2356
Severe hyperphosphataemia and short bowel syndrome in a haemodialysis patient
Alford, H., Farrington, K., Vilar, E.
Department of Renal Medicine, Lister Hospital Stevenage
INTRODUCTION: Patients with short bowel syndrome have high nutritional and hypertonic fluid requirements to prevent malnutrition and dehydration. Conversely, haemodialysis patients are likely to require dietary phosphate restriction. Little evidence to inform best practice exists where the requirements to maintain high protein and calorie intake appear antagonistic to phosphate control. We present a unique case of severe refractory hyperphosphataemia in the context of short bowel syndrome posing considerable management difficulties and provides insight into intestinal phosphate absorption.
SYNOPSIS: A 33 year old female with a previous total colectomy for ulcerative colitis developed small bowel obstruction and ischaemia requiring resection, leaving 250cm of small bowel. Irreversible acute kidney injury developed during the peri-operative period with complete anuria requiring chronic haemodialysis. Following a period of clinical stability, long term artificial nutrition was not required. Weight was maintained with a high calorie, high protein diet of 35kCal/kg/day and 1.2g protein/kg/day (assessed by three day food diary analysis with Diet Plan 6). Phosphate intake was assessed at 1200mg/day (16mg phosphate/g protein), exceeding dialysis recommendations of 800-100mg/day. Severe hyperphosphataemia developed with phosphate levels 2-4.9mmol/L. Phosphate binders were tried sequentially and in combination, including calcium-based, lanthanum carbonate and sevelamer hydrochloride. Proton pump inhibitors and anti-motility agents were given concurrently. Wide variation in serum albumin was noted (see graph), higher plasma phosphate levels being associated with higher albumin. These fluctuations were attributed to hydration status and normal saline infusions of 0.5-1 litre per dialysis session were commenced. Despite an initial phosphate reduction with these measures, adequate phosphate control could not be achieved.
DISCUSSION:
Various mechanisms may have contributed to hyperphosphataemia. Maintenance of protein intake prevented adequate reduction in dietary phosphate. Severe shortening of the bowel and rapid transit time may have provided inadequate time for phosphate binding and may have reduced the effectiveness of binders. Though the effectiveness of sevelamer may be potentiated by proton pump inhibitors, that of calcium-based binders may be attenuated. Volume depletion may also have contributed. In animal studies, phosphate absorption is thought to be dependent on sodium co-transporters in the duodenum and jejunum, and to a much lesser extent in the ileum (including NaPi-IIb). We hypothesise chronic sodium and water depletion may lead to these co-transporters retaining sodium and therefore, phosphate. A further possible mechanism is a reduction in endogenous secretion of phosphate by the intestine. This case of intractable hyperphosphataemia may provide insights into mechanisms of phosphate transport in the bowel and phosphate binder action.