A rare case of refractory ascites due to aortic regurgitation delaying peritoneal dialysis catheter removal after renal transplantation

Abstract

Introduction

Removing the peritoneal dialysis (PD) catheter after transplantation is necessary in order to improve quality of life after transplantation. However, there is no consensus on the best timeframe of PD-catheter removal in transplanted patients. Early removal can lead to the absence of dialysis access in case of graft failure. However, late removal is associated with significant infectious risk given the immunosuppression. Herein, we describe an exceptional case of refractory ascites secondary to aortic regurgitation in a cirrhotic patient, delaying the removal of his PD catheter.
Case report
We describe the case of a 49-year old patient, with Child B cirrhosis and end-stage kidney disease on chronic peritoneal dialysis who benefited from kidney transplantation. The scheduled PD catheter flushes were marked by the drainage of ascitic fluid, leading to the postponement of the PD catheter removal. The ascites, thought to be secondary to his long-known cirrhosis, was refractory to optimal drug treatment and the PD catheter was used to remove ascites periodically. As a transjugular intrahepatic portosystemic shunt was planned, a severe aortic regurgitation was diagnosed. After aortic valve replacement, the ascites completely disappeared, and the PD catheter could be removed.
Discussion
Heart failure represents only 3% of all refractory ascites. Furthermore, left-side heart failure causing ascites but without signs of right-side heart failure has only been described once in the medical literature. Patients with ascites and kidney failure on PD can safely be managed through the PD catheter instead of recurrent paracentesis. However, in transplanted patients especially, keeping the catheter in place brings significant infectious risk.
Conclusion
We described an unusual case of refractory ascites after renal transplantation, due to aortic valve regurgitation. This case highlights the importance of weighing the pros and cons of early PD catheter removal, as PD catheter might be useful as a means of removing ascites.

Peritoneal dialysis (PD) accounts for 11% of renal replacement therapy among end-stage kidney disease (ESKD) patients[1]. An increasing number of PD patients eventually undergo kidney transplantation (KT), therefore raising the question of PD catheter removal. However, there is no agreement regarding the best timing to remove the peritoneal dialysis catheter after transplantation. Catheter infection and peritonitis are the major complications of keeping a catheter for longer, especially in transplanted patients on immunosuppressive drugs[2]. It has been suggested that the best period to remove a PD catheter would be between the 30th and 45th day post-transplant[3]. However, no consensus exists in the current medical literature[4]. In fact, in exceptional circumstances, the catheter might never be removed due to unexpected clinical conditions such as recurrent ascites. Herein, we present the case of a PD patient suffering from recurrent ascites after a kidney graft.

Case report

We report the case of a 49-year-old Armenian patient, primarily admitted for a kidney transplantation in July 2018. He presented anuric ESKD on PD due to antiphospholipid syndrome (APS) nephropathy and lupus nephritis diagnosed in 2010. The patient has no history of PD-associated peritonitis. The patient received on a daily basis 4 exchanges (2 L of glucose 1.36% and Nutrineal®) over 8 hours on automated peritoneal dialysis, associated with a long dwell of 1.5L icodextrin. He is also known for high blood pressure, hyperlipidemia, and a MTHFR gene mutation. Our patient presented heart thrombi in 2010 and had a CHILD B cirrhosis secondary to hepatitis C virus infection, auto-immune hepatitis, and presinusoidal portal hypertension due to supra-hepatic veins thrombosis (Budd-Chiari syndrome), along with esophageal varices and portal cavernoma. There is no history of smoking nor chronic alcohol consumption.

After a routine pre-transplant workup, including a cardiac ultrasound without significant valvular dysfunction, doppler ultrasound of the neck and lower limb vessels, electrocardiogram, and pulmonary function tests, he benefited from a deceased donor kidney transplant in 2018 after 8 years of PD treatment and presented immediate graft function with plasmatic creatinine 4.7 mg/dl on day three and 1.7 mg/dl on day eleven. He recovered normal kidney function after three weeks and left the hospital. His daily treatments were Tacrolimus, mycophenolate mofetil, aethylprednisolone, aspirin, acenocoumarol, furosemide, lercanidipine, Tamsulosin, pantoprazole, B9 vitamins and NaHCO3. The removal of the PD catheter was planned in our nephrology unit in ambulatory care. Our institution’s protocol, in accordance with the transplant center we collaborate with, stipulates that the peritoneal dialysis catheter should be removed approximately 1 month after transplantation. We then require the assistance of our vascular surgery colleagues to remove this catheter in the operating room.

During the next four months, the catheter was flushed twice on a weekly basis and despite not infusing the patient with dialysate, about 1.85 liters of transudate ascites was drained every two days through the peritoneal catheter. Clinical examination showed large abdominal wall venous collaterals, no palpable nodes, muted cardiopulmonary auscultation, no abdominal pain nor lower limb edema at that time. Laboratory tests showed no sign of decompensated cirrhosis (serum albumin of 32 g/l (normal range: 40-49 g/l), Prothrombin time 75% (normal range: 70-100%), c-reactive protein 7mg/l (normal range: <10 mg/l), total bilirubin 1.0 mg/dl (normal range: < 1.2 mg/dl). A liver magnetic resonance imaging and CT scan (Figure 1) revealed perihepatic ascites, central fibrosis, and preserved permeability of the supra-hepatic veins but signs of chronic obstruction of the portal vein.

Figure 1.Abdominal computed tomography revealing perihepatic and abdominal ascites. The peritoneal dialysis catheter is still in place.

Figure 2.Doppler echocardiography revealed a severe transvalvular aortic regurgitation.

A FibroScan with a fibrosis score of F2 indicates moderate liver fibrosis. A gastroscopy confirmed the presence of varicose veins and global gastropathy due to portal hypertension. A Holter monitor did not reveal any arrhythmia. The patient was put on oral furosemide and spironolactone. Given that the ascites was recurrent despite optimal drug treatment, a multidisciplinary staff considered placing a transjugular intrahepatic portosystemic shunt (TIPS). The pre-intervention trans-thoracic and trans-esophageal echocardiogram (Figure 2) unexpectedly showed a severe aortic regurgitation due to degenerative valve disease and a dilated left ventricle (Vtd 208,2ml with norms 50-90 mL/m2) with preserved left and right ventricles ejection fractions, without dilated right cavities and without pericardial effusion. The patient had his aortic valve replaced by a mechanical valve almost one year after his transplantation. Our patient underwent 1 episode of staphylococcus aureus peritonitis with evidence of tunnelitis. He had to be hospitalized for IV vancomycin and cephalosporine. A final 350 ml of ascitic fluid was removed 12 months after kidney transplantation. The PD catheter was removed 4 months later. The patient did not relapse his ascites in 3 years.

Discussion

Kidney transplantation is known to decrease the mortality of patients suffering from end-stage kidney disease (ESKD), helping patients to return to an almost normal life after peritoneal dialysis (PD). This freedom comes with setting the patient free from all devices used for dialysis, including the peritoneal catheter.

Ascites is a pathological accumulation of fluid in the peritoneal cavity. This condition is known in numerous pathologies and has a broad, transversal, and multidisciplinary differential diagnosis[5]. Considering cirrhosis and cancers are responsible for approximately 90% of all ascites, clinicians sometimes overlook rarer causes as right heart failure, tuberculosis, and pancreatic diseases. Notably, ESKD has also been associated with recurrent ascites[6].

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