Abstract
Parasitic infections do not usually present with rapidly progressive renal failure but can provoke glomerular lesions which are mostly proliferative. In filarial infection, glomerular involvement is usually mild and transient, and presentation with renal failure is rare. We report occult filariasis presenting as rapidly progressive renal failure due to immune-complex mediated membranoproliferative glomerulonephritis. Our patient responded to treatment with diethylcarbamazine and a short course of steroid. This case highlights the importance of thorough workup to identify the cause and consideration of filariasis in an endemic area.
Keywords
Case report
A 45-year woman with no prior co-morbidity presented with complaints of facial and body swelling for 4 weeks. Examination revealed hypertension with a blood pressure of 160/90 mm of Hg and anasarca.
Laboratory investigations showed an anaemia (Hb 76 g/L), total leucocyte count 6 × 109/L (neutrophils 55%, lymphocytes 30%, monocytes 4%, eosinophils 11%), absolute eosinophil count 0.726 × 109/L, platelet count 197 × 109/L, serum urea 35.70 mmol/L, serum creatinine 194.48 µmol/L, serum total proteins 52.00 g/L, serum albumin 26.00 g/L, serum cholesterol 6.92 mmol/L and serum triglycerides 2.41 mmol/L. Urinalysis revealed 4 + proteinuria, many red blood cells and pus cells. Urine protein excretion was 5.2 g/day. Complement levels C3 0.87 g/L (range: 0.90–1.80 g/L) and C4 0.10 g/L (range 0.12–0.42 g/L) were low. Anti-nuclear antibodies (ANA), myeloperoxidase and proteinase 3 anti-neutrophil cytoplasmic antibodies (ANCA) were negative. Serology for hepatitis B surface antigen, hepatitis C virus and human immunodeficiency virus was negative. An ultrasound examination showed normal-sized kidneys with a normal Doppler study. Chest radiography, ECG and echocardiography were normal.
Light microscopic examination of percutaneous ultrasound-guided renal biopsy core revealed 11 glomeruli showing a membranoproliferative (MPGN) pattern of glomerular injury (Figure 1). Immunofluorescence microscopy showed granular immune-complex deposits of IgG3 (3 + ), C3 (3 + ), C1q (2+), kappa (3+) and lambda (3+), light chains in capillary wall and mesangium and was negative for IgA, IgM, IgG1, IgG2, IgG4.
Renal biopsy. (a) Photomicrograph showing thickened glomerular basement membrane with mesangial and endocapillary cell proliferation and accentuation of lobular pattern of capillary tuft (PAS stain, 40×). (b) Photomicrograph showing a glomeruli with mesangial and endocapillary hypercellularity, accentuation of lobular pattern of tufts and thickened capillaries (H&E, 400×). (c) Photomicrograph showing the thickened glomerular basement membrane with focal splitting and double contouring (silver methenamine stain, 40×). (d) Direct immunofluorescence microscopy shows glomerular, mesangial and capillary wall granular staining (3+) for IgG.
Her serum tested positive for filarial antigen by immunochromatography and filarial antibody by Immunodot test, although repeated peripheral blood film examination including a diethylcarbamazine (DEC) provocation test did not reveal microfilaria.
She was treated with DEC 100 mg three times daily for 21 days and prednisolone 40 mg orally once daily for 14 days, which was tapered and stopped after 2 months; supportive therapy with antihypertensive and diuretics was continued.
On subsequent follow-up, unilateral right lower limb oedema became apparent. A 99 m Tc-sulphur colloid lymphoscintigraphy revealed a partial lymphatic obstruction in the right lower limb (Figure 2). After 3 months of treatment, the patient was normotensive with a serum creatinine of 79.56 µmol/L, 24-h urine protein of 0.120 g/day, and with no active urinary sediments.
99m Tc-sulphur colloid lymphoscintigraphy of the index case showing a partial lymphatic obstruction in the right lower limb.
At 12 months follow-up, she remained asymptomatic with normal renal function.
Discussion
Although 45% of untreated microfilaremic patients have renal pathology manifested as microscopic haematuria (35%) and/or proteinuria (20%), 1 presentation of a rapidly progressive renal failure (RPRF) is rarely described. 2
Our case presented with RPRF, which is commonly attributed to other forms of glomerulonephritis. Negative serological tests, and a kidney biopsy consistent with immune-mediated MPGN, compelled us to consider chronic infection or antigenaemia as a cause of RPRF. Residence in an endemic area and mild peripheral eosinophilia raised the suspicion of occult filariasis as a cause.
Serological tests to detect circulating Wuchereria bancrofti antigens by immunochromatographic card tests have high sensitivity and specificity and are useful in diagnosing such patients. 3
Renal abnormalities in filariasis arise mainly due to two mechanisms: (a) mechanical damage to the glomeruli and (b) immune-complex deposition. Glomerular disease associated with filariasis is predominantly immune complex mediated 4 and the most common pathology described is diffuse mesangial hyperplasia, although membranous nephropathy has also been described.2,5 Clinical presentation of chyluria and rare instances of finding microfilaria in the renal biopsy specimen have also been described. 6
Our patient responded to DEC and a short course of steroids along with supportive treatment. Steroids were added because of the severe nature of renal injury. Paradoxical increase in proteinuria or decline in kidney function has been reported following initiation of DEC. 1 Interestingly, our patient continued to have mild non-pitting oedema despite the resolution of anasarca. Lymphangiography revealed obstruction of lymphatics in the right lower limb, presumably due to filariasis.
Footnotes
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.