Scandinavian Journal of Infectious Diseases

ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19

Acute Glomerulonephritis Complicating Australia Antigen-Negative Viral Hepatitis Robert V. Hague To cite this article: Robert V. Hague (1975) Acute Glomerulonephritis Complicating Australia Antigen-Negative Viral Hepatitis, Scandinavian Journal of Infectious Diseases, 7:4, 277-279, DOI: 10.3109/inf.1975.7.issue-4.10 To link to this article: http://dx.doi.org/10.3109/inf.1975.7.issue-4.10

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Date: 17 April 2016, At: 13:06

Scand J Infect Dis 7: 277-279, 1975

Case Report

Acute Glomerulonephritis Complicating Australia Antigen-negative Viral Hepatitis ROBERT V. HAGUE From The Royal Hospital, Sheffield, England

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ABSTRACT. A case of acute glomerulonephritis complicating Australia antigen-negative hepatitis in a 17-year-old man is described. The literature relating the onset of glomerulonephritis to virus infection is general, and to that of hepatitis in particular, is reviewed.

INTRODUCTION Subclinical renal involvement occurs commonly in acute viral hepatitis, the changes in renal function usually being transient (5). Occasionally, glomerulonephritis occurs in association with persisting Australia (Au) antigenaemia (4, 12). This paper reports a patient in whom an attack of acute nephritis complicated Au antigen-negative hepatitis.

CASE REPORT A 17-year-old male developed anorexia, nausea, general tiredness and pruritus in December 1972, which lasted for 2 weeks. These symptoms returned in March 1973, but were then associated with deep jaundice, dark urine and pale stools. He had also lost weight and had noticed considerable sweating. There was no history of contact with a jaundiced patient, nor of exposure to drugs or chemicals. He had been tattooed 12 months previously. There had been no recent sore throat. On examination in May 1973 he was deeply jaundiced and there were pumerous scratch marks on his skin as a result of the pruritus. The liver was slightly enlarged and he was afebrile. The blood pressure was 130/85 and there was no abnormality in the cardiovascular, respiratory or central nervous systems. Investigations performed in May indicated viral hepatitis. Serum bilirubin was greater than 10 mg/lOO ml (normal 0-1.0), serum aspartate aminotransferase (SOOT) 1300 U/ml (normal 0-30), serum alanine aminotransferase (SOPT) 1200 U/ml (normal 0-30), and alkaline phosphatase 15 King U (normal 3-15). The serum albumin was 2.8 g/lOO ml (normal 3.5-5.5), IgO 2600 mg/lOO ml (normal 500-1600), IgM 215 mg/lOO ml (normal 37-170), and IgA 300 mg/lOO ml (normal 125-424). Immunoelectrophoresis and immunodiffusion methods for detecting Au antigen were negative. Immunodiffusion,

electrophoresis and haemagglutination techniques failed to detect antibodies to Au antigen. Tests for antinuclear factor, anti mitochondrial antibody, smooth muscle antibody and alpha fetoprotein were negative. Hb was 14.5 g/l 00 ml, WBC 5 OOO/mm 3 , platelets 225 OOO/mm 3 , a blood film normal. Blood urea and serum electrolytes were normal. Urinalysis revealed a trace of protein in one of two samples tested and a midstream urine specimen showed no abnormality on microscopy and no growth on culture. The subsequent clinical course of the patient is shown in Fig. I. As the jaundice was subsiding and he was improving symptomatically, it was not felt that a liver biopsy was indicated. However, by mid-June he began to feel tired, his face, hands and legs became swollen and he noticed some backache and shortness of breath. His weight increased by 9 kg and examination revealed marked ankle and sacral oedema, ascites, bilateral pleural effusions and pulmonary oedema. The jugular venous pressure was raised and the blood pressure had risen to 190/120. Blood urea was 77 mg/lOO ml (normal 20-50) and urine 24 hour protein output 8.6 g. Microscopy of the urinary deposit revealed 4 WBC/HPF, 3 RBC/HPF and hyaline and granular casts. A chest X-ray revealed an enlarged heart and pulmonary oedema. Serum creatinine was 1.4 mg/lOO ml (normal 0.7-1.4), and creatinine clearance 30 ml/min (normal >80). Hb was 11.5 g/IOO ml, and ESR 47 mm/l hr. A throat swab was normal and the slide agglutination test for leptospirosis was negative. The antistreptolysin 0 (ASO) titre and serum cholesterol were normal. The hepatic enzymes were still slightly elevated (SOOT 33 U/ml and SOPT 41 Ujml), and the serum albumin was still reduced at 3.3 g/lOO ml. He was given frusemide in doses up to 500 mg daily and within 6 days his weight had fallen to normal. His hypertension was quickly controlled by frusemide and methyldopa 250 mg 3 times daily, and both drugs were withdrawn within a week. His blood urea rose transiently to 110 mg/lOO ml, but quickly returned to normal. Liver function tests returned completely to normal by the end of July. Proteinuria and mild hypertension persisted for sevScand J Infect Dis 7

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R. V. Hague

SERUM BILIRUBIN (mg. per 100m!.)

BLOOD UREA I mg. per 100ml.)

URINE PROTEIN (g. per 24 hr. )

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BODY WEIGHT I kg.)

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Fig. I. Changes in serum bilirubin,

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eral months, but by December, 1974 no protein was detectable in his urine and he was normotensive. It was not, therefore, felt justifiable to do a renal biopsy.

DISCUSSION Over recent years it has become increasingly apparent that subclinical renal involvement occurs in many viral infections which predominantly affect other tissues. Renal changes in the form of haematuria and proteinuria have been observed in patients infected with mumps (9, 14), and with echoviruses (II, 16). Glomerulonephritis has been noted on renal biopsy in coxsackievirus (2), adenovirus (3), and vaccinia virus infections (8). More recently acute nephritis has been noted in association with infectious mononucleosis (15). Acute viral hepatitis is a multisystem disease (5). Renal morphological and functional alterations are common, the former being represented by interstitial oedema, swelling of the tubular epithelium and segmental proliferative glomerular changes. The latter are represented by reduced renal concentrating ability, proteinuria, haematuria, pyuria and cylindruria. These changes are usually of minor degree and short-lived. Gross renal function, as determined by the blood urea and serum creatinine, is usually normal, but creatinine clearance is occasionally reduced. Increased protein excretion occasionally persists for as long as 4 months after the acute episode, but recovery, both functional and histological, is usually complete. There is some evidence that the renal changes may be a consequence of the renal deposition of immune comScand J Infect Dis 7

I

JULY

-1

blood urea, urine protein and body weight from May to July, 1973 (+represents results of" Albustix" (Ames) testing of urine for protein.)

plexes and it has been suggested that a chronic process could occasionally be initiated leading to a more serious impairment of renal function in some patients (7). It is not clear whether pre-existing renal disease can be worsened by an attack of acute viral hepatitis. It is generally accepted that deposition of immune complexes in glomeruli is related to the development of glomerulonephritis (6), and it is thought to be those situations in which there is a relatively poor antibody production with persistent circulation of antigen-antibody complexes which cause nephritis. There is much evidence that virus antibody complexes can lead to glomerulonephritis in animals, but so far there is little evidence for its occurrence in man (13). To date there are only a few reports incriminating the virus of hepatitis in the development of persisting glomerulonephritis. In one, membranous glomerulonephritis occurred as a sequel to posttransfusion hepatitis (4). The renal disease revealed itself clinically after many months of continued hepatic activity. Immunofluorescent staining of the kidney tissue showed glomerular deposits of Au antigen, IgG and complement in a pattern characteristic of immune complex deposition. A more recent report (12) describes a similar case in which persistent viral hepatitis was associated with the development of a membranoproliferative glomerulonephritis with deposition of Au antigencontaining complexes in the glomeruli. In both cases the renal involvement was associated with persisting hepatic disease and Au antigenaemia.

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Acute nephritis complicating hepatitis Recently a high incidence of Au antigencontaining immune complexes was noted in kidney biopsy material obtained from children with various forms of glomerulonephritis without clinically apparent liver disease (I). The case described here differs from those previously reported in that the nephritis presented itself clinically when the patient had recovered from the hepatitis and his liver function tests had almost returned to normal. Its interest also lies in the fact that it would appear to be the first report describing glomerulonephritis occurring in association with Au antigen-negative hepatitis. How often persisting renal disease follows viral hepatitis is not clear and it may be that viral infections playa greater part than is recognised in the production of renal disease in man (10, 13).

ACKNOWLEDGEMENTS I would like to thank Dr C. E. Davies for permission to investigate his patient and Dr D. R. Cullen and Dr M. Platts for helpful advice and criticism.

279

10. Leading article: Virus infection of the kidney and urinary tract. Lancet I: 19, 1974. I!. Mary, A. S. & Swallow, J. H.: An epidemic of ECHO 6 virus infection. Postgrad Med J 46: 265, 1970. 12. Myers, B. D., Griffel, B., Naveh, D., Jankielowitz, T. & Klajman, A.: Membrane-proliferative glomerulonephritis associated with persistent viral hepatitis. Am J Clin Pathol 59: 222, 1973. 13. Smith, R. D. & Aquino, J.: Viruses and the kidney. Med Clin North Am 55: 89, 1971. 14. Utz, J. P., Houk , V. N. & Alling, D. W.: Clinical and laboratory studies of mumps. N Engl J Med 270: 1283, 1964. 15. Woodroffe , A. J., Row, P. G., Meadows, R. & Lawrence, J. R.: Nephritis in infectious mononucleosis. QJMed43:451,1974. 16. Yucloglu, A. M., Berkovich , S. & Minkowitz , S.: Acute glomerulonephritis associated with ECHO virus type 9 infection. J Pediatr 69: 603, 1966.

Address for reprints: R. V. Hague, The Royal Hospital, West Street, Sheffield S1 3SR, England

REFERENCES

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Brzoska, W. J., Krawczynski, K., Nazarewicz, T., Morzycka, M. & Nowoslawski, A.: Glomerulo-

nephritis associated with hepatitis-B surface antigen immune complexes in children. Lancet 2: 477, 1974. Burch, G. E. & Colcolaugh, H. L.: Progressive coxsackie viral pancarditis and nephritis. Ann Intern Med 71:963,1969. Chany, C., Lepine, P., Lelong, M., Le-tan-Vinh, S. P. & Virat, S.: Severe and fatal pneumonia in infants and young children associated with adenovirus infections. AmJ Hyg67:367, 1958. Combes, B., Stastny, P., Shorey, J., Eigenbrodt, E. H., Barrera, A., Hull, A. R. & Carter, N. W.: Glomerulonephritis with deposition of Australia antigen-antibody complexes in glomerular basement membrane. Lancet 2: 234, 1971. Conrad, M. E., Szhwartz , F. D. & Young, A. A.: Infectious hepatitis-A generalised disease. A study of renal, gastrointestinal and hematologic abnormalities. Am J Med 37: 789, 1964. Dixon, F. J.: The pathogenesis of glomerulonephritis. Am J Med 44: 493, 1968. Eknoyan, G., Gyorkey, F., Dichoso, C., MartinesMaldonado, M., Suki, W. W. & Gyorkey, P.: Renal morphological and immunological changes associated with acute viral hepatitis. Kidney Int I: 413, 1972. Herbut, P. A.: Diffuse glomerulonephritis following revaccination for smallpox. Am J Pathol 20: lOll, 1944. Hughes, W. T., Steigman, A. J. & Delong, H. F.: Some implications of fatal nephritis associated with mumps. Am J Dis Child III: 297, 1%6. Scand J Infect Dis 7

Acute glomerulonephritis complicating Australia antigen-negative viral hepatitis.

A case of acute glomerulonephritis complicating Australia antigen-negative hepatitis in a 17-year-old man is described. The literature relating the on...
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