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Changes in serum leptin levels in chronic renal failure patients with metabolic acidosis
1Division of Nephrology, Peking Union Medical College Hospital, Beijing, China.
Objective:
To examine the relationship between serum leptin levels (SLL) and metabolic acidosis in patients with chronic renal failure (CRF).
Design:
SLL in control patients and in predialysis patients with CRF were measured and compared. SLL before and after correction of acidosis in patients with CRF were also compared.
Patients And Controls:
Twenty-five patients with CRF (10 men and 15 women) aged 51.2 +/- 10.4 years and control patients (healthy subjects, 23 men and 25 women) aged 42.1 +/- 12.6 years were studied.
Intervention:
Five percent sodium bicarbonate (NaHCO(3), 2 to 3 mL/kg) was intravenously infused on the morning of the first day of treatment. NaHCO(3) was taken orally at a dosage of 50 to 200 mg/kg/d for 3 to 5 days thereafter.
Main Outcome Measure:
SLL before and after NaHCO(3) treatment was measured by radioimmunoassay, and blood gas was measured before and after correction of metabolic acidosis in patients with CRF.
Results:
SLL in the normal control group (n = 48) was 10.04 +/- 7.0 ng/mL and was realated to body mass index (BMI) (P =.0331). SLL in men (n = 23) was lower than that in female controls (n = 25, P <.01). SLL in patients with CRF (n = 25) before (plasma HCO(3)(-), 13.03 +/- 3.05 mmol/L) and immediately after improvement of metabolic acidosis (plasma HCO(3)(-), 18.35 +/- 4.21 mmol/L) was 14.52 +/- 9.27 ng/mL and 15.34 +/- 11.89 ng/mL (P >.05), respectively. SLL measured 3 to 5 days after treatment for metabolic acidosis (plasma HCO(3)(-), 20.46 +/- 4.03 mmol/L) was 19.33 +/- 14.58 ng/mL, which was significantly higher than that in the normal control group and that in acidotic patients before NaHCO(3) treatment (P <.01).
Conclusions:
SLL in acidotic patients with CRF were comparable to that in control subjects, and SLL was significantly increased after correction of metabolic acidosis in patients with CRF. The preliminary results suggest that hyperleptinemia in patients with CRF may be masked by metabolic acidosis and that metabolic acidosis may inhibit leptin synthesis or secretion. Further studies are needed to clarify the mechanisms.