Duplicated ureters are the most common congenital malformation of the upper urinary tract, but there are few reports on the transplantation of kidneys with duplicated ureters. We introduce different techniques for the ureteroneocystostomy of double ureters and long-term results. We specifically detail the experience of two patients with duplicated ureters at Bong Seng Memorial Hospital from March 1995 to May 2012. In our first case, the top technique of spatulating and suturing duplicated ureters was applied with the bottom technique for double ureteroneocystostomy. The operation time was 4 hours and 45 minutes, while the ureteroneocystostomy took 32 minutes. In the second case a double-armed 4.0 Vicryl suture was placed on each tip of the ureter and both needles passed from the inside out through the bladder wall. The ureters were pulled into the bladder and the suture was tied on the serosa of the bladder. The operation time was 3 hours and 50 minutes, while the ureteroneocystostomy took 15 minutes. Neither urological complications nor urinary tract infections were observed in the follow-up period and no double-J stent was needed. We therefore conclude that these two techniques are available procedures for handling duplicated ureters, with the technique applied in the second case particularly time-effective.
Follow-Up Studies ; Handling (Psychology) ; Humans ; Kidney ; Kidney Transplantation ; Needles ; Polyglactin 910 ; Serous Membrane ; Stents ; Sutures ; Transplants ; Ureter ; Urinary Bladder ; Urinary Tract ; Urinary Tract Infections

PURPOSE: This report presents our experience of the renal transplatation of a long term dysfunctional contracted bladder and its outcome. METHODS: Between March 1996 and May 2006, 425 cases of renal transplantation were performed in our medical center. We found 14 chronic renal failure patients having dysfunctional contracted bladder (DFCB) that was diagnosed through the preoperative voiding cystourethrogram. DFCB was defined as the maximal urinary bladder volume less than 100 mL. No surgical or medical preparation was done before and after renal transplantation. In 8 out of 14 cases, extravesical ureteroneocytostomy (EVUC) was conducted and the Lich's EVUC was done for the other 6 cases. Double J ureteral stent was not employed in any cases. RESULTS: The mean age of the recipients was 41.4 years. The mean capacity of these bladder was 72.1 mL (range 20 to 100 mL). Of the 14 cases, thirteen had living donor related transplantation and one received cadaveric kidney. Postoperative complication was occurred in one case, which was bleeding. There was no evidance of urinary tract complication. All patient excluding of one patient who had the episodesof chronic rejection were stable throughout the entire follow up period. CONCLUSION: DFCB in renal translpantation had no adverse effect on successful outcome in transplant operation deposite no preoperative preparation, especially cadaveric donor transplatation, it may, however, need a delicate surgical skills to perform EVUC.
Cadaver ; Follow-Up Studies ; Hemorrhage ; Humans ; Kidney ; Kidney Failure, Chronic ; Kidney Transplantation* ; Living Donors ; Postoperative Complications ; Stents ; Tissue Donors ; Ureter ; Urinary Bladder* ; Urinary Tract

Acute antibody-mediated rejection is the major cause of graft failure in the early stage of kidney transplantation. Preoperative treatment and early diagnosis of acute rejection is very important to prevent graft loss in sensitized patients. High panel reactive antibody (PRA) means a likelihood of acute rejection, and the recipient of high PRA needs adequate pretreatment for kidney transplantation. However, there is not sufficient time and chances for desensitization in deceased kidney transplants. We report a successful renal transplant outcome in a 47-year-old-woman with high PRA levels (Class I 97.5%, Class II 36.7%). The cross match was negative on the CDC (ELISA) and flowcytometric methods. Plasma exchange was performed on the recipient before transplantation (fresh frozen plasma replacement, 1.3 plasma volume) and immediately after plasma exchange she was given 200 mg of rituximab. She received basiliximab and methyl prednisolone induction therapy and was maintained on steroids, mycophenolate mofetil, and tacrolimus. Graft function was normal immediately after transplantation, but decreased urinary output and elevated serum creatinine was noted on POD 5. On POD 6, a graft biopsy revealed acute cellular rejection (Type IIa) and antibody-mediated rejection (Type II). On 9~13 days after transplantation, additional plasma exchange was performed every other day, and steroid pulse therapy was performed 3 times. After normalization of urinary output and serum creatinine, the patient was discharged and is being followed up on. In conclusion, immunologically careful preparation and pretransplant treatment may be needed on the negative cross match in cadaveric kidney recipients with high levels of PRA.
Antibodies, Monoclonal ; Antibodies, Monoclonal, Murine-Derived ; Biopsy ; Cadaver ; Centers for Disease Control and Prevention (U.S.) ; Creatinine ; Early Diagnosis ; Graft Rejection ; Humans ; Immunization ; Kidney ; Kidney Transplantation ; Mycophenolic Acid ; Plasma ; Plasma Exchange ; Prednisolone ; Recombinant Fusion Proteins ; Rejection (Psychology) ; Rituximab ; Steroids ; Tacrolimus ; Tissue Donors ; Transplants

Acute antibody-mediated rejection (AMR) developing simultaneously with acute cellular rejection has been rarely reported as a long-term complication of renal transplantation, and it can present on top of another chronic pathology affecting the graft. A 51-year-old female patient with chronic kidney disease of unknown etiology received renal transplantation 12 years ago from a living unrelated donor with 3 HLA mismatches. She received induction therapy with methylprednisolone and was maintained on steroids, mycophenolate mofetil and cyclosporine A (CsA). For a period of twelve years post-transplantation, she was clinically and biochemically stable. She presented with a rise in serum creatinine (SCr.) from 1.3 mg/dL to 2.4 mg/dL but did not have proteinuria. Graft biopsy revealed findings suggestive of acute cellular rejection on top of antibody-mediated rejection (type II) and chronic calcineurin inhibitor toxicity. Panel reactive antibody (PRA) test levels were 3.6%, 91.7% for class I and II respectively. The patient was treated with high-dose methylprednisolone for 3 days but serum creatinine was not fully normalised. After 2 weeks from initial methyl-PDS pulse therapy, she received intravenous immunoglobulin, plasma exchange and anti-CD20 (rituximab). Cyclosporine was changed to tacrolimus. She achieved a complete response, and SCr. was maintained at 1.3 mg/dL without proteinuria. Follow-up PRA test levels were 0%, 75% for class I and II. Current therapies have had considerable success in reversing mixed, acute humoral and cellular rejection since it is being identified quickly and treated aggressively. The best use of rituximab to treat AMR should be evaluated in controlled trials using dosing strategies that include longer courses or retreatment schedules.
Antibodies, Monoclonal, Murine-Derived ; Appointments and Schedules ; Biopsy ; Calcineurin ; Creatinine ; Cyclosporine ; Female ; Follow-Up Studies ; Graft Rejection ; Humans ; Immunoglobulins ; Immunoglobulins, Intravenous ; Kidney Transplantation ; Methylprednisolone ; Middle Aged ; Mycophenolic Acid ; Plasma Exchange ; Plasmapheresis ; Proteinuria ; Rejection (Psychology) ; Renal Insufficiency, Chronic ; Retreatment ; Rituximab ; Steroids ; Tacrolimus ; Transplants ; Unrelated Donors

Kidney transplantation (KTP) lowers the mortality and morbidity of patients with end-stage renal disease. Post-transplantation infection and antibody mediated rejection (AMR) are the most common complications. Hepatitis B surface antigen (HBsAg) positive carrier donors and high anti A/B antibody titer ABO incompatible KTP could lead to recipient hepatitis B virus (HBV) infection and AMR. Here, we report a case of successful KTP in a 41-year-old male with a high titer of ABO incompatible and HBsAg positive donor. He underwent seven rounds of plasmapheresis, low dose intravenous immunoglobulin and rituximab treatment to inhibit antibody production and remove antibodies from the serum, after which he was administered anti-viral agent for HBV prophylaxis. The recipient maintained successful allograft function for 6 months after transplantation; therefore, we report that desensitization and anti-viral treatment achieved successful outcome in a 1:512 anti A/B antibody titer ABO incompatible and hepatitis B carrier donor KTP.
Adult ; Allografts ; Antibodies ; Antibody Formation ; Hepatitis B Surface Antigens ; Hepatitis B virus ; Hepatitis B* ; Hepatitis* ; Humans ; Immunoglobulins ; Kidney Failure, Chronic ; Kidney Transplantation* ; Kidney* ; Male ; Mortality ; Plasmapheresis ; Rituximab ; Tissue Donors

Polyoma virus (PV) nephropathy is a known cause of graft loss after renal transplantation. In a renal transplant patient suspected of graft rejection, it is important to discriminate between PV induced interstitial nephritis and acute cellular rejection, because of similar pathologic findings. After the loss of the first allograft secondary to PV nephropathy, transplant graft nephroureterectomy before retransplantaton may have an influence in the recurrence of PV nephropathy. However, this question has not been completely resolved. Case: A 23-year-old male underwent first renal transplantation from his HLA haploidentical 25 year-old-sister. His renal function had been good with cyclosporine, steroid and azathioprine until 9 months after transplantation, when his serum creatinine level rose to 2.2 mg/dL. A renal biopsy revealed features of tubulitis and we confirmed PV nephropathy through a positive PV monoclonal antibody reaction to inclusion body. After gradual loss of graft function, he underwent hemodialysis. After 48 months of hemodialysis, the patient underwent cadaveric renal retransplantation without transplant graft nephroureterectomy. Thrombocytopenia and suspected delayed graft function occurred after 2 days of transplantation. A graft biopsy revealed thrombotic microangiopathy. Improved graft function was attained after a temporary stop of tacrolimus and ATGAM(R) bridging therapy. The patient is maintaining satisfactory graft function 33 months after retransplantation without clinical and serological evidence of recurrent PV infection.
Allografts ; Azathioprine ; Biopsy ; Cadaver ; Creatinine ; Cyclosporine ; Delayed Graft Function ; Graft Rejection ; Humans ; Inclusion Bodies ; Kidney Transplantation ; Male ; Nephritis, Interstitial ; Polyomavirus* ; Recurrence ; Renal Dialysis ; Tacrolimus ; Thrombocytopenia ; Thrombotic Microangiopathies ; Transplants* ; Young Adult

Transplant renal artery stenosis (TRAS) is an important cause of hypertension, allograft dysfunction, and graft loss. Patient and allograft survival rates are lower in patients with TRAS. Causes of TRAS include acute rejection, cytomegalovirus infection, calcineurin inhibitor toxicity, atherosclerosis of recipient, and/or donor. Technical problems due to surgery are a common cause of early TRAS. A 62-year-old male in end stage renal disease received kidney transplant surgery. There was 5/6 mismatch of human leukocyte antigen and the panel reactive antibody of patient was class I 0% and class II 0%. End to side anastomosis was done between the graft's renal artery and the patient's common iliac artery. His serum creatinine was measured at 6.4 mg/dL before transplantation but his serum creatinine level did not fall below 2.6 mg/dL at 5 days postoperative. His blood pressures was 160/90~180/100 mmHg. There was a significant TRAS (about 80% luminal narrowing) at the arterial anastomosis site on the renal magnetic resonance angiography. We performed percutaneous transluminal angioplasty (PTA) for the stenotic lesion. The balloon angioplasty was done with a 5 mm balloon and low pressure (8 mmHg, nominal pressure was 10 mmHg) at the stenotic lesion. The arterial pressure gradient was 8 mmHg (recipient's common iliac arterial pressure, 147/73 mmHg; poststenotic segmental renal arterial pressure, 139/70 mmHg) just before the balloon angioplasty. After PTA, the arterial pressure gradient became 3 mmHg (recipient's common iliac arterial pressure, 157/66 mmHg; poststenotic segmental renal arterial pressure, 154/65 mmHg). The arterial size and blood flow recovered to within normal range and serum creatinine level was normal after PTA. PTA using low pressure and a small balloon was safe and effective modality in treating early TRAS.
Allografts ; Angioplasty ; Angioplasty, Balloon* ; Arterial Pressure ; Atherosclerosis ; Calcineurin ; Creatinine ; Cytomegalovirus Infections ; Humans ; Hypertension ; Iliac Artery ; Kidney ; Kidney Failure, Chronic ; Kidney Transplantation ; Leukocytes ; Magnetic Resonance Angiography ; Male ; Middle Aged ; Phenobarbital ; Reference Values ; Renal Artery Obstruction* ; Renal Artery* ; Survival Rate ; Tissue Donors ; Transplants