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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2019  |  Volume : 30  |  Issue : 6  |  Page : 1461-1463
Toxocariasis and nephrotic syndrome


Department of Internal Medicine, Military Hospital of Tunis, Montfleury, Tunis, Tunisia

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Date of Submission19-Nov-2018
Date of Acceptance18-Dec-2018
Date of Web Publication9-Jan-2020
 

   Abstract 


We describe a case of toxocariasis as a rare cause of nephrotic syndrome in an adult woman. This rare association was confirmed by elevated Toxocara-specific immunoglobulin M titers. Renal biopsy was not done because of prolonged activated partial thromboplastin time. Our patient was treated with prednisone and albendazole. These treatments resulted in partial remission of renal symptoms as well as the abatement of the Toxocariasis infection. The relationship between toxocariasis infection and glomerular disease is still unclear. In the literature, exceptional renal impairment secondary to toxocariasis have been described, especially in children. To the best of our knowledge, this is the second case of nephrotic syndrome associated with toxocariasis in adults.

How to cite this article:
Ariba YB, Abid R, Battikh R, Louzir B, Labidi J. Toxocariasis and nephrotic syndrome. Saudi J Kidney Dis Transpl 2019;30:1461-3

How to cite this URL:
Ariba YB, Abid R, Battikh R, Louzir B, Labidi J. Toxocariasis and nephrotic syndrome. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Jan 20];30:1461-3. Available from: http://www.sjkdt.org/text.asp?2019/30/6/1461/275494



   Introduction Top


Toxocariasis is a helminthic zoonosis with a worldwide distribution, and until now, it continues to be an almost unknown disease among the general population and even among health professionals. Infection can present with a wide clinical spectrum varying from asymptomatic to severe organ injury.[1] There are three major clinical syndromes associated with human toxocariasis; covert toxocariasis, ocular larva migrans, and visceral larva migrans. Visceral larva migrans is the most prevalent type of the disease and the classical presentation includes fever, hepatomegaly, and eosinophilia (>500/mm3).[2] Renal involvement has been only rarely reported.

In this case report, we describe a 69-year-old woman presenting with nephrotic syndrome with coincident toxocariasis infection.


   Case Report Top


A 69-year-old woman was on follow-up in the cardiology department since 2012 for mitro-aortic valvulopathy with atrial fibrillation requiring anticoagulant therapy. She was hospitalized in the Cardiothoracic Surgery Department for surgical treatment of her valvulopathy. On admission, she was noted to have lower limb edema, and laboratory parameters showed features of nephrotic syndrome. She was, therefore, transferred to our department to evaluate the glomerulopathy. There was a history of pruritus lasting for one year.

Physical examination revealed mild pallor of the skin and conjunctivae, significant lower limb edema, and scratching lesions. The body temperature was 36.5°C. There was no lymphadenopathy or hepatosplenomegaly. The patient was eupnoeic and respiratory auscultation was unremarkable. Her blood pressure was 110/70 mm Hg, heart rate was 80 bpm, and cardiac examination revealed a holo-systolic murmur heard at the apex, with radiation into the axilla with jugular veins distension but without the hepato-jugular reflux. Urinalysis showed pH 6, specific gravity 1025, hemoglobin 1+, protein 3+, and the absence of nitrites and leukocytes. Proteinuria was recorded as 5.91 g/24 h. Fractional excretion of sodium was <1%. Multiple stool, blood, and urine cultures were negative.

Complete blood count showed hematocrit 27.1%, hemoglobin 9.1 g/dL, white blood cell count 8.300/mm3 with neutrophils 4600/mm3, lymphocytes 1800/mm3, monocytes 500/mm3 and eosinophils 1300/mm3, and platelet count 338,000/mm3. The erythrocyte sedimentation rate was 37 mm in 1 h and the C-reactive protein was negative. Liver functions were normal. Serum creatinine was 255 μmol/L, and urea was 21.2 mmol/L. Total serum proteins were 52 g/L, albumin 28 g/L, αL globulins 2.3 g/L, α2 globulins 8.4 g/L, β globulins 6.4 g/L, gamma globulins 6.2 g/L, calcium 2.48 mmol/L, cholesterol 4.6 mmol/L, and triglycerides 2.2 mmol/L. The measurement of serum immunoglobulins was IgG 7.6 g/L, IgA 1.98 g/L, and IgM 0.48 g/L.

There was no serological evidence for a recent viral infection from HBV, HCV, CMV, or HIV. Serological tests were also negative for leishmaniosis, schistosomiasis, hydatidosis but was strongly positive for toxocariasis. Enzyme-linked immunosorbent assay for toxocaral antibodies showed 1.9 U (>1.1) and the Western blot was also positive. Thyroid hormone levels were normal. Antinuclear, antineutrophil cytoplasmic antibodies, and cryoglobulins were all negative. Tumor markers (ACE, CA19-9, CA15-3, CA-125, and AFP) were also negative. Abdominal and pelvic ultrasounds and computed tomography scans of the brain were unremarkable. Ultrasound of the heart was normal. Endoscopy of the stomach and duodenum was unremarkable. A percutaneous biopsy of the left kidney was indicated but was not performed because of prolonged activated partial thromboplastin time despite discontinuation of anticoagulation.

On the basis of the strong serological positivity for toxocariasis and the marked eosino-philia, diagnosis of visceral larva migrans syndrome was made and the nephrotic syndrome was attributed to toxocariasis. The patient was treated with prednisone (1 mg/kg per os daily) and with albendazole (10 mg/kg per os twice a day for 7 days). The steroid treatment resulted in the complete disappearance of eosinophilia and negativity of the toxocara serology. After one month of pred-nisone therapy, total serum protein was 53 g/L, albumin was 29.5 g/L, and proteinuria had decreased to 1.69 g/24 h. However, the patient has not come for follow-up since April 2013.


   Discussion Top


Toxocariasis is a multi-systemic disease of parasitic zoonosis that occurs, especially in young children.[3] In adults, toxocariasis is unusual and infections appear to be mild or subclinical, but may provoke positive serological tests and sometimes, persistent eosinophilia.[4] Many infections caused by Toxocara are asymptomatic, reaching 44.4% and systemic toxocariasis manifests around 15.5% of diagnosed cases. Because of the variability of signs and symptoms of the disease, in 1988, toxocariasis was divided into two main types: visceral larva migrans and ocular toxocariasis. Between 1992 and 1993, a third clinical form called covert toxocariasis was described in seropositive patients, gastrointestinal disturbances, weakness, and lethargy. Myocarditis, nephritis, and involvement of the central nervous system have also rarely been described.[5] In a report on pediatric patients from Egypt, toxocara infection was found in 10.7% of patients presenting with renal disease. Two of these patients had nephrotic syndrome; however, a kidney biopsy was not performed.[6] In another case report, nephrotic syndrome in a seven-year-old boy coincident with Toxocara canis infection was described and remission of renal symptoms was obtained after steroids treatment and abatement of the Toxocara infection. In this case, a biopsy was performed and it was consistent with minimal change disease and the nephrotic syndrome responded to corticosteroids.[7] In an adult case report, cortico-resistant nephrotic syndrome was described in a 41-year-old woman.[8] Renal remission was obtained after the ciclosporin introduction. Our case is the second case reported in adults. In mice infected with toxo-cara, the predominant renal lesion is mesan-gioproliferative glomerulonephritis. Immuno-histochemical studies established that renal alterations were associated with glomerular deposits of IgG, IgM, and third component of complement (C3).[9]


   Conclusion Top


The relationship between toxocariasis and glomerular disease is still unclear. Some authors suggested that immunomediated mechanism might possibly be involved in the genesis of kidney damage observed in this parasitic zoonosis. Toxocariasis should be considered as a possible cause, although rare of nephrotic syndrome, especially in the presence of a marked eosinophilia.

Conflict of interest: None declared.



 
   References Top

1.
Roldán WH, Cavero YA, Espinoza YA, Jiménez S, Gutiérrez CA. Human toxocariasis: A seroepidemiological survey in the Amazonian city of Yurimaguas, Peru. Rev Inst Med Trop Sao Paulo 2010;52:37-42.  Back to cited text no. 1
    
2.
Ecevit Ç, Bağ Ö, Vergin C, Öztürk A. Visceral larva migrans presenting with hypereosino-philia. Turkiye Parazitol Derg 2013;37:58-60.  Back to cited text no. 2
    
3.
Arango CA. Visceral larva migrans and the hypereosinophilia syndrome. South Med J 1998;91:882-3.  Back to cited text no. 3
    
4.
Demirci M, Unlü M, Fidan F, Kaya S. Eosinophilic pneumonia due to toxocariasis: An adult case report. Turkiye Parazitol Derg 2012;36:258-9.  Back to cited text no. 4
    
5.
Carvalho EA, Rocha RL. Toxocariasis: Visceral larva migrans in children. J Pediatr (Rio J) 2011;87:100-10.  Back to cited text no. 5
    
6.
Nada SM, Abazza BE, Mahmoud LA, Habeeb YS, Hussein HF, Amer OT. Toxocariasis as a cause of renal disease in children in Sharkia Governorate, Egypt. J Egypt Soc Parasitol 1996;26:709-17.  Back to cited text no. 6
    
7.
Shetty AK, Aviles DH. Nephrotic syndrome associated with Toxocara canis infection. Ann Trop Paediatr 1999;19:297-300.  Back to cited text no. 7
    
8.
Zotos PG, Psimenou E, Roussou M, Kontogiannis S, Panoutsopoulos A, Dimopoulos AM. Nephrotic syndrome as a manifestation of Toxocara canis infection. Nephrol Dial Transplant 2006;21:2675-6.  Back to cited text no. 8
    
9.
Casarosa L, Papini R, Mancianti F, Abramo F, Poli A. Renal involvement in mice experimenttally infected with Toxocara canis embryonated eggs. Vet Parasitol 1992;42:265-72.  Back to cited text no. 9
    

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Correspondence Address:
Yosra Ben Ariba
Department of Internal Medicine Military, Hospital of Tunis, Montfleury, Tunis
Tunisia
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DOI: 10.4103/1319-2442.275494

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    Abstract
   Introduction
   Case Report
   Discussion
   Conclusion
    References
 

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