ORIGINAL ARTICLEChronic dehydration may impair renal function in patients with chronic intestinal failure on long-term parenteral nutrition
Introduction
Used for the first time in 1970, long-term parenteral nutrition (LTPN) has improved the survival prognosis of patients with chronic intestinal failure. However, this technique presents many well-known complications such as catheter infections or thrombosis, hepatitic or metabolic bone disturbances. More recently, a few studies have also described renal function impairment.1, 2, 3 Buchman et al.1 reported a decrease in creatinine clearance of 3.5±6.3% per year (0.6–14.5%) in 29 of their 33 patients using the Cockcroft formula. A degradation of inulin clearance was noted in 9 of 16 short-bowel patients by Boncompain et al.2 In a study by Mourkazel et al.3 all of their cohort of 13 children (9±4.9 years) on total parenteral nutrition had a decrease in plasma DTPA clearance (diethylenetriamine pentaacetic acid). These authors evaluated many factors such as age, nephrotoxic medications, bacteraemic or fungaemic episodes, amino acid load and parenteral nutrition duration. However, the aetiology of this renal dysfunction remains largely unknown.
Patients with severe intestinal failure, particularly those with massive intestinal resection, have high losses of fluid and electrolytes (high-output jejunostomy, fistulae, diarrhoea). The volume of such losses is often difficult to evaluate, especially in home patients. Their compensation, either by oral or intravenous route, could therefore be insufficient. Sodium depletion is probably underestimated in these patients. We advanced the hypothesis that part of the renal function impairment in patients with chronic intestinal failure on LTPN could be secondary to sodium depletion.
The aim of this study was to evaluate renal function in patients with chronic intestinal failure on LTPN (more than 6 months) and the role of sodium depletion among other factors in renal dysfunction.
Section snippets
Materials and methods
This prospective study was conducted according to the 1975 Helsinski declaration as revised in 1983.
Results
Concerning renal function, 21/40 LTPN patients (52.5%) had a decrease in GFR of 20% or more compared with normal values for age. The mean reduction of GFR was 38±15%. Measured creatinine clearance gave a similar evaluation of renal function (Table 1). Estimated clearance by Cockcroft formula, corrected or not for body surface area of 1.73 m2, was also significantly different between the two groups but was generally underestimated with major variations (from −39% to +54% in Group 1, from −66%
Discussion
In the present study, renal impairment was frequent and found in 52.5% of our patients with chronic intestinal failure on LTPN. Previous renal diseases and biological signs of dehydration explained most renal alteration. The majority of the cases of renal failure (71%) were related to biological signs of sodium depletion without clinical symptoms. These biological signs were the strongest predictor of decreased glomerular filtration in LTPN patients.
Before we discuss our results and
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