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Sodium citrate for filling haemodialysis


catheters.
ARTICLE in NEPHROLOGY DIALYSIS TRANSPLANTATION NOVEMBER 1999
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Ramon Romero
Autonomous University of Barcelona
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Sodium citrate for filling haemodialysis catheters


Sir,
Patients dialysed via a catheter frequently present problems
of obstruction and decreased flow. Different anticoagulant
(1 and 5% heparin [1], urokinase [2], tPA [3] and oral
anticoagulants [4]) have been used to ensure the patency of
these catheters; however, no standardized protocol exists for
avoiding thrombosis and the risk of bleeding. We use 5%
heparin when correct flow with 1% heparin is difficult to
maintain. Purchase and Gault described the use of sodium
citrate for filling a Permcath catheter in a patient allergic to
heparin [5].
The aim of the present work was to demonstrate the
usefulness of sodium citrate at 46.7% for maintaining dialysis
catheters permeable, particularly in patients with bleeding
problems. Sodium citrate was compared with 5% heparin in
the same catheter. We used 5 ml sterile monodoses of 46.7%
sodium citrate.
In all cases filling was performed by the administration of
20 ml of physiologic saline into each lumen of the catheter
and later the anticoagulant under study (sodium citrate

Nephrol Dial Transplant (1999) 14: 2532

Fig. 1. Coagulation study prothrombin time (PT ) in patients on


catheter haemodialysis. Comparison when the catheter was filled
with different anticoagulants: sodium citrate or 5% heparin (normal
parameter: PT 70100%).

Fig. 2. Coagulation study partial thromboplastin time (PTT ) in


patients on catheter haemodialysis. Comparison on filling with
different anticoagulants: sodium citrate or 5% heparin (normal
parameter: PTT 2040 s).

46.7% vs heparin 5%). The amount of anticoagulant administered corresponded to the volume of the catheter lumen.
The protocol was applied in 10 patients with acute renal
failure on conventional haemodialysis with double-lumen catheter. In all cases, 2500 IU of dalteparin were used during
haemodialysis. Four catheters were inserted into the right
jugular vein and six in the internal femoral vein. Samples were
taken peripherally 60 min after the haemodialysis session.
Sixty minutes after filling of the catheter, coagulation
status remained unchanged (prothrombin time 85%; partial
thromboplastin time 37 min 6 s) in patients in whom sodium
citrate was used, thereby avoiding the risk of bleeding,
whereas it was altered in 100% cases when 5% heparin was
used (prothrombin time 64.7%, partial thromboplastin time
90 s) (Figures 12).
Mean blood flow of 287 ml/min was maintained after 2
weeks of follow-up in catheters filled with sodium citrate.
No patient presented alkalosis or hypocalcaemia resulting
from sodium citrate administration.
Despite the difficulty in establishing a single filling protocol
for haemodialysis catheters which avoids flow blockage and
the risk of bleeding, we recommend filling the catheter with
sodium citrate 46.7%.
Department of Nephrology
Hospital Universitari Germans
Trias i Pujol
Badalona
Spain

B. Bayes
J. Bonal
R. Romero

Nephrol Dial Transplant (1999) 14: 2533


1. Trivedi HS, Twardowski ZJ. Use of double-lumen dialysis catheters. Loading with locked heparin. ASAIO J 1997; 43: 900903
2. Twardowski ZJ. The clotted central vein catheter for haemodialysis. Nephrol Dial Transplant 1998; 13: 22032206
3. Paulsen D, Reisoether A, Aasen M, Fauchals P. Use of tissue
plasminogen activator for reopening of clotted dialysis catheters.
Nephron 1993; 64: 468470
4. Wing AJ, Curtis JR, De Wardener HE. Reduction of clotting in
Scribner shunts by long-term anticoagulation. Br Med J 1967;
3: 143145
5. Purchase L, Gault MH. Hemodialysis with a Permcath kept open
with streptokinase and later citrate in a heparin-sensitive patient.
Nephron 1991; 58: 119120

Is tissue factor a mediator of fibrin deposition in


glomerular pathology?
Sir,
Coagulation activation and fibrin deposition have been associated with inflammatory glomerular diseases in man and
laboratory animals. Fibrin deposition has been observed
within and around the glomerulus and is thought to play a
major pathogenetic role in the development and the progression of the disease [1,2].
Glomerular epithelial cell proliferation has been favoured
as a possible cause of local coagulation activation [3].
However, it has been suggested that the source of glomerular
procoagulant activity (PCA) in glomerular pathology could
either be blood or resident glomerular cells. Of the inflammatory cells that infiltrate glomeruli, lymphocytes and
neutrophils exhibit no PCA [4]. On the other hand, glomerular fibrin deposition (GFD) is dependent on leukocyte
accumulation [5]. When rabbits are treated with Mustinehydrochloride they develop severe leukopaenia. This prevents
glomerular macrophage accumulation and GFD without any
functional alteration of the host coagulation factors [5].
Mononuclear cells are known to be a potent source of
PCA. Increased expression of PCA by monocytes or macrophages in several inflammatory conditions is an established
phenomenon [4]. Similarly, isolated glomeruli from humans
and animals with some forms of glomerular disease express
high levels of PCA [6 ]. Both mononuclear and intrinsic
glomerular cells from cultured isolated glomeruli were shown
to express increased PCA [6,7]. Macrophage accumulation
progressively declined and eventually disappeared as the
glomerulonephritis (GN ) phase resolved [7]. This suggests
that the PCA is mainly derived from infiltrating mononuclear
leukocytes and intrinsic glomerular cells.
The PCA generated in renal disease was initially thought
to activate the extrinsic pathway of the coagulation cascade
via at least three different mechanisms: (i) tissue thromboplastin or factor VIIaneither of these components alone has
any PCA [8], (ii) prothrombinase and (iii) platelet factor
III. The haemostatic system has recently seen recognition of
tissue factor ( TF ) pathway inhibitor, which has led to a
revised understanding of the blood coagulation cascade.
Coagulation can only significantly proceed through a
TF-dependent pathway. TF is a single-chain integral plasma
membrane glycoprotein. It forms a complex with factor

2533

VII/VIIa with the subsequent activation of both factors X


and IX. Thus, TF is the primary trigger of thrombin generation and fibrin formation [8]. In glomerular disease this is
supported by: (i) the exclusion of the involvement of factor
VIII in GFD [9], (ii) the correlation between TF in glomerular supernatants and thromboxane B2 formation in platelets
[10] and (iii) the increase in antigenic TF level in animals
with induced-GN [11]. Therefore, irrespective of the source,
it is reasonable to suggest that TF is the primary trigger of
fibrin formation in GN-associated GFD.
In patients with GN, TF is also liberated in urine where
levels are thought to be clinically important, particularly in
those with immune-complex GN [12].
In conclusion, TF is implicated in glomerular pathology.
Achievements in developing therapeutic measures have been
modest. Manipulation of clotting activity through TF expression may have an impact in managing patients with glomerular disease. Understanding the mechanisms leading to
abnormal TF expression might lead to strategies for reducing
and/or preventing its induction in these conditions. It is an
area, which warrants further investigation.
University Department of
B. A. Lwaleed
Haematology
Southampton University Hospitals
Tremona Road
Southampton
UK
1. Hancock W, Atkins R. Activation of coagulation pathways and
fibrin deposition in human glomerulonephritis. Semin Nephrol
1985; 5: 6977
2. Silva FG, Hoyer J, Pirani CL. Sequential studies of glomerular
crescent formation in rats with anti-glomerular basement membrane-induced glomerulonephritis and the role of coagulation
factors. Lab Invest 1984; 53: 404415
3. Heptinstall RH. Pathology of the Kidney, 2nd ed. Little, Brown
& Co, Boston: 1974: 376
4. Rivers RPA, Hathaway WE, Weston WL. The endotoxininduced coaglant activity of human monocytes. Br J Haematol
1975; 30: 311316
5. Holdsworth SR, Tipping PG. Macrophage-induced Glomerular
Fibrin Deposition in Experimental Glomerulonephritis in the
Rabbit. J Clin Invest 1985; 76: 13671374
6. Yamabe H, Yoshikawa S, Ohsawa H et al. Tissue factor by
cultured rat glomerular epithelial cells. Nephrol Dial Transplant
1993; 8: 519523
7. Thomson NM, Holdsworth SR, Glasgow EF, Atkins RC. The
macrophage in the development of experimental crescentic glomerulonephritis. Am J Pathol 1979; 94: 223235
8. Nemerson Y. The tissue factor pathway of blood coagulation.
Semin Haematol 1992; 29: 170176
9. Hoyer JR, Michael AF, Hoyer LW. Immuno-fluorescent localization of anti-haemophilic factor antigen and fibrinogen in human
renal disease. J Clin Invest 1974; 53: 13751384
10. Ardaillou R, Bens M, Edgington TS. Glomerular tissue factor
stimulates thromboxane synthesis in human platelets via thrombin generation. Kidney Int 1992; 41: 361368
11. Tipping PG, Erlich JH, Apostolopoulos J, Mackman N,
Loskutoff D, Holdsworth SR. Glomerular tissue factor expression in crescentic glomerulonephritis. Correlations between antigen, activity, and mRNA. Am J Pathol 1995; 147: 17361748
12. Lwaleed BA, Bass PS, Chisholm M, Francis JL. Urinary tissue
factor levels in glomerulonephritis: A potential marker of glomerular injury. J Clin Pathol 1997; 50: 336340

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