Journal Information
Vol. 39. Issue. 2.March - April 2019
Pages 111-222
Vol. 39. Issue. 2.March - April 2019
Pages 111-222
Letter to the Editor
DOI: 10.1016/j.nefroe.2019.03.004
Open Access
Prolonged activated partial thromboplastin time without coagulopathy in peritoneal dialysis
Tiempo parcial de tromboplastina activado prolongado sin coagulopatía subyacente en diálisis peritoneal
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Alba Santos Garcíaa,
Corresponding author
albasantosgarcia@gmail.com

Corresponding author.
, Isabel Millán del Vallea, Leonidas Cruzado Vegaa, Rosalía Ruiz Ferrúsa, Diana Tordera Fuentesa, Alejandra Sabater Belmara, Romina Valenciano Morenoa, Angela Mompel Sanjuanb
a Servicio de Nefrología, Hospital General Universitario de Elche, Elche, Alicante, Spain
b Servicio de Hematología, Hospital General Universitario de Elche, Elche, Alicante, Spain
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Tables (1)
Table 1. Coagulation study performed with Sysmex CS-5100 automated analyser, with Pathromtin® reagent.
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Dear Editor,

The activated partial thromboplastin time (aPTT) is the time required for fibrin to appear after mixing plasma with substitutes for platelet phospholipids. It is used as screening for alteration in the intrinsic and common coagulation pathways, to monitor treatment with heparin sodium and to determine the presence of lupus anticoagulant.1,2

Coagulation abnormalities are often due to pre-analysis anomalies3 or incorrect sample collection. Moreover, aPTT is prolonged with deficiency of the coagulation factors involved, with lupus anticoagulant or in heparin therapy.

We present the cases of two patients on peritoneal dialysis (PD) (cases 1 and 2) who, on the day they were called to receive a kidney transplant, were found to have prolongation of aPTT. In both patients, four repeat coagulation tests were similar (Table 1). Possible interference was ruled out, as well as poor sample extraction. After assessment by haematology, two vials of prothrombin complex and one bag of fresh frozen plasma were administered, with no change in the intrinsic pathway values, so they were rejected for kidney transplantation. Reviewing the patients from our unit, we found that cases 3 and 4 had the same problem. All the cases were male, aged from 53 to 69, on continuous ambulatory PD with a nocturnal exchange of Extraneal. Patient 2 was being treated with acenocoumarol and received vitamin K to reverse its effect; the rest of the patients had no previous history or medication that interfered with coagulation.

Table 1.

Coagulation study performed with Sysmex CS-5100 automated analyser, with Pathromtin® reagent.

  Case 1  Case 2  Case 3  Case 4  Normal range 
aPTT; s  90.3  64.3  86.6  71.3  25–38 
aPTT; ratio  2.91  2.07  2.89  2.38  0.5–1.2 
Prothrombin time; s  13.7  15.7  12.5  11.8   
Quick ratio; %  79  61  83  100  70–100 
INR  1.1  1.3  1.1  1–1.3 
Clotting factors; %
Factor II  84.6  NA  99  110  70–120 
Factor V  155.9    184  118  70–120 
Factor VII  197.1    185  166  55–170 
Factor VIII  285.0    315  314  60–150 
Factor IX  241.9    182  219  60–150 
Factor X  121.5    115  118  70–120 
Factor XI  186.3    118  210  60–150 
Factor XII  127.3    171  171  60–150 
Von Willebrand factor; %
Activity  249.7  NA  349  192  40–150 
Antigen  271.2    482  178  45–150 
Platelet function; s
Collagen/adrenaline  101  NA  170  150  85–165 
Collagen/ADP  71    104  129  71–118 

ADP: adenosine diphosphate; aPTT: activated partial thromboplastin time; INR: international normalised ratio; NA: not available.

After exhaustive study, coagulation abnormalities inherent to each patient were ruled out (Table 1). The coagulation study was performed with a Sysmex CS-5100 automated coagulation analyser, with Pathromtin® SL as reagent. When the reagent was changed to Actin® FS (Siemens, Marburg, Germany), the aPTT returned to normal. Samples from the affected patients had been saved, verifying the normality of the intrinsic pathway with the new reagent.

In the cases presented, there was interference from the laboratory reagent causing the false lengthening of the aPTT. It is interesting the fact that we have found several cases, all of them in PD patients. After studying 70 haemodialysis patients and 80 patients with chronic kidney disease (CKD) stages G3b, 4 and 5, we found no patients on haemodialysis or with CKD with the same interference.

Patients on PD with icodextrin are known to be subject to laboratory interferences: there may be falsely elevated blood glucose readings4 and measured plasma amylase levels decrease.5 However, to date, no interference with coagulation tests has been reported.

The only common factor found in our series is continuous ambulatory PD and treatment with icodextrin, although it is true that not all patients with icodextrin have had the same interference.

Reagents for measuring aPTT are composed of an activator and phospholipids (of synthetic or animal origin). The sensitivity and specificity for aPTT reagents to heparin and coagulation factors vary depending on their origin, their properties and the total concentration of phospholipids, even if the same activator is used.6,7 The reagents used by our laboratory are differentiated according to the surface activator they use: silicon dioxide (Pathromtin® SL) or ellagic acid (Dade Actin® FS). They have a strong correlation coefficient, but comparability is low.8 Our hypothesis is that the metabolites of icodextrin can competitively interfere in the binding of silicon dioxide surface activator, preventing the correct reading of the aPTT.

We would like to inform all nephrologists of this situation, as the laboratory interference had significant repercussions: cases 1 and 2 could not have a kidney transplant until the complete coagulation study was performed.

Nephrologists therefore need to be aware that a prolonged aPTT may indicate the existence of a bleeding disorder, be associated with an increased risk of thrombosis (due to lupus anticoagulant) or lack any thrombotic or haemorrhagic implications (in patients with PD it may be the result of interference with the laboratory reagent).

References
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A.H. Schmaier.
Contact activation: a revision.
Thromb Haemost, 78 (1997), pp. 101-107
[2]
R.D. Langdell, R.H. Wagner, K.M. Brinkhous.
Effect of antihemophilic factor on one-stage clotting tests; a presumptive test for hemophilia and a simple one-stage antihemophilic factor assay procedure.
J Lab Clin Med, 41 (1953), pp. 637-647
[3]
D.M. Adcock, D.C. Kressing, R.A. Marlar.
Minimum specimen volume requirements for routine coagulation testing: dependence on citrate concentration.
Am J Clin Pathol, 109 (1998), pp. 595-599
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J. Plum, S. Gentile, C. Verger, R. Brunkhorst, U. Bahner, B. Faller, et al.
Efficacy and safety of a 7.5% icodextrin peritoneal dialysis solution in patients treated with automated peritoneal dialysis.
Am J Kidney Dis, 39 (2002), pp. 862-871
[5]
R. Wang, L. Skoufos, L. Martis.
Glucose monitoring for diabetic patients using icodextrin.
Perit Dial Int, 24 (2004), pp. 296-297
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Lipid compostion of seven APTT reagents in relation to heparin sensitivity.
Br J Haematol, 106 (1999), pp. 801-808
[7]
A. Denis-Magdelaine, A. Flahaultb, E. Verdya.
Sensivity of sixteen APTT reagents for the presence of lupus anticoagulants.
Haemostasis, 25 (1995), pp. 98-105
[8]
L. Derek, M. Zivkovic, D. Hasperger, J. Juricek, Z. Romic.
Comparability of Pathromtin SL, Dade Actin FS i STA Cephascreen reagents for activated partial thromboplastin time measurement.
Biochem Med, 18 (2009), pp. 81-87

Please cite this article as: Santos García A, Millán del Valle I, Cruzado Vega L, Ruiz Ferrús R, Tordera Fuentes D, Sabater Belmar A, et al. Tiempo parcial de tromboplastina activado prolongado sin coagulopatía subyacente en diálisis peritoneal. Nefrologia. 2019;39:210–211.

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