Association of metabolic syndrome with kidney function and histology in living kidney donors

Abstract

The selection of living kidney donors is based on a formal evaluation of the state of health. However, this spectrum of health includes subtle metabolic derangements that can cluster as metabolic syndrome. We studied the association of metabolic syndrome with kidney function and histology in 410 donors from 2005 to 2012, of whom 178 donors were systematically followed after donation since 2009. Metabolic syndrome was defined as per the NCEP ATPIII criteria, but using a BMI > 25 kg/m(2) instead of waist circumference. Following donation, donors received counseling on lifestyle modification. Metabolic syndrome was present in 50 (12.2%) donors. Donors with metabolic syndrome were more likely to have chronic histological changes on implant biopsies than donors with no metabolic syndrome (29.0% vs. 9.3%, p < 0.001). This finding was associated with impaired kidney function recovery following donation. At last follow-up, reversal of metabolic syndrome was observed in 57.1% of donors with predonation metabolic syndrome, while only 10.8% of donors developed de novo metabolic syndrome (p < 0.001). In conclusion, metabolic syndrome in donors is associated with chronic histological changes, and nephrectomy in these donors was associated with subsequent protracted recovery of kidney function. Importantly, weight loss led to improvement of most abnormalities that define metabolic syndrome.

Keywords: Body mass index; kidney transplant; living donor; metabolic syndrome; nephrosclerosis; outcomes.

Figure 1. Frequencies of histological abnormalities (either glomerulosclerosis, interstitial fibrosis/tubular atrophy or arteriosclerosis) in donors with and without metabolic syndrome at the time of donation

Chronic histological changes were characterized by the following: (1) >5% global glomerulosclerosis, (2) any interstitial fibrosis with tubular atrophy and (3) any arteriosclerosis, and scored the number of any histological changes as 0, 1, 2 and 3.

Figure 2. Estimated GFR at each time point in donors with and without metabolic syndrome (A); and percent change in estimated GFR from baseline to 1 month postdonation, from within 1 month postdonation to within 12 months of follow-up and from within 1 month postdonation to 2 years postdonation in donors with and without metabolic syndrome at the time of donation (B)

eGFR_CKD–EPI = estimated glomerular filtration rate by the Chronic Kidney Disease Epidemiology Collaboration equation. *p < 0.001: compared to eGFR_CKD–EPI at 1 month postnephrectomy in donors without metabolic syndrome by the matched-paired Student’s t-test. ^†p < 0.05: compared to eGFR_CKD–EPI at 1 month postnephrectomy in donors with metabolic syndrome by the matched-paired Student’s t-test.

Figure 3. Estimated GFR_CKD–EPI at each time point in donors with and without chronic histological changes on implant biopsy (A); and percent change in estimated GFR_CKD–EPI from baseline to 1 month postdonation, from within 1 month postdonation to within 12 months of follow-up, and from within 1 month postdonation to 2 years postdonation in donors with and without chronic histological changes on implant biopsy (B)

eGFR_CKD–EPI = estimated glomerular filtration rate by the Chronic Kidney Disease Epidemiology Collaboration equation. *p < 0.001: compared to eGFR_CKD–EPI at 1-month postnephrectomy in donors without chronic histological changes on implant biopsy by the matched-paired Student’s t-test.

Figure 4. Proportion of donors who developed metabolic syndrome at follow up and donors who reversed the condition following donation

MetS, metabolic syndrome.

Figure 5. Scatter plots depicting the associations between BMI changes from pre- to postdonation and each of the metabolic syndrome components

BMI, body mass index; SBP, systolic blood pressure; TG, triglyceride; HDL, high-density lipoprotein; FBG, fasting blood glucose.