Creative Biolabs provides complement-focused nephropathy research services for programs investigating immune-complex glomerular injury, alternative-pathway dysregulation, thrombotic microangiopathy, podocyte and tubular damage, renal complement deposition, genotype or autoantibody-driven disease, translational biomarkers, and complement-targeted therapeutics. We support experimental planning, sample and pathway qualification, renal cell and tissue models, mechanism-of-action studies, candidate testing, and integrated data interpretation.
Discuss Your Nephropathy Research ProgramOur services are designed for nephrology programs that need to determine which complement pathway is active, whether dysregulation is systemic or kidney-localized, how a genetic variant or autoantibody changes regulation, and whether a therapeutic candidate produces pathway-selective renal protection.
Classical, lectin, alternative, and terminal-pathway profiling; activation-product and deposition assays; functional genetics; complement autoantibody studies; renal cell and tissue models; biomarker panels; and candidate efficacy evaluation.
C3 glomerulopathy, immune-complex glomerulonephritis, IgA nephropathy, lupus nephritis, membranous nephropathy, complement-mediated HUS/TMA, FSGS, transplant-associated injury, and project-defined renal disease models.
Feasibility assessment, control and matrix planning, assay qualification, study execution, raw and processed data, statistics, images, mechanistic interpretation, biomarker or candidate ranking, and next-step recommendations.
We can begin with pre-analytical risk review, matrix testing, pathway screening, and a staged biomarker plan.
The same plasma marker can reflect different renal mechanisms. Our study design connects soluble pathway activity to the kidney compartment where complement is deposited, regulated, or converted into inflammatory and cytotoxic injury.
Immune complexes, aberrant IgA, damaged endothelium, exposed matrix, ischemia, glycated surfaces, infection-related signals, or transplant-associated injury initiate complement.
C3 convertase formation, factor B and factor D activity, properdin stabilization, nephritic factors, or insufficient factor H and factor I regulation sustain pathway output.
C3 fragments, C4d, immunoglobulin-associated complement, and C5b-9 accumulate in glomerular, tubular, interstitial, or vascular compartments.
C3a/C5a signaling, endothelial activation, podocyte stress, mesangial inflammation, tubular injury, thrombosis, proteinuria, sclerosis, or fibrosis define the phenotype.
Is low C3 caused by consumption? Does a patient sample stabilize C3 or C5 convertase? Is C5b-9 generated systemically or on renal cells? Does factor H-related protein competition reduce surface regulation? Which pharmacodynamic marker changes before the renal phenotype?
Complement-depleted and reconstituted serum, heat-inactivated matrix, pathway-selective buffers, wild-type and variant regulators, autoantibody-positive and negative samples, target-specific inhibitors, inactive or isotype controls, and rescue experiments.
Disease labels alone do not define the assay. We align pathway emphasis, sample matrix, renal compartment, controls, and efficacy endpoints with the proposed driver and disease stage.
Profile alternative-pathway dysregulation, C3 nephritic factors, factor H and FHR balance, genetic variants, convertase stability, C3 fragment deposition, and terminal-pathway activity.
Explore C3 glomerulopathy researchStudy endothelial complement activation, regulatory variants or antibodies, C5a and C5b-9 formation, thrombosis-related endpoints, and rescue by proximal or terminal inhibitors.
Explore HUS complement researchAssess classical, lectin, and alternative pathway contributions in IgA nephropathy, lupus nephritis, membranous nephropathy, and project-defined immune-complex models.
Explore glomerulonephritis researchConnect IgM/C3 deposition, soluble activation products, podocyte stress, permeability, proteinuria-related conditions, and sclerosis or fibrosis endpoints in FSGS-related research.
View C3b deposition assaysInvestigate complement activation on tubular epithelial cells or matrix under hypoxic, oxidative, glycated, toxic, or protein-overload stress and quantify inflammatory or viability outcomes.
Explore cell-based complement evaluationEvaluate donor-specific or project-defined antibody-mediated complement activation, endothelial deposition, C4d and C5b-9, inflammatory signaling, and inhibitor response.
View complement inhibition assaysAssay modules can be commissioned independently or combined into a staged study. Conditions are harmonized across modules so pathway, deposition, and kidney-cell results can be interpreted together.
Establish whether the sample or candidate changes net complement capacity.
Build a fit-for-purpose serum, plasma, urine, or supernatant panel.
Determine whether activation reaches the kidney cell or tissue compartment of interest.
Move from a suspected complement abnormality to functional evidence.
Connect pathway modulation to a renal effect rather than a soluble marker alone.
Quantify potency, selectivity, rescue, and the relationship between pharmacodynamics and renal protection.
Gene-panel findings can be linked to variant expression, regulator activity, convertase control, deposition, and kidney-cell protection.
Purified and reconstituted systems isolate complement regulation; renal cells and advanced models test whether that mechanism produces a relevant tissue response. Model qualification precedes candidate comparison.
Defined proteins, wild-type or variant regulators, depleted and reconstituted serum, convertase components, immune complexes, nephritic-factor concepts, modified matrix, and benchmark inhibitors.
Podocytes, mesangial cells, glomerular endothelial cells, endothelial–podocyte interfaces, complement-sensitive surfaces, permeability, inflammatory activation, and thrombotic readouts.
Proximal or distal tubular epithelial cells, hypoxic or oxidative injury, protein-overload and glycated contexts, complement deposition, viability, inflammatory mediators, and fibrosis-related endpoints.
Kidney organoids, tissue slices or explants, glomerular and TMA-related concepts, ischemia–reperfusion, antibody-mediated injury, disease-relevant animal models, and pharmacodynamic endpoints.
Collection tube, anticoagulant, processing delay, temperature, storage, freeze–thaw history, hemolysis, proteinuria, renal function, ex vivo complement activation, urine concentration normalization, matrix interference, species compatibility, and sample volume are reviewed before testing.
We use milestone-based testing so a candidate advances only when its effect is linked to the intended complement node and reproduced in a renal context with appropriate activity, specificity, and toxicity controls.
C1s, MASP-2, C3, factor B, factor D, properdin, C3 convertase, or amplification-loop inhibition.
C5, C5a, C5aR, C6–C9, membrane attack complex, or downstream inflammatory signaling.
Factor H, factor I, soluble CR1, surface-targeted regulation, replacement, engineered regulator, or variant rescue.
Antibodies, proteins, peptides, aptamers, small molecules, nucleic-acid tools, gene-delivery concepts, and project-defined modalities.
The final package is selected according to the target, renal compartment, candidate format, intended route, and the biological claim required for advancement.
Representative controls include vehicle, inactive analog, isotype, heat-inactivated matrix, depleted and reconstituted serum, pathway-selective standards, cell-health controls, non-renal cells, and rescue with a functional complement regulator.
Combine biochemical engagement, pathway function, complement deposition, activation biomarkers, and kidney-cell protection at matched candidate concentrations.
These original studies illustrate three complementary research patterns: functional regulation and renal-surface deposition in C3 glomerulopathy, a urinary complement regulator associated with IgA nephropathy progression, and paired plasma–urine complement profiling in FSGS.
Slagle and colleagues combined patient FH/FHR measurements, genotype analysis, renal-cell C3b deposition, and heparan-sulfate binding studies. The work demonstrates how circulating regulator balance and local surface chemistry can be evaluated in one disease-mechanism program.
View research via DOI
Liu and colleagues measured urinary CFH in a longitudinal IgA nephropathy cohort and related it to eGFR, proteinuria, histologic severity, and renal outcome. The design illustrates the value of matrix-aware complement biomarkers combined with established renal measures.
View research via DOI
Huang and colleagues quantified C3a, C5a, sC5b-9, C4d, C1q, MBL, and Bb in biopsy-proven primary FSGS. The study shows how multi-analyte profiling can connect complement activation with proteinuria, renal dysfunction, fibrosis, treatment response, and outcome.
View research via DOIWe provide complement pathway and activation-product profiling, C3 and C5b-9 deposition assays, functional genetic and autoantibody studies, renal cell and tissue models, serum/plasma/urine biomarker analysis, and complement-targeted candidate evaluation for glomerular, vascular, tubular, and transplant-related research contexts.
Programs can be designed for C3 glomerulopathy, complement-mediated HUS and thrombotic microangiopathy, IgA nephropathy, lupus nephritis, membranous nephropathy, other immune-complex glomerulonephritides, FSGS-related complement questions, tubular injury, and transplant-associated renal injury.
Yes, subject to sample suitability and project requirements. A study can pair soluble pathway activity with urinary biomarkers, tissue deposition, renal cell phenotype, genotype, and candidate response. Collection and processing variables are reviewed because ex vivo complement activation and urine concentration can materially affect interpretation.
Yes. Genetic findings and suspected autoantibodies can be linked to protein expression, binding, factor H or factor I regulation, convertase stability, C3b degradation, pathway output, renal-surface deposition, endothelial or renal-cell injury, and rescue by a functional regulator or inhibitor.
Options include C3a, C5a, Ba/Bb, iC3b/C3d, sC5b-9, C3, C4, C1q, factor B, factor D, properdin, factor H, factor I, FHR proteins, C4d, pathway functional activity, and C3-fragment or membrane attack complex deposition. The panel is selected according to disease mechanism and matrix.
Yes. Candidates can be tested for target engagement, pathway selectivity, activation-product reduction, renal-surface deposition, endothelial or podocyte protection, permeability, inflammatory and thrombotic outputs, and toxicity in cell, co-culture, organoid, explant, or project-defined preclinical models.
Please provide the renal disease context, suspected complement pathway or target, available sample and species, kidney compartment, candidate format and amount, concentration range, benchmark, biomarker and phenotype endpoints, timeline, and the decision the data must support. Unknown items can be addressed in a feasibility phase.
Complement Activity/Function Assay Products
Learn More
Complement Testing Services
Learn More
Complement Therapeutics Featured Products
Learn More
Complement Therapeutics Services Brochure
Learn More
Aptamer Development PLATFORM
Learn More
ComPLETTM Hemolysis Assay Solutions
Learn More