Abstract: FR-PO882
Combination of Acanthocyturia and Elevated Serum IgA Level for the Diagnosis of IgA Nephropathy
Session Information
- IgA Nephropathy: Clinical, Outcomes, and Therapeutics
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Zarm, Ayaa M., Ochsner Medical Center, New Orleans, Louisiana, United States
- Stark, Ana Isabel, Ochsner Medical Center, New Orleans, Louisiana, United States
- Kovacic, Rosemary, Ochsner Medical Center, New Orleans, Louisiana, United States
- Kanduri, Swetha Rani, Ochsner Medical Center, New Orleans, Louisiana, United States
- Velez, Juan Carlos Q., Ochsner Medical Center, New Orleans, Louisiana, United States
Group or Team Name
- Ochsner Group.
Background
Serum IgA level (sIgA) has been assessed as a clinical test for the diagnosis of IgA nephropathy (IgAN). Its performance has been modest with sensitivity (SENS) and specificity (SPEC) around 65%. However, studies had tested its performance independently of urinary findings. We hypothesized that idenitfication of acanthocyturia by microscopic examination of the urinary sediment (uSEDI) may increase the pre-test probability of IgAN and, therefore, the diagnostic yield of sIgA may improve when utilized in cases where acanthocyturia is present.
Methods
We prospectively collected data of patients seen in nephrology consultation who had a urine specimen subjected to uSEDI as part of the clinical evaluation over a 5-yr period. Within this cohort, we identified cases in which: 1) urinary acanthocytes were identified by uSEDI; 2) a kidney biopsy was perfomed; and 3) sIgA was obtained as part of the diagnostic work up. Normal range of sIga for our hospital laboratory is 40-350 mg/dL. We assessed the diagnostic performance of sIgA.
Results
Among 801 patients assessed by uSEDI, 240 (30%) underwent kidney biopsy. Urinary acanthocytes were identified in 96 (40%), and 49 (51%) had sIgA measured. Mean age was 53 years, 45% women, 71% white and 27% black. Median serum creatinine was 2.2 (0.6-19.2) mg/dL. Diagnosis was IgAN in 22 (24%), pauci immune glomerulonephritis (GN) in 18 (20%), lupus GN in 8 (9%), other proliferative or infection-related GN (IRGN) in 9 (10%), and thin basement membrane nephropathy in 5 (5%). One case was IgA-dominant IRGN. Median sIgA was higher in IgAN or IgA-dominant IRGN than in others (360 vs 253 mg/dL, p=0.012). Using the laboratory normal range, sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of elevated sIgA for identifying IgAN (or IgA-dominant IRGN) were 53%, 68%, 42% and 77%. The AUROC for sIgA for IgAN diagnosis was 0.74 (95% CI 0.59-0.88, p=0.013). The optimal cuttoff was 327 mg/dL. Notably, all IgAN cases were ≥ 230 mg/dL.
Conclusion
sIgA performs modestly as a diagnostic test for IgAN. Adjusting the cutoff to a level within normal range increases the NPV. We suggest that in patients with acanthocyturia, sIgA may be part of the serological work up.