Renal Vein Stenosis With Transudative Ascites From Graft After Renal Transplantation With Good Response After Percutaneous Stent Placement M.S. Pan, R.H. Wu, D.P. Sun, Y.F. Tian, and M.J. Chen ABSTRACT Ascites sometimes occurs as a result of technical complications of transplant surgery or other medical reasons, including hepatic, cardiac, or oncologic pathology. Renal vein stenosis after renal transplant resulting in transudative ascites is rare; thus there are few if any data on such cases. Stent implantation seems to be a safe and elective approach to treatment of this rare condition. We present the case of a 22-year-old woman in whom massive ascites developed 33 months after renal transplantation. After the analysis of the ascites ﬂuid and exclusion of transplant artery stenosis, graft rejection, infection, portal hypertension, and other possible etiologies, the ﬁnal diagnosis of graft renal vein stenosis with transudative ascites derived from the graft was made based on imaging studies, including Doppler ultrasonography and computed tomography. The patient underwent angiographic stent placement, and the ascites markedly improved after the procedure. Renal vein stenosis complicated with ascites after renal transplantation is highly unusual; the patient’s response to angiographic stent placement was beneﬁcial, with satisfactory resolution of the blockage and ascites.
immunosuppression regimen consisting of prednisolone (5 mg) 0.5 of 1 tablet daily, mycophenolic acid (180 mg) 2 tablets twice daily, and tacrolimus (1 mg) 2 tablets every 12 hours (maintaining a serum tacrolimus level of about 3.5 ng/mL). The laboratory blood workup revealed a serum blood urea nitrogen to creatinine ratio of 23 to 1.4 mg/dL, glucose level of 116 mg/dL, aspartate aminotransferase to alanine aminotransferase ratio of 19 to 20 IU/L, albumin level of 3.8 g/dL, total to direct bilirubin ratio of 0.43 to 0.15 mg/dL, and plasma white blood cell count of 6200/mL. Antiehepatitis C virus and hepatitis B surface antigen were negative. Routine urinalysis showed no hematuria, proteinuria, or pyuria, and the patient was not pregnant. A 24-hour urine total protein level was 1139 mg/d. The ascites analysis revealed a hazy ﬂuid with 340 red cells and 100 white cells/high-power ﬁeld, with a differential of 3 segmented neutrophils and 89 lymphocytes. Cytologic analysis revealed no malignant cells, and a culture of the ascites ﬂuid was negative for acid-fast bacilli; polymerase chain reaction for tuberculosis also was
A 22-year-old woman with immunoglobulin A nephropathye associated end-stage renal disease underwent continuous ambulatory peritoneal dialysis for 3 years while waiting for a kidney donor. She received a deceased-donor cadaveric kidney from a 46-year-old man who died of a head injury after a car accident in November 2008. She presented with persistent, massive ascites; abdominal fullness and distention developed after she had experienced good allograft function for 33 months. At that time, she was taking an
From the Division of General Surgery, Department of Surgery (M.S.P., D.P.S., Y.F.T., M.J.C.) and the Department of Radiology (R.H.W.), Chi-Mei Medical Center, Tainan, Taiwan. Address reprint requests to Ming-Jenn Chen, MD, No. 901, Zhonghua Road, Yongkang District, Tainan City 710, Taiwan (ROC). E-mail: [email protected]
ENAL TRANSPLANTATION complications leading to ascites are rare , and the causes include graft rejection, graft decapsulation, lymphocele, leakage of the anastomosis and/or vascular complications, ureteral perforation, transudation from the graft kidney, and infection secondary to immunosuppression [2e8]. Vascular complications are relatively rare and include renal artery or vein stenosis, renal graft arterial or venous thrombosis, and arterial injury such as arteriovenous ﬁstula, intrarenal pseudoaneurysm, and arterial dissection . Balloon angioplasty and stent placement for treatment of renal vein stenosis seems to be a safe and effective approach to treatment . We present a rare case of renal vein stenosis of a renal graft leading to massive ascites 33 months after transplantation.
0041-1345/14/$esee front matter http://dx.doi.org/10.1016/j.transproceed.2013.09.051 598
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RENAL VEIN STENOSIS WITH TRANSUDATIVE ASCITES
Fig 1. Computed tomographic angiography disclosed perie graft-kidney ﬂuid collection (arrowhead); dilation of the graft renal vein (black arrow), and massive ascites (white arrow). negative. No bacterial growth in the ascites ﬂuid was detected. The biochemical analyses of the ascites ﬂuid revealed an albumin level of 0.5 g/dL, creatinine of 1.31 mg/dL, and lactate dehydrogenase of 14 IU/L. The serum ascites-albumin gradient ratio was 3.3. A renal biopsy was performed, and no graft rejection was evident. A chest radiograph showed no abnormality, and the heart size was normal. Echocardiography showed good left ventricular function without cardiac chamber dilatation or signiﬁcant pericardial effusion. Despite the normalcy of most laboratory assessments, abdominal Doppler ultrasonography showed massive ascites without any change in graft size or patency of the transplanted renal artery and vein. The resistance indices of the arcuate artery, interlobar artery, segmental artery, and renal artery anastomoses were all 0.7. Computed tomographic angiography showed perirenal ﬂuid collection around the transplanted kidney, no evidence of graft renal arterial stenosis, but a dilated graft renal vein, with an abrupt decrease in caliber at the anastomosis to the internal iliac vein (Fig 1). Based on these image ﬁndings, the diagnosis was graft renal vein stenosis resulting in perirenal ﬂuid collection, ascites, and multiple tiny subcapsular infarctions. Digital subtraction angiography of the renal artery revealed multiple tortuous drainage or collateral veins in the perirenal space (Fig 2). Percutaneous transluminal angioplasty also showed focal 80% stenosis at the anastomosis of the renal vein and right internal iliac vein (Fig 3). The stenotic site was dilated with an 8-mm balloon catheter followed by the placement of a 12-mm 6-cm self-expanding metallic stent (Maris, Medtronic, Minneapolis, Minnesota, United States). After the procedure, the patient’s ascites remained detectable by abdominal sonography, but the volume decreased gradually (Fig 4) over the next 6 months and no ascites recurrence was detected.
Ascites can be classiﬁed based on its underlying pathophysiology, including portal hypertension, hypoalbuminemia,
Fig 2. Digital subtraction angiography of the renal artery revealed multiple tortuous drainage paths or collateral veins (black arrow) in the perirenal space.
peritoneal disease, and other etiologies. The patient in this case report showed no speciﬁc clinical symptoms, signs, laboratory ﬁndings, or image ﬁndings that would lead to the ﬁnal diagnosis. Her main symptom was abdominal fullness without abdominal pain. No general malaise or recent body weight loss was noted. Physical examination was abdominal distention without tenderness. No fever, jaundice, dysuria, or tachycardia was noted. Laboratory studies, including ascites and urine analyses, found no liver function impairment, infection, heart function impairment, malnutrition, or thyroid function impairment. Abdominal sonography and abdominal computed tomography revealed no cirrhosis, portal vein stenosis, or bile duct dilatation; the only ﬁnding was ascites. Further research into possible causes of her massive ascites led to a report by Marko et al. of posterenal transplantation complications leading to ascites . The possible causes of ascites were graft rejection [2,3], graft decapsulation , lymphocele , leak of anastomosis/ vascular complications, ureteral perforation , transudation from the graft kidney , and infection secondary to immunosuppression . A renal biopsy showed no graft rejection. Graft decapsulation, lymphocele leakage of the main artery anastomoses, transudation, and infection were all eliminated as possible causes of the ascites. Computed tomographic angiography to survey blood vessel status showed no signs of graft renal artery stenosis, but a dilated graft renal vein with an abrupt decrease in the caliber at the site of anastomosis to the internal iliac vein. Posttransplantation graft renal vein stenosis with transudative ascites was then diagnosed.
PAN, WU, SUN ET AL
Fig 3. (A) Percutaneous transluminal angioplasty showed a bird beakelike stenosis (white arrow) at the anastomosis of the renal vein and right internal iliac vein. The pressure gradient between the renal vein and internal iliac vein was more than 5 mm Hg. (B) The stenosis was dilated, and the stent was placed.
Surgical complications of kidney transplantation may severely affect graft survival so that surgical intervention is needed. All complications must be diagnosed quickly and treated appropriately to minimize morbidity and mortality. Reported vascular complications include renal artery, renal graft arterial or venous thrombosis, and arterial injury such as arteriovenous ﬁstula, intrarenal pseudoaneurysm, and arterial dissection . Posttransplantation renal venous complications are relatively rare, and they often appear like acute vein thrombosis during the ﬁrst week after renal transplantation . Posttransplantation renal vein stenosis is considered to be extremely rare. It is associated with
Fig 4. Abdominal sonography performed 6 months after stent placement. The ascites subsided markedly.
surgical complications such as hematoma, lymphocele, or torsion. Other possible causes include acute graft rejection , local infection , or arteriovenous ﬁstulae resulting from high-pressure turbulent ﬂow in the renal allograft . The clinical symptoms and signs are not speciﬁc to graft renal vein stenosis. The patient presented with persistent ascites due to renal vein stenosis, which may not have been reported previously. Radiologic examinations such as Doppler ultrasonography, magnetic resonance angiography, or computed tomographic angiography should be considered to diagnose renal vein stenosis. These sophisticated imaging ﬁndings enabled the diagnosis of graft renal vein stenosis, resulting in perirenal ﬂuid collection and ascites diagnosis to be made. The treatment of the venous stenosis requires either surgical reconstruction or venoplasty with or without endovascular stent placement. Compared with surgical treatment, endovascular interventions have the beneﬁts of minimal invasiveness, fewer complications, less morbidity, and less mortality . With respect to interventional techniques, venoplasty without stent placement is described in an individual case report of poor results due to rapid restenosis . In contrast, there were some case reports published in which venoplasty with stent placement resulted in good longterm outcomes [16,17]. Currently, there are no prospective studies or retrospective reviews of postekidney transplantation renal vein stenosis, possibly because renal vein stenosis after kidney transplantation is extremely rare; renal artery stenosis is much more frequently reported . In this case, the patient’s ascites improved gradually after venoplasty with stent placement. The stent functioned well, and no restenosis was found. Catheter drainage of the ascites ﬂuid was not indicated, and the patient’s symptoms and signs
RENAL VEIN STENOSIS WITH TRANSUDATIVE ASCITES
of ascites subsided slowly over time. The ascites did not subside entirely, which could have been due to the growth of collateral perirenal veins with stenosis. Nonetheless, the long-term result was satisfactory for the patient.
Diagnosis of posterenal transplantation ascites can be difﬁcult, and all possible causes should be evaluated. Currently, only a few case reports of renal vein stenosis are available; thus, posterenal transplantation renal vein stenosis leading to ascites is extremely rare. Venoplasty with stent placement was an effective treatment for graft renal vein stenosis in this case and appeared to be the best treatment option. Nonetheless, further study and analysis of renal vein stenosis treatments and outcomes, including surgical and interventional procedures, would beneﬁt future patients.
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