Fishbane S, Natke E, Maesaka JK
Role of volume overload in dialysis-refractory
hypertension
Am J Kidney Dis
(Aug) 28:257-261 1996

The role of volume overload in the hypertension of dialysis patients
is controversial. We know that blood pressure in 50 % of dialysis
patients either stays the same or increases during dialysis. Because
there is sympathetic overactivity in dialysis patients, perhaps in
many ESRD patients fluid is not involved in the genesis of
hypertension. There are data on both sides. For example, at ASN
1995, Katzarski
et al demonstrated a large rebound in the blood volume after short (3
hour) dialysis. Also, Bergstrom's group previously had shown that in
patients being dialyzed using the Tassin regimen (6-8 hour dialysis
sessions) IVC diameter was lower 24 hours after dialysis as opposed to
IVC diameter in patients undergoing "short" treatments. The Tassin
patients have good survivals, good blood pressure control, and low
requirement for antihypertensive medications.
In a contrarian view,
also at the 1995 ASN, Luik and colleagues
found that blood pressure only increased in 3/10 patients who were
deliberately volume loaded by altering dry weight. Using the CRIT-
LINE monitor,
Steuer et al presented data at the 1996 ASAIO meeting suggesting
that increased fluid removal from patients who were apparently volume
overloaded based on intradialytic hematocrit measurements did not
lower the blood pressure.
In the present paper, Fishbane et al used predialysis plasma ANP
levels as a marker for volume overload. Levels were compared in 12
normotensive HD patients, 12 hypertensive patients whose BP normalized
with fluid removal, and 9 patients with dialysis refractory
hypertension. Patients with "cardiac disease", which I understand as
meaning primarily CHF, were excluded.
Plasma ANF levels in normotensive HD patients averaged about 240
pg/ml and did not change with HD. In the dialysis sensitive
hypertensives, plasma ANF was much higher, about 800 pg/ml, but
decreased to a mean of 160 pg/ml by the end of dialysis.
Surprisingly, in the dialysis resistant group, plasma ANF was quite
high, mean 1730 pg/ml, and remained at 1940 pg/ml postdialysis,
despite removal of an average of 3.1 L of ultrafiltrate. Six of the 9
volume resistant hypertensives were subjected to extensive UF. In 3
of these 6, dry weight was successfuly reduced by about 2.7 kg and BP
became volume responsive. Plasma ANF levels in these "responders"
now decreased with dialysis, from about 1100 pg/ml predialysis to 250
postdialysis. In the other 3 patients, attempted reductions in dry
weight were accompanied by severe cramps or intradialytic hypotension.
Comment: This is a landmark study in that it casts doubt on the
idea that volume resistant hypertension in ESRD patients really
exists. It may be that the combination of the relatively high sodium
and chloride dialysate used today associated with short treatments,
maintains many patients in a covert overhydrated state. It would be
fascinating to see if apparently volume resistant hypertensives had a
"flat line" hematocrit profile during dialysis, and if reduction of
dry weight based on intradialytic hematocrit monitoring would improve
their plasma ANF levels. Plasma ANF might conceivably become a useful
clinical tool to assess fluid overload in ESRD patients. Much further
work needs to be done in this very important area. (John T.
Daugirdas, M.D., University of Illinois at Chicago)