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Intrarenal Complement Activation as a marker of kidney injury and treatment response in lupus nephritis

Award Number: K23AR085758
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 06/01/2026
PERIOD OF PERFORMANCE END DATE: 05/31/2031

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Intrarenal Complement Activation as a marker of kidney injury and treatment response in lupus nephritis - ABSTRACT The complement system is known to play a central role in the pathogenesis of lupus nephritis (LN), one of the most severe manifestations of systemic lupus erythematosus (SLE). Mortality rates for SLE patients with LN is almost four-fold higher than those without LN. Over 50% of LN patients do not respond to standard treatment and are more likely to progress to end-stage-kidney-disease. Given the critical role of complement in LN, we hypothesize that non-responders have complement-driven inflammation as a major source of kidney injury. With the arrival of complement blockade in LN, this study addresses the unmet need to gain insight into complement- mediated kidney injury in LN and to identify non-invasive complement markers of treatment response. Emerging data suggest that complement components are synthesized inside the kidney and are linked to kidney damage. Studies in mice showed specific kidney cell populations express complement genes, which can lead to kidney injury by cytokine production contributing to inflammation, stimulation of extracellular matrix, and activation of the renin angiotensin system. However, intrarenal complement activation in LN patients is not well characterized. It is important to localize the site of complement production inside the LN kidney to ensure drugs can reach their correct targets and identify new markers of treatment response. Our overall hypothesis is that intrarenal complement activation is associated with disease activity, kidney damage and nonresponse to standard treatment in LN. Our hypothesis is based prior studies where we showed membrane attack complex deposition in kidney tubules of LN patients was associated with interstitial fibrosis/tubular atrophy (IFTA), a histologic marker of kidney damage. In addition, we found that tubular complement gene expression and urinary complement protein levels were significantly elevated in LN patients with IFTA as compared to those without IFTA. These increases correlated with fibrosis-related signaling pathways, such as TGF-β expression, further highlighting the role of complement in kidney injury. To investigate our central hypothesis, we will 1) investigate intrarenal complement gene expression signatures in the LN kidney tissue and correlate with kidney damage and treatment response (Aim 1), and 2) compare serum and urine complement protein profiles between responders and non-responders in a prospective LN cohort (Aim 2). This translational study is significant because there are complement-targeting therapies that may be used in patients with evidence of intrarenal complement activation in kidney tissue and urine, which promise individualized medicine. The support from a K23 will enable Dr. Wang to develop expertise in lupus, LN complement biology, biomarker development, cohort building and the application of omics approaches to study autoimmune diseases as she transitions to an independent investigator with expertise in the field of lupus.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $177,984 )
2026	2026	ALBERT EINSTEIN COLLEGE OF MEDICINE	1300 MORRIS PARK AVE	BRONX	NY	10461	BRONX	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	5/12/2026	NEW	$177,984
														Subtotal = $177,984

Grand Total All Awards = $177,984

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Intrarenal Complement Activation as a marker of kidney injury and treatment response in lupus nephritis

Award Number: K23AR085758

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 06/01/2026

PERIOD OF PERFORMANCE END DATE: 05/31/2031

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