M. Boncompain-gerard et al., Renal function and urinary excretion of electrolytes in patients receivingcyclic parenteral nutrition, J PARENT EN, 24(4), 2000, pp. 234-239
Background: Long-term parenteral nutrition (LTPN) has been shown to induce
renal impairment and hone demineralization. However, the mechanism of both
injuries has not been clarified. Methods:: This prospective study was perfo
rmed 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) parent
eral 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 m(2) and ERPF was 412 +/- 31 mL
/min/1.73 m(2). Decreased GFR was present in 9 patients. There was no relat
ion between renal function and age or the duration of LTPN. Urine volume an
d excretion of urea, creatinine, sodium, magnesium, and phosphate but not p
otassium increased significantly in nocturnal urine compared with diurnal u
rine. On the basis on 24-hour calciuria, 7 patients were normocalciuric (NC
a) whereas 9 were hypercalciuric (HCa). Both had excessive nocturnal calciu
ria, but only the HCa group had diurnal hypercalciuria, the calcium supply
being identical. Bone mineral density (BMD) was slightly, although not sign
ificantly, higher in NCa group, but in all patients BMD correlated signific
antly with calciuria. Serum parathyroid hormone and vitamin D were not diff
erent in the two groups. Conclusions: In patients receiving LTPN, renal fun
ction is frequently impaired, by a mechanism which remains unclear. In noct
urnal cyclic mode of nutrition, urinary volume and electrolyte excretion oc
curred predominantly during the infusion, but some patients have diurnal hy
percalciuria. In these patients a defect in renal calcium reabsorption or m
ore likely the inability of Lune to retain the infused calcium may be respo
nsible for bone demineralization.