Are these panels validated for clinical diagnosis of acute kidney injury?

No. All panels are for research use only (RUO). They are suitable for preclinical nephrotoxicity research, clinical AKI biomarker studies, and drug safety assessment. They are not validated for clinical AKI diagnosis or patient management. While KIM-1, NGAL, Clusterin, and Osteoactivin are FDA-qualified for preclinical rat nephrotoxicity assessment, this qualification is for drug development context-of-use, not clinical diagnosis.

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MSD Kidney Injury / Nephrotoxicity Panels

MSD V-PLEX

Nephrotoxicity · Drug Safety · Multi-Site

MSD Kidney Injury Panel — KIM-1, NGAL & Cystatin C Assay

Q: Should I use urine or plasma for kidney injury biomarkers?

Urine is preferred for most nephrotoxicity biomarkers. KIM-1, NGAL, Clusterin, Osteoactivin, TFF3, and Calbindin are directly released from injured tubular cells into urine — urinary concentrations reflect local kidney injury more directly than plasma. NGAL can be measured in both urine and plasma — plasma NGAL reflects both renal and systemic sources. For research protocols, spot urine normalized to urinary creatinine is the standard approach. For preclinical rat studies, the FDA qualification data used urine normalized to creatinine. Contact us for matrix-specific collection and normalization guidance.

Monitor drug-induced kidney injury across glomerular, proximal tubular, distal tubular, and collecting duct nephron segments — using MSD multiplex panels that include FDA-recognized nephrotoxicity biomarkers (KIM-1, NGAL, Clusterin, Osteopontin) qualified by the PSTC/C-Path consortium for preclinical drug safety assessment.

Traditional kidney safety markers — serum creatinine and BUN — rise only after ~50% of nephron function is lost. They are late, insensitive, and confounded by muscle mass, diet, and hydration. MSD kidney injury panels detect site-specific tubular damage hours to days before functional decline: KIM-1 is the most specific proximal tubular injury marker — upregulated within hours of toxic or ischemic insult; NGAL/Lipocalin-2 is the most sensitive — elevated in urine within 2–6 hours across multiple AKI etiologies; Clusterin indicates tubular regeneration; Osteopontin reflects tissue remodeling. By measuring these across nephron segments simultaneously — glomerular (Cystatin C), proximal tubular (KIM-1, NGAL, Clusterin, α-GST, Osteoactivin), and distal tubular/collecting duct (Calbindin, TFF3) — a single 25 µL urine or plasma sample provides a nephron-segment-resolved injury map that histopathology alone cannot deliver.

Inquire About Kidney Panels View Panel Configurations

Beyond Creatinine — Next-Generation Nephrotoxicity Biomarkers

In 2008, the Predictive Safety Testing Consortium (PSTC), led by the FDA's Critical Path Institute (C-Path), submitted qualification data to the FDA and EMA for a panel of urinary kidney injury biomarkers. Both agencies subsequently issued guidance accepting KIM-1, Clusterin, NGAL, Osteopontin, Albumin, β2-Microglobulin, and Cystatin C as biomarkers of drug-induced kidney injury in preclinical safety studies — enabling their inclusion alongside traditional histopathology and clinical chemistry in IND-enabling toxicology programs. This regulatory recognition transformed kidney safety assessment: for the first time, molecular biomarkers could complement (or in some cases precede) the histopathological reference standard, providing quantitative, temporal, and reversible-readout data that terminal histopathology cannot provide.

 Kidney Injury Biomarkers — Site-Specific Detection & Regulatory Status
KIM-1/HAVCR1 (Proximal Tubule): the most specific proximal tubular injury marker. Transmembrane glycoprotein upregulated on apical membrane of injured proximal epithelial cells within hours of toxic or ischemic insult. FDA/EMA-recognized for preclinical rat nephrotoxicity. Measured in both our Human 7-Plex and Rat 4-Plex.
NGAL/LCN2 (Proximal Tubule): the most sensitive AKI marker — elevated in urine within 2–6 hours across multiple etiologies (ischemic, toxic, septic). FDA/EMA-recognized. Measured in Human 6-Plex and Rat 4-Plex. Also measurable in plasma for systemic vs. renal source discrimination.
Clusterin (Proximal & Distal Tubule): pro-survival glycoprotein upregulated during tubular regeneration. FDA/EMA-recognized. More sensitive and specific than serum creatinine or BUN for detecting drug-induced tubular damage. Measured in both Human panels.
Cystatin C (Glomerular): freely filtered cysteine protease inhibitor — urinary elevation indicates impaired proximal tubular reabsorption. Independent of muscle mass, unlike creatinine. FDA/EMA-recognized.
Osteoactivin/GPNMB (Proximal Tubule): lysosomal protein induced by proximal tubular stress. FDA/EMA-recognized for preclinical rat studies.
Calbindin & TFF3 (Distal Tubule/Collecting Duct): Calbindin is a calcium-binding protein decreased in distal tubular injury. TFF3 is a mucosal protective factor decreased in collecting duct injury. Both provide site-specific distal nephron assessment not available from standard markers.

Kidney Injury Panel Configurations

Panel	Plex	Biomarkers	Species	FDA/EMA Biomarkers
Human Kidney Injury 6-Plex	6	A2M, Clusterin, Cystatin C, NGAL/LCN2, RBP4, Serpin A1	Human	Clusterin, Cystatin C, NGAL
Human Kidney Injury 7-Plex	7	Calbindin, Clusterin, α-GST, HAVCR1/KIM-1, Osteoactivin, TFF3, VEGF-A	Human	KIM-1, Clusterin, Osteoactivin
Rat Kidney Injury 4-Plex	4	Albumin, NGAL/LCN2, HAVCR1/KIM-1, Osteopontin	Rat	KIM-1, NGAL, Osteopontin, Albumin

Additional human panels (up to 24+ analytes including EGF, TIMP-1, RBP4, Renin, Uromodulin, FABP1, Collagen IV, α-1-Microglobulin, IL-18, IP-10, MCP-1) and mouse/canine species panels are available from the MSD catalog. Contact us for expanded panel configurations. All services are for research use only.

Nephron-Segment-Resolved Kidney Injury Assessment

Glomerular Injury

Markers: Cystatin C, Albumin, VEGF-A. Cystatin C is freely filtered and reabsorbed — urinary elevation indicates impaired proximal tubular reabsorption. Albumin indicates glomerular barrier integrity loss. VEGF-A reflects podocyte health. Glomerular injury is the hallmark of diabetic nephropathy, glomerulonephritis, and antibody-mediated rejection.

Proximal Tubular Injury

Markers: KIM-1, NGAL, Clusterin, Osteoactivin, α-GST, RBP4. The proximal tubule is the most common site of drug-induced nephrotoxicity due to high metabolic activity, drug transporter expression, and concentration of filtered xenobiotics. KIM-1 and NGAL are the earliest and most sensitive indicators of proximal tubular damage.

Distal Tubule & Collecting Duct

Markers: Calbindin, TFF3, Osteopontin. Distal tubular injury is less common than proximal but characterizes specific drug toxicities (amphotericin B, lithium, calcineurin inhibitors). Site-specific distal markers distinguish tubular from glomerular injury and provide mechanistic insight into the nephron location of toxicity.

Electrochemiluminescence for Kidney Biomarker Detection

Advantages for Nephrotoxicity Assessment

Multiplex nephron-segment mapping in one well: proximal tubular (KIM-1, NGAL, Clusterin, α-GST), glomerular (Cystatin C, Albumin), and distal tubular (Calbindin, TFF3) markers measured simultaneously — providing a complete nephron injury map from 25 µL.
FDA-recognized biomarker panel: the same biomarkers qualified by the PSTC/C-Path consortium (2008) and accepted by FDA and EMA for preclinical nephrotoxicity assessment — enabling regulatory-context-appropriate data for IND-enabling studies.
Urine or plasma — single platform: the same MSD panels work for both matrices. Urine is preferred for tubular injury markers (direct release from injured cells); plasma NGAL can help distinguish systemic from renal sources.
Wide dynamic range: albumin spans >4 orders of magnitude from normal (<30 µg/mL) to nephrotic (>300 µg/mL). ECL accommodates this without the dilution adjustments that narrow-range assays require.

Kidney Injury Assay Specifications

TechnologyMSD V-PLEX

PanelsHuman 6/7-Plex + Rat 4-Plex

FDA BiomarkersKIM-1, NGAL, Clusterin, Osteopontin, Albumin, Cystatin C

Sample Volume25 µL per well

Dynamic Range3–4+ logs per analyte

Preferred MatrixUrine (spot, creatinine-normalized)

Acceptable MatrixEDTA Plasma

Urine NormalizationAll biomarkers reported as /mg uCr

Intra-Assay CV<10%

Plate Format96-well MULTI-ARRAY

SpeciesHuman, Rat

Regulatory ContextPSTC/C-Path FDA/EMA-recognized

Sample Collection Notes

Urine — uCr normalization essential to correct for flow rate variation.
EDTA plasma for NGAL/Cystatin C; process within 1h at 4°C.
Serial pre-dose + on-treatment timepoints for preclinical toxicology.

Kidney Injury Panel Service Details

Service Package

Item	Full Service	Notes
Sample Processing & Creatinine Normalization	Included	uCr normalization for all urinary biomarkers
Standard Curves	8-point, per analyte	Recombinant protein calibrators
QC Samples	Multi-level, duplicate	With documented acceptance criteria
Data Report	With nephron-segment summary	Biomarker/uCr ratios + QC metrics
Raw ECL Data	Included	Per-well, per-spot signal values

For Research Use Only. Not for diagnostic procedures.

How to Get Started

Select Panel

Choose human (6 or 7-Plex) or rat (4-Plex) based on species and coverage needs. Expanded panels available.

Collect & Ship

Spot urine or EDTA plasma. Serial pre-dose + on-treatment timepoints. Ship on dry ice with creatinine measurement.

Receive Nephrotoxicity Data

Receive quantitative biomarker data with uCr normalization, nephron-segment summary, and QC documentation.

Kidney Injury Detection: MSD vs Traditional Methods

Feature	MSD (Kidney Injury Panel)	Serum Creatinine / BUN	Individual ELISA (×N)
Detection Timing	Hours after injury (KIM-1, NGAL)	Days after injury — ~50% nephron loss	Hours — but one marker at a time
Nephron Site Resolution	Glomerular + proximal + distal — multiplex	None — functional only, not site-specific	One site per assay
Regulatory Recognition	FDA/EMA-recognized biomarkers (PSTC/C-Path 2008)	Standard clinical chemistry	Variable
Sample Volume	25 µL — all markers in one well	~50–100 µL per test	100 µL × N markers
Urine Creatinine Normalization	Included — all urinary biomarkers/uCr	N/A — serum-based	User-performed

What You Receive

Nephron-segment-resolved quantitative report — glomerular, proximal tubular, and distal tubular/collecting duct biomarkers with per-analyte QC metrics, standard curve parameters, and LOD/LLOQ values (Excel + PDF)
Urinary biomarker/uCr ratios — all urinary biomarkers normalized to urinary creatinine concentration with documented normalization factors
Raw ECL data — per-well, per-spot signal values with plate layout maps and individual standard curve plots
FDA/EMA biomarker status documentation — regulatory context for PSTC/C-Path-qualified biomarkers to support IND-enabling study data packages
Methods summary — formatted for manuscript Methods sections with panel catalog references and creatinine normalization protocol

Why Choose Electrochemiluminescence for Kidney Biomarker Testing

FDA-recognized biomarkers in a single multiplex: KIM-1, NGAL, Clusterin, and Osteopontin are qualified by the PSTC/C-Path consortium and accepted by FDA/EMA for preclinical nephrotoxicity assessment — all measured simultaneously from 25 µL
Hours, not days — earlier detection than creatinine: NGAL rises within 2–6 hours and KIM-1 within hours of toxic or ischemic insult, while serum creatinine requires days and ~50% nephron loss to detect change
Nephron-segment injury mapping: glomerular (Cystatin C, Albumin), proximal tubular (KIM-1, NGAL, Clusterin, α-GST), and distal tubular/collecting duct (Calbindin, TFF3) markers in one panel — identifying not just that the kidney is injured, but which segment
MSD kidney injury panels are the established standard in preclinical safety: the same V-PLEX platform and FDA-recognized biomarkers (KIM-1, NGAL, Clusterin, Osteopontin) are widely documented in published nephrotoxicity research — providing analytical precedent and regulatory-context familiarity
Expands from rat 4-Plex to human 24+ analyte panels: start with the core FDA-recognized panel for preclinical rat studies; expand to comprehensive human panels as programs advance to clinical development on the same ECL platform

Supporting Publications

Dieterle F, Sistare F, Goodsaid F, et al. (2010) Nature Biotechnology. 28(5):455–462. "Renal biomarker qualification submission: a dialog between the FDA-EMEA and Predictive Safety Testing Consortium." DOI: 10.1038/nbt.1625 · PMID: 20436457

Bonventre JV, Vaidya VS, Schmouder R, et al. (2010) Nature Biotechnology. 28(5):436–440. "Next-generation biomarkers for detecting kidney toxicity." DOI: 10.1038/nbt0510-436 · PMID: 20458311

Vaidya VS, Ozer JS, Dieterle F, et al. (2010) Kidney International. 78(11):1105–1113. "Kidney injury molecule-1 outperforms traditional biomarkers of kidney injury in preclinical biomarker qualification studies." DOI: 10.1038/ki.2010.310 · PMID: 20736987

Haase M, Bellomo R, Devarajan P, et al. (2009) Journal of the American Society of Nephrology. 20(8):1667–1674. "Accuracy of Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Diagnosis and Prognosis in Acute Kidney Injury: A Systematic Review and Meta-analysis." DOI: 10.1681/ASN.2009020161 · PMID: 19578007

References for informational context. For Research Use Only.

Kidney Injury & Nephrotoxicity Panel FAQ

Should I use urine or plasma for kidney injury biomarkers?

Urine is preferred for most tubular injury markers. KIM-1, NGAL, Clusterin, Osteoactivin, Calbindin, and TFF3 are directly released from injured tubular cells into urine — urinary concentrations reflect local kidney injury more directly than plasma. NGAL can be measured in both urine and plasma — plasma NGAL may reflect systemic sources (neutrophil activation, infection) in addition to renal injury. For research protocols, spot urine normalized to urinary creatinine (uCr) is the standard approach, consistent with the PSTC/C-Path FDA qualification data that used urine normalized to creatinine. Albumin should be measured in urine for kidney injury assessment. Cystatin C can be measured in either matrix.

What does it mean that these biomarkers are "FDA-recognized"?

In 2008, the Predictive Safety Testing Consortium (PSTC), led by the FDA's Critical Path Institute (C-Path), submitted urinary biomarker qualification data to both the FDA and EMA for a panel of kidney injury biomarkers including KIM-1, NGAL, Clusterin, Osteopontin, Albumin, β2-Microglobulin, and Cystatin C. Both agencies issued guidance accepting these biomarkers as indicators of drug-induced kidney injury in preclinical (IND-enabling) safety studies. This means sponsors can include MSD kidney injury panel data alongside traditional histopathology and clinical chemistry in regulatory submissions for preclinical programs. Our panels measure these FDA-recognized biomarkers in the same multiplex format used in the qualification studies. All services are for research use; biomarker data intended to support regulatory submissions should be discussed during study design to ensure appropriate documentation and QC standards are implemented.

Why measure multiple kidney biomarkers instead of just KIM-1 or NGAL alone?

Different biomarkers report on different nephron segments and injury mechanisms. KIM-1 is the most specific proximal tubular marker but does not detect glomerular or distal tubular injury. NGAL is the most sensitive but can be elevated from non-renal sources (plasma NGAL). Clusterin indicates tubular regeneration — distinguishing ongoing injury from recovery. Calbindin and TFF3 report on distal segments that KIM-1 and NGAL miss. A multi-marker panel provides a nephron-segment-resolved injury map — revealing not just that injury occurred, but which segment, how severely, and whether regeneration is underway. Relying on a single marker provides a binary signal; multiplex provides mechanistic insight into the site and nature of kidney injury.

How are urinary biomarkers normalized — and why is this necessary?

Urinary biomarker concentrations vary with urine flow rate and dilution — a concentrated morning urine sample will have higher apparent biomarker levels than a dilute sample, even if the same amount of biomarker was released from the kidney. Creatinine normalization (uCr) corrects for this by dividing each biomarker concentration by the urinary creatinine concentration from the same sample, yielding values in pg or ng per mg creatinine. This is the standard method used in the PSTC/C-Path FDA qualification data, and we perform it for all urinary biomarkers with documented creatinine concentrations in the data report.

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