Mycoplasma pneumoniae respiratory infections are occasionally associated with extrarespiratory manifestations. 1 This organism can affect children of all ages. 2 Renal involvement is rare, and it usually presents as an acute nephritis that may be manifested simultaneously with the other symptoms or 5 to 10 days later. 3
We present a case of a 6-year-old boy with acute nephritis occurring concomitantly with respiratory tract infection caused by M. pneumoniae and review the pertinent literature.
A 6-year-old boy was admitted to the Pediatric Nephrology Clinic because of painless macrohematuria. Three days earlier he had developed a fever (39°C) that lasted for 24 h and was associated with coryza and nonproductive cough that persisted until admission.
The clinical and laboratory data are shown in Table 1. Chest roentgenogram revealed peribronchial infiltrates. Ultrasound examination of the kidney was normal. On admission the anti-streptolysin O titer was 200 IU/ml, and it remained essentially unchanged during the following 2 weeks. The pharyngeal culture revealed normal bacterial flora.
An enzyme-linked immunosorbent assay (Alphadia SA/NY) was used for the detection of specific anti-M. pneumoniae IgM and IgG antibodies. The results were expressed as the ratio of the optical density value of the sample to the cutoff value and were considered positive when this ratio was >1.1, equivocal when it was 0.9 to 1.1 and negative when <0.9. In our patient the IgM was equivocal on admission and increased to pathologic values 15 days later (ratios 1.0 and 1.6, respectively). The IgG antibody was negative on admission and positive 15 days later (ratio 2.6). The direct and indirect Coombs reaction was negative. The IgM and IgG antibodies for Coxiella burnetii, Rickettsia conorii and Chlamydia pneumoniae were negative.
The child was treated with erythromycin orally for 10 days. He never developed edema or hypertension, and the macrohematuria subsided 2 days after admission, followed by microhematuria which persisted for the following 2 months. The proteinuria resolved after 10 days and the C3 returned to normal in 35 days (1,170 mg/l). The anti-M. pneumoniae IgM antibodies were positive 4 months later (ratio 1.3), becoming negative 6 months later, whereas the IgG remained positive (ratio 3.9). The child was asymptomatic on follow-up at 6 months.
Acute postinfectious glomerulonephritis (GN) in childhood is usually caused by group A beta-hemolytic Streptococcus, but it can be caused by other infections. 4 It can appear simultaneously with bacterial pneumonia (pneumococcal, staphylococcal) and pneumonia caused by C. pneumoniae, Coxiella burnetii, Nocardia5 and M. pneumoniae. 3 In our patient the clinical presentation of the child was compatible with M. pneumoniae infection which was subsequently proved by the detection of borderline positive specific IgM antibodies on admission that increased 15 days later, as well as the parallel appearance of IgG antibodies. The PCR for M. pneumoniae in nasopharyngeal swab is most useful as a rapid diagnostic test, but it was not available in our laboratory. Radiographically there were peribronchial infiltrates but no evidence of pneumonia. Most (75%) M. pneumoniae infections present with minor respiratory symptoms (pharyngitis, tracheobronchitis), ∼20% are asymptomatic and only 3 to 10% of infected patients develop pneumonia. 1, 6
The diagnosis of acute GN in our case was supported by the sudden onset of macrohematuria, proteinuria and granular casts in the urine. Red blood cell casts are diagnostic of glomerular origin of hematuria. 7
Acute poststreptococcal GN typically presents 7 to 14 days after group A beta-hemolytic streptococcal infection and only rarely in fewer than 7 days. 4 In our patient the illness appeared just 3 days before the presentation of nephritis, and the fever subsided spontaneously within 24 h without antibiotics. This clinical course of our patient, in combination with the laboratory findings that were incompatible with conventional bacterial infection, makes the presence of a poststreptococcal GN highly unlikely.
Although M. pneumoniae-associated GN is rare, a few cases have been reported in children, the clinical characteristics of which are summarized in Table 2. 3, 8–11 Glomerulonephritis can appear either concomitantly with other symptoms or 5 to 10 days later. 3 In cases with renal involvement persistence of anti-M. pneumoniae IgM and IgG antibodies has been reported, 3 as in our patient. In the study by Saïd et al., 3 four of the six reported children were boys. Predominance of boys has also been reported by Srivastava et al. 5 in cases with pneumonia-associated acute glomerulonephritis. However, the number of reported children is too small to confirm the male predominance.
The C3 serum complement was initially decreased in 4 of 10 reported children and subsequently normalized in one of them, whereas in 3 of 4 it remained persistently low. 3, 8, 11 In these 3 children renal biopsy revealed membranoproliferative glomerulonephritis (MPGN) types I (1 patient) and II (2 patients), and all 3 progressed to chronic renal failure and end-stage renal failure. 8, 11 Our patient is the second reported case in whom the initially low C3 was only transient, and its rapid normalization was associated with an excellent clinical outcome. Because of the rapid clinical and laboratory improvement, a renal biopsy was not performed in our patient. Proteinuria resolved within 10 days, and microhematuria resolved within 2 months, a finding similar to those in other reported cases. 3, 9, 10 In a child with acute renal failure reported by Saïd et al., 3 the glomerular filtration rate returned to normal in 2 months, whereas the microhematuria resolved after 36 months. MPGN is the most frequent lesion found in patients with mycoplasmal infection in whom the acute nephritis is associated with persistently low C3. 3
The pathogenesis of GN associated with M. pneumoniae infection is unclear. In the study by Saïd et al., 3 the PCR was negative, and immunofluorescence studies failed to detect M. pneumoniae antigen in the renal parenchyma. The authors argued that this does not necessarily rule out the role of this microorganism, because the pathogenesis of postinfectious GN is more likely based on immunologic mechanisms. 3 An immune reaction against the glomeruli could be supported by the detection of anti-M. pneumoniae antibodies by immunofluorescence in the glomeruli. The antigen involved could be mycoplasmal or a cross-reacting renal antigen. Searches for M. pneumoniae antigen by immunofluorescence in the renal biopsies were negative in the study by Saïd et al. 3 Circulating immune complexes, containing either mycoplasmal or autologous antigen, are likely to participate in the pathogenetic mechanism. 3 These complexes have been reported in mycoplasmal extrarespiratory infections, but no specific mycoplasmal antigen has been detected 12 except for cases with central nervous system and liver involvement, in which specific mycoplasmal and autologous antigens were detected. 12, 13
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