No abstract

Background and Aims Encapsulating peritoneal sclerosis (EPS) is a life-threatening complication of long-term peritoneal dialysis (PD). Causative factors are the chronic exposure to bioincompatible PD and peritonitis episodes. Pro-inflammatory state and oxidative stress associated with chronic uremia may further accelerate these pathomechanisms. Clinical symptoms are, essentially, signs of intestinal obstruction. Treatments commonly used are corticosteroids, tamoxifen, immunosuppressants like azathioprine, mycophenolate mofetil (MMF), or mTOR inhibitors which has fibrinolytic properties and may help with reducing inflammation. In the last ten years, the incidence of SEP in kidney transplant recipients has increased, but few cases have been reported. Given the rare nature of this pathology, we decided to publish the cases of two EPS happening after kidney transplantation (KT). Case report We report the cases of two male patients aged 46 and 25 with a history of chronic renal failure, who benefited of continuous ambulatory peritoneal dialysis (CAPD) for three years. The first patient was switched to haemodialysis (HD) for sub-dialysis, with one episode of peritonitis and one episode of catheter infection. The second patient had three episodes of peritonitis complicated by asymptomatic EPS, hence its transfer to HD. Our two patients presented, at 30 and 40 days post KT, an episode of acute intestinal obstruction with abdominal scans fitting with a mechanical bowel obstruction on an encapsulating peritonitis without signs of complication. Both patients were on corticosteroid therapy (15 and 17.5 mg/day) combined with MMF and Calcineurin inhibitors (CNIs) (Tacrolimus). Medical measures were not effecient. Surgical treatment was then considered. During the operation, a classical picture of EPS was found characterized by a thin cocoon-like sclerotic membrane encasing the small bowel. A complete resection of the encapsulating sclerotic membrane and total adhesiolysis were performed, with an immediate improvement on the clinical level. No recurrence was noted for both patients at 5 and 24 months respectively. Conclusion The specificities of our patients compared to the reported cases were the short duration of the PD and the relatively young age. In fact, some studies demonstrated an increased incidence of EPS in younger patients. In addition, this complication has declared itself despite corticosteroid therapy. Some case reports have demonstrated an increase in the incidence of SEP in kidney transplant patients, suggesting the possible implication of CNIs which have a profibrotic effect and may promote peritoneal matrix accumulation.

Background and Aims Inherited thrombophilia can be defined as a genetically determined predisposition to develop thromboembolic complications. Inherited prothrombotic risk factors include antithrombin deficiency, protein C and protein S deficiencies, activated protein C resistance due to Leiden factor V mutation, inherited hyperhomocysteinemia, prothrombin G20210A variant, dysfibrinogenemia and elevated factor VIII levels. Method We report the case of a patient with history of bilateral renal artery stenosis who presented with renal artery bypass thrombosis related to an inherited thrombophilia. Results We report a case of 40-year-old male patient who presented with extremely high blood pressure and hypokalemia without other biological abnormalities. The duplex ultrasound showed bilateral renal stenosis with chronic occlusion of the right renal artery and a tight stenosis of the left renal artery estimated at 50%. Renal angiography confirmed the bilateral stenosis, associated to a small right kidney. Renal scintigraphy with DMSA showed normal left renal function and right renal function estimated at 2%. The therapeutic decision was to perform an aorto-renal bypass surgery by the saphenous vein.After renal artery bypass the blood pressure improved markedly, maintaining this result at 12 months follow-up at clinical examination and duplex ultrasound. One year later, the patient presented with high blood pressure. The duplex ultrasound showed a stenosis of the bypass with a double stenosis of the left aorto renal bypass on renal angioscanner. The patient underwent angioplasty of the venous bridge with implantation of 2 stents with improvement of blood pressure after angioplasty. Six months later, the patient presented an unbalanced blood pressure, the ultrasound control with a vascular Doppler showed a stenosis at the stent. The antihypertensive treatment was increased, a thrombophilia balance was requested concluding a combined protein C and protein S deficiency. Conclusion An etiological assessment should be carried out systematically in the event of thrombosis occurring before the age of 40 or in the case of iterative venous or arterial thrombosis. A genetic study where appropriate and a family screening are then recommended.

No abstract

No abstract