Nephro! Dial Transplant (1991) 6: 518-520 © 1991 European Dialysis and Transplant Association-European Renal Association
Nephrology Dialysis Transplantation
Case Report
J. H. Campbell1, G. Warwick2, M. Boulton-Jones2, A. McLay3, B. Jackson3 and R. D. Stevenson1 Departments of 'Respiratory Medicine, 2Renal Medicine and 3Pathology, Glasgow Royal Infirmary, Glasgow, UK
Introduction
anaemia (Hb 10.5 g/dl), normal white cell count, proteinuria (+ + + ) and haematuria on dipstick urinalysis, Mycoplasma pneumoniae infection remains an import- and hypoalbuminaemia (24 g/1). Intravenous ampicillin ant cause of community acquired pneumonia [1]. and erythromycin (2 g each daily) were started, but over Although a wide range of extrapulmonary manifest- the following week he developed progressive renal ations [2] have been described, its association with failure (urea 20 mmol/1, creatinine 610 jumol/1) and glomerulonephritis has been only sporadically reported increasingly heavy proteinuria (4.9-6.8 g/24 h). Serology revealed positive complement fixation test to [3-5]. Mycoplasma pneumoniae (titre 1:256) and influenza B, We describe the case of a 69-year-old man who suggesting recent infection. C4, C3 and C3d were presented with right-upper-lobe pneumonia and seronormal, antistreptolysis O titre was less than 200. Tests logical evidence of Mycoplasma pneumoniae and for antinuclear cytoplasmic antibody and antiglomeruinfluenza B infection who developed rapidly progressive lar basement membrane were negative. Fibreoptic glomerulonephritis and nephrotic syndrome. bronchoscopy was normal. In view of the deteriorating renal function a percutaneous renal biopsy was performed on day 6. This showed a diffuse proliferative glomerulonephritis with a Case Report few glomeruli showing crescent formation (7%) (Fig. 1). Ultrastructural examination showed scanty subenIn May 1988 a 69-year-old man presented with a 6-week dothelial and mesangial electron-dense deposits history of exertional breathlessness, expectoration of together with focal intraluminal monocyte aggregation. scanty sputum and fever. There had been no response to This pattern, together with the immunohistochemical a course of antibiotics at home. He had smoked 20 findings of scattered foci of granular loop IgM and C3, cigarettes per day since the age of 20. There was no raised the possibility of a postinfectious glomerulonephrelevant past history. On admission a chest X-ray ritis of the type usually encountered in deep-seated showed right upper lobe consolidation. Relevant labor- visceral infections [7]. The patient's renal function atory investigations demonstrated mild renal failure deteriorated further and he required dialysis. A second with urea (7.4 mmol/1) and creatinine (130 /zmol/1), renal biopsy performed on day 26, showed progression of the original lesion with solid tufts, diffuse proliferCorrespondence and offprint requests to: Dr J. H. Campbell, Department of Respiratory Medicine, Glasgow Royal Infirmary, 16 Alex- ation, and four active crescent out of 13 glomeruli. andra Parade, Glasgow G31 2ES, UK. Immunosuppressive therapy was started with methyl-
Downloaded from http://ndt.oxfordjournals.org/ at New York University on April 13, 2016
Rapidly Progressive Glomerulonephritis and Nephrotic Syndrome Associated with Mycoplasma pneumoniae Pneumonia
Glomerulonephritis, Nephrotic Syndrome, and Mycoplasma pneumoniae
519
revealed an ulcerated colonic diverticulum, which was the likely origin of infection. Sections of the kidney revealed some focal glomerular hypercellularity and healing crescents, the overall picture being of a resolving rather than active glomerulonephritis.
Comment
prednisolone (1 g i.v. x 3), cyclophosphamide (3 mg/ kg), and plasma exchange ( x 6 ) . Repeat chest X-ray showed resolution of the upper lobe consolidation but he remained oliguric and dialysis dependent. Ten weeks after starting dialysis urine volumes and renal function had improved sufficiently to stop immunosuppressive treatment and dialysis (BP 170/98, urea 20.4 mmol/1, plasma creatinine 480 \ano\l\, albumin 33 g/1, dipstick proteinuria ++). Four months later he was readmitted with an E. coli septicaemia and left lower lobe pneumonia. Review 2 weeks before this emergency admission had revealed BP 160/105, dipstick proteinuria + + , urea 12.5 mmol/1, creatinine 310 jumol/1, and plasma albumin 38 g/1. He died shortly after admission. Postmortem examination
Downloaded from http://ndt.oxfordjournals.org/ at New York University on April 13, 2016
Fig. 1. Renal biopsy, day 6. Light-microscopy showing glomerulus characterised by proliferative features associated with early crescent formation (arrows). H & E x 390.
Dumas et al [3] were the first to draw attention to the association of Mycoplasma pneumoniae infection and renal disease, describing two cases of pneumonia associated with membranoproliferative glomerulonephritis (although concomitant streptococcal infection may have been the cause). Von Bonsdorff et al [4] reported similar histology in a 20-year-old man with mycoplasma pneumonia and no significant ASO titre. Vitullo et al [5] in 1978 reported a case of acute proliferative glomerulonephritis associated with Mycoplasma pneumoniae infection in which mycoplasma, IgG and C3 were deposited along the glomerular capillary walls and in the mesangium. They concluded that the renal disease was due to mycoplasma-induced immune complex nephritis. Other workers have described an association with IgA nephropathy [6] or tubulointerstitial nephritis [8]. In all published cases to date the renal failure was mild and self-limiting, no patient requiring dialysis or specific therapy other than adequate treatment of the mycoplasma infection. Acute glomerulonephritis has also been described in association with deep-seated infection [7]. Beaufils reported that the glomerulonephritis in these patients closely parallels the course of infection [7]. Delayed or inadequate treatment of the underlying infection was associated with progression of the renal disease. In contrast, our patient developed acute glomerulonephritis with nephrotic syndrome which progressed despite adequate antibiotic therapy and resolution of the pneumonic illness. Evidence for mycoplasma infection in this man was the significant complement fixation titre (1:256) and the response to erythromycin. The titre to influenza B suggests a concomitant infection but it seems unlikely that this significantly contributed to his illness. We were unable to identify mycoplasma antigen in the biopsy specimens but the temporal relationship of the development of his renal disease with the pneumonic illness and the lack of any evidence for an alternative aetiology supports the view that they were causally linked. To our knowledge, this is the first report of acute glomerulonephritis and nephrotic syndrome developing in association with Mycoplasma pneumoniae infection in which the renal disease progressed despite adequate treatment of the mycoplasma infection and required immunosuppressive therapy.
J. H. Campbell et al
520
References 1. MacFarlane JT, Finch RG, Ward MJ, Macrae AD. Hospital study of adult community acquired pneumonia. Lancet 1982; 2: 255-258 2. Ali NJ, Sillis M, Andrews BE, Jenkins PF, Harrison BDW. The clinical spectrum and diagnosis of Mycoplasma penumoniae infection. QJ Med 1986; 277: 241-251 3. Dumas R, Bascoul P, Baldet A, Serra A, Roux J, Jean R. Glomerulonephritic membrano-proliferative et maladie mycoplasmique. Arch Fr Pediatr 1976; 33: 783 4. Von Bonsdorff M, Ponka A, Torproth T. Mycoplasmal pneumonia
associated with mesangiocapillary glomerulonephritis type II (Dense deposit disease). Acta Med Scand 1984; 216: 427-429 Vitullo BB, O'Regan S, de Chandarevian JP, Kaplan BS. Mycoplasma pneumonia associated with acute glomerulonephritis. Nephron 1978; 21: 284-288 Kanayoma Y, Shiota K, Kotumi K et al. Mycoplasma pneumoniae pneumonia associated with IgA nephropathy. Scand J Infect Dis 1982; 14: 231-233 Beaunls M, Morel-Maroger L, Sraer JD, Kanfer A, Kourilsky O, Richet G. Acute renal failure of glomerular origin during visceral abscesses. N EnglJ Med 1976; 295: 185-189 Pasternack A, Helin H, Vanttinen T, Jarventie G, Vesikori T. Acute tubulointerstitial nephritis in a patient with Mycoplasma pneumoniae infection. Scan J Infect Dis 1979; 11: 85-87 Received for publication 16.10.90 Accepted in revised form 19.2.91 Downloaded from http://ndt.oxfordjournals.org/ at New York University on April 13, 2016
Nephrology Dialysis Transplantation
Case Report
J. H. Campbell1, G. Warwick2, M. Boulton-Jones2, A. McLay3, B. Jackson3 and R. D. Stevenson1 Departments of 'Respiratory Medicine, 2Renal Medicine and 3Pathology, Glasgow Royal Infirmary, Glasgow, UK
Introduction
anaemia (Hb 10.5 g/dl), normal white cell count, proteinuria (+ + + ) and haematuria on dipstick urinalysis, Mycoplasma pneumoniae infection remains an import- and hypoalbuminaemia (24 g/1). Intravenous ampicillin ant cause of community acquired pneumonia [1]. and erythromycin (2 g each daily) were started, but over Although a wide range of extrapulmonary manifest- the following week he developed progressive renal ations [2] have been described, its association with failure (urea 20 mmol/1, creatinine 610 jumol/1) and glomerulonephritis has been only sporadically reported increasingly heavy proteinuria (4.9-6.8 g/24 h). Serology revealed positive complement fixation test to [3-5]. Mycoplasma pneumoniae (titre 1:256) and influenza B, We describe the case of a 69-year-old man who suggesting recent infection. C4, C3 and C3d were presented with right-upper-lobe pneumonia and seronormal, antistreptolysis O titre was less than 200. Tests logical evidence of Mycoplasma pneumoniae and for antinuclear cytoplasmic antibody and antiglomeruinfluenza B infection who developed rapidly progressive lar basement membrane were negative. Fibreoptic glomerulonephritis and nephrotic syndrome. bronchoscopy was normal. In view of the deteriorating renal function a percutaneous renal biopsy was performed on day 6. This showed a diffuse proliferative glomerulonephritis with a Case Report few glomeruli showing crescent formation (7%) (Fig. 1). Ultrastructural examination showed scanty subenIn May 1988 a 69-year-old man presented with a 6-week dothelial and mesangial electron-dense deposits history of exertional breathlessness, expectoration of together with focal intraluminal monocyte aggregation. scanty sputum and fever. There had been no response to This pattern, together with the immunohistochemical a course of antibiotics at home. He had smoked 20 findings of scattered foci of granular loop IgM and C3, cigarettes per day since the age of 20. There was no raised the possibility of a postinfectious glomerulonephrelevant past history. On admission a chest X-ray ritis of the type usually encountered in deep-seated showed right upper lobe consolidation. Relevant labor- visceral infections [7]. The patient's renal function atory investigations demonstrated mild renal failure deteriorated further and he required dialysis. A second with urea (7.4 mmol/1) and creatinine (130 /zmol/1), renal biopsy performed on day 26, showed progression of the original lesion with solid tufts, diffuse proliferCorrespondence and offprint requests to: Dr J. H. Campbell, Department of Respiratory Medicine, Glasgow Royal Infirmary, 16 Alex- ation, and four active crescent out of 13 glomeruli. andra Parade, Glasgow G31 2ES, UK. Immunosuppressive therapy was started with methyl-
Downloaded from http://ndt.oxfordjournals.org/ at New York University on April 13, 2016
Rapidly Progressive Glomerulonephritis and Nephrotic Syndrome Associated with Mycoplasma pneumoniae Pneumonia
Glomerulonephritis, Nephrotic Syndrome, and Mycoplasma pneumoniae
519
revealed an ulcerated colonic diverticulum, which was the likely origin of infection. Sections of the kidney revealed some focal glomerular hypercellularity and healing crescents, the overall picture being of a resolving rather than active glomerulonephritis.
Comment
prednisolone (1 g i.v. x 3), cyclophosphamide (3 mg/ kg), and plasma exchange ( x 6 ) . Repeat chest X-ray showed resolution of the upper lobe consolidation but he remained oliguric and dialysis dependent. Ten weeks after starting dialysis urine volumes and renal function had improved sufficiently to stop immunosuppressive treatment and dialysis (BP 170/98, urea 20.4 mmol/1, plasma creatinine 480 \ano\l\, albumin 33 g/1, dipstick proteinuria ++). Four months later he was readmitted with an E. coli septicaemia and left lower lobe pneumonia. Review 2 weeks before this emergency admission had revealed BP 160/105, dipstick proteinuria + + , urea 12.5 mmol/1, creatinine 310 jumol/1, and plasma albumin 38 g/1. He died shortly after admission. Postmortem examination
Downloaded from http://ndt.oxfordjournals.org/ at New York University on April 13, 2016
Fig. 1. Renal biopsy, day 6. Light-microscopy showing glomerulus characterised by proliferative features associated with early crescent formation (arrows). H & E x 390.
Dumas et al [3] were the first to draw attention to the association of Mycoplasma pneumoniae infection and renal disease, describing two cases of pneumonia associated with membranoproliferative glomerulonephritis (although concomitant streptococcal infection may have been the cause). Von Bonsdorff et al [4] reported similar histology in a 20-year-old man with mycoplasma pneumonia and no significant ASO titre. Vitullo et al [5] in 1978 reported a case of acute proliferative glomerulonephritis associated with Mycoplasma pneumoniae infection in which mycoplasma, IgG and C3 were deposited along the glomerular capillary walls and in the mesangium. They concluded that the renal disease was due to mycoplasma-induced immune complex nephritis. Other workers have described an association with IgA nephropathy [6] or tubulointerstitial nephritis [8]. In all published cases to date the renal failure was mild and self-limiting, no patient requiring dialysis or specific therapy other than adequate treatment of the mycoplasma infection. Acute glomerulonephritis has also been described in association with deep-seated infection [7]. Beaufils reported that the glomerulonephritis in these patients closely parallels the course of infection [7]. Delayed or inadequate treatment of the underlying infection was associated with progression of the renal disease. In contrast, our patient developed acute glomerulonephritis with nephrotic syndrome which progressed despite adequate antibiotic therapy and resolution of the pneumonic illness. Evidence for mycoplasma infection in this man was the significant complement fixation titre (1:256) and the response to erythromycin. The titre to influenza B suggests a concomitant infection but it seems unlikely that this significantly contributed to his illness. We were unable to identify mycoplasma antigen in the biopsy specimens but the temporal relationship of the development of his renal disease with the pneumonic illness and the lack of any evidence for an alternative aetiology supports the view that they were causally linked. To our knowledge, this is the first report of acute glomerulonephritis and nephrotic syndrome developing in association with Mycoplasma pneumoniae infection in which the renal disease progressed despite adequate treatment of the mycoplasma infection and required immunosuppressive therapy.
J. H. Campbell et al
520
References 1. MacFarlane JT, Finch RG, Ward MJ, Macrae AD. Hospital study of adult community acquired pneumonia. Lancet 1982; 2: 255-258 2. Ali NJ, Sillis M, Andrews BE, Jenkins PF, Harrison BDW. The clinical spectrum and diagnosis of Mycoplasma penumoniae infection. QJ Med 1986; 277: 241-251 3. Dumas R, Bascoul P, Baldet A, Serra A, Roux J, Jean R. Glomerulonephritic membrano-proliferative et maladie mycoplasmique. Arch Fr Pediatr 1976; 33: 783 4. Von Bonsdorff M, Ponka A, Torproth T. Mycoplasmal pneumonia
associated with mesangiocapillary glomerulonephritis type II (Dense deposit disease). Acta Med Scand 1984; 216: 427-429 Vitullo BB, O'Regan S, de Chandarevian JP, Kaplan BS. Mycoplasma pneumonia associated with acute glomerulonephritis. Nephron 1978; 21: 284-288 Kanayoma Y, Shiota K, Kotumi K et al. Mycoplasma pneumoniae pneumonia associated with IgA nephropathy. Scand J Infect Dis 1982; 14: 231-233 Beaunls M, Morel-Maroger L, Sraer JD, Kanfer A, Kourilsky O, Richet G. Acute renal failure of glomerular origin during visceral abscesses. N EnglJ Med 1976; 295: 185-189 Pasternack A, Helin H, Vanttinen T, Jarventie G, Vesikori T. Acute tubulointerstitial nephritis in a patient with Mycoplasma pneumoniae infection. Scan J Infect Dis 1979; 11: 85-87 Received for publication 16.10.90 Accepted in revised form 19.2.91 Downloaded from http://ndt.oxfordjournals.org/ at New York University on April 13, 2016
