The role of saline hydration in reversing aggravated azotemia in long-term kidney transplant patients

Abstract

Background Unexplained azotemia is frequently encountered in long-term kidney transplant (KT) patients, and subtle hypovolemia may contribute to it. We investigated the possibility of relieving the azotemia by saline hydration, and characterized responders whose renal dysfunction was stabilized. |Methods Fifty-four long-term KT patients with recently aggravated azotemia were given saline intravenously: 0.9% saline 5 mL/kg over 1 hour, followed by 0.9% saline 1 mL/kg/hr over 12 hours, and 0.45% saline 1 L over the next 24 hours. Serum and urine data were collected and analyzed to assess responses. |Results Among the total patients, saline hydration relieved azotemia: BUN (46.9 ± 17.2 vs 39.3 ± 15.4 mg/dL, P < 0.01) and serum creatinine (2.9 ± 1.1 vs 2.5 ± 1.1 mg/dL, P < 0.01) on Day 1 versus Day 0. In 38 patients serum creatinine did not increase in the following month (70%, responders). Compared with the non-responders, the responders had a higher urine-to-plasma creatinine ratio (41.1 ± 26.6 vs 21.2 ± 13.8, P < 0.01) and lower fractional excretion of sodium (1.9 ± 1.8 vs 4.3 ± 4.5%, P < 0.01), uric acid (11.0 ± 9.0 vs 20.1 ± 10.3%, P < 0.01) and urea (33.8 ± 13.1 vs 54.9 ± 43.0%, P < 0.05) on admission. Multiple logistic regression analysis revealed that responding was independently associated with lower fractional excretion of uric acid (OR, 0.925; 95% CI, 0.857 - 0.998). |Conclusions Saline hydration has a stabilizing effect on allograft dysfunction in a subset of KT patients. Fractional excretion of uric acid may predict responsiveness to saline hydration.; Conclusions Saline hydration has a stabilizing effect on allograft dysfunction in a subset of KT patients. Fractional excretion of uric acid may predict responsiveness to saline hydration.