Home About us Current issue Ahead of Print Back issues Submission Instructions Advertise Contact Login   

Search Article 
Advanced search 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 199 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 

Table of Contents   
Year : 2013  |  Volume : 24  |  Issue : 2  |  Page : 364-365
Effect on early graft function of high-dose desmopressin in transplant recipients with bleeding disorders

1 4th Pediatric Department, Aristotle University of Thessaloniki, Thessaloniki, Greece
2 Nephrology Department, Birmingham Children's Hospital NHS Foundation Trust, Birmingham, United Kingdom

Click here for correspondence address and email

Date of Web Publication26-Mar-2013

How to cite this article:
Tramma D, O'Brien C, Hulton SA. Effect on early graft function of high-dose desmopressin in transplant recipients with bleeding disorders. Saudi J Kidney Dis Transpl 2013;24:364-5

How to cite this URL:
Tramma D, O'Brien C, Hulton SA. Effect on early graft function of high-dose desmopressin in transplant recipients with bleeding disorders. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2022 May 23];24:364-5. Available from: https://www.sjkdt.org/text.asp?2013/24/2/364/109604
To the Editor,

Early allograft function after cadaveric renal transplantation can be affected by many factors such as prolonged cold ischemia, cause of death and the physiological states associated with brain death. [1] Diabetes insipidus is common among potential donors following brain injury, and may be associated with hypovolemia, hyponatremia and hypotension. The use of desmopressin (DDAVP) to limit these consequences is advised in that DDAVP can be given to brain-dead donors without any effect on renal function, but may be controversial in that the use of desmopressin during organ procurement is associated with a higher rate of primary non-function of renal allografts. [2],[3]

High-dose DDAVP shortens the bleeding time in uremia. In patients with chronic renal failure, the clearance of DDVAP decreases to approximately one-quarter and the terminal half-life is prolonged two to three times. [4]

We report a case of a 13-year-old girl with end-stage renal failure and neurological and developmental problems secondary to presumed mitochondrial dysfunction. She experienced significant hemorrhage after a diagnostic kidney biopsy and other routine surgical procedures. She was noted to have a prolonged bleeding time (greater than 20 min and a correction to 13 min after a DDVAP dose). Other clotting parameters were normal. The hematologist's advice was to use high-dose DDVAP (two doses of 300 ng/kg by intravenous injection) during any future surgical procedures. She underwent cadaveric kidney transplantation and received one dose of DDAVP at the time of surgery. The cold ischemia time was 14.4 h and there was no intraoperative hypotension recorded. She was noted to have deayed graft function of more than two weeks that required hemodialysis. Her graft biopsy at day 10 showed acute tubular necrosis without evidence of acute rejection. Delayed renal graft function occurs in about 30% of recipients from deceased donors, refers to the lack of graft function immediately after transplant secondary to ischemia-reperfusion injury and/or immunological causes and is characterized by acute tubular necrosis upon biopsy. The kidney is particularly susceptible to ischemic injury following transplantation. [5]

After reperfusion of the ischemic kidney, arterioles exhibit increased reactivity to vasoconstrictive agents such as endothelin, angiotensin II and adenosine. Microvascular dysfunction occurs after acute renal ischemic injury, mainly through an imbalance between vasoconstrictors and vasodilators. Thus, renal tissue hypoxia promotes initial tubular damage leading to acute organ dysfunction. [6]

Desmopressin is prescribed routinely as a hemostatic agent, useful for its vasoconstrictive effect. [7] Experimental data suggest that vasopressin induces acute non-oliguric renal failure due to contraction in glomerular mesangial cells, with no spontaneous recovery of vasopressin-injured kidneys. [8] DDAVP stimulates platelet and endothelial P-selectin expression, with resultant endothelial activation. [6] Thrombogenesis after aspirin use is faster and more distinct when desmopressin is added. [9]

As far as we are aware, there are no data about the effect of desmopressin in kidney recipients when used as a hemostatic agent during transplantation. We propose that the vasoconstrictive effect of DDAVP would aggravate renal tissue hypoxia.

Because no other risk factor for delayed graft function was established in our patient, we focused on the use of high-dose DDAVP during the transplantation procedure, and wish to alert other clinicians to the possible role of this drug in delaying graft function.

   References Top

1.Koo DD, Welsh KI, Mclaren AJ, Poake JA, Morris JP, Fuggle VS. Cadaver versus living donor kidneys: Impact of donor factors on antigen induction before transplantation. Kidney Int 1999;56:1551-9.  Back to cited text no. 1
2.Guesde R, Barrou B, Leblanc I, et al. Administration of desmopressin in brain-dead donors and renal function in kidney recipients. Lancet 1998;10:1178-81.  Back to cited text no. 2
3.Hirschl MM, Matzner MP, Huber WO, et al. Effect of desmopressin substitution during organ procurement on early allograft function. Nephrol Dial Transplant 1996;11:173-6.  Back to cited text no. 3
4.Ruzicka H, Björkman S, lethagen S, Stemer G. Pharmacokinetics and antidiuretic effect of high-dose desmopressin in patients with chronic renal failure. Pharmacol Toxicol 2003;92:137-42.  Back to cited text no. 4
5.Bronzatto EJ, da Silva Quadros KR, Santos RL, Alves-Filho G, Mazzali M. Delayed graft function in renal transplant recipients: Risk factors and impact on 1-year graft function: A single centre analysis. Transplant Proc 2009; 41: 849-51.  Back to cited text no. 5
6.Legrand M, Mik GE, Johannes T, Payen D, Ince C. Renal hypoxia and dysoxia after reperfusion of the ischemic kidney. Mol Med 2008; 14:502-16.  Back to cited text no. 6
7.Manucci PM. Desmopressin: A non transfusional hemostatic agent. Annu Rev Med 1990; 41:55-64.  Back to cited text no. 7
8.Heidbreder E, Zollner T, Schafferhans K, Götz R. Atrial natriuretic peptide reverses experimental acute renal failure induced by arginine desmopressin. Miner Electrolyte Metab 1990; 16:48-53.  Back to cited text no. 8
9.Peter F, Benkovic C, Muehlberger T, et al. Effects of desmopressin on thrombogenesis in aspirin-induced platelet dysfunction. Br J Haematol 2001;117:658-63.  Back to cited text no. 9

Correspondence Address:
Despoina Tramma
4th Pediatric Department, Aristotle University of Thessaloniki, Thessaloniki
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.109604

Rights and Permissions


    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  


 Article Access Statistics
    PDF Downloaded307    
    Comments [Add]    

Recommend this journal