- Email: [email protected]
Filarial chyluria as a cause of acute urinary retention
FILARIAL CHYLURIA AS A CAUSE OF ACUTE URINARY RETENTION ROBERT
H. SHERMAN,
LAURENCE
M.D.
B. GOLDMAN,
RALPH W. DEVERE
M.D.
WHITE,
M.D.
From the Department of Urology, University of California, Davis, and Kaiser Permanente Medical Group, Sacramento, California
ABSTRACT-An adult male with acute urinary retention had spontaneous resolution after passage of a proteinaceous clot. He admitted to passing milky urine intermittently over the past twenty years. A history of hydrocele with associated lymphadenitis in a patient who emigrated porn Australia was suspicious for a parasitic etiology. Urinalysis, lymphangiography, and positive indirect hemagglutination studies confirmed the diagnosis of filarial chyluria.
Chyluria refers to the passage of milky white urine composed of intestinal lymphatic fluid and is due to lymphourinary communication. When analyzed, chylous urine is found to contain lipid, protein, and cellular moieties made of emulsified medium-chained fatty acids (chylomicrons), cholesterol, albumin, fibrinogen, red blood cells, and occasionally microfilaria (when due to parasitic infection). Lymphocytes are an essential diagnostic requirement. l The etiology of chyluria was first proposed in 1862 by Carter, who postulated a lymphatic blockage at the level of the thoracic duct, causing lymphatic hypertension and retrograde flow of lymph into the urinary system via a fistulous communication. This is essentially correct with the exception of the level of proposed blockage. Anatomic dissection and cinelymphangiography have documented that an enormous system of lymphovenous collaterals develops in the event of thoracic duct obstruction. In addition, ligation of the thoracic duct has never induced chyluria in animal experiments. It has been confirmed at autopsy that lymphorenal fistulization develops due to ob-
struction of the ipsilateral para-aortic lymphatic channels above the renal hilum. Lymphatic hypertension, under normal anatomic conditions, is shunted into venous channels, preventing rupture into other organ systems. However, with disruption of lymphatic architecture, venous runoff is curtailed and aberrant fistulization develops with subsequent chylous leak. Chyluria can be divided into two groups. Parasitic chyluria commonly is seen in areas of endemic filariasis and is usually due to Wuchereria bancrofti infestation. Nonparasitic chyluria is caused by lymphatic aneurysm, pregnancy, or acute lymphatic obstruction due to trauma, tuberculosis, syphilis, or retroperitoneal tumor or abscess. Chyliform urine (false chyluria) is seen in lipiduria (from fat embolism, diabetic neuropathy, or fatty degeneration of any bladder or renal growth), rupture of a caseating tuberculous cavity or may be confused with pyuria. 2-4Differentiation largely depends on careful history and physical examination, urinalysis, and, most important, a lymphangiogram.
642
UROLOGY
/ JUNE1987
/ VOLUMEXXIX,NUMBER6
FIGURE 1. Lymphangiograms show (A) dilatation of collateral lymphatic circulation (arrows), and (B) abnormal lymph nodes displaying large filling defects (white arrow) and dilated pericalyceal lymphatics bilaterally (black arrows).
Case Report A seventy-two-year-old white man in acute urinary retention was admitted to the urology service. There was no obstructive or irritative voiding symptoms, recent trauma, or documented neoplasm. He admitted to a twentyyear history of passing milky white urine episodically. When present, it began around midmorning and persisted throughout the day. When supine for several hours, his urine returned to an amber color, only to recur after several hours of ambulation. He denied gross hematuria, dysuria, weight loss, or constitutional symptoms. Past surgical history included a right hydrocelectomy with associated bilateral inguinal node swelling and tenderness occurring approximately thirty years ago. The patient denied postoperative complications, and his adenopathy resolved “with medications.” He has resided in Northern California for fifteen years, having emigrated from Eastern Australia. Physical examination was remarkable for a distended and tender bladder. There was no adenopathy, edema, or hydrocele. Spontaneous passage of a proteinaceous clot per urethra relieved his obstructive symptoms, following which his urine was seen to be milky white. A gelatinous plug had settled to the bottom of the specimen cup. Analysis revealed protein (4 + ) with 4-8 white and 3-5 red blood cellslhpf. No bacteria or casts were seen. Sudan III stain was
UROLOGY
i JUNE1987
/ VOLUMEXXIX,NUMBER6
positive for the presence of urinary fat. Urine cultures for routine bacteria and tuberculosis were negative. Creatinine, blood urea nitrogen, and complete blood count were normal; however, a differential white blood cell count showed 19 per cent eosinophils. Serum albumin and total protein were slightly below the lower limits of normal. Although microfilariae were not found in either urine or blood smears, indirect hemagglutination studies were positive for the presence of antifilarial antibodies. An intravenous pyelogram was unremarkable. A lymphangiogram showed segmental dilatation of varices in both iliac and right paracaval lymphatics as well as prominent paracalyceal channels bilaterally. Collateral lymphatic channels were obvious. The para-aortic lymph nodes were abnormal, some displaying large filling defects (Fig. 1). Thoracic duct was patent. The urine cleared over a twelve-hour period, and the patient was discharged and prescribed a low-fat diet. Follow-up examination was unretern. l1 Benzopyrone, a medication for chronicand uroflow studies ruled out persistent bladder outlet obstruction. Comment Filariasis refers to a variety of conditions caused by infestation with nematodes. The most common of these parasites is Wuchereria bancrofti with others being Brugia, Echinococcus, Cysticercus, and Ascaris species. The
643
disease is transmitted via a mosquito and is endemic to tropical and subtropical countries where vector infestation is heavy. The life cycle of these parasites proceeds from man to mosquito and back through a series of larval stages. The worm matures to adulthood in the salivary gland of the mosquito. Once injected through the human epidermis, the parasites migrate to and multiply within the lymphatic system. They release microfilariae in a circadian fashion (usually at night), at which time a blood smear may document their presence. Microfilaremia (carrier state) is detected in only lo-40 per cent of cases. 5,6It is the local reaction toward the adult worms within the lymphatic system, not the microfilaremia, that causes all pathologic reactions within the host. The course of the disease can be divided into three phases. The latent (or incubation) period lasting months to years is subclinical and represents a low-grade allergic reaction to exoantigens contained on live worms. The lymphangiectasis which ensues is mild, reversible, and usually remits spontaneously. The second (or acute) phase represents a full-blown allergic (Arthus) response to the somatic antigens of dead worms. This causes granulomatous lymphangitis and lymphadenitis. Presenting symptoms include fever, weight loss, funiculoepididymitis, orchitis, filarial abscess, genital edema or adjacent thrombophlebitis. An acute hydrocele is common and of interest is the fact that these do not transilluminate. The third (or chronic) phase occurs five to twenty years after the primary infestation. Recurrent localized inflammatory reactions destroy existing collateral lymphatic channels, causing progressive fibrosis of previously edematous tissues.’ Ultimately, obliteration of lymphatic vessels occurs with subsequent lymphatic hypertension, the clinical expression of which depends on the degree and location of insult. Rupture of a lymphatic varix may occur in the pericardium, pleura, peritoneum, intestines, and joint spaces. Rupture in the urinary tract (usually at the level of the calyceal fornices) produces chyluria. This usually presents episodically, varying with the amount of fat ingested, occasionally with posture or following physical exertion, or may be associated with conditions predisposing to urostasis, such as pregnancy or benign prostatic hypertrophy. The incidence of detectable chyluria among patients with chronic filariasis is l-2 per cent,3 and of these, only 10 per cent display obstruc-
tive symptoms5 Elephantiasis of leg, scrotum, or penis is the hallmark of this stage. Massive urinary protein loss can cause a nephrotic syndrome or frank anasarca. Superinfection is common, and bacterial prophylaxis is recommended. Diagnosis of filariasis is suspected with the proper symptomatology in endemic areas and confirmed by the detection of microfilariae in peripheral blood smear, chylous urine, or hydrocele fluid. Analysis of chylous urine confirms its lymphatic components. Eosinophilia is common. Calcification of lymphatic channels or hydrocele sacs occurs frequently and may be noted on plain films of the abdomen. Sudan III administered orally stains chylous particles in the urine bright orange. Complement fixation and skin tests exist. Dirofilaria immitis contains surface antigens common to all filarial worms and comprises the basis for an indirect hemagglutination test. Antibodies are noted up to twenty years after active disease. When chyluria exists, cystoscopic examination may document the renal unit involved, especially following the administration of a highfat diet, which exacerbates chylous leak. Intravenous pyelography may document obstruction or pyelonephritic changes, but rarely identifies fistulous communications. Lymphangiography remains the roentgenographic procedure of choice to confirm both lymphatic involvement as well as sites of pyelolymphatic fistulae.8Te Typically, in the early stages of disease, the lymphatic tree is dilated, tortuous, and lengthened compared with the unaffected side. With advanced disease, mottled defects of the nodes and even skipped lymphatic chains are frequently seen. Similar findings may be noted in advanced carcinoma and malignant lymphomas. Treatment is a function of the stage and severity of disease and is divided into medical and surgical management. Low-fat diets consisting of short-chain fatty acids are suggested since these are absorbed via the portal rather than the lymphatic system. Diethylcarbamazine is the drug of choice in filarial disease and has been purported to destroy and/or sterilize female worms.1° In addition, microfilariae are sensitized so that they become more susceptible to phagocytosis by the reticuloendothelial system.” Benzopyrone, a medication for chronicstage disease, enhances the resorption of accumulated interstitial protein (the cause of lymphedema), thereby diminishing the tissue
644
UROLOGY
/
JUNE 1987
I
VOLUME XXIX, NUMBER 6
swelling. l2 However, because of the episodic nature of the disease, it becomes difficult to assess the efficacy of any therapeutic measure. Although the majority of cases resolve spontaneously or with medical treatment, refractory disease may require surgical intervention. l3 With regard to chyluria, various sclerosing agents introduced into the renal pelvis have been proposed in the hope of chemically cauterizing the fistulous tracts.12 Endoscopic cauterization has been advised in the event of lymphovesical fistulization. Capsulectomy with stripping of the renal pedicle lymphatics is advocated by Torres and Estrada.14 Some recommend ligation of lymphatic varices,12 while others suggest nephrectomy in symptomatic cases. In addition, both retrograde pyelography and lymphangiography have documented therapeutic effects in curtailing or even eliminating chylous leak.5J5 Filariasis has been virtually nonexistent in the United States. However, with increasing immigration, its prevalence is sure to climb. Knowledge of the disease will facilitate its diagnosis and management. Sacramento,
UROLOGY
I JUNE 1987
4301 X Street California 95817 (DR. SHERMAN)
/ VOLUME
XXIX, NUMBER
6
References 1. Date A, Padankatti T, Vaska PH, and Shastry JCM: Lymphocytopenia in chyluria, Trans R Sot Trop Med Hyg 74: 137 (1980). 2. Bai KI, Sastry VN, and Subbaiah DV: Chyluria in childhood, Indian Pediatr 14: 229 (1977). 3. ‘Klousia JW, McClennan BL, and Semerjian BS: Chyluria: a case report and brief literature review, J Urol 117: 393 (1977). 4. Johnston DW: Chyluria: case report and review of literature, Ann Intern Med 12: 931 (1955). 5. Shankar PJ, Gandhi GM, and Rao MS: Clinical and lymphangiographic studies in haematochyluria, J Assoc Physicians India 23: 553 (1975). 6. Saigo C: A study of filariasis in Okinawa, Kuwamotos IGK z 15: 173 (1939). 7. Okamoto K, and Ohi Y: Recent distribution and treatment of filarial chyluria in Japan, J Urol 129: 64 (1983). 8. Gagnon JH: Lymphangiography in filarial chyluria, J Can Assoc Radio1 25: 319 (1974). 9. Callahan DH, Graf EC, Gersack J, and Turbow AM: Lymphangiography and simultaneous excretory urography as a diagnostic aid in chyluria, J Urol 93: 417 (1965). 10. Von Lichtenberg F, and Lehman JS: Parasitic diseases of the genitourinary system, in Harrison JH, et al (Eds): Campbell’s Urology, ed 4, Philadelphia, WB Saunders Company, 1-615, 1978. 11. Zerner J, and Barber HRK: Puerperal chyluria, NY State J Med 77: 414 (1977). 12. Yamauchi S: Chyluria, in Kaufman JJ,: Current Urologic Therapy, Philadelphia, WB Saunders Company, 1980, p 54. 13. Mahadevan R: Surgical aspects of filariasis, Trop Doct 8: 28 (1978). 14. Torres LF, and Estrada J Jr: Experiences in the treatment of chyluria, J Urol 87: 73 (1962). 15. Akisada M, and Tani S: Filarial chyluria in Japan, Radiology 90: 311 (1968).
645
H. SHERMAN,
LAURENCE
M.D.
B. GOLDMAN,
RALPH W. DEVERE
M.D.
WHITE,
M.D.
From the Department of Urology, University of California, Davis, and Kaiser Permanente Medical Group, Sacramento, California
ABSTRACT-An adult male with acute urinary retention had spontaneous resolution after passage of a proteinaceous clot. He admitted to passing milky urine intermittently over the past twenty years. A history of hydrocele with associated lymphadenitis in a patient who emigrated porn Australia was suspicious for a parasitic etiology. Urinalysis, lymphangiography, and positive indirect hemagglutination studies confirmed the diagnosis of filarial chyluria.
Chyluria refers to the passage of milky white urine composed of intestinal lymphatic fluid and is due to lymphourinary communication. When analyzed, chylous urine is found to contain lipid, protein, and cellular moieties made of emulsified medium-chained fatty acids (chylomicrons), cholesterol, albumin, fibrinogen, red blood cells, and occasionally microfilaria (when due to parasitic infection). Lymphocytes are an essential diagnostic requirement. l The etiology of chyluria was first proposed in 1862 by Carter, who postulated a lymphatic blockage at the level of the thoracic duct, causing lymphatic hypertension and retrograde flow of lymph into the urinary system via a fistulous communication. This is essentially correct with the exception of the level of proposed blockage. Anatomic dissection and cinelymphangiography have documented that an enormous system of lymphovenous collaterals develops in the event of thoracic duct obstruction. In addition, ligation of the thoracic duct has never induced chyluria in animal experiments. It has been confirmed at autopsy that lymphorenal fistulization develops due to ob-
struction of the ipsilateral para-aortic lymphatic channels above the renal hilum. Lymphatic hypertension, under normal anatomic conditions, is shunted into venous channels, preventing rupture into other organ systems. However, with disruption of lymphatic architecture, venous runoff is curtailed and aberrant fistulization develops with subsequent chylous leak. Chyluria can be divided into two groups. Parasitic chyluria commonly is seen in areas of endemic filariasis and is usually due to Wuchereria bancrofti infestation. Nonparasitic chyluria is caused by lymphatic aneurysm, pregnancy, or acute lymphatic obstruction due to trauma, tuberculosis, syphilis, or retroperitoneal tumor or abscess. Chyliform urine (false chyluria) is seen in lipiduria (from fat embolism, diabetic neuropathy, or fatty degeneration of any bladder or renal growth), rupture of a caseating tuberculous cavity or may be confused with pyuria. 2-4Differentiation largely depends on careful history and physical examination, urinalysis, and, most important, a lymphangiogram.
642
UROLOGY
/ JUNE1987
/ VOLUMEXXIX,NUMBER6
FIGURE 1. Lymphangiograms show (A) dilatation of collateral lymphatic circulation (arrows), and (B) abnormal lymph nodes displaying large filling defects (white arrow) and dilated pericalyceal lymphatics bilaterally (black arrows).
Case Report A seventy-two-year-old white man in acute urinary retention was admitted to the urology service. There was no obstructive or irritative voiding symptoms, recent trauma, or documented neoplasm. He admitted to a twentyyear history of passing milky white urine episodically. When present, it began around midmorning and persisted throughout the day. When supine for several hours, his urine returned to an amber color, only to recur after several hours of ambulation. He denied gross hematuria, dysuria, weight loss, or constitutional symptoms. Past surgical history included a right hydrocelectomy with associated bilateral inguinal node swelling and tenderness occurring approximately thirty years ago. The patient denied postoperative complications, and his adenopathy resolved “with medications.” He has resided in Northern California for fifteen years, having emigrated from Eastern Australia. Physical examination was remarkable for a distended and tender bladder. There was no adenopathy, edema, or hydrocele. Spontaneous passage of a proteinaceous clot per urethra relieved his obstructive symptoms, following which his urine was seen to be milky white. A gelatinous plug had settled to the bottom of the specimen cup. Analysis revealed protein (4 + ) with 4-8 white and 3-5 red blood cellslhpf. No bacteria or casts were seen. Sudan III stain was
UROLOGY
i JUNE1987
/ VOLUMEXXIX,NUMBER6
positive for the presence of urinary fat. Urine cultures for routine bacteria and tuberculosis were negative. Creatinine, blood urea nitrogen, and complete blood count were normal; however, a differential white blood cell count showed 19 per cent eosinophils. Serum albumin and total protein were slightly below the lower limits of normal. Although microfilariae were not found in either urine or blood smears, indirect hemagglutination studies were positive for the presence of antifilarial antibodies. An intravenous pyelogram was unremarkable. A lymphangiogram showed segmental dilatation of varices in both iliac and right paracaval lymphatics as well as prominent paracalyceal channels bilaterally. Collateral lymphatic channels were obvious. The para-aortic lymph nodes were abnormal, some displaying large filling defects (Fig. 1). Thoracic duct was patent. The urine cleared over a twelve-hour period, and the patient was discharged and prescribed a low-fat diet. Follow-up examination was unretern. l1 Benzopyrone, a medication for chronicand uroflow studies ruled out persistent bladder outlet obstruction. Comment Filariasis refers to a variety of conditions caused by infestation with nematodes. The most common of these parasites is Wuchereria bancrofti with others being Brugia, Echinococcus, Cysticercus, and Ascaris species. The
643
disease is transmitted via a mosquito and is endemic to tropical and subtropical countries where vector infestation is heavy. The life cycle of these parasites proceeds from man to mosquito and back through a series of larval stages. The worm matures to adulthood in the salivary gland of the mosquito. Once injected through the human epidermis, the parasites migrate to and multiply within the lymphatic system. They release microfilariae in a circadian fashion (usually at night), at which time a blood smear may document their presence. Microfilaremia (carrier state) is detected in only lo-40 per cent of cases. 5,6It is the local reaction toward the adult worms within the lymphatic system, not the microfilaremia, that causes all pathologic reactions within the host. The course of the disease can be divided into three phases. The latent (or incubation) period lasting months to years is subclinical and represents a low-grade allergic reaction to exoantigens contained on live worms. The lymphangiectasis which ensues is mild, reversible, and usually remits spontaneously. The second (or acute) phase represents a full-blown allergic (Arthus) response to the somatic antigens of dead worms. This causes granulomatous lymphangitis and lymphadenitis. Presenting symptoms include fever, weight loss, funiculoepididymitis, orchitis, filarial abscess, genital edema or adjacent thrombophlebitis. An acute hydrocele is common and of interest is the fact that these do not transilluminate. The third (or chronic) phase occurs five to twenty years after the primary infestation. Recurrent localized inflammatory reactions destroy existing collateral lymphatic channels, causing progressive fibrosis of previously edematous tissues.’ Ultimately, obliteration of lymphatic vessels occurs with subsequent lymphatic hypertension, the clinical expression of which depends on the degree and location of insult. Rupture of a lymphatic varix may occur in the pericardium, pleura, peritoneum, intestines, and joint spaces. Rupture in the urinary tract (usually at the level of the calyceal fornices) produces chyluria. This usually presents episodically, varying with the amount of fat ingested, occasionally with posture or following physical exertion, or may be associated with conditions predisposing to urostasis, such as pregnancy or benign prostatic hypertrophy. The incidence of detectable chyluria among patients with chronic filariasis is l-2 per cent,3 and of these, only 10 per cent display obstruc-
tive symptoms5 Elephantiasis of leg, scrotum, or penis is the hallmark of this stage. Massive urinary protein loss can cause a nephrotic syndrome or frank anasarca. Superinfection is common, and bacterial prophylaxis is recommended. Diagnosis of filariasis is suspected with the proper symptomatology in endemic areas and confirmed by the detection of microfilariae in peripheral blood smear, chylous urine, or hydrocele fluid. Analysis of chylous urine confirms its lymphatic components. Eosinophilia is common. Calcification of lymphatic channels or hydrocele sacs occurs frequently and may be noted on plain films of the abdomen. Sudan III administered orally stains chylous particles in the urine bright orange. Complement fixation and skin tests exist. Dirofilaria immitis contains surface antigens common to all filarial worms and comprises the basis for an indirect hemagglutination test. Antibodies are noted up to twenty years after active disease. When chyluria exists, cystoscopic examination may document the renal unit involved, especially following the administration of a highfat diet, which exacerbates chylous leak. Intravenous pyelography may document obstruction or pyelonephritic changes, but rarely identifies fistulous communications. Lymphangiography remains the roentgenographic procedure of choice to confirm both lymphatic involvement as well as sites of pyelolymphatic fistulae.8Te Typically, in the early stages of disease, the lymphatic tree is dilated, tortuous, and lengthened compared with the unaffected side. With advanced disease, mottled defects of the nodes and even skipped lymphatic chains are frequently seen. Similar findings may be noted in advanced carcinoma and malignant lymphomas. Treatment is a function of the stage and severity of disease and is divided into medical and surgical management. Low-fat diets consisting of short-chain fatty acids are suggested since these are absorbed via the portal rather than the lymphatic system. Diethylcarbamazine is the drug of choice in filarial disease and has been purported to destroy and/or sterilize female worms.1° In addition, microfilariae are sensitized so that they become more susceptible to phagocytosis by the reticuloendothelial system.” Benzopyrone, a medication for chronicstage disease, enhances the resorption of accumulated interstitial protein (the cause of lymphedema), thereby diminishing the tissue
644
UROLOGY
/
JUNE 1987
I
VOLUME XXIX, NUMBER 6
swelling. l2 However, because of the episodic nature of the disease, it becomes difficult to assess the efficacy of any therapeutic measure. Although the majority of cases resolve spontaneously or with medical treatment, refractory disease may require surgical intervention. l3 With regard to chyluria, various sclerosing agents introduced into the renal pelvis have been proposed in the hope of chemically cauterizing the fistulous tracts.12 Endoscopic cauterization has been advised in the event of lymphovesical fistulization. Capsulectomy with stripping of the renal pedicle lymphatics is advocated by Torres and Estrada.14 Some recommend ligation of lymphatic varices,12 while others suggest nephrectomy in symptomatic cases. In addition, both retrograde pyelography and lymphangiography have documented therapeutic effects in curtailing or even eliminating chylous leak.5J5 Filariasis has been virtually nonexistent in the United States. However, with increasing immigration, its prevalence is sure to climb. Knowledge of the disease will facilitate its diagnosis and management. Sacramento,
UROLOGY
I JUNE 1987
4301 X Street California 95817 (DR. SHERMAN)
/ VOLUME
XXIX, NUMBER
6
References 1. Date A, Padankatti T, Vaska PH, and Shastry JCM: Lymphocytopenia in chyluria, Trans R Sot Trop Med Hyg 74: 137 (1980). 2. Bai KI, Sastry VN, and Subbaiah DV: Chyluria in childhood, Indian Pediatr 14: 229 (1977). 3. ‘Klousia JW, McClennan BL, and Semerjian BS: Chyluria: a case report and brief literature review, J Urol 117: 393 (1977). 4. Johnston DW: Chyluria: case report and review of literature, Ann Intern Med 12: 931 (1955). 5. Shankar PJ, Gandhi GM, and Rao MS: Clinical and lymphangiographic studies in haematochyluria, J Assoc Physicians India 23: 553 (1975). 6. Saigo C: A study of filariasis in Okinawa, Kuwamotos IGK z 15: 173 (1939). 7. Okamoto K, and Ohi Y: Recent distribution and treatment of filarial chyluria in Japan, J Urol 129: 64 (1983). 8. Gagnon JH: Lymphangiography in filarial chyluria, J Can Assoc Radio1 25: 319 (1974). 9. Callahan DH, Graf EC, Gersack J, and Turbow AM: Lymphangiography and simultaneous excretory urography as a diagnostic aid in chyluria, J Urol 93: 417 (1965). 10. Von Lichtenberg F, and Lehman JS: Parasitic diseases of the genitourinary system, in Harrison JH, et al (Eds): Campbell’s Urology, ed 4, Philadelphia, WB Saunders Company, 1-615, 1978. 11. Zerner J, and Barber HRK: Puerperal chyluria, NY State J Med 77: 414 (1977). 12. Yamauchi S: Chyluria, in Kaufman JJ,: Current Urologic Therapy, Philadelphia, WB Saunders Company, 1980, p 54. 13. Mahadevan R: Surgical aspects of filariasis, Trop Doct 8: 28 (1978). 14. Torres LF, and Estrada J Jr: Experiences in the treatment of chyluria, J Urol 87: 73 (1962). 15. Akisada M, and Tani S: Filarial chyluria in Japan, Radiology 90: 311 (1968).
645