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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2008  |  Volume : 19  |  Issue : 4  |  Page : 651-657
Early Non-Immunological Post Transplant complications: A Single Center Experience

Department of Nephrology, Al-Karamah Teaching Hospital, Baghdad, Iraq

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To assess non-immunological complications affecting renal transplant patients in the first six months after transplantation in Al-Karama hospital, Baghdad, Iraq, we studied 68 patients (49 males, 19 females) attending the clinic during the year 2006. Forty six (67%) patients received kidneys from related and 22 (33%) from unrelated donors. The patients revealed the following complications: post transplant hypertension in 28 (41%) patient, infection (mostly bacterial) in 27 (37%), new onset diabetes in 11 (16%), calcineurin inhibitor toxicity in 10 (14%), anemia in 8 (12%), surgical complications in 7 (10%), slow graft recovery in 4 (6%), cardiovascular complications in 3 (4%), and Kaposi sarcoma in 2 (2.9%).Transient hyperglycemia, hypertension, infection and diabetes mel­litus were the commonest early complications of renal transplantation. The incidence of complications is comparable to the average reported in the literature, especially in this region of the world.

Keywords: Renal, Transplantation, Hypertension, Tumor, Hyperglycemia, Infections, Diabetes, Cardiovascular, Graft

How to cite this article:
Jabur WL, Mohammed Saaed HM, Abdulla K. Early Non-Immunological Post Transplant complications: A Single Center Experience. Saudi J Kidney Dis Transpl 2008;19:651-7

How to cite this URL:
Jabur WL, Mohammed Saaed HM, Abdulla K. Early Non-Immunological Post Transplant complications: A Single Center Experience. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2022 Nov 27];19:651-7. Available from: https://www.sjkdt.org/text.asp?2008/19/4/651/41334

   Introduction Top

Adverse outcome for some transplant reci­pients, including peri-operative mortality and graft rejection are encountered in various degrees in all centers around the world. [1] In Iraq, there are several centers for kidney transplantation.

We conducted this study to evaluate short­term non-immune complications during the first six months after renal transplantation in patients followed up in our center, which is one of the biggest transplant centers in the country.

   Patients and Methods Top

We studied 68 patients (49 (60%) males, 19 (40%) females) who received renal trans­plantation and attended Al-Karama trans­plant clinic, Baghdad, Iraq, for follow up in the second half of 2005 and first half of 2006. Sixty one (90%) patients received their allografts in our center. Age of pa­tients ranged from 13 to 50 years. Before transplantation all patients underwent re­gular hemodialysis for periods ranging from 2 months to 2 years.

In most patients the cause of renal failure was unknown. Otherwise, renal stone di­sease, diabetes mellitus, systemic lupus ery­thematosus, polycystic kidney disease and chronic glomerulonephritis were the main causes.

Forty six (67%) patients had related do­nors with 50% or more HLA histocompa­tibility, while 22 (32%) patients had unre­lated donors with HLA histocompatibility of 25% or zero. No cadaver transplantation is performed in Iraq. We used Basiliximab for induction and triple maintenance therapy that included prednisolone, cyclosporine and azathioprin or prednisolone, tacrolimus and mycophenolate mofetil (MMF) depen­ding on whether the patient is high risk or not. Adjuvant therapeutics for all patients included deltiazem, simvastatin, trimetho­prim, gancyclovir, and Alfa-calcidol.

The term slow graft recovery was used to describe grafts that did not function prompt­ly in the immediate days after operation so that serum creatinine remained above 3 mg/dl during the first week, but dialysis was not needed. [2] On the other hand, delayed graft function was used to describe grafts that did not function properly so that dialysis was needed during the first week after operation. [2]

Serum levels of cyclosporine and tacroli­mus was available only for few patients who could afford doing it outside the coun­try. Our criteria to diagnose calcineurin inhibitor toxicity was renal impairment in the presence of high serum level (C2 level more than 300 ng/ml for cyclosporine and a trough level more than 20 ng/ml for tacrolimus) if available. Otherwise, we de­pended on the following criteria that inclu­ded blood urea to creatinine ratio more then 40, improvement of renal function within 2-4 days after decreasing the dose of calcineurin inhibitor, absence of clinical signs of rejection such as local tenderness and oliguria, hyperkalemia, and hypertension.

Two readings of blood pressure above 140/90 within one week indicated post transplant hypertension if the patient was normotensive before operation or was hy­pertensive but his blood pressure was well controlled by treatment before operation and deteriorated despite continuing the same treatment. [3],[4]

We adopted the definition of post trans­plant diabetes of American Diabetes Asso­ciation and World Health Organization (WHO), which state that new onset dia­betes mellitus (NODM) is diagnosed with two measurements of fasting blood sugar of 126 mg/dl or above. [5] However, we de­fined post transplant hyperglycemia as ele­vated blood glucose during the first few days post transplantation and normalized there-after without additional therapy. In all of them pre operative history of dia­betes mellitus was negative.

   Results Top

[Table 1] shows the various complications encountered in the first six months after transplantation. Four (6%) patients had slow graft recovery. There was no case of de­layed graft function. Ten patients (14%) were diagnosed as having renal impairment se­condary to calcineurin inhibitors; in all of them, renal function normalized after re­adjustment of dose.

Twenty eight (41%) patients whose blood pressure was well controlled by treatment before surgery developed post transplant hypertension. In most of them, hypertension was moderate to severe requiring two or three antihypertensive drugs. They were treated with calcium channel blocker del­tiazem or long acting nifedipine plus angio­tensin converting enzyme inhibitors (ACEI) or B-Blockers adjusted to heart rate and renal function. Accelerated hypertension (diastolic blood pressure above 120 mm mercury in the absence of end organ da­mage) was seen in three (12%) patients. Malignant hypertension (diastolic pressure above 120 mm. mercury with signs of end organ damage) was not encountered.

Eleven (16%) patients developed post transplant diabetes mellitus. In all of them blood sugar was controlled with oral hypo­cemic agents without insulin; onset was in the 1st week in one patient and during the sixth month in the rest. Thirty five (51%) patients developed hyperglycemia in the first few days after transplantation, which normalized spontaneously. None of the patients in either group was a known diabetic before transplantation.

[Table 2] shows the surgical complications in 7 (10%) patients; urinary leak in 4 pa­tients necessitating re-implantation in one, Lymphocele in 2 (3%), and renal artery thrombosis in one.

[Table 3] shows that 25 (37%) patients de­veloped infection during the first 6 months. Among these, 6 developed acute pyeloneph­ritis; 2 of them associated with renal im­pairment. In one of these patients the diag­nosis was made by renal biopsy performed to exclude rejection. Other cases of infec­tion included 3 patients with herpes zoster, 2 with newly acquired pulmonary tuber­culosis, and one who converted to CMV positive state 2 months after transplantation.

Three (4%) patients developed acute coronary syndrome (unstable angina); one in the first post operative day, the other after three weeks, and the third after one month.

Eight (12%) patients were anemic through­out the first six months. Hemoglobin level ranged from 9-11 g/dl. The anemia was normochromic normocytic in 7 patients and macrocytic in one. There was no apparent cause for the anemia.

Two (2.9%) patients developed skin Kaposi sarcoma, and one (l.5%) patient developed hemolytic uremic syndrome. His renal func­tion improved with reduction of cyclos­porine dose.

   Discussion Top

Post transplant hypertension is very com­mon with an incidence of more than 50% in most centers. [3],[4],[6] It is also an important determinant of graft survival. [6] The incidence of 41% uncontrolled hypertension in our study was not unexpected. In addition, the drugs we used have been shown to have comparable efficacies. [7]

Our patients who developed NODM were all euglycemic before transplantation. They developed hyperglycemia within the first month after transplantation. The probable risk factors are higher doses of calcineurin inhibitors and steroids in our protocol. A similar incidence was reported by some [8],[9] and a higher incidence by others. [10] In USRDS (US Renal Data System) registry [11] the incidence was 16-24% with significant correlation with a Tacrolimus based immu­nosuppression protocol.

In our study, 51% developed post-trans­plant transient hyperglycemia; 4 (11%) of them only developed NODM later on. In Mathew et al [10] study the glucose tolerance was abnormal in 42% of the patients, of those only 18% developed NODM although they had done the glucose tolerance test 2­ 6 weeks post-transplantation. Transient hy­perglycemia is mostly related to the dose of steroids and cyclosporine. The higher incidence of NODM in Mathew's study probably reflects the higher incidence of diabetes mellitus in the general population in India. We did not perform glucose tole­rance tests to exactly assess the prevalence of impaired glucose tolerance. The impor­tance of hyperglycemia and its probable relation to future diabetic state is still debatable and need further study.

The incidence of slow graft recovery in our study was low, and probably related to vascular surgical difficulties due to size in­compatibility or vascular anomaly. No case of delayed graft function or acute tubular necrosis was encountered. The fact that we only do live donor transplantation seems to contribute to this result. The incidence of both is higher in centers performing de­ceased kidney transplantation, even in pre­emptive transplantation. [1],[12],[13] Incidence of 18% was reported by some. [14]

Acute reversible calcineurin inhibitor toxi­city was observed in 14% of our patients. This high incidence is probably due to the high dose of the calcium inhibitors in our transplant protocol. Renal impairment was accompanied with anemia and hypertension; all were corrected when the dose of cal­cineurin inhibitors was adjusted.

Acute pyelonephritis was the most fre­quent infection, accounting for 24% of all infections. A similar incidence was reported by Al-Wakeel [15] in Saudi Arabia. It oc­curred early in the [1] post-transplantation pe­riod. Canivet et al [6] reported reflux in 9 (52%) of their 17 patients with pyeloneph­ritis demonstrated by radioisotope mictura­ting cystography. No ureteric stenosis or vesico-ureteric reflux could be demonstra­ted by micturating cystography in our pa­tients, and this discrepancy may be related to the higher sensitivity of the radioisotope method compared to the radiological mic­turating cystography.

Bacterial pneumonia was observed in 3 (12% of the cases with infection) patients. A similar incidence was reported by Al­Wakeel. [15] Cholecystitis occurred in one patient and was mild. No stones were encountered, unlike the cases of Sarkio et al [17] which caused significant morbidity and mortality with and without gallstones.

Cytomegalovirus (CMV) disease was diag­nosed in one patient. Other studies reported higher incidence (5-20%). [18] This is pro­bably attributable to Gancyclovir prophy­laxis that we applied to all our patients for the first three months and is comparable to the findings of Sagedal et al [18] who conclu­ded that pre-emptive treatment of CMV infection is associated with very low risk of CMV disease. It may also be related, as was suggested by some, [19] to using Basili­ximab instead of OKT3 for induction of immunosuppression.

Two patients developed hepatitis and were HBs Ag positive after transplanta­tion, and one patient developed hepatitis C seroconversion. These satisfactorily low rates are probably related to the fact that we only accept virologically negative candi­dates for transplantation. Finally, post trans­plant herpes zoster was observed in three patients.

Our results showed a significantly higher incidence of bacterial than viral infections in the first six months after transplantation (77% vs. 28%) which is similar to the expe­rience in Saudi Arabia. [15] The North Ame­rican Pediatric Renal Transplant Coopera­tive Study (NAPRTCS) data demonstrated equal incidence of viral and bacterial in­fections. [19] The difference is probably rela­ted to the difference in age and geographic location.

Pulmonary tuberculosis was diagnosed in 2 (2%) patients. Although their past history was negative for tuberculosis we feel the condition was more likely a reactivation rather than a new infection because it oc­curred early after transplantation. In compa­rison, the incidence was 5% in Al-Wakeel [15] and Shankar et al studies; [20] mostly miliary tuberculosis.

Anemia was observed in 8 (12%) patients. In comparison, the incidence was higher in Nampoory et al study [21] from Kuwait (52%) and the cause was related to erythropoietin deficiency or resistance, which might also be the cause in our patients. Yorgin et al [22] reported an 80% incidence of anemia in transplanted children and young adults du­ring the first 6 months after transplantation. The causes were multiple including allo­graft failure, drug effect, iron deficiency and bone disease.

Surgical complications were reported in 7(9%) patients. Al-Wakeel [15] study found 18.4% incidence of lymphocele and urinary leak, while renal artery thrombosis oc­curred in one patient. In addition, Samhan et al [23] found 9.5% incidence of lymphocele in recipients of deceased allografts.

Kaposi sarcoma was diagnosed in 2 (3%) patients; both developed lesions limited to the skin and improved by discontinuation of MMF or azathioprine and optimization of cyclosporine, tacrolimus, and steroids. The incidence was comparable to other regional studies, [15],[24] however, higher than that in western countries and America; the inci­dence parallels that of the HHV8 in the general population. [25]

Calcineurin related hemolytic uremic syn­drome incidence was 1.5%, and it was treated conservatively by reducing the dose of cyclosporine and optimization of MMF and prednisolone. Ardalan found 3­ 14% incidence. [26]

We conclude that our study found that post transplant hyperglycemia was the com­monest early complication of renal trans­plantation. The incidence of post transplant hypertension and new onset diabetes mel­litus was comparable to that in other parts of the Middle East and worldwide. Bac­terial infection predominated the early in­fections after transplantation.

   References Top

1.Wolf R. The state of kidney transplantation in the United States. Semin Dial 2005;18 (6):453-5.  Back to cited text no. 1    
2.Amend WJ, Vincenti F, Tomlanovich S. The first three post-transplant months. In: Danovitch GM, ed. Handbook of kidney transplantation, 4th ed, CHIPS, Texas, 2005. p. 219.  Back to cited text no. 2    
3.Kasiske BL, Vazquez MA, Harmon WE, et al. Recommendations for the outpatient surveillance of renal transplant recipients. J Am Soc Nephrol 2000;11(15):S1-86.  Back to cited text no. 3    
4.Midtvedt K, Hartmann A. Hypertension after kidney transplantation: Are treatment guide­lines emerging? Nephrol Dial Transplant 2002;17(7):1166-9.  Back to cited text no. 4    
5.Kamar N, Marriat C, Delahousse M, et al. Diabetes mellitus after kidney transplan­tation: a French multi-center observational study. Nephrol Dial Transplant 2007;22 (7):1986-93.  Back to cited text no. 5    
6.Fernandez-Fresnedo G, Palomar R, Francisco AL, et al. Hypertension and long term survival: effect of early glomerular filtration. Nephrol Dial Transplant 2001; 16(1):105-9.  Back to cited text no. 6    
7.Formica RN, Friedman AL, Lober MI, Smith JD, Eisen T, Bia MJ. A randomized trial comparing Losartan with Amlodipine as initial therapy for hypertension in the early post transplant period. Nephrol Dial Transplant 2006;21(5):1389-94.  Back to cited text no. 7    
8.Midtvedt K, Hartmann A, Lund K, Bjerkely BL. Insulin resistance is a common denominator of post-transplant diabetes mellitus and impaired glucose tolerance in renal transplant recipients. Nephrol Dial Transplant 1998;13(2):425-9.  Back to cited text no. 8    
9.Addous A, Mohammed AS, Ismail G, Al­Hashemy A. Post-transplant diabetes mellitus in kidney recipients with special reference to association with HLA Antigens. Saudi J Kidney Dis Transpl 2000;11(4):559-62.  Back to cited text no. 9    
10.Mathew JT, Rao M, Job V, Ratnaswamy S, Jacob CK. Post-transplant hyperglycaemia: A study of risk factors. Nephrol Dial Transplant 2003;18(1):164-71.  Back to cited text no. 10    
11.First MR. Improving long-term renal transplant outcomes with Tacrolimus: speculation vs evidence. Nephrol Dial Transplant 2004;19(Supp 6):17-22.  Back to cited text no. 11    
12.Kasiske BL, Snyder JJ, Matas AJ, Ellison MD, Gill JS, Kausz AT. Pre-emptive kidney transplantation: the advantage and the advantaged. J Am Soc Nephrol 2002; 13(5):1358-64.  Back to cited text no. 12    
13.Mateu LM, Calabuig AS, Plaza LC, Esteve AF. Acute rejection and late renal transplant failure: risk factors and prog­nosis. Nephrol Dial Transplant 2004;19 (Suppl.3):38-42.  Back to cited text no. 13    
14.Cantarovich D, Giral-Classe M, Hourmant M, et al. Prevention of acute rejection with antithymocyte globulin, avoiding cortico­steroids, and delayed cyclosporin after renal transplantation. Nephrol Dial Transplant 2000;15(10):1673-6.  Back to cited text no. 14    
15.Al-Wakeel J, Mitwalli AH, Tarif N, et al. Living unrelated renal transplant: Outcome and issues. Saudi J Kidney Dis Transpl 2000;11(4):553-8.  Back to cited text no. 15    
16.Canivet E, Wampach H, Brandt B, et al. Assessment of radioisotopic micturating cystography for the diagnosis of vesico­ureteric reflux in renal transplant reci­pients with acute pyelonephritis. Nephrol Dial Transplant 1997;12(1):67-70.  Back to cited text no. 16    
17.Sarkio S, Salmela K, Kyllonen L, Rosliakova M, Honkanen E, Halme L. Complications of gallstone disease in transplantation patients. Nephrol Dial Transplant 2007;22 (3):886-90.  Back to cited text no. 17    
18.Sagedal S, Nordal K, Hartmann A, et al. Pre-emptive therapy of CMV pp65 antigen positive renal transplant recipients with oral ganciclovir: A randomized, comparative study. Nephrol Dial Transplant 2003;18 (9):1899-908.  Back to cited text no. 18    
19.Dharnidharka VR, Stablein DM, Harmon WE. Post-transplant infections now exceed acute rejection as cause of hospitalization: A report of the NAPRTCS. Am J Transplant 2004;4(3):384-9.  Back to cited text no. 19    
20.Shankar MS, Aravindan AN, Sohal PM, et al. The prevalence of tuberculin sensitivity and energy in chronic renal failure in an endemic area: tuberculin test and the risk of post-transplant tuberculosis. Nephrol Dial Transplant 2005;20(12):2720-4.  Back to cited text no. 20    
21.Nampoory MR, Johny KV, al-Hilali N, Seshadri MS, Kanagasabhapathy AS. Ery­thropoietin deficiency and relative resis­tance cause anemia in post-renal transplant recipients with normal renal function. Nephrol Dial Transplant 1996;11(1):177-81.  Back to cited text no. 21    
22.Yorgin P, Belson A, Sanchez J, et al. Unexpectedly high prevalence of post transplant anemia in pediatric and young adult renal recipients. Am J Kidney Dis 2002;40(6):1306-18.  Back to cited text no. 22    
23.Samhan M, Al-Mousawi M. Lymphcele following renal transplantation. Saudi J Kidney Dis Transpl 2006;17(1):34-7.  Back to cited text no. 23    
24.Emiroglu R, Moray G, Sevmis S, Sozen M, Biligin N, Haberal M. Long term results of pediatric renal transplantation at one center in Turkey. Transplant Proc 2005;37(2):675-8.  Back to cited text no. 24    
25.Sweny P. Infection and cancer following renal transplantation. Saudi J Kidney Dis Transpl 2006;17(2):189-99.  Back to cited text no. 25    
26.Ardalan MR. Review of thrombotic microangiopathy (TMA) and post-renal transplant TMA. Saudi J Kidney Dis Transpl 2006;17(2):235-44.  Back to cited text no. 26    

Correspondence Address:
Wael Latif Jabur
Department of Nephrology, NMC Specialty Hospital, P.O. Box 7832, Dubai, UAE

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Source of Support: None, Conflict of Interest: None

PMID: 18580032

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