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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2020  |  Volume : 31  |  Issue : 5  |  Page : 1101-1105
Catching the Worm Early: An Atypical Case of Bancroftian Filarial Nephropathy

1 Department of Nephrology, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of General General Pathology, Christian Medical College, Vellore, Tamil Nadu, India

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Date of Web Publication21-Nov-2020


Filarial glomerular disease has been attributed to circulating immune complex deposition. We report here a rare manifestation of filarial nephropathy with microfilariae documented in glomerular capillaries in addition to immune complex glomerulonephritis, thus suggesting that direct toxicity may also contribute to the pathogenesis of this entity.

How to cite this article:
Krishnakumar A, Valson AT, Duhli N, Mohapatra A, Tulsidas KS, Varughese S. Catching the Worm Early: An Atypical Case of Bancroftian Filarial Nephropathy. Saudi J Kidney Dis Transpl 2020;31:1101-5

How to cite this URL:
Krishnakumar A, Valson AT, Duhli N, Mohapatra A, Tulsidas KS, Varughese S. Catching the Worm Early: An Atypical Case of Bancroftian Filarial Nephropathy. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2022 Aug 10];31:1101-5. Available from: https://www.sjkdt.org/text.asp?2020/31/5/1101/301177

   Introduction Top

Glomerular diseases secondary to parasitic infections are common in the Indian subcontinent. Filarial infections usually cause renal disease manifesting as chyluria, whereas parenchymal diseases are quite rare.[1] Common glomerular pathologies in filariasis include mesangial proliferative glomerulonephritis (GN) and acute proliferative and exudative glomerulonephritis with eosinophilic predominance.[2] However, most glomerular pathologies have been attributed to immune complex deposition in the kidneys.[3] In this case report, we report the presence of microfilarial forms in the glomerular capillaries, which we hypothesize may also contribute to the pathogenesis of bancroftian filarial glomerular disease.

   Case Report Top

A 55-year-old man from Jharkhand with no known prior comorbidities had an acute febrile illness that lasted for three days. The fever was high grade and intermittent, with chills and rigors, and no other localizing symptoms or signs. The fever settled after taking a non-steroidal anti-inflammatory drug (NSAID) that was prescribed by the general practitioner in his locality. A couple of days later, he noticed generalized swelling of his body, especially in the periorbital region. This was also accompanied by foamy urine and a decreased urine output. There was no history of a sore throat or skin lesions and no change in the color of urine. For the above symptoms, he was evaluated elsewhere and was found to have a serum creatinine of 1.6 mg/dL and urine dipstick positive for albumin. He was empirically started on oral prednisolone at a dose of 1 mg/kg once daily by his local practitioner without a renal biopsy. He had completed a 10-day course of oral steroids before he presented to the emergency department of our hospital with another episode of fever. On examination, the patient was febrile (temperature 99.4°F) had anasarca, and his blood pressure was 160/90 mm Hg. Systemic examination was unremarkable. Preliminary laboratory investigations were as follows: total leukocyte count: 15,200/mm3, differential count: neutrophils: 79%, lymphocytes: 9%, monocytes: 10%, and eosinophils: 2%; serum creatinine: 1.3 mg/dL, and blood urea 190 mg/dL. Serum electrolytes were within normal limits. Urine microscopy showed 52 red blood cells (RBCs)/high power field (HPF), 8 white blood cells/HPF, and dipstick protein 2+, with 24 h urine protein excretion of 1.21 g/day. Urine phase-contrast microscopy showed 60% dysmorphic RBCs, which was suggestive of glomerular hematuria. A peripheral blood smear sent as part of the routine workup for acute febrile illness was positive for microfilaria of Wuchereria bancrofti, and subsequently, microfilariae were also demonstrated in urine smears [Figure 1]. Further evaluation revealed normal complement levels (C3, C4). Serological tests for the anti-nuclear antibody (ANA), anti-DNAse B, and antistreptolysin O were also negative. The patient was prescribed a course of diethylcarbamazine (DEC).
Figure 1: Wet mount smear of urine showing microfilarial organism.

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A renal biopsy was performed [Figure 2] and [Figure 3] five days after the start of DEC therapy with a provisional diagnosis of acute filarial glomerulonephritis. The biopsy showed 18 glomeruli displaying mesangial matrix expansion, accentuation of lobulation, mesangial and endocapillary cell proliferation, neutrophilic infiltration, karyorrhectic nuclear debris, focal capillary wall reduplication, and peripheral capillary wall thickening. Many glomerular capillary loops showed microfilarial forms. The extraglomerular compartment showed interstitial expansion with edema and mild infiltrates of mononuclear cells as well as tubular dilatation with hyaline casts. The vascular compartment showed arteriosclerosis. Immunofluorescence microscopy showed focal capillary wall deposits of IgG (2+), but C3, C1q, and C4 were negative.
Figure 2: A glomerulus with focal proliferation of endocapillary cells, neutrophilic infiltration and intracapillary microfilarial forms (arrow) PAS, ×400.

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Figure 3: A glomerulus with focal proliferation of endocapillary cells and intra-capillary microfiliarial forms (arrow) (H and E ×400).

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Despite a transient worsening of edema after initiation of DEC, serum creatinine decreased to 0.96 mg/dL and urine protein/creatinine ratio was 0.08 one week after the kidney biopsy, suggesting resolution of disease.

   Discussion Top

Filarial parasites belong to the Filarioidea superfamily. More than a hundred species are known, but only eight species affect humans.[4] Among them, Wuchereria bancrofti, Onchocerca volvulus, Loa loa, and Brugia malayi have been associated with renal involvement.

The definitive host is the adult human. The viviparous female worms reside in the lymphatic system and liberate microfilariae into the blood and subcutaneous tissue. They remain dormant for weeks to months until they are ingested by the respective vectors. The microfilariae then become filariform larvae, which mature into adult forms when they infect a new host.

Inflammatory damage in the lymphatic system is principally caused by adult worms. Pathologic changes are due to the parasite's direct effects as well as the host's inflammatory response. It has been hypothesized that the death of the worm precipitates granulomatous inflammation and fibrosis of lymphatic vessels.

On the other hand, extralymphatic manifestations are caused by microfilariae and parasite antigens that are cleared rapidly by the lungs (causing tropical pulmonary eosinophilia), kidneys (causing renal damage), and the reticuloendothelial system (causing hepatomegaly, splenomegaly, lymphadenopathy, cutaneous skin reactions, and granulomas).

Renal disease usually manifests as chyluria, microscopic hematuria (35%), and/or proteinuria (20%).[5] Whereas, the common compartment involved is the interstitium; the presence of both hematuria and proteinuria is indicative of glomerular involvement. The pathologic manifestations were initially thought to be due to direct mechanical damage to the glomeruli by the circulating adult worm, but the current consensus is that the pathology is due to the deposition of immune complexes in the glomerular basement membrane.[5]

The classic pathologic feature is an eosinophilic proliferative GN, as described by Date et al.[2] However, mesangioproliferative GN, membranoproliferative GN, minimal change disease and collapsing focal segmental glomerulosclerosis have also been described.[6] Our patient had an acute immune-complex mediated glomerulonephritis, as evidenced by diffuse endocapillary proliferation with capillary wall deposition of IgG and focal capillary wall thickening. Because hematuria, proteinuria, and renal dysfunction were present at the initial presentation, a direct toxic effect of microfilariae is likely. It has been reported that in patients with filarial fever, the metabolic activity of adult worms is increased so that there is an increase in the number of microfilariae and filarial antigens in circulation, leading to the heightened immune complex formation as well as direct toxic effects like tubulointerstitial disease.[7] The presence of microfilariae in both peripheral blood and urine in our patient at presentation lends further support to this hypothesis. However, eosinophilic infiltration and interstitial inflammation may have been attenuated due to treatment with oral prednisolone prior to biopsy. Steroid co-administration with DEC has been shown to reduce the incidence of treatment-related side effects in patients with a high microfilarial load. Hence, it is conceivable that by damping host immune response, the course of oral steroid our patient received at his hometown may have promoted microfilarial multiplication. We hypothesize that because the steroid course was discontinued by the patient prior to presenting at our center, which may have resulted in a rebound inflammatory response to the circulating microfilariae resulting in the immunological and direct toxic effects apparent on the biopsy. The biopsy findings are not consistent with NSAID-mediated kidney injury, which was the other possible differential diagnosis in this case.

Microfilariae in the renal biopsy specimen are a rare finding, though microfilariae have been demonstrated in renal arterioles, glomerular capillaries, peritubular capillaries, tubules and the interstitium.[6],[8] The unusual feature in this patient was that he had circulating intracapillary microfilariae, despite initiation of DEC before biopsy. DEC acts by causing a loss of the microfilarial sheath and subsequent apoptosis, leading to microfilarial death.[9] It is important to note that DEC has a lower microfilaricidal effect when compared to ivermectin,[10] and treatment response may therefore be delayed. This explains how microfilariae were still visible in the renal biopsy specimen despite DEC therapy. Treatment with DEC also kills adult worms residing in the lymphatics and exacerbates renal abnormalities due to enhanced immune complex formation from the filarial antigens released from dead worms. This, however, is not an indication to stop DEC therapy, as DEC-induced hematuria and/or proteinuria is transient, and continued treatment reduces microfilarial population resulting in complete resolution of abnormal renal findings, especially in patients with non-nephrotic proteinuria.[11] There is no literature regarding the role of steroids in the treatment of filarial immune complex-mediated glomerulonephritis, but therapeutic apheresis has been described as a means to reduce filarial antigen load before initiation of DEC.[12] Our patient showed dramatic response to DEC with complete normalization of renal function and resolution of hematuria and proteinuria within one week of starting DEC.

In conclusion, in patients hailing from a filaria endemic area with renal involvement in the form of haematuria and/or proteinuria, an immune complex GN should be considered. We hypothesize that both direct and immune complex-mediated mechanisms may be responsible for the renal dysfunction and pathological abnormalities seen in filarial nephropathy.

   Declaration of Patient Consent Top

The authors certify that they have obtained the appropriate patient consent form. In the form the patient has given his/her consent for his/her images and other clinical information to be reported in the journal. The patient understands that his/her name and initials will not be published and due efforts will be made to conceal his/her identity, but anonymity cannot be guaranteed.

Conflict of interest: None declared.

   References Top

Ray DS, Thukral S. Microfilariae in the kidney. Trop J Med Res 2017;20:101-3.  Back to cited text no. 1
  [Full text]  
Date A, Gunasekaran V, Kirubakaran MG, Shastry JC. Acute eosinophilic glomerulonephritis with Bancroftian filariasis. Postgrad Med J 1979;55:905-7.  Back to cited text no. 2
Prasad GB, Reddy MV, Harinath BC. Immune complexes and immunoglobulins involved in human filariasis. Indian J Med Res 1983;77: 813-6.  Back to cited text no. 3
Klion AD. Filarial infections in travelers and immigrants. Curr Infect Dis Rep 2008;10:50-7.  Back to cited text no. 4
Dreyer G, Ottesen EA, Galdino E, et al. Renal abnormalities in microfilaremic patients with Bancroftian filariasis. Am J Trop Med Hyg 1992;46:745-51.  Back to cited text no. 5
Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO Clinical Practice Guideline for Glomerulonephritis. Kidney Int Suppl 2012;2: 139-274.  Back to cited text no. 6
Langhammer J, Birk HW, Zahner H. Renal disease in lymphatic filariasis: Evidence for tubular and glomerular disorders at various stages of the infection. Trop Med Int Health 1997;2:875-84.  Back to cited text no. 7
Ray DS, Thukral S. Microfilariae in the kidney. Trop J Med Res 2017;20:101.  Back to cited text no. 8
  [Full text]  
Florencio MS, Peixoto CA. The effects of diethyl-carbamazine on the ultrastructure of microfilariae of Wuchereriabancrofti. Parasitology 2003;126:551-4.  Back to cited text no. 9
Stolk WA, VAN Oortmarssen GJ, Pani SP, et al. Effects of ivermectin and diethylcarbamazine on microfilariae and overall microfilaria production in Bancroftian filariasis. Am J Trop Med Hyg 2005;73:881-7.  Back to cited text no. 10
Dreyer G, Ottesen EA, Galdino E, et al. Renal abnormalities in microfilaremic patients with Bancroftian filariasis. Am J Trop Med Hyg 1992;46:745-51.  Back to cited text no. 11
Muylle L, Taelman H, Moldenhauer R, Van Brabant R, Peetermans ME. Usefulness of apheresis to extract microfilarias in management of loiasis. Br Med J (Clin Res Ed) 1983; 287:519-20.  Back to cited text no. 12

Correspondence Address:
Arvind Krishnakumar
Department of Nephrology, Christian Medical College, Vellore, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.301177

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