Scandinavian Journal of Infectious Diseases
ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19
Acute Tubulointerstitial Nephritis in a Patient with Mycoplasma Pneumoniae Infection Amos Pasternack, Heikki Helin, Tuomo Vånttinen, Greta Jårventie & Timo Vesikari To cite this article: Amos Pasternack, Heikki Helin, Tuomo Vånttinen, Greta Jårventie & Timo Vesikari (1979) Acute Tubulointerstitial Nephritis in a Patient with Mycoplasma Pneumoniae Infection, Scandinavian Journal of Infectious Diseases, 11:1, 85-87, DOI: 10.3109/ inf.1979.11.issue-1.15 To link to this article: http://dx.doi.org/10.3109/inf.1979.11.issue-1.15
Published online: 02 Jan 2015.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=infd19 Download by: [RMIT University Library]
Date: 08 May 2016, At: 11:37
Scand J Infect Dis 1 I : 85-87, 1979
Case Report
Acute Tu bulointerstitial Nephritis in a Patient with Mycoplasma pneumoniae Infection AMOS P A S T E R N A C K , HEIKKI HELIN, TUOMO V A N T T I N E N , G R E T A JARVENTIE and TIM0 VESIKARI
Downloaded by [RMIT University Library] at 11:37 08 May 2016
From the Departments of Clinical and Biomedical Sciences, University of Tampere, and Tampere Central Hospital, Tampere, Finland
ABSTRACT. A 26-year-old man developed pneumonia, hepatitis and biopsy-verified acute tubulointerstitial nephritis coinciding with a rise and fall of complement-fixing antibodies to Mycoplasma pneumoniae. M. pneumoniae antigenic material and complement (C3) in the renal interstitium were shown by immunohistochemical techniques. A causal relationship between M. pneumoniae infection and the renal lesion is suggested.
INTRODUCTION Acute tubulointerstitial nephritis is seen in association with various systemic infections (6). W e report a case in which Mycoplasma pneumoniae infection was considered to b e the cause of acute tubulointerstitial nephritis. This etiologic association has not hitherto been recognized.
CASE REPORT A previously healthy 26-year-old man was admitted to hospital complaining of abdominal pain, backache and fever of about 12 h duration. Local tenderness was observed in the renal area. An intravenous pyelogram showed symmetric, slightly delayed excretion without signs of obstruction. A chest X-ray film showed patchy pneumonic infiltrations on the right side. Blood pressure was 150/80 mmHg. Rectal temperature was 39.1"C. Laboratory investigations showed hemoglobin 132 g/l; serum creatinine 175 pmol/l; ESR 44 mmlh; alanine aminotransferase 36 U/l; serum complement levels C 3 1.0 g/l, C 4 0.5 g/l; antinuclear antibodies negative; antistreptolysin-0 titre 450; urinary protein 4.95 g/24 h; erythrocytes 8-12/high power field, leukocytes 5-8/high power field. Urinary bacterial culture was negative. Complementfixing (CF) antibodies to M. pneumoniae were detected in serum at a dilution of 1 : 32. Ampicillin was started at admission and given for 12 days in a dose of 2 g/day. The patient had fever up to 39.0"C during the first 9 days. On the 10th to 14th day a chest X-ray, serum creatinine, urinary sediment and urinary protein were normal. The M. pneumoniae C F antibody titre had risen to 256. 12 days after admission serum alanine aminotransferase was 97
U/l and aspartyl aminotransferase 52 U/l. Both enzymes were normal 1 month later. Four months later the M. pneumoniae antibody titre was 32 and the antistreptolysin-0 titre 450. Renal biopsy was performed on the 5th day after admission. Glomeruli were normal in light and electron microscopy and in the immunofluorescent study. In the interstitium there was patchy oedema and infiltration with mononuclear cells and some polymorphonuclears (Fig. 1). Deposits of C 3 were seen in arterioles and in the interstitium at the sites of the cellular infiltration. Some tubuli were atrophic or partly destroyed and contained erythrocytes. In a search for M. pneumoniae antigenic material possibly present in the renal lesion, the following indirect immunoperoxidase technique was used (3). Paraffin sections of the biopsy specimen were incubated with paired sera from a case of acute M. pneumoniae infection (acute stage serum with no demonstrable M. pneumoniae C F antibodies and convalescence serum with a CF antibody titre of 1024). The sections were then incubated with peroxidase-labelled anti-human-IgG serum followed by the diaminobenzidine reaction. A positive reaction was observed with the high-titre serum in areas corresponding to those where immunofluorescence showed the C 3 deposits (Fig. 1). Negative reactions were obtained with the serum not having demonstrable M. pneumoniae antibodies and with the peroxidase-labelled anti-human-IgG serum alone.
DISCUSSION This patient had clinically reversible pneumonia, hepatitis and tubulointerstitial nephritis coinciding with a rise a n d fall of antibodies t o M. pneumoniae. Sccind J Itifecr Dis I I
Downloaded by [RMIT University Library] at 11:37 08 May 2016
86
A . Pasternack et a l .
Fig. I. Photomicrograph of renal biopsy specimen showing interstitium with inflammatory cellular infiltration and ) black tubular destruction (left part, H and E, ~ 2 0 5 and
reaction product after staining with Mycoplasma pneumoniae convalescence serum and peroxidase-labelled antihuman-IgC serum (right part, x330).
M. pneumoniae, although usually regarded as a respiratory pathogen, may cause infections that involve other organs. Gastroenteritis, hepatitis, periand myocarditis, and central nervous system infections as well as dermatologic, musculoskeletal and hematological manifestations have been described (1). Moreover, M. pneumoniae has been isolated from the blood of a patient with septicemia (2). M. arthritidis has caused experimental pyelonephritis in rats (5). M. salivarium has been isolated from the renal cortex of a patient with focal glomerulonephritis and chronic focal pyelonephritis (4). In our patient the presence of M. pneumoniae antigenic material and C 3 in the renal interstitium suggests a causal relationship between the pathogen and the renal lesion. Other possible causes of acute
tubulointerstitial- nephritis (dehydration or shock, hemolysis, toxins or drugs, epidemic nephropathy) are excluded by the history, clinical findings and course of the disease.
REFERENCES 1. Murray, H. W., Masur, H., Senterfit, L. B. & Roberts,
R. B.: The protean manifestations of Mycoplasma pneumoniae infection in adults. Am J Med 58:229, 1975. 2. Naftalin, J. M., Wellish, G., Kahana, Z. & Diengott, D.: Mycoplasma pneumoniae septicemia. JAMA 228: 565, 1974. 3. Nakane, P. K. & Pierce, G. B.: Enzyme-labelled antibodies for light and electron microscopic localization of tissue antigens. J Cell Biol33: 307;- 1967. 4. Pachas, W. N.: The role of Mycoplasma in some unusual conditions of the kidney and the urinary tract. Ann NY Acad Sci 170: 786, 1970.
Nephritis in m y c o p l a s m a infection
81
5. Thomsen, A. C., Rosendal, S. & Thomsen, 0. F.: Mycoplasmosis: Experimental pyelonephritis in rats. Acta Pathol Microbiol Scand (A) 81: 379, 1973. 6. Zech, P., Bouletreau, R., Moskovtchenko, J. F., Beruard, M., Favre-Bulle, S., Blanc-Brunat, N. & Traeger, J.: Infection in acute renal failure. In: Advances in nephrology, p. 231 (ed. J. Hamburger, J. Crosnier & M. H. Maxwell). Year Book Medical Publishers, Chicago 1971.
Downloaded by [RMIT University Library] at 11:37 08 May 2016
Address for reprints: A . Pasternack, M.D., Department of Clinical Sciences, University of Tampere, Teiskontie 35, SF-33520 Tampere 5 2 , Finland
Scand J Itfect Dis I I
ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19
Acute Tubulointerstitial Nephritis in a Patient with Mycoplasma Pneumoniae Infection Amos Pasternack, Heikki Helin, Tuomo Vånttinen, Greta Jårventie & Timo Vesikari To cite this article: Amos Pasternack, Heikki Helin, Tuomo Vånttinen, Greta Jårventie & Timo Vesikari (1979) Acute Tubulointerstitial Nephritis in a Patient with Mycoplasma Pneumoniae Infection, Scandinavian Journal of Infectious Diseases, 11:1, 85-87, DOI: 10.3109/ inf.1979.11.issue-1.15 To link to this article: http://dx.doi.org/10.3109/inf.1979.11.issue-1.15
Published online: 02 Jan 2015.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=infd19 Download by: [RMIT University Library]
Date: 08 May 2016, At: 11:37
Scand J Infect Dis 1 I : 85-87, 1979
Case Report
Acute Tu bulointerstitial Nephritis in a Patient with Mycoplasma pneumoniae Infection AMOS P A S T E R N A C K , HEIKKI HELIN, TUOMO V A N T T I N E N , G R E T A JARVENTIE and TIM0 VESIKARI
Downloaded by [RMIT University Library] at 11:37 08 May 2016
From the Departments of Clinical and Biomedical Sciences, University of Tampere, and Tampere Central Hospital, Tampere, Finland
ABSTRACT. A 26-year-old man developed pneumonia, hepatitis and biopsy-verified acute tubulointerstitial nephritis coinciding with a rise and fall of complement-fixing antibodies to Mycoplasma pneumoniae. M. pneumoniae antigenic material and complement (C3) in the renal interstitium were shown by immunohistochemical techniques. A causal relationship between M. pneumoniae infection and the renal lesion is suggested.
INTRODUCTION Acute tubulointerstitial nephritis is seen in association with various systemic infections (6). W e report a case in which Mycoplasma pneumoniae infection was considered to b e the cause of acute tubulointerstitial nephritis. This etiologic association has not hitherto been recognized.
CASE REPORT A previously healthy 26-year-old man was admitted to hospital complaining of abdominal pain, backache and fever of about 12 h duration. Local tenderness was observed in the renal area. An intravenous pyelogram showed symmetric, slightly delayed excretion without signs of obstruction. A chest X-ray film showed patchy pneumonic infiltrations on the right side. Blood pressure was 150/80 mmHg. Rectal temperature was 39.1"C. Laboratory investigations showed hemoglobin 132 g/l; serum creatinine 175 pmol/l; ESR 44 mmlh; alanine aminotransferase 36 U/l; serum complement levels C 3 1.0 g/l, C 4 0.5 g/l; antinuclear antibodies negative; antistreptolysin-0 titre 450; urinary protein 4.95 g/24 h; erythrocytes 8-12/high power field, leukocytes 5-8/high power field. Urinary bacterial culture was negative. Complementfixing (CF) antibodies to M. pneumoniae were detected in serum at a dilution of 1 : 32. Ampicillin was started at admission and given for 12 days in a dose of 2 g/day. The patient had fever up to 39.0"C during the first 9 days. On the 10th to 14th day a chest X-ray, serum creatinine, urinary sediment and urinary protein were normal. The M. pneumoniae C F antibody titre had risen to 256. 12 days after admission serum alanine aminotransferase was 97
U/l and aspartyl aminotransferase 52 U/l. Both enzymes were normal 1 month later. Four months later the M. pneumoniae antibody titre was 32 and the antistreptolysin-0 titre 450. Renal biopsy was performed on the 5th day after admission. Glomeruli were normal in light and electron microscopy and in the immunofluorescent study. In the interstitium there was patchy oedema and infiltration with mononuclear cells and some polymorphonuclears (Fig. 1). Deposits of C 3 were seen in arterioles and in the interstitium at the sites of the cellular infiltration. Some tubuli were atrophic or partly destroyed and contained erythrocytes. In a search for M. pneumoniae antigenic material possibly present in the renal lesion, the following indirect immunoperoxidase technique was used (3). Paraffin sections of the biopsy specimen were incubated with paired sera from a case of acute M. pneumoniae infection (acute stage serum with no demonstrable M. pneumoniae C F antibodies and convalescence serum with a CF antibody titre of 1024). The sections were then incubated with peroxidase-labelled anti-human-IgG serum followed by the diaminobenzidine reaction. A positive reaction was observed with the high-titre serum in areas corresponding to those where immunofluorescence showed the C 3 deposits (Fig. 1). Negative reactions were obtained with the serum not having demonstrable M. pneumoniae antibodies and with the peroxidase-labelled anti-human-IgG serum alone.
DISCUSSION This patient had clinically reversible pneumonia, hepatitis and tubulointerstitial nephritis coinciding with a rise a n d fall of antibodies t o M. pneumoniae. Sccind J Itifecr Dis I I
Downloaded by [RMIT University Library] at 11:37 08 May 2016
86
A . Pasternack et a l .
Fig. I. Photomicrograph of renal biopsy specimen showing interstitium with inflammatory cellular infiltration and ) black tubular destruction (left part, H and E, ~ 2 0 5 and
reaction product after staining with Mycoplasma pneumoniae convalescence serum and peroxidase-labelled antihuman-IgC serum (right part, x330).
M. pneumoniae, although usually regarded as a respiratory pathogen, may cause infections that involve other organs. Gastroenteritis, hepatitis, periand myocarditis, and central nervous system infections as well as dermatologic, musculoskeletal and hematological manifestations have been described (1). Moreover, M. pneumoniae has been isolated from the blood of a patient with septicemia (2). M. arthritidis has caused experimental pyelonephritis in rats (5). M. salivarium has been isolated from the renal cortex of a patient with focal glomerulonephritis and chronic focal pyelonephritis (4). In our patient the presence of M. pneumoniae antigenic material and C 3 in the renal interstitium suggests a causal relationship between the pathogen and the renal lesion. Other possible causes of acute
tubulointerstitial- nephritis (dehydration or shock, hemolysis, toxins or drugs, epidemic nephropathy) are excluded by the history, clinical findings and course of the disease.
REFERENCES 1. Murray, H. W., Masur, H., Senterfit, L. B. & Roberts,
R. B.: The protean manifestations of Mycoplasma pneumoniae infection in adults. Am J Med 58:229, 1975. 2. Naftalin, J. M., Wellish, G., Kahana, Z. & Diengott, D.: Mycoplasma pneumoniae septicemia. JAMA 228: 565, 1974. 3. Nakane, P. K. & Pierce, G. B.: Enzyme-labelled antibodies for light and electron microscopic localization of tissue antigens. J Cell Biol33: 307;- 1967. 4. Pachas, W. N.: The role of Mycoplasma in some unusual conditions of the kidney and the urinary tract. Ann NY Acad Sci 170: 786, 1970.
Nephritis in m y c o p l a s m a infection
81
5. Thomsen, A. C., Rosendal, S. & Thomsen, 0. F.: Mycoplasmosis: Experimental pyelonephritis in rats. Acta Pathol Microbiol Scand (A) 81: 379, 1973. 6. Zech, P., Bouletreau, R., Moskovtchenko, J. F., Beruard, M., Favre-Bulle, S., Blanc-Brunat, N. & Traeger, J.: Infection in acute renal failure. In: Advances in nephrology, p. 231 (ed. J. Hamburger, J. Crosnier & M. H. Maxwell). Year Book Medical Publishers, Chicago 1971.
Downloaded by [RMIT University Library] at 11:37 08 May 2016
Address for reprints: A . Pasternack, M.D., Department of Clinical Sciences, University of Tampere, Teiskontie 35, SF-33520 Tampere 5 2 , Finland
Scand J Itfect Dis I I
