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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 2  |  Page : 320-322
Membranous glomerulopathy associated with idiopathic hypereosinophilic syndrome

Department of Internal Medicine, Hedi Chaker Hospital, Sfax, Tunisia

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Date of Web Publication9-Mar-2010


Renal involvement is rarely reported and little is known about the renal morpho­logic changes in the idiopathic hypereosinophilic syndromes. We reported a case of a 52-year-old man with idiopathic hypereosinophilic syndrome associated with membranous glomerulopathy. The eosinophilia and the proteinuria greatly improved with corticosteroid treatment. We review the literature regarding the nephropathy of this hematologic disorder.

How to cite this article:
Frigui M, Hmida M, Jallouli M, Kechaou M, Frikha F, Bahloul Z. Membranous glomerulopathy associated with idiopathic hypereosinophilic syndrome. Saudi J Kidney Dis Transpl 2010;21:320-2

How to cite this URL:
Frigui M, Hmida M, Jallouli M, Kechaou M, Frikha F, Bahloul Z. Membranous glomerulopathy associated with idiopathic hypereosinophilic syndrome. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2022 Aug 9];21:320-2. Available from: https://www.sjkdt.org/text.asp?2010/21/2/320/60203

   Introduction Top

The idiopathic hypereosinophilic syndromes (IHES) are rare hematologic disorders charac­terized by persistent eosinophilia without an identifiable underlying cause. Some patients have only minor symptoms and require no treatment; others have severe disease from organ involvement, especially cardiac and neu­rological, as well as hematologic derangement. [1]

Renal involvement is rarely reported and lit­tle is known about the renal morphologic cha­nges in this disease. [2] A case of an IHES with a nephrotic syndrome due to membranous glo­merulopathy, is presented here.

   Case Report Top

A 52-year-old white man diagnosed with hy­pereosinophilia at another hospital 7 months ago, presented to us with lower limb edema. On physical examination, blood pressure was 120/70 mmHg, heart rate 80/mn. Pitting edema of lower limbs was noted and the remainder of the physical examination was unremarkable. His white blood cell count was 39500 /mL, eosinophils 32500/mL, hemoglobin 11.1 g/dL and platelets 424000/mL. 24 hour urine protein excretion was in the range of 5.4 to 7.2 g/day without hematuria. The plasma protein was 55 g/L and the albumin was 22 g/L. Serum creati­nine was 78 µmol/L. Echocardiography revealed left ventricle diastolic dysfunction with hypo­kinesia of the interventricular septum. Compu­terized tomography of the chest was normal as well as abdominal ultrasound. Examination of the stool for parasites was negative. Antinuclear, anti-double stranded DNA, anti-Sm, pANCA, cANCA, anti-RNP, rheumatoid factor, anti-Ro and anti-La antibodies were all negative. C3, C4 components of complement system and im­munoglobulin A, M and G levels were within normal ranges. Total IgE level was 300 IU/mL (normal< 200). VDRL and serology for hydatid disease were negative. Bone marrow biopsy was performed, revealing 35% eosinophils and immature eosinophil precursors. Marrow blasts were mildly increased accounting for 6% of the bone marrow differential count. Chromo­some studies on the bone marrow aspirate re­vealed no chromosomal abnormalities. The RT­PCR was negative for the FIP1L1-PDGFRA transcript. There was no T-cell population with abnormal phenotype. The percutaneous kidney biopsy specimen disclosed typical histopatho­logical findings of a membranous nephropa­thy. There was no mononuclear inflammatory infiltrates in the interstitium. Tubules were nor­mal. There were IgG, IgM and C3 epimembra­nous deposits on immunofluoresence micros­copic examination. Based upon the medical re­cord, physical examination findings and labo­ratory data, he was diagnosed as having IHES associated with a membranous nephropathy. He was given prednisone 60 mg daily, furose­mide (40 mg twice a day) and captopril. Pred­nisone dose was progressively tapered after 6 weeks. Three months after the beginning of the treatment, his white blood cell count was 12000/mL and eosinophils 450/mL. The pro­teinuria decreased to 0.7 g/day.

   Discussion Top

Renal involvement with eosinophilia can oc­cur in angiolymphoid hyperplasia, drug-indu­ced reactions, cholesterol embolization, immu­noallergic responses, eosinophilic helminthic infection, malignant blood dyscrasias, neoplas­tic process and systemic necrotizing vasculi­tis. [3] The present case had no history of any medication before beginning of his complaints, and no evidence of cholesterol embolization in the renal biopsy specimen. Examination of the stool for parasites and hydatic cyst serology were negative. He was also negative for mye­loproliferative syndromes, especially the chro­nic eosinophilic leukaemia, and lymphoproli­ferative syndromes fulfilling the diagnostic cri­teria of IHES defined by Chusid and Dale in 1975. [4] Renal involvement in IHES is rarely observed. [2],[5] No case of kidney involvement was reported in 50 patients with IHES. [6] The kidney involvement in the IHES can present as pro­teinuria [7] or renal failure. [1],[5] There is little infor­mation on renal histology in this syndrome. Me­sangial expansion, [3] thickned glomerular base­ment membrane, [7] proliferative glomeruloneph­ritis, [4],[8] crescentic glomerulonephritis, [9] immuno­tactoid glomerulopathy, [2] glomerular sclerosis, [5] interstitial nephritis with eosinophilic infil­trates [7] and ischemic lesions secondary to in­trarenal thrombi [4],[10],[11] are the most renal histo­logical changes reported by the authors. Our patient is the second case of membranous glo­merulonephritis with IHES.

The first case was reported by Lanfranchi et al. [12] They reported the presence of glomerular sclerosis and eosinophilic interstitial infiltrates contrary to our patient where interstitium was spared.

Different histopathologic findings have been reported on immunofluorescence microscopic examination of the renal biopsy specimens from the patients with IHES.

No immunoglobulin deposits were detected in some cases. [5],[13] On the other hand, the pre­sence of immune complex depositions in the kidney was shown by other authors. [9],[14]

In the present case, there were IgG, IgM and C3 depositions on immunofluorescence mic­roscopic examination of the biopsy specimen.

Our immunofluorescence microscopic findings, along with the previous reports, [7],[9],[14] may indi­cate an immunological origin for kidney invol­vement in IHES.

In conclusion, further reports on the renal his­topathological changes seen in IHES cases diagnosed are expected to report significant contributions towards establishing the renal involvement in this disease, and clarifying the mechanisms responsible for renal changes.

   References Top

1.Ambarus V, Cosovanu A. The evolutionary cha­racteristics of the hypereosinophilic syndrome. Rev Med Chir Soc Med Nat Iasi 1998;102:69­-75.  Back to cited text no. 1      
2.Choi YJ, Lee JD, Yang KH, Kim BK, Bang BK, Shim SI. Immunotactoid glomerulopathy associated with idiopathic hypereosinophilic syndrome. Am J Nephrol 1998;18:337-43.  Back to cited text no. 2  [PUBMED]    
3.Guidicelli CP, Didelot F, Duvic C, Desrame J, Herody M, Nedelec G. Eosinophilia and renal pathology. Med Trop 1998;58(Suppl4):477-81.  Back to cited text no. 3      
4.Chusid MJ, Dale DC, West BC, Wolff SM. The hypereosinophilic syndrome: Analysis of fourteen cases with review of the literature. Medicine 1975;54:27.  Back to cited text no. 4      
5.Motellon JL, Bernis C, Garcia-Sanchez A, Gruss E, Traver JA. Renal involvement in the hyper­eosinophilic syndrome. Nephrol Dial Transplant 1995;10:401-3.  Back to cited text no. 5      
6.Fauci AS, Harley JB, Roberts WC, Ferrans VJ, Gralmick HR, Bhorson BH. The idiopathic hypereosinophilic syndrome: Clinical, pathophy­siologic and therapeutic considerations. Ann Intern Med 1982;97:78.  Back to cited text no. 6      
7.Bulucu F, Can C, Inal V, Baykal Y, Erikci S. Renal involvement in a patient with idiopathic hypereosinophilic syndrome. Clin Nephrol 2002; 57(2):171-2.  Back to cited text no. 7      
8.Hardy WR, Anderson RE. The hypereosino­philic syndromes. Ann Intern Med 1968;68: 1220-9.  Back to cited text no. 8  [PUBMED]    
9.Richardson P, Dickinson G, Nash S, Hoffman L, Steingard R, Germain M. Crescentic glome­rulonephritis and eosinophilic interstitial infil­trates in a patient with hypereosinophilic syn­drome. Postgrad Med J 1995;71:175-8.  Back to cited text no. 9      
10.Date A, Parameswaran A, Bhaktaviziam A. Renal lesions in the obliterative cardiomyopathies: endomyocardial fibrosis and Loffler's endo­carditis. J Pathol 1983;140:113-22.  Back to cited text no. 10  [PUBMED]    
11.Spry CJF, Davies J, Tai PC, Oslen EG, Oakley CM, Goodwin JF. Clinical features of fifteen patients with the hypereosinophilic syndrome. Q J Med 1983;205:1-2.  Back to cited text no. 11      
12.Spry CJ, Davies J, Tai PC, Oslen EG, Oakley CM, Goodwin JF. Clinical features of fifteen patients with the hypereosinophilic syndrome. Q J Med 1983;205: 1-2  Back to cited text no. 12      
13.Nakahara C, Kamoda T, Kinugasa H, et al. Simultaneous onset of nephritic syndrome and insulin-dependent diabetes mellitus in a case with hypereosinophilie syndrome. Clin Nephrol 2000;53:312-3.  Back to cited text no. 13  [PUBMED]    
14.Reuss JA, Olbermann M. Hypereosinophilic syn­drome. Dtsch Med Wochenschr 1983;108: 778-82.  Back to cited text no. 14  [PUBMED]    

Correspondence Address:
Makram Frigui
Department of Internal Medicine, Hedi Chaker Hospital, 3029 Sfax
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Source of Support: None, Conflict of Interest: None

PMID: 20228521

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