Bilateral Renal Artery Embolization in a Case With Severe Proteinuria Secondary to Amyloidosis in a Hemodialysis Patient

Written By: Sam Savage

Published Date: August 8, 2007 Last Edited: August 8, 2007

By Turgut, Faruk Kanbay, Mehmet; Kaya, Arif; Uz, Burak; Akcay, Ali

Keywords: Amyloidosis, embolization, proteinuria Abbreviations: FMF = familial Mediterranean fever; NS = nephrotic syndrome

Abstract

Amyloid-associated protein (secondary, reactive) amyloidosis occurs most frequently as a complication of chronic inflammatory disease. Renal involvement with amyloidosis is common and proteinuria is often the first symptom. We submit a case with severe proteinuria and hypoalbuminemia, and end-stage renal disease secondary to bronchiectasis-related amyloidosis. Bilateral embolization of the renal arteries was performed to prevent loss of albumin.

Introduction

Bronchiectasis is a consequence of inflammation and destruction of the structural components of the bronchial wall. It may sometimes be associated to secondary amyloidosis. Secondary amyloidosis results from the extracellular deposition of fibrillar amyloid protein in various organs secondary to chronic inflammation. Proteinuria is often the first symptom associated with systemic amyloidosis. Involvement of kidneys can lead to severe proteinuria and in time can lead to end-stage kidney disease. We report a case with chronic renal failure secondary to bronchiectasis-related amyloidosis, with severe proteinuria and hypoalbuminemia. Bilateral embolization of the renal arteries was performed to prevent loss of albumin.

Case report

A 35-year-old man was admitted to the hospital with dyspnea and generalized pitting edema. He had a history of chronic kidney failure secondary to bronchiectasis-related AA type amyloidosis. He was under a regular hemodialysis program three times per week. On physical examination, he had clubbing, widespread ralles in the lungs, ascites and anasarca. The laboratory parameters of the patient are shown in Table I; 24-h protein excretion was 15 g/day. Although albumin infusions were given, the albumin levels decreased gradually. On his seventh day of hospital admission, his albumin level decreased to 0.8 mg/dl. He did not improve with general measures. Bilateral renal artery embolization was planned to prevent loss of albumin. High-density alcohol was injected via the right femoral artery catheter to the bilateral renal arteries. No complication was observed during the procedure. The levels of albumin started to increase without replacement. Generalized edema and dyspnea improved. Two months after the embolization, albumin level was 4.2 g/dl and he was under a regular hemodialysis program.

Discussion

Amyloid deposition may be either a primary process or secondary to various diseases and may be localized to one specific site or generalized throughout the body. Familial Mediterranean fever (FMF) is the leading cause of AA amyloidosis in our country and tuberculosis, bronchiectasis and chronic arthritis are other important underlying conditions [1]. In our case, secondary amyloidosis developed after frequent pulmonary infections in childhood and, eventually, end-stage renal disease occurred. The association of amyloidosis and bronchiectasis has been reported previously in the literature [2]. Renal involvement results in nephrotic syndrome (NS) which is characterized by heavy proteinuria, hypoalbuminemia and edema. Complications of NS that may require treatment include edema, thromboembolism and malnutrition. In our case albumin level decreased to 0.8 g/dl, although albumin was given intravenously. The patient had peripheral and pulmonary edema and there was no possibility for specific th crapy. The main goal of NS therapy is to prevent glomerular protein leakage and to decrease edema. In this state, it is usually not possible to prevent the decrease in serum albumin levels. This can be partly achieved by administering angiotensinconverting enzyme inhibitors, lowering the protein content of the diet, and cautiously using nonsteroidal anti- inflammatory agents [3]. Bilateral nephrectomy was the only available therapy before the development of interventional radiological techniques for the unsuccessful cases. The literature reports good results when renal embolization is applied to the nephrotic syndrome [4,5]. Bilateral renal artery embolization was planned to keep albumin levels within the normal range, although this technique has undesirable adverse side-effects, including the post-infarction syndrome (flank pain, fever, vomiting), hypertension, and embolization [6,7] . After the procedure, none of these complications occurred in our patient, the albumin levels increased and the symptoms of hypoalbuminemia improved. In addition, it is well known that mortality and morbidity are high in patients with hypoalbuminemia. Hence, we speculate that embolization should be seriously considered as soon as possible in hemodialysis patients with NS. We, therefore, report this case to emphasize that causes of chronic kidney failure with severe proteinuria can be evaluated relatively early for renal embolization.

Table I. Laboratory parameters of die patient.

References

1. Tuglular S, Yalcinkaya F, Paydas S, Oner A, Utas C, Bozfakioglu S, Ataman R, Akpolat T, Ok E, Sen S, Dusunsel R, Evrenkaya R, Akoglu E. A retrospective analysis for aetiology and clinical findings of 287 secondary amyloidosis cases in Turkey. Nephrol Dial Transplant 2002;17:2003-2005.

2. Akcay S, Akman B, Ozdemir H, Eyuboglu FO, Karacan O, Ozdemir N. Bronchiectasis-related amyloidosis as a cause of chronic renal failure. Ren Fail 2002;24:815-823.

3. Palmer BF. Nephrotic edema – pathogenesis and treatment. Am J Med Sci 1993;306:53-67.

4. Olivero JJ, Frommer JP, Gonzalez JM. Medical nephrectomy: die last resort for intractable complications of die nephrotic syndrome. Am J Kidney Dis 1993;21:260-263.

5. Kuhn C, Sonntag F, Runge M, Vogel H. Nephrotic syndrome as indication for one-stage bilateral renal embolization. Dtsch Med Wochenschr 1982; 107:461 ->>64.

6. Gang DL, Dole KB, Adelman LS. Spinal cord infarction following dierapeutic renal artery embolization. JAMA 1977; 237:2841-2842.

7. Lumerman JH, Smidi AD. Complete and partial renal infarction. Lesson 16. AUA Update Series; 1997. p. 186.

FARUK TURGUT1, MEHMET KANBAY1, ARIF KAYA2, BURAK UZ2, & AXI AKCAY1

1 Department of Nephrology, Fatih University School of Medicine, Ankara, Turkey and 2 Department of Internal Medicine, Fatih University School of Medicine, Ankara, Turkey

Correspondence: Dr. Mehmet Kanbay, 35. sokak 81/5 Emek 06490, Ankara, Turkey. Tel: +90 312 440 06 06. E-mail: drkanbaytoyahoo.com

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