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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2014  |  Volume : 25  |  Issue : 4  |  Page : 890-892
Rare association of IgA nephropathy with nephrotic syndrome in a patient with eosinophilic gastritis


1 Department of Nephrology, Davita Nephrolife, Bangalore, India
2 Department of Gastroenterology, Davita Nephrolife, Bangalore, India

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Date of Web Publication24-Jun-2014
 

How to cite this article:
Panchangam V, Manjunath S M. Rare association of IgA nephropathy with nephrotic syndrome in a patient with eosinophilic gastritis. Saudi J Kidney Dis Transpl 2014;25:890-2

How to cite this URL:
Panchangam V, Manjunath S M. Rare association of IgA nephropathy with nephrotic syndrome in a patient with eosinophilic gastritis. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2021 Nov 29];25:890-2. Available from: https://www.sjkdt.org/text.asp?2014/25/4/890/135203
To the Editor,

Eosinophilic gastritis (EG) is an extremely un­common disorder. [1],[2] The disease is characte­rized by eosinophilic infiltration of various layers of the gastrointestinal tract in the absence of any known cause of eosinophilia. [3],[4] The infil­tration may be mucosal, serosal or in the mus-cularis area, causing variability in presentation like gastric outlet obstruction and abdominal pain. [5]

We herewith report on a 22-year-old unmarried female who presented with anasarca of 15 days duration and one episode of painless gross hematuria. There was no associated upper respi­ratory infection or gastrointestinal symptoms. No history of any drug intake or food allergy was elicited.

She reportedly had episodes of vomiting and pain in the epigastrium two years earlier, and was diagnosed to have EG on endoscopic gas­tric mucosal biopsy. The biopsy sample was negative for Helicobacter pylori, colonoscopy was unremarkable and stool was negative for ova or cyst. Her complete blood count, renal function test, liver function tests and serum IgE levels were normal. She was treated with aza-thioprine and steroids in tapering dose and was receiving azathioprine 50 mg per day at the current presentation.

The patient denied any history of gastritis, food allergy, joint pains or history suggestive of secondary glomerular disease. She was normo-tensive and investigations revealed a 24-h urine protein of 5.4 g with numerous red cells on urine microscopy; the serum total cholesterol was 422 mg/dL, blood urea was 23 mg/dL, serum creatinine was 0.8 mg/dL and serum albumin was 2.8 g/dL. Serological work-up was negative for anti-nuclear antibodies, human immunodeficiency virus, hepatitis B and hepa­titis C; complement C3 and C4 levels were nor­mal and anti-neutrophil cytoplasmic antibodies (ANCA), both p-ANCA and c-ANCA, as well as anti-double stranded DNA were negative.

A kidney biopsy was performed and renal histology showed features suggestive of IgA nephropathy with +++ IgA deposits in the me-sangium and unremarkable blood vessels and capillaries [Figure 1], [Figure 2] and [Figure 3]. Electron micros­copy was suggestive of mesangial deposits of IgA with effacement of foot process.
Figure 1: IgA deposits in the mesangium.

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Figure 2: Mesangial cellularity and unremarkable capillary loops on light microscopy.

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Figure 3: Eosinophilic infiltration of the gastric mucosa and submucosa.

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The clinical and histopathological findings were suggestive of IgA nephropathy with neph-rotic syndrome. She was started on predni-solone 1 mg/kg for six weeks and azathioprine was continued at 50 mg/day. At the end of three weeks, she had biochemical and clinical remis­sion of the nephrotic state. She completed six weeks of prednisolone and was then switched to 60 mg alternate day for the next six weeks. Following this, the steroids were tapered over the next six months.

Presently, the patient is on azathioprine 50 mg/day for the last one year with no gastric symptoms or relapse of hematuria or the neph-rotic syndrome.

EG is an extremely uncommon disorder, [1],[2] and is characterized by eosinophilic infiltration of various layers of the gastrointestinal tract in the absence of any known cause of eosinophilia. [3],[4] Eosinophila and high IgE levels are seen in most cases, and these patients are initially treated with high-dose steroids. However, the disease usually recurs after withdrawal of ste-roids. [1] Other therapeutic options include immu-nosuppressive drugs like azathioprine, leuko-triene inhibitors and immunomodulators like alfa interferon. These medications have shown variable degrees of success in induction and maintenance of remission. [3]

The prognosis of EG is considered benign with a waxing and waning course. There are case reports of IgA nephropathy occurring in patients with EG along with gluten-sensitive enteropathy, both of which are IgA-related di­seases. No case reports of isolated eosinophilic gastritis with IgA nephropathy or renal involve­ment exist till now. [3] Although these diseases are idiopathic, recent investigations support the role of eosinophils and T helper-2 cytokines. [2],[6] In addition, eosinophils can mediate pro-inflamma­tory effects. Finally, eosinophils can serve as major effector cells, inducing tissue damage and dysfunction by releasing toxic granule pro­teins (major basic protein, eosinophilic cationic protein, eosinophil peroxidase and eosinophil-derived neurotoxin) and lipid mediators, which are cytotoxic. [2],[6],[7]

 
   References Top

1.Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol 2004;113:11-28.  Back to cited text no. 1
[PUBMED]    
2.Matsushita M, Hajiro K, Morita Y, Takakuwa H, Suzaki T. Eosinophilic gastroenteritis involving the entire digestive tract. Am J Gastroenterol 1995;90:1868-70.  Back to cited text no. 2
    
3.Jackson S, Moldoveanu Z, Kirk KA, et al. IgA-containing immune complexes after challenge with food antigens in patients with IgA nephro-pathy. Clin Exp Immunol 1992;89:315-20.  Back to cited text no. 3
    
4.Rostoker G, Petit-Phar M, Delprato S, et al. Mucosal immunity in primary glomerulonephritis: II. Study of the serum IgA subclass repertoire to food and airborne antigens. Nephron 1991;59:561-6.  Back to cited text no. 4
    
5.Chaudhary R, Shrivastava RK, Mukhopadhyay HG, Diwan RN, Das AK. Eosinophilic gastritis-an unusual cause of gastric outlet obstruction. Indian J Gastroenterol 2001;20:110.  Back to cited text no. 5
    
6.Jaffe JS, James SP, Mullins GE. Evidence for an abnormal profile of interleukin-4 (IL-4), IL-5, and gamma-interferon (gamma-IFN) in peri­pheral blood T cell is from patients with allergic eosinophilic gastroenteritis. J Clin Immunol 1994;14:299-309.  Back to cited text no. 6
    
7.Kelly KJ. Eosinophilic Gastroenteritis. J Pediatr Gastroenterol Nutr 2000;30 Suppl:S28-35.  Back to cited text no. 7
[PUBMED]    

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Correspondence Address:
Vidyashankar Panchangam
Department of Nephrology, Davita Nephrolife, Bangalore
India
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DOI: 10.4103/1319-2442.135203

PMID: 24969211

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  [Figure 1], [Figure 2], [Figure 3]



 

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