August 1998, Volume 48, Issue 8

Original Article

Effect of Dialysis on Bleeding Time in Chronic Renal Failure

Mohammed Luqman Butt  ( Department of Haematology, Bolan Medical College, Quetta. )
Tahir Shafi  ( Department of Medicine, Sheikh Zayed Hospital, Lahore. )
Iftekhar Farooqi  ( Department of Pathologist, Baqai Medical College, Karachi. )
Moinuddin  ( Sahiwal, Department of Haematology, Baqai Medical College, Karachi. )


Renal failure is associated with severe haemorrhagic complications. Platelets play an important role in coagulation and their dysfunction may be responsible for the bleeding tendency in these patients. Sixty patients with advanced renal failure were investigated for bleeding tendency due to platelet dysfunction. The pre-dialysis platelet count was 46 to 325x109IL) (mean 166x10 9/L), Post-dialysis platelet count was 60 to 310x109IL, (mean 172x109/L) Pre-dialysis mean bleeding time (BT) was 4.95±0.27 minutes (range 1.30 to 20 minutes), Thirty-three patients (55%) had prolonged BT before dialysis. Mean BT in all patients after dialysis was 2.46±0.24 minutes (range 1.15 to 10 minutes). BT was corrected in 27(81.8%) out of 33 patients with prolonged BT before dialysis. In 6 patients (10%) it remained prolonged. This improvement in BT after dialysis was statistically significant (p value <0.001). Both peritoneal and hemodialysis resulted in significant improvement in bleeding time (JPMA 48:242,1998).


Severe haemorrhagic complications in the course of uremia due to renal failure have long been reported1. The advent of dialysis has definitely lowered the incidence of the most severe haemorrhagic event, but bleeding still remains a major problem for uremic patients especially while undergoing surgezy or invasive procedures2,3.
Quantitative and qualitative defects of platelets were suggested on the basis of prolonged bleeding time and other investigations. Bleeding time is the test that provides an overall measures of the primaiy hemostatic plug formation and is now generally accepted as the best laboratory parameter of clinical bleeding. This study was designed to find out the incidence of prolonged bleeding time in patients with chronic renal failure, the effect of dialysis prolongedbleeding time and to compare the effect of two methods of dialysis.

Patients and Methods

A total of sixty patients were included in the study irrespective of age, sex orethnic group. All these patients were suffenng from advanced renal failure. Half of them underwent acute peritoneal dialysis and the other half were on regular hemodialysis. The diagnosis of advanced renal failure was confirmed by clinical and laboratory parameters. Platelet counts and bleeding time were perfonned before initiation of dialysis and 6 hours after the dialysis was completed to allow time for disappearance of action of heparin given during dialysis. Bleeding time was done by Duke’s method.
Duke’s method
Ear lobe was warmed and 3 mm deep puncture was made with a disposable lancet. As soon as the puncture was made, stop watch was started. At 15 seconds interval the drop of blood which had exuded from the wound was absothed into a filter paper without touching the surface of the ear. The time takenforbleedingto ease fromthis standarized wound was the bleeding time. Normal range by this method is 1-3.5 minutes. Value of 4 minutes or above was considered abnormal.


Total sixty patients were included in this study. Forty fourpatients were males and 16 females. Theiragevaried from 15 to 68 years.

Table I shows causes of renal failure in these patients. Hypertension, diabetes mellitus and chronic glomerulonephritis were leading causes of renal failure.
The incidence of bleeding from different sites in these patients is depicted in Table II.

Hematuria and epistaxis were the most common, present in 11 patients each. Hematuna could have been due to underlying primary renal pathology in some patients.
Pre-dialysis platelet count was 46 to 325x109/L (mean 166x109/L). Post-dialysis count was 60 to 360x109/L (mean 172x109L) which was not statistically different from pre-dialysis count.
Thirty-three patients out of 60 (66.7%) showed abnormally prolonged bleeding time (BT)before dialysis. Of these 20 were from the peritoneal dialysis and 13 from the hemodialysis group. After dialysis only 6 (10%) showed pronged BT (Table III).

Sixteen out of 20 (80%) patients in peritoneal dialysis group and 2 out of 3 (84.6%) patients with prolonged BT in hemodialysis group showed improvement in BT alter dialysis (P value <0.001). Mean BT was 4.95±0.72 before dialysis. Post-dialysis BT improved to 2.46±0.24 minutes (Pvalue <0.001). Effect oftwo types ofdialysis onBT are shown in Table IV.

In peritoneal dialysis group pre and post-dialysis mean BT was 5.78±0.81 and 2.43±0.81 respectively (P<0.001). Similarly in hemodialysis group pre and post-dialysis mean BT was 4.12±0.39 and 2.50±0.30 respectively (P<0.001). Pre-dialysis BT was lower in the hemodialysis group as these patients were getting regular hemodialysis and were not severely uremic. Onthe other hand patients in peritoneal dialysis group had dialysis for the first tune and they were more uremic.


Prolonged bleeding time is afrequentfinding inpatients of chromc renal failure. In uremic patients there is impainnent of platelet function which is based upon the availability of storage pool and the platelete phospholipid5.
Aggregation studies using various agents have demonstrated such defects in platelet aggregation6. There is evidence that impaired vessel wall and platelet interaction mediated by prostacyclin and Von Willebrand Factor(VWF) is an important defect responsible for bleeding tendencies in uremic patients7,8. Aggregation studies have demonstrated decreased sensitivity of platelets to the aggregating agents like adenosine phosphate, epinephrine and collagen in vitro9. Platelet factor-3 availability is also abnormal in chronic renal failure10,11. Some dialyzable compounds like guanidino-succinic acid, phenol and several other hydroxy phenolacetic acids have been implicated in various hematological abnormalities in renal failure12,13. With frequent dialysis platelet abnormality can be corrected and normal hemostasis maintained, suggesting that the observed defects am due to inhibition of platelet function by retained metabolites.
None of our patients had thrombocytopenia severe enough to cause haernorrhagic complications. Mild thrombocytopenia was noticed in 3 out of 12 patients (25%) by Lewis et al5, in 8 out of 33 patients by Cheney et al4 and in 3 out of 29 patients with uremia by Evans et al15. Nancy et al6. Ivanovich et al16. Mannucci et al17 and Bloomm et al’s reported normal platelet count in uremic patients.
Bleeding time was prolonged in55% of ourpatients and was corrected with hemodialysis in 81.8% and in 80% with peritoneal dialysis. Ourfindings are in agreement with most of the reports in literature.8,14,15,19,20.
The study concluded that the incidence of prolonged bleeding time in chronic renal failure was 55% and a significant decrease was observed in the bleeding time after dialysis. Statistical analysis proved bothtechniques of dialysis i.e., hemodialysis and peritoneal dialysis to have the same efficacy.


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2. Janson PA, Jubelirer SJ. Weinstein Mi eta!. Treatment of the bleeding tendency inuraemiawithcryoprecipitate. N. Engl. J. Med., 1980;303:1318-22.
3. Smith MC and Dunn MJ. Impaired platelet thromboxane production in renal failure. Nephron, 1981,29:133-7.
4. Hougie C. Bleeding time. In: Williams, WJ, Beutler E, Erslev AJ, et al. Haematology. 3rd ed. Singapore, McGraw-Hill, 1986, p. 167!.
5. Lewis JH, Zucker MB, Ferguson JH. Bleeding tendency in uraemia.Blood, 1956;11:1073-76.
6. Nenci GG, Berrettini M, Agnelli G et al. Effect of peritoneal dialysis, hemodialysis , kidney transplantation on platelet function. Nephron, 1979;23:287-92.
7. Kazatchkine M, Sultan Y, Caen JP et a!. Bleeding in renal failure: A possible cause. Br. Med. J., 1976;2612-5.
8. Remuzzi G, Cavenaghi AE, Mecca G et al. Prostacyclin like activity, bleeding in renal failure Lancet, 1977,2:1195-7.
9. Minno GD, Martinez J, Makean ML et a!. Platelet dysfunction in uraemia, multifaceted defect partially corrected by dialysis. Am.i. Med., 1985;79:552-9.

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