Determinants associated with the correction of glomerular hyper-filtration one year after bariatric surgery

Increased adipokine production and hyperfiltration may explain the links between obesity and chronic kidney disease. Indeed, hyperfiltration may precede a subsequent accelerated decline of kidney function in these patients. Glomerular filtration rate decreases after bariatric surgery in young obese patients with hyperfiltration.

Our aim was to identify the factors associated with this decrease 1 year after bariatric surgery.

We used data from a prospective cohort of severely obese patients who underwent bariatric surgery in Nice University Hospital.

We analyzed 175 patients before and 1 year after bariatric surgery. Low-grade inflammation was evaluated by serum C-reactive protein levels. Lean body mass and fat body mass were estimated by bioelectric impedance analysis. Body surface area was assessed by the Du Bois formula. Serum creatinine levels were used to estimate glomerular filtration rate by the chronic kidney disease-epidemiology collaboration (CKD-EPI) equation. Glomerular filtration rate was de-adjusted from standard body surface area and then divided by lean body mass to calculate the decrease in hyperfiltration and to separate the patients into 2 groups: above or below the median decrease of hyperfiltration after bariatric surgery.

The factors associated with a large correction of hyperfiltration were baseline C-reactive protein levels (10.0 ± 5.8 mg/L versus 12.7 ± 7.4 mg/L, P = .01) and brachial circumference (41 ± 4 cm versus 44 ± 5 cm, P = .006). A high fat mass reduction rate was significantly associated with a substantial hyperfiltration reduction after bariatric surgery (P<.001) independently of sex and surgical procedure.

The correction of hyperfiltration is associated with a high reduction rate of fat mass after bariatric surgery but may be limited by low-grade inflammation.