Hyperphosphataemia and related mortality.

strongly positive for toxocariasis. Enzyme-linked immuno-sorbent assay for toxocaral antibodies showed 2.7 U (>1.1). Antinuclear, antineutrophil cytoplasmic antibodies, cryoglo-bulins and immune complexes were all negative. Computed tomography scans of the lungs, brain and abdomen were unremarkable. A bone marrow aspirate and biopsy revealed increased cell infiltration of the bone marrow with the predominance of eosinophils and a normal caryotype. Endoscopy of the stomach and duodenum was unremarkable and biopsy showed eosinophilic infiltration. Ultrasound of the heart and ophthalmoscopy were normal. A percutaneous biopsy of the left kidney was performed. Histopathological examination revealed 29 glomeruli with diffuse thickening of the glomerular capillary wall with spikes and podocyte hypertrophy, patchy tubular cell swelling and patchy tubular atrophy with loss of the brush border and absence of interstitial inflammatory cell infiltrate. Immunofluorescence showed fine granular IgG(þ), C3d(þ) and IgM(þ) deposits in the capillary wall and also IgM(þ) deposits in the mesangium, while IgA, C1q and C4 were negative. This was consistent with membranous glomerulo-nephritis stage 0 ! I. The mesangial deposits suggested a secondary cause. On the basis of the strong serological positivity for toxocariasis and the marked eosinophilia, diagnosis of VLM syndrome was made. The nephrotic syndrome was attributed to toxocariasis. The patient was treated with prednisone (1 mg/kg p.o. daily) for the marked eosinophilia and with albendazole (10 mg/kg p.o. twice a day for 7 days). The steroid treatment resulted in the complete disappearance of eosinophilia and fever within 48 h. The patient was discharged from hospital in good clinical condition. After 1 month of prednisone therapy, total serum protein was 5.4 g/dl, albumin 2.8 g/dl and proteinuria had decreased to 1.5 g/24 h. Two months later, while still under prednisone therapy (0 6 mg/kg), proteinuria increased to the level of 2 g/24 h. At this point, ciclosporin was initiated at a dose of 3 mg/kg and prednisone was slowly tapered over the next 2 months, then stopped. Two months after ciclosporin treatment, proteinuria was 300 mg/24 h and 5 months after ciclosporin introduction, nephrotic syndrome is still in remission. Toxocara infection can cause three distinct clinical syndromes in humans: VLM, OLM and covert toxocariasis. Myocarditis, nephritis and involvement of CNS have been described. In a report on paediatric 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. In another case …