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| Year : 2010 | Volume
: 21
| Issue : 3 | Page : 533-534 |
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| Regional citrate anticoagulation for hemodialysis: A safe and efficient method |
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Faical Jarraya1, Khaled Mkawar1, Khawla Kammoun1, Abdelhamid Hdiji1, Somaya Yaich1, Mahmoud Kharrat1, Khaled Charfeddine1, Mohamed Ben Hmida1, Hichem Mahfoudh1, Fatma Ayedi2, Jamil Hachicha1
1 Department of Nephrology, Sfax University Hospital, Sfax, Tunisia
2 Department of Biochemistry, Sfax University Hospital, Sfax, Tunisia
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| Date of Web Publication | 26-Apr-2010 |
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How to cite this article:
Jarraya F, Mkawar K, Kammoun K, Hdiji A, Yaich S, Kharrat M, Charfeddine K, Hmida MB, Mahfoudh H, Ayedi F, Hachicha J. Regional citrate anticoagulation for hemodialysis: A safe and efficient method. Saudi J Kidney Dis Transpl 2010;21:533-4 |
How to cite this URL:
Jarraya F, Mkawar K, Kammoun K, Hdiji A, Yaich S, Kharrat M, Charfeddine K, Hmida MB, Mahfoudh H, Ayedi F, Hachicha J. Regional citrate anticoagulation for hemodialysis: A safe and efficient method. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2022 Aug 12];21:533-4. Available from: https://www.sjkdt.org/text.asp?2010/21/3/533/62710 |
To the Editor,
Regional citrate anticoagulation (RCA) was proposed by Pinnik et al as an alternative to heparin for intermittent hemodialysis (HD), [1] was first used by Morita et al. in 1961. [2] More recently, it is used for continuous hemodialysis [3] in high risk bleeding patients. Citrate achieves anticoagulation by forming complexes with ionized calcium. During HD, the citrate effect is most likely confined to the extra corporeal system because about 60% of the formed citrate complexes are removed from the blood by the dialyzer. Citrate that leaves the dialyzer and enters the patient's circulation is rapidly metabolized in the tricarboxylic acid pathway, predominantly in the liver and skeletal muscle. [4] Hypertonic trisodium citrate (TSC) was mainly used in the literature. It seems to be efficient with no systemic anticoagulation. However, it can result in hypernatremia or hypercalcemia. In addition, the combination of TSC and bicarbonate dialysate produces a profound metabolic alkalosis. [5]
We report our experience with 26 (17 men, mean age was 52 ± 13 years and mean dialysis duration was 54 ± 43 months) regular HD patients without risk for bleeding over 26 hemodialysis sessions. All hemodialysis sessions lasted four hours, and were carried out with acetate dialysate using Gambro AK 95 and Fresenius 4008B monitors and disposable polysulfone (FreseniusTM) dialyzers. RCA was performed by continuous infusion of sterile 510 mM TSC in the arterial line at a rate of 0.68 mmol/min. A calcium- and magnesiumfree dialysate containing 29.5 mmol acetate after 35-fold dilution was used. To correct the induced calcium loss, calcium-chloride was infused in the venous line at rates of 0.18 mmol/ min. All clinical manifestations were noted during the dialysis session. Laboratory checkup was made at the start, at 2 hours, between citrate injection site and dialyzer (arterial), between calcium injection site and patient (venous) and at the end of the session.
Hypotension was noted in 4 (15%) patients and hypocalcaemia related clinical manifestations in 3 (12%) cases. Although there was no total dialyzer clotting, partial clotting was noted in 5(19%) cases. Premature dialysis session discontinuation was required for 3 patients due to recurrent hypotension one, clinical manifestations attributed to hypocalcemia but not confirmed at blood analysis in another, and intolerance to acetate and or citrate in a third one. Biochemical tests showed neither alterations of sodium nor of calcium blood levels at the end of the dialysis session. Serum bicarbonate increased at the end of dialysis sessions but without reaching an alkalemic state. Activated partial thromboplastin time (APTT) increased after citrate administration (T2a: 124 ± 5 min) and return to a normal range (T2v: 28 ± 7 min) after calcium chloride infusion. At the end of dialysis session, the mean APTT was at 27 ± 3 min (matches the baseline values). There no more nursing time spent while using this method of anticoagulation than the regular HD with heparin.
Our study shows that RCA with TSC was a safe and simple method for anticoagulation in our HD patients as shown by others without compromising efficiency of dialysis or more inconvenience to staff in comparison to stan dard HD. [6],[7],[8],[9],[10],[11] Many protocols required the use of a dialysate with or without calcium. [12],[13],[14] We support the use of calcium-free dialysate since it is more securable to use with RCA. We believe that RCA can be considered for chronic HD patients who are not only at risk of bleeding if they have pre-morbid vascular abnormalities, such as intestinal arterio-venous malformations, diabetic proliferate retinopathy, malignant hypertension, and polycystic kidney disease in addition to heparin induced throm bocytopenia. [10]
 Acknowledgment | |  |
This work was supported by a grant from Hedi Chaker Hospital, Sfax University Hospital, Tunisia. We are grateful to Dr. Philippe Moriniere for his advices.
| References | | |
| 1. | Pinnick RV, Wiegmann TB, Diederich DA. Regional citrate anticoagulation for hemodialysis in the patient at high risk for bleeding. New Engl J Med 1983;308:258-61.  [PUBMED] |
| 2. | Morita Y, Johnson RW, Dorn RE, Hall D. Regional anticoagulation during hemodialysis using citrate. Am J Med Sci 1961;242:32-43. |
| 3. | Gabutti L, Marone C, Colucci G, Duchini F, Schonholzer C. Citrate anticoagulation in continuous venovenous hemodiafiltration: A metabolic challenge. Intensive Care Med 2002;28:1419-25. |
| 4. | Von Brecht JH, Flanigan MJ, Freeman RM, Lim VS. Regional anticoagulation: Hemodialysis with hypertonic trisodium citrate. Am J Kidney Dis 1986; 8:196-201 |
| 5. | Collart F, Wens R, Dratwa M. Regional anticoagulation with sodium citrate: Chronic utilization in the hemodialysis patient. Nephrologie 1993;14:151-4. [PUBMED] |
| 6. | Unver B, Sunder-Plassmann G, Horl WH, Apsner R. Long-term citrate anticoagulation for high-flux haemodialysis in a patient with heaprin-induced thrombocytopenia type II. Acta Med Austriaca 2002;29:146-8. |
| 7. | Faber LM, de Vries PM, Oe PL, van der Meulen J, Donker AJ. Citrate haemodialysis. Neth J Med 1990;37:219-24. [PUBMED] |
| 8. | Brecht JH, Flanigan MJ, Freeman RM, Lim VS. Regional anticoagulation: Hemodialysis with hypertonic trisodium citrate. Am J Kidney Dis 1986;8: 196-201. [PUBMED] |
| 9. | Van Der Meulen J, Janssen MJ, Langendijk PN, Bouman AA, Oe PL. Citrate anticoagulation and dialysate with reduced buffer content in chronic hemodialysis. Clin Nephrol 1992;37:36-41. |
| 10. | Janssen MJ, Huijgens PC, Bouman AA, Oe PL, Donker AJ, Van der Meulen J. Citrate versus heparin anticoagulation in chronic haemodialysis patients. Nephrol Dial Transplant 1993;8:1228-33. [PUBMED] [FULLTEXT] |
| 11. | Flanigan MJ, Pillsbury L, Sadewasser G, Lim VS. Regional hemodialysis anticoagulation: hypertonic trisodium citrate or anticoagulant citratedextrose-A. Am J Kidney Dis 1996;27:519-24. [PUBMED] [FULLTEXT] |
| 12. | Janssen MJ, Huijgens PC, Bouman AA, Oe PL, Van Der Meulen J. Citrate anticoagulation and divalent cations in hemodialysis. Blood Purif 1994;12:308-16. [PUBMED] |
| 13. | Wiegmann TB, MacDougall ML, Diederich DA. Long-term comparisons of citrate and heparin as anticoagulants for hemodialysis. Am J Kidney Dis 1987;9:430-5. [PUBMED] |
| 14. | Evenepoel P, Maes B, Vanwalleghem J, Kuypers D, Messiaen T, Vanrenterghem Y. Regional citrate anticoagulation for hemodialysis using a conventional calcium-containing dialysate. Am J Kidney Dis 2002;39:315-23. [PUBMED] [FULLTEXT] |
Correspondence Address:
Faical Jarraya
Department of Nephrology, Sfax University Hospital, Sfax
Tunisia
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 20427885 
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