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1986, overall 1 -year graft survival improved for transfused and nontransfused, cyclosporine-treated and conventionally treated patients. Opelz’s data showed that for 3 consecutive years, success rates for nontransfused patients were nearly as good (no sta- tistically significant differences) as those for trans- fused patients in both cadaver and 1 haplotype matched living related transplants. Donor specific transfusion conferred no additional benefit.

The UCLA registry data also showed a diminished “transfusion effect” from 12%* in 1980 to 3%* in 1988-1989. The optimal number of required trans- fusions has also declined from 5-10 to 2-3, and the percentage of patients transplanted without transfu- sion has increased from 10% (1984) to 34% (1989). However, the UCLA registry data continue to show a significant transfusion effect at 1 year that is great- est for black and Asian recipients (6%-7%),* HLA- DR mismatched recipients (4%),* pediatric donor kidneys ( lo%),* and second cadaver transplant sur- vival (lo%).*+

Of greater concern are the possible long-term ef- fects of blood transfusions. Nontransfused patients may have greater risk and seventy of early rejection episodes in the first year,* and a higher subsequent graft loss rate after the first year.

There is clearly an effect of blood transfusion on immunity and the effect is long lasting. However, a 3%-5% improvement in 1-year graft survival may not confer sufficient benefit for the added risk of human immunodeficiency virus infection, hepatitis C infection, and development of lymphocytotoxic

* Difference from nontransfused. t Transfusion had to occur prior to the first transplant to confer benefit on the second transplant. $ Nontransfused versus transfused: risk of early rejection: 42% versus 26%: 1-year survival rate among those with rejection: 56% versus 67%; I-year survival rate among those without rejection: 83% versus 89%.

antibodies. Some centers have abandoned a trans- fusion policy. The final answer will emerge when the number of nontransfused recipients increases and more accurate analysis of long-term benefits is avail- able.

The use of red blood cell and platelet leukocyte filters results in a 2 to 3 log reduction in the number of leukocytes transferred with each transfusion (i.e., from 1 to 3 x lo9 leukocytes to 5107 leukocytes). This degree of leukocyte depletion appears to be sufficient to prevent transmission of cytomegalovi- rus, but is sufficient only to delay but not to prevent lymphocytotoxic antibody formation. (Filters have not been approved for prevention of graft versus host disease.)

The blood transfusion policy at Oregon Health Sciences University is the following:

1. Clinically necessary transfusions (for anemia) are given with American Red Cross approved leukocyte filters.

2. One “protocol” transfusions is given to all trans- plant recipients (identical, haplo-identical, and zero-matched living related and unrelated and cadaveric recipients).

3. Donor-specific transfusions are not given.

Mary Meyer, Portland, OR

References I . Cecka JM, Toyatome A: The transfusion effect, in Clinical Trunsplanrs.

edited by Terasaki P. The Regents of the University of California, 5:335-341, 1989

2. Opelz G. To transfuse or not before transplantation. Edited by Moms PJ, Tilney N. Philadelphia, W. B. Saunders Co., 2:77-85, 1988

~~

9: One protocol transfusion is equivalent to one unit packed red blood cells (or more ifgiven at any time in the past) or 5 leukocyte- poor units (leukocyte filtered).

Frequency of Vascular Access Stenoses

A number of screening studies using venous pres- sures or recirculation values have shown a high fie- quency of vascular access stenoses. However, I have never seen a study that reports thefvequency of such stenoses in an unscreened hemodialysis patient pop- ulation. Do such data exist?

Yes, they do. Vascular access stenoses are ex- tremely common.

In 1989, all 46 chronic hemodialysis patients at the Medical College of Pennsylvania underwent ven- ography of their dialysis accesses (1). Our dialysis population had 10 arteriovenous native fistulas, 32 polytetrafluoroethylene arm grafts and 4 polytetra- fluoroethylene thigh grafts. There were 56 discrete lesions found with multiple lesions in 26% of pa- tients. Thirty eight of 46 patients had access stenoses

greater than 40%. These stenoses were subdivided into five types with the following incidences: proxi- mal vein, 36%; venous anastomosis, 25%; subclavian vein, 23%; arterial anastomosis, 11%; and intimal hyperplasia in graft, 5 %.

The high frequency of stenotic lesions we found is in agreement with previous retrospective studies showing that outflow stenoses are the most common cause for access failure (2-4). Venous injury due to previous cannulations or other trauma (e.g., surgical) coupled with turbulent blood flow may predispose to intimal and medial hyperplasia (5). Stenosis oc- curred in 82.6% of our patients, but the incidence of graft clotting during our study period of 1 year was only 37%. Thus, in our experience, not all stenoses lead to immediate access failure. Therefore, nonin- vasive predictors of impending access failure are

286 DIALYSIS CLINIC

graft function. ASAIO Abstr 19:23, 1990 2. Glanz S, Bashist B, Gordon DH, Butt K, Adamsons R: Angiography

of upper extremity access fistulas for dialysis. Radiology 143:45-52, 1982

needed’ posed as noninvasive predictors (6).

pressures have been pro-

J~~~ L ~ ~ , philadelphia, PA 3. Connolly JE, Brownell DA, Levine EF, McCart M: Complications of

4. Bell D, Rosenthal J: Arteriovenous graft life in chronic hemodialysis.

5 . Nelson EW: Venous access techniques. Urologic Clinics of North

6 . Schwab SJ, Raymond JR, Saeed M, Newman GE, Dennis PA, Bollinger RR: Prevention of hemodialysis fistula thrombosis early detection of venous stenosis. Kidney Int 36:707-711, 1989

renal dialysis access procedures. Arch Surg 119:1325-1328, 1984

ArchSurg 123:1169-1172, 1988

References America. 13:415-481, 1982

1. Dev D, Lee J, Ball D, Dubyanskite A, Elivera H, Ahmed Z Venog- raphy, venous resistance and stressed venous resistance in predicting

Effect of Blood Flow on Venous Pressure

Increasing dialyzer blood flow from 300 to 400 mllmin using a 15-gauge needle causes a big jump in venous pressure. How much of this is related to resistance in the needle and how much to resistance in the access? Do fistulae and grafts dger?

In vitro, at a blood flow of 300 ml/min, the pressure drop through a 15-gauge needle (at a hem- atocrit of 28%) is 95 mm Hg increasing to 152 mm Hg at a blood flow of 400 ml/min. Thus, there is an increase of 60 mm Hg in “venous” pressure from the flow-induced increase in resistance through the needle.

Pressure within the fistula is a function of intra- fistula flow and any underlying abnormality with pressures lower in a native access than in a synthetic access (1). In the absence of any stenoses distal to the venous return needle and with extracorporeal flow a small fraction of total fistula flow, the incre- ment in venous pressure noted with increasing dialy-

zer blood flow is mostly due to the resistance in the needle and should be the same in native and syn- thetic accesses. It is unclear whether this would be the case if venous stenoses were present since extra- corporeal flow might constitute a larger fraction of total access flow altering longitudinal pressure dissi- pation and vessel wall compliance. In other words, we don’t know whether a large increase in venous pressure with increased blood flow is a sign of access stenosis, although there is reason to suspect it might be the case.

Anatole Besarab, Philadelphia, PA

References I . Michael H, Dorrell S. Besarab A, Moritz M: Vascular dialysis accesses:

determinants of measured venous pressure and relationship to intra- access venous pressure (Abstract). J Am Soc Nephrol 1:369. 1990

Hemolysis Due to Central Vein Hemodialysis Catheters

Hemolysis due to central vein hemodialysis cath- eters has been reported. How prevalent is this prob- lem and what factors account for its development?

Chronic, mild hemolysis is known to play a part in the anemia of end-stage renal failure (1). On the other hand, acute hemolysis due to central vein hemodialysis catheters (CVHC) has been docu- mented in only two papers (2, 3). Nand et al. (2) described nine patients, while Korzets et al. (3) added one further case to the literature. All 10 patients had an acute drop in hemoglobin levels and the presence of fragmented red blood cells and schistocytes on a peripheral blood smear, supporting the diagnosis of acute intravascular hemolysis. Other biochemical parameters were consistent with an acute hemolytic process. Finally, in 9 of the 10 patients, an improve- ment in hemoglobin levels was documented with the

removal of the hemodialysis catheter. The prevalence of hemolysis due to CVHC re-

mains unknown. However, the widespread use of CVHC coupled with the paucity of reports dealing with an associated hemolysis probably means that hemolysis from these catheters is rather rare. How- ever, two further points are worthy of consideration. First, hemolysis associated with CVHC may go un- recognized, and, therefore, its frequency may be underestimated. Second, and much more important, acute hemolysis due to CVHC is a treatable and reversible cause of acute anemia in the hemodialysis patient. Therefore, hemolysis should always be sought when an unexplained fall in hemoglobin lev- els occurs when using CVHC. If diagnosed, and when other possible causes of acute hemolysis in patients undergoing hemodialysis are ruled out (4, 5), then the catheter should be promptly removed.