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Nephrol Dial Transplant (2000) 15: 2063
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Oxford Textbook of Clinical Nephrology, 2nd edn. Oxford.
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medullary sponge renal disorders. In: Schrier RW, Gottschalk
CW, eds. Disease of the Kidney. 6th edn, vol. 1. Little Brown,
Boston, MA: 1997; 499–520
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kidney associated with congenital hemihypertrophy. J Am Soc
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Dietary salt intake and blood pressure control in
haemodialysis patients
Sir,
Krautzig et al. [1] reported a decrease in predialysis blood
pressure in eight patients when dialysate sodium was reduced
from 140 to 135 mmol/l, with a dietary salt restriction of no
more than 6 g/day. In contrast, Kooman et al. [2] reported
subsequently that predialysis blood pressure in six patients
did not change significantly when dialysate sodium was
reduced from 140 to 136 mmol/l, but no other dietary
interventions were performed.
In the present study we modified dietary sodium intake
but did not change dialysate sodium. We compared patients
at a midweek haemodialysis session on their usual salt intake
with the same patients at a midweek haemodialysis session
after having ingested a low-salt diet. Fifteen dialysis patients,
eleven male and four female, were studied. Dialysis parameters and dry body-weight were kept constant. We measured
predialytic plasma conductivity and intradialytic sodium
mass transfer with non-invasive sensor (Diascan, Hospal )
by automatic conductivity measurement at the dialysate inlet
and outlet. Mean intradialytic sodium mass transfer was
347±117 mmol with usual salt intake and 241±83 mmol
with salt restriction, P<0.001 (Student’s t test, paired data).
This was equivalent to a salt intake of 10.21±3.4 vs
7.09±2.4 g/day respectively, P<0.001. Initial plasma conductivity was 14.31±0.22 (usual sodium intake) vs
14.18±0.17 mS/cm (salt restriction), P<0.01. Predialysis
systolic blood pressure decreased with dietary salt restriction
from 138.7±16 to 131.8±16 mmHg (P<0.01), diastolic
pressure from 79.3±13 to 75.0±12 mmHg (P<0.05), and
mean arterial pressure from 99.1±12 to 93.9±12 mmHg
(P<0.01). Interdialytic weight gain decreased with salt
restriction from 2.26±0.73 to 1.78±0.52 kg (P<0.001)
whereas post-dialysis weight did not change, (66.05±11.9 to
66.05±11.8 kg, NS ).
Our results are in agreement with both reports cited above
and point to the important role of salt intake in the pathogenesis of hypertension in haemodialysis patients. We agree with
Scribner’s personal opinion that antihypertensive medications do not control blood pressure well in such patients [3].
We believe that an appropriate management of hypertension
in this patient population can only be obtained if it includes
a large dialysis dose allowing the removal of vasoconstrictor
substances, the achievement of an adequate dry weight, and
the inclusion of dietary sodium restriction. The excellent
results of blood pressure control at the Tassin centre in
2063
France [4] are obtained without drugs, via a high dialysis
dose ( Kt/V>1.7), together with dietary salt restriction
(<5 g/day).
Automatic measurement of sodium mass transfer during
the dialysis session is a practical tool for the control of
dietary salt intake in individual haemodialysis patients, in
particular in hypertensive patients. It allows one to proceed
to accurate and continuous dietary interventions for each
patient.
Nephrology Department
Hospital General de Castellón
Castellón
Spain
F. Maduell
V. Navarro
1. Krautzig S, Janssen U, Koch KM, Granolleras C, Shaldon S.
Dietary salt restriction and reduction of dialysate sodium to
control hypertension in maintenance haemodialysis patients.
Nephrol Dial Transplant 1998; 13: 552–553
2. Kooman JP, Hendriks EJM, van den Sande FM, Leunissen
KML. Dialysate sodium concentration and blood pressure control
in haemodialysis patients ( letter). Nephrol Dial Transplant 2000;
15: 554
3. Scribner BH. Can antihypertensive medications control BP in
haemodialysis patients: yes or no? Nephrol Dial Transplant 1999;
14: 2599–2601
4. Charra B, Calemard E, Ruffet M et al. Survival as an index of
adequacy in dialysis. Kidney Int 1992; 41: 1286–1291
Post-renal transplant obstruction caused by
cytomegalovirus ureteritis
Sir,
Cytomegalovirus (CMV ) infection is the leading cause of
infectious complications following renal transplantation. The
risk of developing the disease depends on many factors, most
importantly the donor and recipient CMV serology status
pre-transplant and the level of immunosuppression [1].
We report an unusual case of CMV tissue-invasive disease
found incidentally when investigating a patient with posttransplant renal obstruction.
Case. A 45-year-old Caucasian man was admitted for his
third cadaveric renal transplant. He had end-stage renal
failure secondary to reflux nephropathy and began CAPD
aged 29. After 7 months he received his first cadaveric
transplant. This was removed on day 10 with histology
consistent with accelerated acute rejection. A second cadaveric transplant 16 months later, failed after 6 years from
biopsy proven chronic rejection. CAPD was recommenced
and continued for the next 7 years.
The donor for his third cadaveric transplant was a 50-yearold woman, with only one DR mismatch. The recipient was,
however, highly sensitized with 70% panel reactive antibodies
(PRA). The donor was CMV IgG seronegative and the
recipient seropositive. The transplant ureter was implanted
into the bladder and a double-J ureteric stent was inserted.
The allograft functioned immediately with serum creatinine
falling from 812 mmol/l to 145 mmol/l at the time of discharge
on day 17.
He was treated with routine cyclosporin A (Neoral )
225 mg b.d., mycophenolate mofetil 1 g b.d. and prednisone
20 mg o.d. In view of his previous transplantations and a
high PRA he was also given induction therapy with basiliximab (Simulect) 20 mg on day 0 and 4.
His initial hospital stay was complicated by a perioperative
cerebral infarct resulting in a dense right hemiplegia and