Pancreatitis after renal transplantation.

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.     

Listeria monocytogenes infection after renal transplantation.

Listeria monocytogenes infection has been observed in 13 patients, of a group of more than 700 renal transplants, treated during the past 13 1/2 years. The infection usually was manifested as bacteremia or meningitis. Twelve of the 13 patients survived the infection; one died of brain-stem herniation due to increased intracranial pressure. The recommended treatment is intravenously given ampicillin sodium.     

Osteoporosis after renal transplantation

This study was performed to determine risk factors associated with osteoporosis that develops after renal transplantation. Sixty-five kidney graft recipients were included in this study. They were divided into four groups according to the time since transplantation: Group 1 (< 1 year; n = 26), group 2 (1-3 years; n = 16), group 3 (3-5 years; n = 12) and group 4 (> 5 years; n = 11). These groups were matched according to probable risk factors for osteoporosis, findings of serum biochemistry, biochemical markers of bone turnover and measurements of bone mineral density. One way ANOVA test and Kruskal-Wallis test were used for statistical analysis. Osteoporosis was found in 22 recipients (33.8%). There were significant differences in recipient age, cumulative steroid dose, and episodes of acute rejection between the four groups. Increasing age, cumulative steroid dose and episodes of acute rejection were found to be risk factors for osteoporosis in our study.     

Hypertension after renal transplantation

With current immunosuppression, elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this are impairment of renal function (secondary to chronic allograft nephropathy or less frequently recurrence of primary renal disease), the use of calcineurin inhibitors as immunosuppressants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenosing lesions of the transplant artery (or the upstream arteries of the recipient), polycytemia, and genetic predisposition to hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, angiotensin converting enzyme inhibitors are indicated in treatment, but given the causal role of sodium retention and graft vasoconstriction, diuretics and calcium channel blockers remain mainstays of antihypertensive treatment in the renal allograft recipient.     

Bacteremia after upper gastrointestinal endoscopy.

During 24 months, 200 upper gastrointestinal endoscopies were performed on 193 patients. Blood cultures were obtained before and five and 30 minutes after the procedure using thiol (50 ml) and trypticase soy broth (100 ml) media. The mean endoscopic time was 34 minutes. Sixteen patients developed bacteremia (8%). Twelve groups of microorganisms were detected in positive blood cultures: Streptococcus (5 species), Lactobacillus sp, Veillonella alcalescens, Staphylococcus aureus, Staph epidermidis, Propioni-bacterium acnes, Corynebacterium acnes, and Bacillus subtilis. Seven patients had positive blood cultures at five and 30 minutes, eight at five minutes, and one at 30 minutes only. There was no clear correlation of bacteremia with the age or previous history of the patient, biopsy, active bleeding, endoscopic time, or findings. A follow-up study of all patients for six months to two years indicated no complications related to endoscopy and/or bacteremia.     

Recurrence of IgA nephropathy after renal transplantation.

With time recurrence of IgA nephropathy in renal allografts may be found in most, if not all patients. However, at the present graft loss due to recurrent IgA nephropathy appears to be of limited importance as compared to other causes. No definite risk factors for recurrent disease and/or graft failure have been identified yet. Although recurrence rates appear to be higher in allografts from living related donors, graft loss rates due to IgA nephropathy are not significantly different. More important, sporadic cases of IgA nephropathy should be excluded in all living related donors.     

Gastric adenocarcinoma after renal transplantation

BACKGROUND/AIMS: Little is known of the characteristics of gastric adenocarcinoma after renal transplantation. This study was performed to find out the incidence and clinicopathological features of gastric adenocarcinoma after renal transplantation in an endemic area for gastric cancer. METHODOLOGY: Between April 1979 and March 2001, fourteen gastric adenocarcinoma patients (0.7%) out of 2000 renal transplant recipients in a single institute were retrospectively reviewed. RESULTS: Gastric adenocarcinoma was identified in 14 recipients (8 males and 6 females; mean age 47.6 years) about 60 months after renal transplantation. Four patients had early gastric cancer; ten patients had cancer in an advanced stage. Eleven patients underwent surgical resection, while three with distant metastasis were treated symptomatically. There was no postoperative mortality. Seven patients survived without evidence of recurrence, whereas four died of recurrence and three of gastric cancer progression. CONCLUSIONS: Renal transplant recipients are at increased risk of gastric adenocarcinoma, the most common malignancy in Korea. With curative surgery, favorable prognosis can be anticipated when the diagnosis is made at an early stage. Regular endoscopic examination for early diagnosis is recommended during the follow-up period after renal transplantation in a gastric cancer endemic area.     

Multiple complications after renal transplantation

This is the case of a 32-year-old male patient, diagnosed with end stage renal disease secondary to a focal and segmental glomerulonephritis. After four years of haemodialysis, he received a renal graft from a cadaveric donor. During the following sixteen years, he developped many different complications. In the early post-transplant period, he developed a severe acute tubular necrosis and two episodes of acute rejection took place, both of them with later recovery. Among the outstanding infectious complications were a virus herpes zoster dorsal infection and a Pseudomonas aeruginosa nosocomial pneumonia. Twelve months later, a series of severe digestive complications took place: cholecystitis that required cholecystectomy, pancreatic pseudocyst which required laparotomy because of an abdominal complication, two separate episodes of upper digestive bleeding that finally required gastric surgery, and an hemorrhagic subphrenic abscess that required a second laparotomy. Currently he has developed a calcified chronic pancreatitis. Moreover, metabolic complications must be mentioned carbohydrate intolerance, cataracts and an avascular bone necrosis, all of them closely related to the immunosuppressive therapy. In spite of these multiple complications, he mantains a good renal function and his quality of life is acceptable.     

Hypertension after successful renal transplantation

Thirty-three renal allograft recipients who had high blood pressure (mean arterial pressure more than 105 mm Hg) at least one year after their successful transplant operation were compared with 23 normotensive kidney transplant recipients (mean arterial pressure less than 105 mm Hg) at the General Clinical Research Center. The patients with higher blood pressure had markedly and significantly higher (96 percent) renal vascular resistance and significantly lower (41 percent) renal plasma flow. Responses to salt loading and restriction were suggestive of marked activity of the renin-angiotensin system as were plasma renin activity measurements. Subsequent follow-up has revealed chronic rejection or renal artery stenosis as a probable cause of hypertension for 11 of the 33 patients. The remaining 22 patients had increased renal vascular resistance and decreased renal plasma flow indistinguishable from that in the 11 patients in whom follow-up revealed a cause for their persistent hypertension; however, 21 of these 22 patients have their native kidneys in place.     

肾移植后输尿管外科并发症

连续９６９例尸体肾移植中，有３３例术后发生输尿管并发症，其中尿漏与输尿管梗阻分别为２１例和１２例。有１１例膀胱输尿管吻合口漏与５例输尿管梗阻在术后早期发生，均与手术操作不当有关，早期手术探查解除诱因后均获治愈。１０例因输尿管坏死导致输尿管缺损尿漏，其中３例在术后２．５－４个月发生输尿管坏死，可能与输尿管排异有关。根据输尿管残留长度分别采用不同的手术方法，替代和弥裤输尿管短缺。８例获得治愈，术后发生     

Glomerular lesions after renal transplantation

Significant changes in glomeruli on light microscopy has been observed in 27 of 109 cadaveric renal allografts which functioned beyond 6 months. Tissue was available for study from all but two allografts. The histologic lesions were classified as follows: recurrent glomerulonephritis, 9 cases (3 focal sclerosis, 2 mesangial immunoglobulin A [IgA] disease, 2 mesangiocapillary glomerulonephritis, 1 dense deposit disease, 1 familial nephritis); de novo glomerulonephritis, 1 case (diffuse proliferative glomerulonephritis with crescents); and glomerular change of uncertain etiology, 17 cases (10 mesangiocapillary, 5 focal sclerosis, 1 focal proliferative and 1 mesangial proliferative). These lesions were not distinguishable on light, fluorescent and electron microscopy from those in patients with spontaneous renal disease. All patients with glomerular lesions had proteinuria, and all but 3 had microscopic hematuria. Glomerular lesions were not significantly associated with early clinical rejection episodes or HLA compatibility. Presensitization of HLA antigens was significantly related to the occurrence of a nonrecurrent glomerular lesion. Vesicoureteral reflux was significantly more frequent in those with glomerular change (14 of 24) than in those without (13 of 48). Glomerular lesions were associated with a higher rate of graft loss due to renal transplant failure; renal function in survivors was significantly worse than in those without glomerular lesions.     

Bacteremia due to Campylobacter in renal transplantation: a case report and review of literature

Campylobacter species are the leading cause of acute bacterial diarrhea in industrialized countries. However, bacteremia is detected in <1% of patients with Campylobacter enteritis and is most likely to occur in patients who are immunocompromised or of older age. To our knowledge, only 2 cases of Campylobacter jejuni bacteremia have been reported in renal transplant recipients (RTRs). We present a case of an RTR with C. jejuni bacteremia presenting as self‐limiting diarrhea followed by fever and cellulitis. The patient was successfully treated with a 2‐week course of imipenem and developed no other complications. We review all cases of Campylobacter bacteremia in RTRs, and discuss clinical presentation and treatment of this potentially fatal disease.     

Chronic granulocytic leukemia after renal transplantation

Chronic granulocytic leukemia (CGL) developed in a 31-year-old man after he underwent a third renal transplant. The leukemia was initially controlled with azathioprine sodium and prednisone therapy, but eventually it entered blast cell crisis. This was controlled with an adult acute lymphocytic leukemia protocol with an excellent response. Despite discontinuing treatment with azathioprine and with the use of busulfan to control the peripheral WBC count, the patient maintained stable renal function for one year following treatment of the blast cell crisis and subsequently died of sepsis. We suggest that CGL after renal transplantation is similar to that observed in the general population and can be treated with the usual chemotherapeutic agents for the disorder without sacrificing renal function.