Grateful to the legendary Sanjeev Sethi for partnering with our team.
Grateful to the legendary Sanjeev Sethi for partnering with our team.
16/16
Bottom line: MCCS and NIH-CI are comparable and add prognostic signal beyond clinical data—with IF/TA doing most of the heavy lifting—and performance was consistent in Class V LN. MCCS may offer a practical edge by aligning chronicity grading across glomerular diseases.
15/16
Robustness check: performance held across key subgroups—including Class V (membranous) LN—with no meaningful interaction effects. In other words: the prognostic signal wasn’t just a proliferative-LN story.
14/16
Clinical pearl: even mild IF/TA mattered—and moderate/severe IF/TA aligned with a striking jump in ESKD risk versus no fibrosis. If you track one chronic lesion meticulously, make it IF/TA.
13/16
Lesion-level insight: IF/TA (interstitial fibrosis/tubular atrophy) was the only component that stayed independently predictive across renal outcomes in multivariable models.
12/16
Decision-curve analysis: adding either NIH-CI or MCCS produced net benefit for identifying 5-year ESKD risk vs clinical variables alone. Translation: chronicity scores capture risk information not visible in routine clinical variables.
11/16
Do these scores add value beyond routine clinical inputs (age/sex/eGFR/proteinuria)?
Yes. Adding either score improved discrimination for PR500, CRR, and ESKD prediction. Mortality prediction didn’t meaningfully improve.
10/16
MCCS grades are especially clinician-friendly: compared with minimal chronicity, severe MCCS (8–10) meant dramatically lower remission and a markedly higher risk of ESKD.
9/16
Core result: higher chronicity = worse renal outcomes.
Each 1-point increase in chronicity → lower remission likelihood and higher ESKD risk. MCCS showed a very similar pattern.
8/16
Cohort snapshot: 307 patients. Within 1 year: PR500 ~47%, CRR ~43%. Over follow-up: ESKD ~20%, deaths ~11%. NIH-CI and MCCS were highly correlated.
7/16
Methods: sex-stratified, age-adjusted Cox models; model discrimination via Harrell’s C-index; plus decision-curve analysis for 5-year ESKD (competing-risk aware).
6/16
Outcomes were clinically grounded:
• PR500 (proteinuria <500 mg/day)
• CRR (PR500 + eGFR within ±15%)
• ESKD (sustained eGFR ≤15 / dialysis / transplant)
• Death
5/16
Design: single-center retrospective cohort (Mayo Clinic), renal specimens 1992–2023, biopsy-proven active LN; first biopsy used. Real-world data with a long runway.
4/16
Two “languages” of chronicity:
• NIH-CI = glomerulosclerosis + fibrous crescents + interstitial fibrosis + tubular atrophy (0–12)
• MCCS = glomerulosclerosis + interstitial fibrosis + tubular atrophy + arteriosclerosis; graded minimal→severe (0–10)
3/16
Why this matters: chronic lesions (glomerulosclerosis, tubular atrophy, interstitial fibrosis) are largely irreversible and track with worse long-term renal outcomes. We need better risk stratification than labs alone.
2/16
New study in Kidney International Reports (2026): “Evaluating Chronicity Scores for Outcomes in Patients With Lupus Nephritis”—with co–senior author Sanjeev Sethi, who reviewed all biopsies.
1/16
In lupus nephritis (LN), “activity” gets the spotlight—but chronic scarring often decides the long game. So: which chronicity score best predicts outcomes—NIH Chronicity Index (NIH-CI) or the Mayo Clinic Chronicity Score (MCCS)?
buff.ly/tvebmPZ