Patient characteristics and outcomes by GN subtype in ESRD

Abstract

Background and objectives: Outcomes-based research rarely focuses on patients with ESRD caused by GN. The hypotheses were that the GN subtype would clinically discriminate patient groups and independently associate with survival after ESRD therapy initiation.

Design, setting, participants, & measurements: Data were extracted from the US Renal Data System for adult patients with incident (1996-2011) ESRD attributed to six GN subtypes: FSGS, IgA nephropathy (IgAN), membranous nephropathy, membranoproliferative glomeruonephritis, lupus nephritis (LN), and vasculitis. ESRD attributed to diabetes and autosomal dominant polycystic kidney disease served as non-GN comparators. Unadjusted and adjusted mortality hazard ratios (aHRs) with 95% confidence intervals (95% CIs) were estimated using Cox regression (reference, IgAN). Models sequentially adjusted for sociodemographic (model 2), comorbidity/laboratory (model 3), and ESRD treatment modality (model 4) variables.

Results: Among 84,301 patients with ESRD attributed to GN, the median age ranged from 39 (LN) to 66 (vasculitis) years, male sex ranged from 18% (LN) to 68% (IgAN), and black race ranged from 7% (IgAN) to 49% (LN). Patients with IgAN had the fewest comorbidities and lowest use of hemodialysis (70.1%). After a median follow-up of 2.5 (interquartile range, 1.0-4.9) years, crude mortality was lowest in IgAN (3.7 deaths/100 person years). Compared to IgAN, adjusted mortality was highest in LN (model 4 aHR=1.75; 95% CI, 1.68 to 1.83) and in diabetes (aHR=1.73; 95% CI, 1.67 to 1.79), and was also higher in all other GN subtypes (membranous nephropathy: aHR=1.23; 95% CI, 1.17 to 1.29; FSGS: aHR=1.37; 95% CI, 1.32 to 1.42; membranoproliferative GN: aHR=1.38; 95% CI, 1.31 to 1.45; vasculitis: aHR=1.51; 95% CI, 1.45 to 1.58) and in autosomal dominant polycystic kidney disease (aHR=1.22; 95% CI, 1.18 to 1.27).

Conclusions: This study exposes substantial heterogeneity across GN subtypes at ESRD therapy initiation and identifies independent associations between GN subtype and post-ESRD mortality. These survival discrepancies warrant further study, and the utility of current research practice to group GN subtypes together when evaluating ESRD outcomes should be questioned.

Keywords: IgA nephropathy; United States Renal Data System; end-stage renal disease; epidemiology and outcomes; glomerulonephritis.

Figure 1.

Flow diagram of cohort assembly. ADPKD, autosomal dominant polycystic kidney disease; DN, diabetes-related ESRD; IgAN, IgA nephropathy; LN, lupus nephritis; MN, membranous nephropathy; MPGN, membranoproliferative GN.

Figure 2.

Kaplan–Meier survival curves. ADPKD, autosomal dominant polycystic kidney disease; DN, diabetes-related ESRD; IgAN, IgA nephropathy; LN, lupus nephritis; MN, membranous nephropathy; MPGN, membranoproliferative GN.

Figure 3.

Unadjusted and adjusted mortality hazard ratios. Model 1 is unadjusted; model 2 is demographic adjusted; model 3 is demographic and comorbidity adjusted; and model 4 is demographic, comorbidity, and ESRD therapy modality adjusted. ADPKD, autosomal dominant polycystic kidney disease; DN, diabetes-related ESRD; IgAN, IgA nephropathy; LN, lupus nephritis; MN, membranous nephropathy; MPGN, membranoproliferative GN.

Figure 4.

Cause of death categories by GN subtype. ADPKD, autosomal dominant polycystic kidney disease; DN, diabetes-related ESRD; IgAN, IgA nephropathy; LN, lupus nephritis; MN, membranous nephropathy; MPGN, membranoproliferative GN.