A 32 year female presented with bilateral pedal edema and decrease in weight for three months, without a history of dysuria, hematuria, hypertension or diabetes. On evaluation blood pressure 126/80 mm Hg, random sugar 116 mg/dL, total protein/albumin = 6.4/2.2 g/L, 24 h urine protein 3.8 g, urine culture was sterile and urine routine examination revealed 3+ urine protein with red blood cells 3–4 per high power field. Other viral (HBsAg, anti-HCV and anti-HIV) and serological markers (ANA, dsDNA, ANCA) and complete blood count was within normal limit. Urine microscopic examination shows numerous live microfilarias (Video linked). Higher magnification revealed sheathed microfilaria having uniformly tapering delicate caudal end with no terminal nuclei (Fig. 1, Fig. 2). On subsequent renal biopsy, histopathology showed features of minimal change diseases. There were no electron dense deposits on electron microscopy (Fig. 3, Fig. 4).
Fig. 1.
Low power microscopy image of live microfilaria.
Fig. 2.
High power microscopy image of live microfilaria showing nuclei till the end and morphology consistent with W. bancrofti.
Fig. 3.
Kidney biopsy showing histologically normal glomeruli and tubulointerstitial compartment (Periodic acid Schiff stain 100×).
Fig. 4.
High power view showing histologically normal glomeruli with patent capillary loops and normal mesangium.
There are two mechanisms by which microfilariae can cause glomerular disease, either by direct physical invasion or as an immune mediated disease. The autoimmune mediated diseases include mesangiocapillary glomerulonephritis (GN), mesangioproliferative GN, membranous GN or collapsing variant of focal segmental glomerulosclerosis [1].
In the present case patient was having turbid urine but not milky white, therefore urine ether test was performed to exclude the presence of chyle in urine. Chyluria in filariasis is usually associated with abnormal retrograde or collateral flow of lymph from intestinal lymphatics into the renal lymphatics. Detection of microfilariae in the chylous urine of otherwise asymptomatic filarial patients has been rarely described [2]. The differential diagnosis of chyluria includes pathological conditions that occlude lymphatic or thoracic ducts, such as those involving parasites (filariasis, echinococcosis, schistosomiasis and ascariasis), tuberculosis, malignancies and the postoperative state (trauma to lymphatics or thoracic duct during surgical procedure) [2].
The lifespan of adult worms is approximately four to five years; however, chyluria can be observed after more than 10 years. Possible reasons for this phenomenon include: (1) irreversible damage to the lymphatic duct (2) the longer survival of adult worms and (3) a non-filarial etiology. Fat intake, pregnancy and exercise are considered to be aggravating factors of chyluria, and these conditions should be avoided, especially in patients with recurrent or prolonged chyluria [2].
Treatment of W. bancrofti infection includes generally, a high-protein diet without fat-containing foods along with the administration of diethylcarbamazine (DEC) (6 mg/day) for two weeks. Conservative treatment of lymphatic filariasis includes bed rest and a fat-restricted diet [3].
Conflicts of interest
No conflicts of interest.
Funding
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Author contribution
Study design, data collections, data analysis, writing, others: Dr Ravi Hari Phulwar, Dr Adarsh Barwad.
Footnotes
Supplementary material related to this article can be found, in the online version, at doi:https://doi.org/10.1016/j.idcr.2018.e00424.
Appendix A. Supplementary data
The following is Supplementary data to this article:
References
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