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We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.<\/strong> <\/p>\nBack to Healio<\/button><\/p>\n<\/div>\n<\/div><\/div>\n<\/p><\/div>\n<\/p><\/div>\n<\/div>\nKey takeaways:<\/h2>\n\nCombination therapy at the outset of lupus nephritis diagnosis can be effective in preventing downstream complications.<\/li>\n Proteinuria is an imperfect biomarker in lupus nephritis.<\/li>\n<\/ul>\nDESTIN, Fla. \u2014 Until biomarkers that can predict treatment response emerge, early and aggressive treatment is recommended in lupus nephritis, according to a presenter at Congress of Clinical Rheumatology East.<\/p>\n
\u201cWe have to be aggressive in lupus nephritis right off the bat because most patients have had untreated disease,\u201d Alfred H<\/b>.<\/b>J<\/b>.<\/b> Kim, MD, PhD<\/b>, <\/b>director of the Washington University Lupus Center, told attendees, here.<\/p>\n
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Alfred H.J. Kim, MD, PhD<\/b>,<\/b> told attendees. <\/i>Image: Rob Volansky | Healio<\/i>
Patients may have waited as long as 5 years between initial presentation and an actual diagnosis of lupus nephritis, according to Kim. It is critical to gain disease control as soon as possible.<\/p>\n
Standard of care for newly diagnosed lupus nephritis generally involves glucocorticoids and mycophenolate mofetil (MMF) or some combination of cyclophosphamide and\/or azathioprine, Kim said.<\/p>\n
\u201cUsing traditional standard of care therapies and then adding belimumab on top is going to improve things, at least in the short term,\u201d Kim said. \u201cTriple therapy does have benefits.\u201d<\/p>\n
The key benefit of belimumab is B-cell depletion. While the data for the B-cell depleter rituximab (Rituxan, Genentech) in lupus nephritis have been suboptimal, the recent FDA approval of the humanized type II anti-CD20 monoclonal antibody obinutuzumab (Gazyva, Genentech) has provided a lift to this approach. \u201cObinutuzumab eliminates nearly all B cells in the kidney,\u201d Kim said. \u201cIt works like a natural killer cell engager.\u201d<\/p>\n
But the jury is still out on the effectiveness of B-cell depletion in lupus nephritis. \u201cYou will hear this argument in the next talk, and then the next, talking about the depth of B-cell depletion, and whether it is clinically important,\u201d Kim said.<\/p>\n
A companion argument pertains to infection risk in patients who have undergone B-cell depletion, according to Kim. He added that vaccine schedules could be problematic in patients who undergo the FDA-approved dosing schedule of obinutuzumab.<\/p>\n
As those parameters are worked out in clinical trials and post-marketing studies, Kim highlighted another critical concern for rheumatologists managing lupus nephritis. \u201cWe have really run into some problems with proteinuria,\u201d he said. <\/p>\n
While proteinuria often defines treatment response in many lupus nephritis trials, Kim suggested the outcome does not often align with biopsy data. Moreover, many patients have low proteinuria but still show signs of proliferative lupus nephritis. <\/p>\n
\u201cProteinuria is problematic for lupus nephritis detection,\u201d Kim said. \u201cIt does not correlate with intrarenal activity.\u201d<\/p>\n
The search for other biomarkers has yielded similarly conflicting results. Kim discussed uIL-16, uCD163 and tenascin C, among others.<\/p>\n
While uIL-16 and uCD163 have shown some potential in defining certain lupus nephritis parameters, Kim said more information is needed.<\/p>\n
\u201cThey have no relationship to chronicity,\u201d he said. \u201cI am not saying that these biomarkers don\u2019t have potential. I am saying we have to be careful not to oversimplify what these biomarkers will mean in the future.\u201d<\/p>\n
Regarding tenascin C, Kim noted that the exact function of the protein is unknown. \u201cBut we know that it correlates with fibrosis,\u201d he said. \u201cIt could be a useful predictor of kidney function loss when measured in urine.\u201d<\/p>\n
As more data emerge on those biomarkers, Kim said the call to be aggressive in treatment. \u201cBe as aggressive as you and the patient are comfortable being,\u201d he said.<\/p>\n
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Sources\/Disclosures<\/h3>\n Source: <\/h2>\n Kim AHJ. The changing landscape of SLE nephritis treatment. Presented at: Congress of Clinical Rheumatology East; April 30-May 3, 2026; Destin, Florida (hybrid meeting).<\/p>\n
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