| Abstract|| |
A 38-years of Bangladeshi woman with a post medical history of treated Bancroftian Filariasis ten years before, presented with chyluria and heavy proteinuria. Percutaneous renal biopsy was consistent with membranous glomerulonephritis. The patient was treated with diethylcarbamazinc (DEC), and later, with azathioprine and prednisolone for the nephrosis. The chyluria disappeared with treatment, but recurred four months later, despite persistent drug therapy. The proteinuria dropped to 2.4 g and 0.2 g/24 hours at two and twelve weeks respectively. After two years of follow-up, the chyluria persisted but the proteinuria remained below 0.2g/24 hours, while plasma proteins remained within normal limits. The patient maintained stable body weight, good general health status, stable renal functions and normal lipid and hepatic profiles. The numerous investigations carried out to elucidate the etiology of the chyluria were not rewarding. The conservative approach for the management of chyuria adopted in this patient seems to be appropriate.
|How to cite this article:|
Al-Anazi AR. Membranous Glomerulonephritis in a Patient Presenting with Chyluria, Probably due to Filariasis: How far should we investigate?. Saudi J Kidney Dis Transpl 1999;10:167-70
|How to cite this URL:|
Al-Anazi AR. Membranous Glomerulonephritis in a Patient Presenting with Chyluria, Probably due to Filariasis: How far should we investigate?. Saudi J Kidney Dis Transpl [serial online] 1999 [cited 2020 Sep 25];10:167-70. Available from: http://www.sjkdt.org/text.asp?1999/10/2/167/37225
| Introduction|| |
Chyluria, the passage of lymphatic fluid into the urine, is a common presentation of filariasis. Filarial infection leads to lymphatic obstruction and may cause different renal disorders. Judicious use of investigations is essential for cost effective management. 
The use of invasive imaging procedures had no effect on either treatment or outcome. 
Here below is a case-report of chyluria, probably filarial in etiology, and membranous glomerulonephritis.
| Case Report|| |
A 38-year old Bangladeshi woman was seen in December 1992 complaining of milky urine intermittently over the previous tow years. One year prior to coming to our hospital, she noticed the onset of dysuria and right loin pain associated with passing pieces of gelatinous tissue in the urine, which was hemochyluric on few occasions. She gave no history of urinary stones or obstruction.
Her past medical history was remarkable for Bancroftian Filariasis in 1982, in her homeland treated with Diethylcarbamazinc (DEC).
Physical examination disclosed a 151-cm tall lady who weighing 69 KG. Her Blood pressure was 110/60 mm Hg and she had moderate pedal edema. She was afebrile, had no lymphadenopathy and abdominal examination showed neither ascites nor organomegaly. The remaining physical examination was unremarkable.
Complete blood count and blood chemistry, including urea nitrogen, electrolytes, liver function test, cholesterol and triglyceride were all within normal limits. Multiple night blood smears and urine collections were negative for filarial. Urine culture was negative for bacteria, mycobacteria and fungi.
The urine appeared milky on inspection Urinary sediment showed 3000 white cells (WBC) and 1000 red cells (RBC) per high power field (HPF). Repeated 24-hours urinary collection showed 9-13 grams of protein. The creatinine clearance was, however, normal.
The finding of high triglycerides in the urine suggested that chyluria was due to chylomicrons. Their presence was confirmed by refrigeration of urine over-night at 4 0 C in upright position which lead to the appearance of a white creamy layer overlying clear urine. Microscopic examination of a Sudan III stained urine specimen confirmed the presence of fat globules. Furthermore, the turbid appearance of the urine did not clear with alkalization but did so with the addit9on of Ether.
The serological profile was within normal limits including hepatitis B surface antigen (HbsAg), antiphospholipid antibodies, titers for syphilis, complement CH50, C3, C4 levels, and immunoelectrophoresis.
Plain abdominal X-ray, ultrasound of the kidneys and computerized tomography scanning of the abdomen and pelvis showed no abnormal findings. Intravenous urography (I.V.U) was normal, and isotope lymphangiogram shoed no obstruction.
Histopathology and culture of the pieces of tissue passed in the urine were unremarkable except for features of chronic inflammation.
The patient was given a three weeks course of DEC. Chyluria disappeared tow months after treatment with DEC then recurred.
During outpatient follow-up, the patient demonstrated persistent hemochyluria and proteinuria.
A renal biopsy was done in April 1993 (16 months after the initial presentation to our hospital) because of the persistent nephritic range proteinuria. The findings were consistent with membranous glomerulonephritis. The patient was started on prednisolone. 1 mg/kg body weight and 100 mg azathioprine per day. She soon developed hyperglycemia, which correlated with the dose of the prednisolone. The corticosteroid part of the therapy was therefore discontinued. Chyluria disappeared again with treatment with azathioprine and prednisolone, but recurred four months later. No lower limb edema occurred on recurrence of chyluria. Proteinuria dropped to 2.4 g and 0.2 g/24 hours, At two and twelve weeks respectively, after treatment with prednisolone and Azathioprine. Despite the persistence of chyluira, the proteinuria remained below 0.2 g/24 hours, while plasma protein remained within normal limits. After two years of follow-up, the patient was still maintaining stable body weight, good general health status stable renal function and normal lipid and hepatic profiles. Her latest urine sediment showed RBC and WBC of 0-5 and 0-2/ HPF, respectively.
| Discussion|| |
Chyluria is one of the late manifestations of the filarial syndrome and has been reported to occur one month to 54 years (average of 20 years) after the acute filarial infestation. ,,
Characterized anatomically by dilated renal lymphatic vessels with functional lymphaticpelvic fistulas. Lymph and emulsified fat may gain access to the urinary tract to give the urine milky appearance and form gelatinous clots. Chyluria occurs because of rupture of lymph vessels as a result of retrograde lymphatic hypertension and dilation in the urinary tract. ,, These clots may cause obstructive uropathy with renal colic and retention of urine. 
In a study of 176 patients, microfilaria caused chyluria in 5.5%.  Our patient presented with intermittent milky urine ten years after acute filarial infestation. She also had proteinuria that was associated with hematuria, loin pain on few occasions. Furthermore, she once passed pieces of gelatinous tissue in urine. Examination of this tissue showed signs of membranous glomerulonephritis found on renal biopsy was probably related to the patient's filariasis in view of the absence of other etiological factors. This is in agreement with other reports. 
Yap HK, et al reported an association of filariasis with glomerulonephritis that caused nephritic syndrome.  Pillay reported chronic glomerulonephritis in renal biopsy results of patients with filariasis.  Waugh demonstrated mesangial deposits of immunoglobulin and complement by using immunoflorescent and electron microscopic studies suggesting an immune complex basis for glomerulonephritis in patients with filariasis.  Ngu and associates reported different renal histopathological abnormalities with filariasis. In a cohort of 21 patients they found four patients (19%) to have membranous glomerulonephritis and 9 (42%) to have membrenoproliferative and mesangial glomerulonephritis. 
Several therapeutic options have been suggested for the chyluria. These include: conservative management with medium chains fatty acids, installation of sclerosing agents into the renal pelvis and surgery.  Recurrence of chyluria was 51.1% after silver nitrate installation and 25.6% after surgical stripping despite excellent short-term results (97.9%).  Treatment with silver nitrate resulted in blockage of the collecting system requiring nephrectomy.  While surgical correction was reported to result in lymphatic-venous anastomosis, ending in ipsilateral renal failure. 
Our patient had hematuria, proteinuria and membranous glomerulopathy, in addition to the recurrent chyluria. During the two years period that elapsed since the first appearance of chyluria, the patient maintained good health status, stable body weight with normal full blood count, renal and hepatic functions with no significant episodes of infection despite persistent chyluria.
The conservative approach practiced in managing this patient seems reasonable. Chyluria may present as a benign condition that can be managed conservatively thus sparing the patients invasive and costly procedures.
| Acknowledgment|| |
We with to thank Ms. Sara Seno for typing this manuscript.
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Awadh R.H Al-Anazi
Department of Medicine, King Khalid University Hospital, P.O. Box 2925, Riyadh 11461