Vascular complications of renal transplantation

From January, 1963, to May, 1979, 600 renal transplants were performed at the Cleveland Clinic. There were 21 vascular complications in this series (3.5 per cent). Arterial complications included renal artery thrombosis in 5 patients, renal artery stenosis in 9 patients, and anastomotic hemorrhage in 2 patients. Venous complications included renal vein thrombosis in 2 patients and hemorrhage in 3 patients. Although vascular complications led directly to graft loss in 10 patients, only 1 resulted in patient death.     

Urologic complications of renal transplantation

The early experience of the University of Miami School of Medicine, Transplant Teanz is presented. Four urologic complications occurring in the first 66 transplants performed are presented in detail, and the method of ureteroneocystostomy is described. A review of the techniques of restoring urinary continuity and their complications is presented. The diagnosis and management of these urologic complications are discussed.     

Colonic complications of renal transplantation

Colonic complications of renal transplantation occur in 1.9 per cent of the cases. In our series of 587 consecutive renal transplants recipients 3 (0.51 per cent) had colonic complications, including 2 with ischemic colitis and 1 with pseudomembranous colitis. A review of 8 large series describing 2,539 additional renal transplant patients revealed 55 with significant colonic complications. The most common complication was ischemic colitis, which occurred in 29 patients, followed by diverticulitis in 17, pseudomembranous colitis in 5, appendicitis in 3, hemorrhagic proctitis in 1, a disrupted appendiceal stump in 1 and fecal impaction in 1. Etiological factors that may be important in the development of these colonic complications are uremia, blood volume redistribution, immunosuppressive therapy, antibiotic therapy, irradiation and previous retroperitoneal surgery.     

Gastrointestinal complications in renal transplantation

One wonders whether the use of cyclosporin, histamine receptor antagonists, low doses of steroids, and early diagnosis and treatment actually modify the incidence, morbidity, and mortality of gastrointestinal (GI) and pancreatic complications in renal transplantation. To find out, we reviewed 614 kidney transplant recipients between January 1984 and December 1988. One hundred patients (16.2%) were found to have GI and/or pancreatic complications in the following distribution: 9.6% gastroduodenal, 1.3% pancreatic, 4% colonic, and 0.4% small bowel. None of the patients presenting a gastroduodenal ulcer had perforation or bleeding. Fifty-five percent of the patients with this complication had a past history of esogastroduodenal disease, compared to 19.6% in recipients without gastroduodenal complications. Some 4.4% of the patients had a small bowel or a colonic complication and four died of peritonitis due to bowel perforation. Mortality was 35% in those having intestinal resection and/or perforation with peritonitis. Sixteen percent of patients with colonic complications had a known history of diverticula, compared to 3% for those without colonic complications. The incidence of GI and/or pancreatic complications in renal transplant recipients remains high and has caused 1.1% of the deaths in our series. Mortality is essentially due to upper GI bleeding, peritonitis following perforation, and infectious colitis. Better detection of gastroduodenal and colonic disease before transplantation seems to be mandatory. Prevention with histamine H2 receptor antagonists and early surgical treatment of complicated colonic diverticula help to reduce the morbidity and mortality in kidney graft recipients.     

Urological complications following renal transplantation

A total of 1016 consecutive renal transplants performed between 1976 and 1990 were analysed retrospectively to determine the incidence of urological complìcations and possible predisposing factors. Some 189 episodes of ureteric obstruction and/or urinary leak occurred in 143 patients (overall incidence 14.1 %). The median annual rate of urinary leak was 5.1%; that of ureteric obstruction was 4.5% pre-1986 and 16.1% post-1986. Sixty-three episodes of urinary leak occurred in 54 patients from 1 day to 3 months post-transplant and 60% involved the distal ureter. Thirty were treated primarily by reconstructive surgery, ten required nephrectomy and three died of associated sepsis. A total of 126 episodes of ureteric obstruction occurred in 104 patients from 1 day to 12 years post-transplant and 86% involved the distal ureter. Prior to 1986, 10/11 patients with ureteric obstruction were treated by reconstructive surgery, but since then 88 (95%) have been treated by percutaneous nephrostomy, with or without stenting, with only one graft lost and no deaths. Children had a significantly increased incidence of ureteric obstruction (P<0.001) whilst male recipients had an increased incidence of urinary leak (P=0.04). More patients with ureteric obstruction than those without had two or more episodes of rejection (P=0.03). No single cause for the increased incidence of ureteric obstruction since 1986 has been identified. Continued attention to technical detail and further study of this trend is warranted.     

Atherosclerotic complications after renal transplantation

Death with functioning graft, the most frequent cause being cardiac death, continues to be the most frequent cause of long-term graft loss. The risk of cardiovascular death in the transplanted patient is lower than in patients with other modalities of renal replacement therapy, but continues to be substantially higher than in the general population. Amongst the factors predicting patient and graft survival are hypertension, dyslipidemia, smoking and possibly hyperhomocysteinemia. It is concluded that lowering of blood pressure to levels far lower than levels accepted in the past, more widespread administration of statines, cessation of smoking and possibly administration of folate should reduce cardiovascular mortality and possibly also influence chronic allograft vasculopathy.