Acid Binding Protein – H-FABP
Cerebral I
Brain-Derived Neurotrophic Factor – BDNF
Glial Fibrillary Acidic Protein – GFAP
Heart-Type Fatty Acid-Binding Protein – H-FABP
Interleukin-6 – IL-6
Cerebral II
C-Reactive Protein – CRP
Neuron Specific Enolase – NSE
Soluble Tumour Necrosis Factor Receptor 1 − sTNFR1
Neutrophil Gelatinase-Associated Lipocalin – NGAL
Chronic Kidney Disease
Fatty Acid Binding Protein-1 – FABP1
Soluble Tumour Necrosis Factor Receptor 1 − sTNFR1
Soluble Tumour Necrosis Factor Receptor 11 − sTNFR 11
Macrophage Inflammatory Protein 1α – MIP-1α
Interleukin-8 – IL-8
Epidermal Growth Factor – EGF
Chronic Kidney Disease II
Complement C3a des Arginine – C3a des Arg
C-Reactive Protein – CRP
Neutrophil Gelatinase-Associated Lipocalin – NGAL
Cystatin C
Cytokine I
Interleukin-1 alpha − IL-1α
Interleukin-1 beta − IL-1β
Interleukin-2 − IL-2
Interleukin-4 − IL-4
Interleukin-6 − IL-6
Interleukin-8 − IL-8
Interleukin-10 − IL-10
Vascular Endothelial Growth Factor − VEGF
Epidermal Growth Factor − EGF
Tumour Necrosis Factor-α − TNF-α
Interferon-γ − IFN-γ
Monocyte Chemotactic Protein-1 − MCP-1
Cytokine III
Interleukin-5 − IL-5
Interleukin-15 − IL-15
Granulocyte Macrophage Colony Stimulating Factor – GM-CSF
Macrophage Inflammatory Protein-1α − MIP-1α
Cytokine IV
Matrix Metalloproteinase-9 − MMP-9
Soluble IL 2 Receptor Alpha − sIL-2Rα
Soluble IL 6 Receptor − sIL-6R
Soluble Tumour Necrosis Factor Receptor 1 − sTNFR1
Soluble Tumour Necrosis Factor Receptor 11 − sTNFR 11
Cytokine V
Interleukin-3 − IL-3
Interleukin-7 − IL-7
Interleukin-13 − IL-13
Interleukin-12p70 − IL-12p70
Interleukin-23 − IL-23
Dehydroepiandrosterone-Sulphate– DHEA-S
Follicle Stimulating Hormone − FSH
Luteinizing Hormone − LH
Sex Hormone Binding Globulin − SHBG
Gastrin 17 − GI7
Pepsinogen I − PGI
Pepsinogen II − PGII
Helicobacter Pylori
Helicobacter pylori – H. pylori
Metabolic Syndrome I
Plasminogen Activator Inhibitor − PAI-1
Interleukin-6 – IL-6
Tumour Necrosis Factor-α – TNF- α
Metabolic Syndrome II
C-Reactive Protein – CRP
Cystatin C
Glial Fibrillary Acidic Protein − GFAP
Glutathione S – Transferase Pi– GSTPi
Heart-Type Fatty Acid-Binding Protein – H-FABP
Interleukin-6 − IL-6
Nucleoside Diphosphate Kinase – NDKA
Parkinson Protein 7 − PARK-7
Soluble Tumour Necrosis Factor Receptor 1 − sTNFR1
Thyroid Free
Free Thyroxine − FT4
Free Tri-iodothyronine − FT3
Thyroid Stimulating Hormone − TSH
Thyroid TBG
Thyroxine Binding Globulin − TBG
Thyroid Total
Thyroid Stimulating Hormone − TSH
Total Tri-iodothyronine − TT3
Total Thyroxine − TT4
Tumour PSA
Total Prostate Specific Antigen – TPSA
Free Prostate Specific Antigen – FPSA
Vitamin D
Vitamin D

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.

Biomarkers Explained

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


“The ability of our new DIKI test to quantitatively detect these early biomarkers associated with kidney damage, enables earlier intervention for treatment, as well as the prevention of further kidney damage. Traditional DIKI diagnostic testing screens for a rise in serum creatinine and decreased urine output, but unfortunately this method of testing is a lagging index of DIKI. The more sensitive biomarkers utilized in the Randox DIKI Biochip are suitable to replace this slow, more laborious and less sensitive testing method.”


John Lamont, Chief Scientist at Randox Laboratories.