scholarly journals Rupture of Renal Transplant

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Shona Baker ◽  
Maria Popescu ◽  
Jacob A. Akoh

Background. Rupture of renal allograft is a rare and serious complication of transplantation that is usually attributed to acute rejection, acute tubular necrosis, or renal vein thrombosis.Case Presentation. LD, a 26-year-old male with established renal failure, underwent deceased donor transplantation using kidney from a 50-year-old donor with acute kidney injury (Cr 430 mmol/L). LD had a stormy posttransplant recovery and required exploration immediately for significant bleeding. On day three after transplant, he developed pain/graft swelling and another significant haemorrhage with cardiovascular compromise which did not respond to aggressive resuscitation. At reexploration, the renal allograft was found to have a longitudinal rupture and was removed. Histology showed features of type IIa Banff 97 acute vascular rejection, moderate arteriosclerosis, and acute tubular necrosis.Conclusion. Possible ways of avoiding allograft rupture include use of well-matched, good quality kidneys; reducing or managing risk factors that would predispose to delayed graft function; ensuring a technically satisfactory transplant procedure with short cold and warm ischemia times; and avoiding large donor-recipient age gradients.

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Deepak Shankar Ray ◽  
Sharmila Thukral

Renal allograft rupture (RAR) is a rare but lethal complication of renal transplantation. It potentially threatens graft and patient survival. RAR is frequently associated with acute rejection, but other causes like renal vein thrombosis and acute tubular necrosis have also been observed. Most commonly a graft nephrectomy is required, but graft repair can also be attempted in selected cases to salvage the graft. Herein, we describe a rare case of spontaneous renal allograft rupture in the early posttransplant period due to acute tubular necrosis. A 42-year-old male, living donor renal allograft recipient, experienced RAR on the sixth posttransplant day. Surgical exploration showed two lacerations of 10 cm and 5 cm length at the upper and mid pole of the kidney. Histologically, the graft demonstrated acute tubular injury; no features of humoral or cellular rejection were identified. The successful management of this complication resulted in the salvage of the patient and the graft. This case demonstrates that early diagnosis and prompt treatment of a life-threatening RAR can salvage the graft.


2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Siddhesh Prabhavalkar ◽  
Agnes Masengu ◽  
Declan O'Rourke ◽  
Joanne Shields ◽  
Aisling Courtney

Acute kidney injury (AKI) is a recognised complication of intravenous pentamidine therapy. A direct nephrotoxic effect leading to acute tubular necrosis has been postulated. We report a case of severe renal allograft dysfunction due to nebulised pentamidine. The patient presented with repeated episodes of AKI without obvious cause and acute tubular necrosis only on renal histology. Nebulised pentamidine was used monthly as prophylaxis forPneumocystis jiroveciipneumonia, and administration preceded the creatinine rise on each occasion. Graft function stabilised following discontinuation of the drug. This is the first report of nebulized pentamidine-induced reversible nephrotoxicity in a kidney allograft. This diagnosis should be considered in a case of unexplained acute renal allograft dysfunction.


2001 ◽  
Vol 16 (1) ◽  
pp. 124-127 ◽  
Author(s):  
Boris Wolfgang Hochleitner ◽  
Reinhold Kafka ◽  
Bernard Spechtenhauser ◽  
Claudia Bösmüller ◽  
Wolfgang Steurer ◽  
...  

2018 ◽  
Vol 29 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Luca Cima ◽  
Francesco Nacchia ◽  
Claudio Ghimenton ◽  
Giovanni Valotto ◽  
Luigino Boschiero ◽  
...  

Background: Acute kidney injury is a treatable entity although difficult to recognize without diagnostic biopsy. We investigated the potential association between clinically defined deceased donors and acute kidney injury with preimplantation histological findings and recipient outcomes. Methods: Kidney biopsies from donors were classified using the Acute Kidney Injury Network criteria and assessed for percentage glomerulosclerosis, tubular atrophy, interstitial fibrosis, and vascular narrowing with the Remuzzi score and for acute tubular necrosis. Differences in incidence rates of delayed graft function (DGF) and cumulative rejection episodes were compared between recipients transplanted with normal and 3 levels of acute kidney injury using the analysis of variance with Bonferroni correction ( P = .0012). Results: Sixteen out of 335 donors showed a severe acute kidney injury level 3 with a median serum creatinine of 458 µmol/L. Fourteen (88%) had 0-3 Remuzzi score and were used for single kidney transplantation and 2 (12%) were used for dual kidney transplantation (score: 4-6). Recipients who received a kidney from a donor with level 3 acute kidney injury had a higher percentage of DGF (47%) without statistical significance ( P = .008). The rate of cumulative rejection (45%) at 2 years was not significantly increased ( P = .09). Conclusions: Recipients receiving level 3 acute kidney injury kidneys, selected with Remuzzi histopathological score and acute tubular necrosis assessment, had a greater incidence of DGF but a similar long-term cumulative rejection compared to no injury and level 1 and level 2 acute kidney injury donors. The application of the histopathological examination allowed expansion of the kidney donor pool.


2012 ◽  
Vol 2012 ◽  
pp. 1-3
Author(s):  
Omkar U. Vaidya ◽  
Todd Buersmeyer ◽  
Rebecca Rojas ◽  
Bart Dolmatch

A 68-year-old Caucasian female with a past medical history of a deceased donor kidney transplant four months prior was admitted with a two-day history of anuria and acute kidney injury. A renal ultrasound demonstrated thrombus in the transplanted kidney's renal vein that extended into the left iliac vein as well as into the left femoral venous system. Catheter-guided tissue thrombolytics were infused directly into the clot. Within twelve hours of initiating thrombolytic infusion, there was brisk urine output. Interval venography demonstrated decreasing clot burden. At the time of discharge her creatinine was 0.78 mg/dL, similar to her baseline value prior to presentation. The patient was noted to have May-Thurner syndrome on intravascular ultrasound (IVUS). Angioplasty followed by stent placement was done. Unique to our case report was the timing of the presentation of renal vein thrombosis (four months after transplant) and the predisposing anatomy consistent with May-Thurner syndrome, which was diagnosed with IVUS and successfully treated with local thrombolytics.


2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Yvelynne P. Kelly ◽  
Astrid Weins ◽  
Melissa Y. Yeung

Hyperoxaluria is an important and underrecognized cause for allograft dysfunction and loss after transplantation. It is potentially treatable if recognized in a timely fashion. Research is ongoing to expand the array of therapeutic options available to treat this. We present a case of a 59-year-old gentleman who underwent deceased donor renal transplantation that was complicated by delayed graft function necessitating continuation of renal replacement therapy. His initial biopsy showed extensive acute tubular necrosis with associated peritubular capillaritis and interstitial nephritis and oxalate crystals in several tubules. Despite receiving methylprednisolone to treat moderate acute cellular rejection, he remained dialysis dependent with minimal urine output. An interval renal allograft biopsy revealed residual acute tubular necrosis with extensive oxalate crystals now visible in many tubules. His plasma oxalate level was concurrently elevated to 19.3 μmol/L (reference range ≤ 1.9 μmol/L). He commenced calcium citrate to manage his hyperoxaluria and ultimately became dialysis independent at 3 weeks after transplantation. This case provides an important example of accelerated oxalate nephropathy as an underappreciated contributor to delayed graft function after renal transplantation. Our accompanying discussion provides an update on current therapeutic measures for managing this challenging condition.


2014 ◽  
Vol 8 (4) ◽  
pp. 130
Author(s):  
Narayan Prasad ◽  
Brijesh Yadav ◽  
Akhilesh Jaiswal ◽  
R.K. Sharma ◽  
Vikas Agarwal

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