P109
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.