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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 6  |  Page : 1258-1261
Renal ablation using bilateral renal artery embolization for treatment of resistant nephrotic syndrome

1 Department of Medicine, Al-Amiri Hospital, Kuwait
2 Department of Medicine, Faculty of Medicine, Kuwait University, Kuwait
3 Department of Clinical Radiology, Al-Amiri Hospital, Kuwait

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Date of Web Publication17-Nov-2012


An 18-year-old man presented with severe nephrotic syndrome due to focal segmental glomerulosclerosis. His disease failed to remit with corticosteroids, calcineurin inhibitors, mycophenolate and rituximab. As his disease progressed with time, his anasarca became more resistant to high-dose combination diuretics and he developed multiple life-threatening bacterial infections. He was subjected to bilateral renal artery embolization with 99.8% alcohol to ablate his kidneys. Subsequently, the patient was maintained on hemodialysis and had normal serum albumin and did not have further infections. The procedure itself was simple and well tolerated, with only a minor post-embolization syndrome.

How to cite this article:
Sallam HE, El-Reshaid K, Varro J. Renal ablation using bilateral renal artery embolization for treatment of resistant nephrotic syndrome. Saudi J Kidney Dis Transpl 2012;23:1258-61

How to cite this URL:
Sallam HE, El-Reshaid K, Varro J. Renal ablation using bilateral renal artery embolization for treatment of resistant nephrotic syndrome. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2022 Aug 17];23:1258-61. Available from: https://www.sjkdt.org/text.asp?2012/23/6/1258/103572

   Introduction Top

Nephrotic syndrome (NS) resistant to corticosteroids and other immunosuppressive agents is a serious medical condition. The unabated protein and immunoglobulin loss can result in generalized edema, predisposition to infections and procoagulable state even prior to the progressive loss in kidney function. [1] In this case report, we present a patient with severe NS due to idiopathic focal segmental glomerulosclerosis in which renal ablation by bilateral renal artery embolization and placement on maintenance hemodialysis was a life-saving measure.

   Case Report Top

An 18-year-old Kuwaiti man was admitted to the renal unit of Al-Amiri Hospital, in May 2004, for generalized edema over the past few weeks. The patient denied any history of fever, joint pains, skin rash and abdominal or chest pains. There was no change in bowel movements or urine color. He did not have significant past medical history of medical illness, allergy, surgery or recent intake of medications. None of his first-degree family members had significant renal disease. On his initial physical examination, he was conscious, fully oriented and in no distress with pain or shortness of breath. Blood pressure was 120/80 mmHg, temperature was normal and weight was 60 kg. He did not have lymphadenopathy, jugular venous distension or goiter. However, he had significant lower limb and sacral edema. Physical examination was unremarkable, except for bilateral pleural effusion and massive ascites. Laboratory investigations showed normal peripheral leucocytic and platelets counts. Hemoglobin was 16 g/L with normal mean corpuscular volume (MCV). Serum sugar, urea, creatinine, electrolytes and liver function tests were normal, except for albumin at 11 g/L. Urine routine showed 2 (+) proteinuria without pyuria or hematuria. Serum cholesterol was 12 mmol/L. Serum TSH was normal. Serum complements (C3 and C4) and protein electrophoresis were normal except for hypo-albuminemia. Anti Nuclear Antibody (ANA), Anti double stranded DNA (anti-ds DNA), Anti Nuclear Cytoplasm Antibody (ANCA), Rheumatoid Factor (RF), hepatitis B surface antigen (HBsAg) and anti-hepatitis C virus (anti-HCV) antibodies were negative. Stool testing for ova, parasites and occult blood was normal. Twenty-four hour urine testing showed normal creatinine clearance, yet protein output was 12 g/day. Chest X-ray confirmed the bilateral pleural effusion. Electrocardiogram was normal. Abdominal and pelvic ultrasound revealed massive ascites, fatty liver and echogenic kidneys (similar to liver and spleen). Percutaneous kidney biopsy was done a few days later. On light microscopy, it showed focal and segmental glomerulosclerosis. Special stains were negative, including Congo red for amyloidosis. Immunoflourescent stains were positive for IgM deposits in the affected glomeruli. The patient was treated initially with corticosteroids (1 mg/kg/day) in addition to angiotensin converting enzyme inhibitor (lisinopril) and high-dose lasix and aldactone to control his anasarca.

Three months later, his laboratory investigations did not change with regards serum albumin and protein excretion. Hence, corticosteroids were tapered down gradually and a calcineurin inhibitor (tacrolimus) was added in a dose of 2 mg twice daily. Moreover, mycophenolate mofetil, in a dose of 1 g twice daily, was added one month later as he did not show improvement. The patient did not show significant change in protein excretion over the next two years. In 2006, his renal function started to deteriorate and his anasarca had increased despite the escalating dosage of diuretics. Magnetic resonance imaging did not show evidence of renal vein thrombosis. At that time, he received 4-weekly infusions of Rituximab (anti-CD20 monoclonal antibody), but did not respond to this therapy. By March 2007, he was almost hospital bound by infections, which included recurrent pneumonia, relapsing urinary tract infections and two severe attacks of spontaneous bacterial peritonitis with septic shock that required ionotropic support. Moreover, his nutritional status was deteriorating and he had already had multiple sessions of ultrafiltration to decrease his symptomatic anasarca. The latter was associated with frequent clotting of the dialysis filters. Tests for hypercoagulable states confirmed that he already had low levels of anti-thrombin III. At that stage, the poor prognosis of his chronic glomerulopathy was discussed with the patient and his family. He was offered trial of medical nephrectomy, in the form of high-dose non-steroidal anti-inflammatory drugs, even at the expense of being on maintenance hemodialysis. The patient agreed but, unfortunately, could not tolerate the severe gastrointestinal side-effects and, moreover, their efficacy was poor.

At this stage, serum creatinine was 224 μmol/ L and serum albumin was 10 g/L. Based on that, the issue of permanent and yet non-surgical approach of renal ablation by bilateral renal artery embolization was raised. After patient's approval, the procedure was carried out by our radiologist. Initially, aortography and selective renal angiography was done. Fortunately, the patient had a single renal artery on both sides. First, the left renal artery was catheterized. The catheter was placed distal to the adrenal branch. Its balloon was inflated and 5 mL of 99.8% alcohol was injected slowly. Ten minutes later, the balloon was deflated and the same technique was repeated on the right side. Subsequently, the abdominal aortography was performed to ensure complete perfusion beyond the proximal segment of both renal arteries with no nontarget embolization [Figure 1]. In the immediate post-operative period and for 48 h, the patient developed, as expected, fever, flank pain and leucocytosis. Subsequently, the patient became anuric with serum creatinine 828 μmol/L and required hemodialysis thrice weekly. Since then, he is well, without infections or focal problems related to his embolization. Two months later, serum albumin had reached 32 g/L. His nutrition is good and he is awaiting kidney transplantation.
Figure 1: Flush aortography before (A) and after (B) chemoembolization of the right renal artery. Note the absence of renal perfusion after embolization indicating successful renal ablation (arrow).

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   Discussion Top

The calculated annual incidence of glomerulonephritis is 34.5 per 100,000 Kuwaiti nationals. [2] Moreover, nearly 10% of those patients have been shown to be resistant to corticosteroids and other immunosuppressive agents. [3] idiopathic nephrotic syndrome (INS), and focal segmental glomerulosclerosis(FSGS) in particular, is a histological expression of diverse processes affecting the renal glomeruli. [4] There is a complex interplay between genetic predisposition, environmental influence and pathogenic factors on the final phenotype expression and its response to pharmacological interventions. [5] Hence, the disease presentation can range from mild proteinuria and slow progression to devastating clinical syndrome, characterized by heavy proteinuria and rapid loss of renal function. Moreover, many types of interventions have been shown to influence the course of the disease, although the response is diverse. [3] Until a specific therapy can be fashioned, it is necessary for the clinician caring for these patients to provide non-toxic and effective measures in controlling the disease.

However, if medical therapy fails to ameliorate the disease, patients are more prone to the serious complications of continuous protein and immunoglobulin loss, which is far from just cosmetic appearance. Serious infections and spontaneous bacterial peritonitis in particular are inevitable life-threatening complications. Unfortunately, even with the progressive loss of the kidney function inherent with such disease, the process is slow and high protein excretion remains a problem. At such a stage, nephrectomy may be the only life-saving measure.

Unfortunately, mortality from bilateral surgical nephrectomy in high-risk patients, such as ours, is as high as 11%, and morbidity may reach 87%. [6] Medical nephrectomy using drugs such as non-steroidal anti-inflammatory may have been useful in certain patients, [7] but, unfortunately, our patient could not tolerate it. Hence, renal ablation using embolization was our second measure. Previous attempts using spongostan, isobutyl-2-cyanoacrylate and mercury led to serious side-effects. [8],[9],[10] Moreover, Giaturco wool coils and autologous clots may recanalize. [7],[11] Absolute alcohol is toxic to the arterial wall and can result in vascular occlusion with thrombus formation without the risk of significant systemic side-effects. It has been previously used in embolization of 27 cases of renal neoplasms, [12] 11 cases of severe hypertension in patients with end-stage renal disease [13] and two isolated cases of anasarca due to amyloidosis. [14] Our case is the first on its use in patients with INS. Our patient is, currently, enjoying a healthy life on hemodialysis and awaiting kidney transplantation in the near future.

   References Top

1.Kaysen GA. Nephrotic syndrome. In Current Therapy in Nephrology and Hypertension; Glassock RJ, ed. St. Lois: Mosby-Year Book; 1998. p. 223-30.  Back to cited text no. 1
2.El-Reshaid W, El-Reshaid K, Kapoor MM, Madda JP. Glomerulopathy in Kuwait: The spectrum over the past 7 years. Ren Fail 2003;25:619-30.  Back to cited text no. 2
3.El-Reshaid K, El-Reshaid W, Madda J. Combination of immunosuppressive agents in treatment of steroid-resistant minimal change disease and focal segmental glomerulosclerosis. Ren Fail 2005;25:523-30.  Back to cited text no. 3
4.Bolton WK, Abdel-Rahman E. Pathogenesis of focal glomerulosclerosis. Nephron 2001;88:6-13.  Back to cited text no. 4
5.Alexopoulos E, Stangou M, Papagianni A, Papadimtriou M. Factors influencing the course and the response to treatment in primary focal segmental glomerulosclerosis. Nephrol Dial Transplant 2000;15:1348-56.  Back to cited text no. 5
6.Keller FS, Coyle M, Rosch J, Dotter CT. Percutaneous renal ablation in end-stage renal disease. Alternative to surgical nephrectomy. Radiology 1986;159:447-51.  Back to cited text no. 6
7.Olivera JJ, Frommer JP, Gonzalez JM. Medical nephrectomy: The last resort for intractable complications of the nephrotic syndrome. Am J Kidney Dis 1993;21:260-3.  Back to cited text no. 7
8.Comelli S, Mioni G, Gaspani D. Renal artery embolization therapy in a case of nephrotic syndrome with massive proteinuria (medical nephrectomy). Radiol Med 1984;6:329-31.  Back to cited text no. 8
9.Henrich WL, Goldman M, Dotter CT, Rosch J, Bennet WN. Therapeutic renal artery occlusion for elimination of proteinuria. Arch Intern Med 1976;136:840-2.  Back to cited text no. 9
10.Avram MM, Lipner HI, Gan AC. Medical nephrectomy. The use of metallic salts for the control of massive proteinuria in the nephrotic syndrome. Trans Am Soc Artif Intern Organs 1976;22:431-8.  Back to cited text no. 10
11.Wu JM, Moorthy AV, Beirne GJ, Grummy AB. Renal infarction with Giaturco wool coils: Use in the management of massive proteinuria. JAMA 1980;243:2425-6.  Back to cited text no. 11
12.Nadalini VF, Zambelli S, Bruttini GP, Pacella M, Giglio C. Renal Artery Embolization with absolute ethanol. J Radiol 1984;65:301-5.  Back to cited text no. 12
13.Golwyn DH, Routh WD, Chen MY, Lorentz WB, Dayer RB. Percutaneous transcatheter renal ablation with absolute ethanol for the uncontrolled hypertension or nephrotic syndrome. Results in 11 patients with end-stage renal disease. JVIR 1997;8:527-33.  Back to cited text no. 13
14.Tikkakoski T, Leppanen M, Turunen J, Anderson S, Sodervik H. Percutaneous transcatheter renal embolization with absolute ethanol for uncontrolled nephrotic syndrome. Acta Radiol 2001;42:80-3.  Back to cited text no. 14

Correspondence Address:
Kamel El-Reshaid
Department of Medicine, Faculty of Medicine, Kuwait University, P. O. Box 24923, 13110 Safat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.103572

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