Journal of Postgraduate Medicine
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Year : 1984  |  Volume : 30  |  Issue : 1  |  Page : 27-32  

ASO titre and serum complement (C3) in post-streptococcal glomerulonephritis.

KJ Shroff, RR Ravichandran, VN Acharya 
 

Correspondence Address:
K J Shroff





How to cite this article:
Shroff K J, Ravichandran R R, Acharya V N. ASO titre and serum complement (C3) in post-streptococcal glomerulonephritis. J Postgrad Med 1984;30:27-32


How to cite this URL:
Shroff K J, Ravichandran R R, Acharya V N. ASO titre and serum complement (C3) in post-streptococcal glomerulonephritis. J Postgrad Med [serial online] 1984 [cited 2020 Dec 5 ];30:27-32
Available from: https://www.jpgmonline.com/text.asp?1984/30/1/27/5489


Full Text



 INTRODUCTION



The concepts regarding the pathology of acute glomerulonephritis have changed considerably over the decades. With the advent of renal biopsy, an invasive procedure, histology has evolved itself as an important tool in the diagnosis and prognosis of glomerulonephritis.[1],[9],[12] However, in post-streptococcal glomerulonephritis (PSGN) the kidney biopsy reveals typical but not pathognomonic features.[3],[8],[15] This paper emphasises the value of combined estimations of ASO titres and C3 levels in the definitive noninvasive diagnosis of PSGN in patients presenting as acute nephritic syndrome.

 MATERIAL AND METHODS



One hundred and fifty one cases of glomerulonephritis followed up in the Nephrology Department of the K.E.M. Hospital, Bombay, were studied during a period of 3 years. The diagnosis of glomerulonephritis was confirmed by kidney biopsy in 101 cases. Fifty cases who had a benign and self-limiting course on clinical and laboratory grounds were not subjected to biopsy. There were 77 males and 74 females with an age range from 2-45 years. Sixty two patients belonged to the group of PSGN and 89 to non-streptococcal glomerulonephritis (NSGN). This group of NSGN included patients of minimal change glomerulonephritis, focal proliferative glomerulo. nephritis, mesangioproliferative glomerulonephritis, membranous glomerulonephritis, focal sclerosing glomerulonephritis and systemic collagenosis. All these patients presented with features of acute nephritic illness. The diagnosis of PSGN was made on the basis of 2 or more of the following criteria- (a) history of preceding sore throat or skin infection; (b) isolation of streptococci from skin or throat; (c) serological evidence of recent streptococcal infection and (d) exudative proliferative glomerulonephritis on renal histology. The diagnosis of NSGN was on the basis of renal histology.

Fifty four patients were studied within a week of apparent or symptomatic onset of the illness and 97 patients were studied at variable intervals after the onset of the disease. ASO titres and C3 levels were estimated in all these patients at the beginning and later on between the periods of 1-5 months, 6-10 months and after 10 months. ASO titre was estimated by a W.H.O. technique.[14] An Indian standard prepared by the Department of Microbiology, Lady Hardinge Medical College, New Delhi was used for the purpose. The C3 was estimated by the single radial immuno diffusion technique.[10] ASO titres were also estimated in 20 healthy controls between the ages of 1-40 years and C3 in 50 healthy controls.

 RESULTS



As seen in [Table 1], in patients having glomerulonephritis whether PSGN or otherwise there is an elevation of ASO titres as compared to the normal population (p < 0.001) at the time of the study. But the elevated titres are significantly higher in the PSGN group than in the NSGN group (p < 0.05). Also the C3 values are lower in both the group of patients of glomerulonephritis. (PSGN: p < 0.01; NSGN: p < 0.05).

However, as shown in [Table 2], at the onset of illness, the elevation of ASO titres and fall in the C3 levels are greater in the PSGN group as compared to the NSGN group (p < 0.01 and p < 0.001 respectively). 96% of the patients belonging to the group of PSGN and 51.7% of patients belonging to the NSGN group showed elevated ASO titres at the onset of the illness.

Follow-up studies

Although at the onset of the illness, the ASO titres are elevated in 96% of the patients belonging to the PSGN group, with advancing time there is a considerable fall in the number of patients having a raised titre [Table 3]. However, in the NSGN group the percentage of patients having raised ASO titres is more or less constant even after a follow up of 2 years.

At the onset of illness, 88% of patients in the PSGN group had significantly low values of C3 which returned to normal in 957o of the patients within 2 months; whereas in the NSGN, no such definite relationship of C3 levels to time interval could be found [Table 4].

 DISCUSSION



The etiologic role of Lancefield Group A streptococci in acute glomerulonenphritis is well established. [3],[4],[5],[8],[15] However, an acute nephritic syndrome clinically resembling that related to streptococcal infection may occur after many other bacterial, viral and parasitic infections. In overcrowded cities like Bombay, streptococcal sore throat is very common and often affects large population in the city. Moreover, in such populations many varieties of the primary glomerulonephritis not known to be related to infections may also present themselves with a picture of acute nephritis (NSGN). Predominant amongst these latter diseases are idiopathic membranoproliferative glomerulonephritis and mesangial proliferative glomerulonephritis. Multisystem diseases like systemic lupus erythematosus, infective endocarditis etc. may also provoke an acute nephritic syndrome. The histological features of PSGN on light microscopy may also be shared by some of these varieties of glomerulonephritis. Hence, the diagnosis of PSGN based on the classical documentation of preceding streptococcal infection may be largely questionable. The antibody response to extracellular products of streptococci, though not protective, are useful markers of recent infection.[11] ASO titre is the most convenient model of antibody because it is easily titrated and more likely to be evaluated after a streptococcal throat infection[8],[13] particularly so, in any smaller centre. This however, may not establish the cause and effect relationship in every case.

In the present study, the ASO titre was elevated in 96% of the subjects in the PSGN group as compared to 51.7% in the NSGN group at the clinical onset of the disease; this may indicate that mere reliance on elevation of ASO titre as a diagnostic aid when presented with a problem of acute nephritic illness can be misleading. A part of the elevation in the NSGN group may be related to the interference of ASO titre estimations by the elevated cholesterol, leading to false positive results;[8] but, in the present study this could not be documented in more than 20 of the NSGN patients. Hinglais et al,[6] in their study of "American individuals", found elevated ASO titre in two patients with NSGN. In overcrowded Bombay city, as already mentioned, both streptococcal sore throat and other non-infectious forms of acute nephritis are quite common and elevated ASO titres in them may be due to non-nephritogenic streptococcal infection.. Hence in such a situation mere elevation of ASO titre alone cannot be taken as diagnostic of PSGN in patients suffering from acute nephritic illness.

One of the most important laboratory parameters utilised in the investigation of patients with acute glomerulonephritis is the serial estimations of complement components. There is ample evidence to suggest prominent involvement of alternative pathway of complement activation in patients with PSGN.[4],[5],[16] In the present series also, C3 was found to be low in 88% of the patients at the onset of illness in the PSGN group. These levels returned to normal in 95% of the patients within a period of 8 weeks. Similar results have been observed by several other workers.[2],[6],[13],[15],[16] On the other hand, in the NSGN group although initially 38% had low C3 values, in only 15% of the patients the C3 levels returned to normal within 8 weeks after the clinical onset of the disease. The combination of raised ASO titres with low values of C3 returning to normal within 8 weeks was seen in 81% of the patients in the PSGN group. Though a similar combination was seen in the NSGN group it involved only 4.5% of patients. Hence the combination estimations of ASO titres and C3 levels done at the clinical onset of acute glomerulonephritis and repeated after 8 weeks helped in the definitive diagnosis of PSGN in large percentage of cases. It further helped in differentiating this group of. patients from acute glomerulonephritis of non-streptococcal origin who would need renal biopsy for the definitive diagnosis and prognosis. This observation becomes particularly useful under Indian conditions where patients are agreeable to simple non-invasive methods of diagnosis as opposed to invasive methods like renal biopsy, which may not even be available in many of the smaller centres.

References

1Badin, J. and Cabin, N.: Path. Bio. (1959): As quoted by Glassock R. J., Cohe, A. H., Bennet, C. M. and Maldonado, M. M.: "Primary Glomerular Diseases in The Kidney" 2nd Edition, Editors--Brenner, B. M., and Rector, F. C., W. B. Saunders Company, Phladelphia 1981., p. 1377.
2Baldwin, D. S., Gluck, M. C:, Schacht; R. G. and Gallo, H.: The long term course of post-streptococcal glo2nerulonephritis. Ann. Intern. Med., 80: 342-358, 1974.
3Dodge, W. F., Spargo, B. H., Travis, L. B., Srivastava, R., Carvajal; H., De Benkelaer, M. D., Langley, M. P. and Menchaca, J. A.: Post-streptococcal glomerulonephritis-a prospective study in children. New Engl. J. Med., 286: 273-278, 1972.
4Fish, A. J., Herdman, R. L., Machael A. F., Pockering, R. J. and Good, R. A.: Epidemic acute glomerulonephritis associated with type 49 streptococcal pyoderma; II-correlative study of light, immunofluorescent and electron microscopic findings. Amer. J. Med., 48: 28-29, 1970.
5Glassock, R. J., Cohen, A. H., Benett, C. M. and Maldonado, M. M.: Primary Glomerular Diseases. In, "The Kidney" 2nd Edition. Editors-Brenner, B. M., Rector, F. C., Jr., W. B. Saunders Company, Philadelphia, 1981, pg. 1373.
6Hinglais, N., Garcia, T. R. and Kleinknocht, D., Long term prognosis in acute glomerulonephritis; The predictive value of early clinical and pathological features observed in 65 patients. Amer. J. Med., 56: 52-60, 1974.
7Kaplan, E. L. and Wannamaker, L. W.: Suppression of ASO response by cholesterol and by lipid extracts of rabbit skin. J. Exp. Med., 144: 754-767, 1976.
8Kassirer, J. P. and Schwartz, W. B.: Acute glomerulonephritis. New Engl. J. Med., 265: 686-692 and 736-740, 1961.
9Lewy, J. E., Salinas-Madrigal, L., Herdson, P. B., Pirani, C. L. and Metioff, J.: Clinicopathologic correlation in acute post-streptococcal glomerulonephritis. Medicine, 50: 453-501, 1971.
10Mancini, G., Carbonara, A. D. and Heremans, J. F.: Immunochemical quantitation of antigens by single radial immunodiffusion. Immunochemistry, 2: 235-237, 1965.
11Nissenson, A. R., Baraff, L. J., Fine, R. N. and Khutson, D. W.: Post-streptococcal acute glomerulonephritis; fact and controversy. UCLA Conference. Ann. Intern. Med., 91: 76-86, 1979.
12Peter, G. and Smith, A. L.: Lancefield Group A streptococcal infection of the skin and pharynx. New Engl. J. Med., 297: 311-317, 1977.
13Popovic-Rolovic, M.: Serum C3 levels in acute glomerulonephritis and postnephritic children. Arch. Dis. Child., 48: 622-626, 1973.
14Rotta, J.: Determination of antistreptolysin, O.: "W.H.O. Manual of Reference Procedures in Streptococcal Bacteriology and Serology". 1976, p. 19.
15Sagel, I., Treser, C., Ty, A., Yoshizawa, N., Kleinberger, H., Ynceoglu, M., Wasserman, E. and Lange, K.: Occurrence and nature of glomerular lesions after Group A streptococci infections in children. Ann. Intern. Med., 74: 492-499, 1973.
16Strife, C. F., McAdam, A. J., McEnery, P. T., Bore, K. E. and West, C. D.: Hypocomplementemic and normocomplementemic acute nephritis in children-a comparison with respect to etiology, clinical manifestations and glomerular morphology. J. Paediatr., 84: 29-38, 1974.

 
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