Intermediate Renal Outcomes, Kidney Failure, and Mortality in Obese Kidney Donors

Abstract

Background: Obesity is associated with the two archetypal kidney disease risk factors: hypertension and diabetes. Concerns that the effects of diabetes and hypertension in obese kidney donors might be magnified in their remaining kidney have led to the exclusion of many obese candidates from kidney donation.

Methods: We compared mortality, diabetes, hypertension, proteinuria, reduced eGFR and its trajectory, and the development of kidney failure in 8583 kidney donors, according to body mass index (BMI). The study included 6822 individuals with a BMI of <30 kg/m², 1338 with a BMI of 30-34.9 kg/m², and 423 with a BMI of ≥35 kg/m². We used Cox regression models, adjusting for baseline covariates only, and models adjusting for postdonation diabetes, hypertension, and kidney failure as time-varying covariates.

Results: Obese donors were more likely than nonobese donors to develop diabetes, hypertension, and proteinuria. The increase in eGFR in obese versus nonobese donors was significantly higher in the first 10 years (3.5 ml/min per 1.73m² per year versus 2.4 ml/min per 1.73m² per year; P<0.001), but comparable thereafter. At a mean±SD follow-up of 19.3±10.3 years after donation, 31 (0.5%) nonobese and 12 (0.7%) obese donors developed ESKD. Of the 12 patients with ESKD in obese donors, 10 occurred in 1445 White donors who were related to the recipient (0.9%). Risk of death in obese donors was not significantly increased compared with nonobese donors.

Conclusions: Obesity in kidney donors, as in nondonors, is associated with increased risk of developing diabetes and hypertension. The absolute risk of ESKD is small and the risk of death is comparable to that of nonobese donors.

Keywords: glomerular filtration rate; hypertension; kidney donation; living donation; obesity; outcomes.

Figure 1.

Study participants.

Figure 2.

Baseline BMI and trend over study period. (A) BMI at donation. (B) BMI by year of donation. Distribution of the predonation BMI were reported by the median and IQR. Distribution of the BMI by year of donation was presented by a scatter plot with regression line. The regression coefficient and 95% CI were reported.

Figure 3.

Trajectory of eGFR (ml/min per 1.73m²) over time. (A) BMI <30 versus 30 kg/m². (B) BMI <30, 30–34.9, >35 kg/m². The trend of eGFR over time is depicted by the cubic spline plots. Difference in eGFR slope between obese and nonobese donors was compared using a generalized linear mixed model. The coefficient (slope) and 95% CI, which represents mean change over time, was reported for each group. The generalized linear mixed model used eGFR as the dependent variable and BMI category as the independent variable, and used a random intercept plus random slope model and unstructured covariance option. The cubic splines were also used to depict the distribution of adjusted hazard ratio of evaluated study outcomes across BMI range. Because the eGFR slope appeared to change direction after 10 years, a subanalysis using the piecewise generalized linear model for years 0–10 and years 10–30 were conducted.

Figure 4.

Cumulative incidence of major outcomes. (A) Mortality. (B) Diabetes. (C) Hypertension. (D) CVD. (E) Proteinuria. (F) ESKD. (G) Composite of ESKD or eGFR<30 ml/min per 1.72m². Kaplan–Meier curve was used for mortality; aHR for mortality obtained from the multivariable Cox proportional hazard model. Adjusted competing risk curves were used for outcomes other than mortality with the subdistribution hazard ratio obtained from the multivariable subdistribution hazard models (Fine and Gray method).

Figure 5.

Cubic spline plot for aHR, by BMI. (A) Nonrenal outcomes, BMI = 25 kg/m² as the reference. (B) Renal outcomes, BMI = 25 kg/m² as the reference. (C) Nonrenal outcomes, BMI = 30 kg/m² as the reference. (D) Renal outcomes, BMI = 30 kg/m² as the reference. aHRs were obtained from the multivariable Cox regression models for individual outcomes.