Dataset Information

Multidisciplinary Lupus Nephritis Clinic Reduces Time to Renal Biopsy and Improves Care Quality.

ABSTRACT:

Objective

Patients with lupus nephritis (LN) have a 26-fold higher mortality rate compared with their peers. Kidney biopsy, the gold standard diagnostic method for LN, may have an average wait time of more than 50 days. Other gaps in quality process measures during LN visits have also been reported. A subspecialty multidisciplinary clinic (MDC) can provide better care and quality in LN; therefore, we aimed to examine how an LN MDC impacted time to biopsy, time to treatment, and other quality measures.

Methods

We included all validated patients with LN who underwent diagnostic kidney biopsies between the 2011 to 2017 pre-MDC period and the 2018 to 2020 post-MDC period. We compared time to biopsy and treatment and quality measures between the two periods and examined factors associated with timely LN diagnosis, defined as a biopsy within 21 days.

Results

During the pre- and post-MDC periods, 53 and 21 patients with LN underwent a diagnostic biopsy, respectively. We found a decrease in the median time to biopsy from 26 days to 16 days after starting the LN clinic (P = 0.014). Beyond clinical factors, the presence of social factors, such as being of a non-White race and having food insecurity, were associated with 54% lower odds of timely diagnosis (adjusted Hazards Ratio [aHR] = 0.46; 95% confidence interval: 0.22-0.93; P = 0.031). We found higher odds of quality measure performance during the post- versus pre-MDC period.

Conclusion

Wait times to diagnose LN decreased by 40% and higher quality measure performance was noted after establishing an LN MDC. Systemic and social barriers predicted delays in diagnosis that may be addressed by MDCs.

SUBMITTER: Garg S

PROVIDER: S-EPMC9274336 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:INTRODUCTION: Among various lupus renal vascular changes, thrombotic microangiopathy (TMA) presented with the most severe clinical manifestations and high mortality. The pathogenesis of TMA in systemic lupus erythematosus (SLE) was complicated. The aim of this study was to assess clinical manifestations, laboratory characteristics, pathological features and risk factors for clinical outcomes of lupus nephritis patients co-existing with renal TMA in a large cohort in China. METHODS: Clinical and renal histopathological data of 148 patients with biopsy-proven lupus nephritis were retrospectively analyzed. Serum complement factor H, A Disintegrin and Metalloprotease with Thrombospondin type I repeats 13 (ADAMTS-13) activity, antiphospholipid antibodies and C4d deposition on renal vessels were further detected and analyzed. RESULTS: In the 148 patients with lupus nephritis, 36 patients were diagnosed as co-existing with renal TMA based on pathological diagnosis. Among the 36 TMA patients, their clinical diagnoses of renal TMA were as followings: 2 patients combining with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome, 2 patients combining with anti-phospholipid syndrome, 2 patients with malignant hypertension, 1 patient with scleroderma and the other 29 patients presenting with isolated renal TMA. Compared with the non-renal TMA group, patients with renal TMA had significantly higher urine protein (7.09±4.64 vs. 4.75±3.13 g/24h, P=0.007) and serum creatinine (159, 86 to 215 vs. 81, 68 to 112 ?mol/l, P<0.001), higher scores of total activity indices (AI) (P<0.001), endocapillary hypercellularity (P<0.001), subendothelial hyaline deposits (P=0.003), interstitial inflammation (P=0.005), glomerular leukocyte infiltration (P=0.006), total chronicity indices (CI) (P=0.033), tubular atrophy (P=0.004) and interstitial fibrosis (P=0.018). Patients with renal TMA presented with poorer renal outcome (P=0.005) compared with the non-TMA group. Renal TMA (hazard ratio (HR): 2.772, 95% confidence interval: 1.009 to 7.617, P=0.048) was an independent risk factor for renal outcome in patients with lupus nephritis. The renal outcome was poorer for those with both C4d deposition and decreased serum complement factor H in the TMA group (P=0.007). CONCLUSIONS: There were various causes of renal TMA in lupus nephritis. Complement over-activation via both classical and alternative pathways might play an important role in the pathogenesis of renal TMA in lupus nephritis.