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| Year : 2010 | Volume
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| Issue : 2 | Page : 320-322 |
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| Membranous glomerulopathy associated with idiopathic hypereosinophilic syndrome |
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Makram Frigui, Mohamed Ben Hmida, Moez Jallouli, Manel Kechaou, Faten Frikha, Zouhir Bahloul
Department of Internal Medicine, Hedi Chaker Hospital, Sfax, Tunisia
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| Date of Web Publication | 9-Mar-2010 |
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 Abstract | | |
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 2020 Oct 26];21:320-2. Available from: https://www.sjkdt.org/text.asp?2010/21/2/320/60203 |
| Introduction | |  |
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 | | |
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 | | |
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 | | |
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| 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. [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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 8. | Hardy WR, Anderson RE. The hypereosinophilic syndromes. Ann Intern Med 1968;68: 1220-9. [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. |
| 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. [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. |
| 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 |
| 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. [PUBMED] |
| 14. | Reuss JA, Olbermann M. Hypereosinophilic syndrome. Dtsch Med Wochenschr 1983;108: 778-82. [PUBMED] |
Correspondence Address:
Makram Frigui
Department of Internal Medicine, Hedi Chaker Hospital, 3029 Sfax
Tunisia
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PMID: 20228521 
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