Pneumonia associated glomerulonephritis is a rare condition that occurs more commonly in adults than in children. To our knowledge there are four published series for pediatric patients including 3, 11, 4 and 6 patients [2-5]. In all of these series glomerulonephritis developed soon after pneumonia; macroscopic hematuria developed after 24-72 hours of hospital admission [2,3,5], but in the study of Schachter , glomerulonephritis developed within six weeks after the infection. In our patient macroscopic hematuria was observed simultaneously with respiratory symptoms and GFR was decreased when she was diagnosed as pneumonia.
Although all of the patients were male in the study of Srivastava , this may be an incidental finding because there are female patients in the other studies and the number of the patients in all series are small to interpretar about this issue. Patients are generally under the age of ten and so was our patient and this may be related to the infectious agent causing pneumonia [2-5].
As in other forms of postinfectious glomerulonephritis in pneumonia-associated glomerulonephritis, the inflammatory process that takes place in the glomeruli is triggered by antigen-antibody reactivity that results in local activity of complement system and of the coagulation cascade .
Hypocomplementemia occurs as a result of activation of alternative complement pathway and it was also a common finding in the series we had reviewed [2,3,5]. Hypocomplementemia was also observed in our patient and returned to normal after 12 weeks at follow up.
Various infectious agents may cause pneumonia associated with glomerulonephritis, mycoplasma pneumonia is the most common microorganism seen in adult series . Streptococcus pneumonia and Chlamydia pneumonia infections may also be associated with glomerulonephritis [2,6-8]. We could not detect the causing microorganism in our patient; blood, pharyngeal swab and urine cultures were all negative. Because the etiology could not be identified and glomerulonephritis occurred synchronously with pneumonia IgA nephropathy was also considered as a differential diagnosis. Our patient had low serum complement 3 levels, marked hypertension and showed a quick resolution of renal impairment. She did not have chronic persistent or recurrent hematuria during follow up. Taken together these findings favored the diagnosis of postinfectious glomerulonephritis rather than IgA nephropathy.
Antistreptolysin O (ASLO) titers were elevated in our patient as reported in other series in the literature. Srivastava reported elevated ASLO titers in 10 of 11 patients in his study . All of the 3 patients and 5 of the 6 patients in the studies of Lechon  and Vila Cots  had also elevated ASLO titers respectively. But none of these authors attributed glomerulonephritis to Streptococcus pyogenes infection because ASLO titers may be affected from many other factors and no universally normal value was applicable. In our patient; pharyngeal swab culture was negative, there was typical clinical, laboratory and radiological findings of pneumonia; therefore our patient was diagnosed as pneumonia associated glomerulonephritis. Because the clinical picture of the patient was mild and anti-neutrophil cytoplasmic antibody was negative we did not consider an immune mediated process which affected lung and kidney simultaneously as seen in Good-Pasture syndrome. Yet this was the first attack of hematuria synchronous with a respiratory tract infection and serum complement 3 level was low IgA was not thought at the forefront.
Diagnosis depends on urine analysis (red blood cells and red blood cell casts, white blood cells, rarely proteinuria), evidence of previous infection (Streptococcal test, pharyngeal swab for viral PCR, etc), renal function tests and serum complement levels. If the patient is presented with a well-defined clinical picture renal biopsy is seldom required . We did not perform renal biopsy because of rapid improvement of renal and respiratory findings with antibiotic and diuretic treatment. Only one child in the study of Srivastava went under renal biopsy which showed proliferative glomerulonephritis without crescents .
Renal prognosis is generally benign and the prognosis is favorable in pneumonia associated APIGN. Antibiotic treatment is required when infection is present at the time of diagnosis . Treatment is usually supportive and directed towards potential complications as hypertension and severe fluid and electrolyte disturbances. Dialysis is rarely required in children for treatment of uremia, hyperkalemia or severe circulatory congestion . Only one child in the study of Srivastava  required dialysis for four days but at follow up blood pressure, urine analysis, serum complements were normalized in 9 patients in whom follow up was available. Renal involvement was also mild in the series of Lechon and Vila Cots respectively [2,5]. In our patient oliguria lasted for only one day and she responded well to diuretics and antibiotics. At follow up renal function tests and urine analysis were completely normal.
As reported in previous series and case reports there is an association between pneumonia and glomerulonephritis although it is very rare. In typical clinical picture basic laboratory investigations may be sufficient; renal biopsy is recommended when normocomplementemia or persistent hypocomplementemia exists or when renal function declines rapidly . In most patients the respiratory and renal prognosis is favorable but clinicians must be aware of the course to make prompt diagnosis and appropriate management and to avoid unnecessary medical intervention.