M Boncompain-Gérard1, D Robert, D Fouque, A Hadj-Aïssa. 1. Service de Réanimation Médicale et Centre Agrée de Nutrition Parentérale de Lyon, Hôpital de la Croix-Rousse, France. hadjaissa@chu-lyon.fr
Abstract
BACKGROUND: Long-term parenteral nutrition (LTPN) has been shown to induce renal impairment and bone demineralization. However, the mechanism of both injuries has not been clarified. METHODS: This prospective study was performed in 16 patients with short bowel syndrome, aged 28 to 63 years, who had received LTPN for 31 +/- 7 months. Urinary excretion of electrolytes were measured before (diurnal, 12 hours) and during (nocturnal, 12 hours) parenteral nutrition. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured in the morning after the nutritional bag supply. RESULTS: Mean GFR was 86 +/- 7 mL/min/1.73 m2 and ERPF was 412 +/- 31 mL/min/1.73 m2. Decreased GFR was present in 9 patients. There was no relation between renal function and age or the duration of LTPN. Urine volume and excretion of urea, creatinine, sodium, magnesium, and phosphate but not potassium increased significantly in nocturnal urine compared with diurnal urine. On the basis on 24-hour calciuria, 7 patients were normocalciuric (NCa) whereas 9 were hypercalciuric (HCa). Both had excessive nocturnal calciuria, but only the HCa group had diurnal hypercalciuria, the calcium supply being identical. Bone mineral density (BMD) was slightly, although not significantly, higher in NCa group, but in all patients BMD correlated significantly with calciuria. Serum parathyroid hormone and vitamin D were not different in the two groups. CONCLUSIONS: In patients receiving LTPN, renal function is frequently impaired, by a mechanism which remains unclear. In nocturnal cyclic mode of nutrition, urinary volume and electrolyte excretion occurred predominantly during the infusion, but some patients have diurnal hypercalciuria. In these patients a defect in renal calcium reabsorption or more likely the inability of bone to retain the infused calcium may be responsible for bone demineralization.
BACKGROUND: Long-term parenteral nutrition (LTPN) has been shown to induce renal impairment and bone demineralization. However, the mechanism of both injuries has not been clarified. METHODS: This prospective study was performed in 16 patients with short bowel syndrome, aged 28 to 63 years, who had received LTPN for 31 +/- 7 months. Urinary excretion of electrolytes were measured before (diurnal, 12 hours) and during (nocturnal, 12 hours) parenteral nutrition. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured in the morning after the nutritional bag supply. RESULTS: Mean GFR was 86 +/- 7 mL/min/1.73 m2 and ERPF was 412 +/- 31 mL/min/1.73 m2. Decreased GFR was present in 9 patients. There was no relation between renal function and age or the duration of LTPN. Urine volume and excretion of urea, creatinine, sodium, magnesium, and phosphate but not potassium increased significantly in nocturnal urine compared with diurnal urine. On the basis on 24-hour calciuria, 7 patients were normocalciuric (NCa) whereas 9 were hypercalciuric (HCa). Both had excessive nocturnal calciuria, but only the HCa group had diurnal hypercalciuria, the calcium supply being identical. Bone mineral density (BMD) was slightly, although not significantly, higher in NCa group, but in all patientsBMD correlated significantly with calciuria. Serum parathyroid hormone and vitamin D were not different in the two groups. CONCLUSIONS: In patients receiving LTPN, renal function is frequently impaired, by a mechanism which remains unclear. In nocturnal cyclic mode of nutrition, urinary volume and electrolyte excretion occurred predominantly during the infusion, but some patients have diurnal hypercalciuria. In these patients a defect in renal calcium reabsorption or more likely the inability of bone to retain the infused calcium may be responsible for bone demineralization.