A case of penumonia and glomerular nephritis

亞東醫院小兒部葉樹人

Summary of History

• Fever treated in LMD but in vain ( under antibiotics) since 06/2/2005, fever persisted

• Progressive dyspnea

• Decreased urine output

• Generalized edema

• Visiting our ES on 06/10/2005

Laboratory Finding_1

• CxR:– Cardiomegaly, boderline– Bilateral pleural effusion

• Mild leukocytosis, elevated CRP• ABG: mild respiratory alkalosis=>hypoxemi

a• Abnormal U/A=> proteinuria and microscop

ic hematuria

Laboratory Finding_2

• Decreased C3 on 06/14, normal on 06/29• ASLO < 25 IU/ml on 06/14 and 06/29• Negative antigen test for pleural effusion• Urine pneumococcal antigen (+)• Normal IgA• Negative ANA

CxR on 6/14:bilateral pleural effuiosn with mild cardiomegaly

CT scan: pneumonia patch with consolidation and pleural effusion

Clues by now

• Pneumonia with pleural effusion, on going

• Partially treated

• Glomerular Nephritis with proteinuria

• Low C3 => recheck normal

• Negative ASLO=> recheck negative

• Pneumococcal antigen test(+)

Pulmonary Renal Syndrome

• Coexistence of pulmonary and renal disease– Specific: vasculitis– Non-specific: pos

t-infection GN, HUS…etc

– Pediatric Pulmonology 29:382–388 (2000)

Post-Streptococcal Glomerular Nephritis (PSGN)

• Throat culture, GAS antigen test

• Low C3, C4 level

• Evidence of Glomerular Nephritis (gross/microscopic hematuria)

• Elevated ASLO

Poststreptococcal glomerulonephritis with pulmonary edema presenting

as respiratory distress

Chih-Yung Chiu · Yhu-Chering Huang ·Kin-Sun Wong · Shao-Hsuan Hsia · Chi-Jen Lin Tzo

u-Yien LinPediatr Nephrol (2004) 19:1237–1240

Background• Acute poststreptococcal glomerulonephritis (P

SGN) is the most common form of postinfectious glomerulonephritis in children and usually follows pharyngitis or pyogenic skin infections

• Gross hematuria, edema, and hypertension are the classic manifestations. Rarely, potentially life-threatening complication of pulmonary edema can occur and require specific aggressive medical therapy

Patient character

• P’ts 2 and 5 had streptococcal pharyngitis and were diagnosed by positive rapid streptococcal antigen test.

• All p’ts presented with dyspneic respirations (6/6) followed by low-grade fever (5/6), cough (5/6), and mild peripheral edema (4/6).

Patient character

• hypertension, mild proteinuria (no more than +2), and microscopic hematuria were found in all six p’ts.

• P’t 6 had high blood pressure exceeding 160/95 mmHg that was complicated by seizures and disturbance of consciousness.

Patient character

• Depressed levels of serum C3 and elevated ASO titers (confirmed the diagnosis of PSGN in all p’ts.

• Reduced serum albumin levels in all p’ts.

• Serum levels of cholesterol and triglyceride were measured in 3 p’ts and no hyperlipidemia was found. Elevated serum creatinine and normal blood urea nitrogen levels were seen in all p’ts

Laboratory character• Renal ultrasound: increased renal echogenicit

y without structural abnormality. • Compared with the convalescent stage, all p’t

s had cardiomegaly and radiographic features of pulmonary edema– Alveolar infiltrates with bilateral pleural effusion wa

s the predominant pattern of pulmonary edema, which was usually misinterpreted as pneumonia at presentation.

Discussion• Gross hematuria, peripheral edema, an

d hypertension are the first clues to diagnosis of PSGN

• Microscopic hematuria and non-specific symptoms such as low-grade fever, cough, sore throat, or abdominal pain may be neglected by the physicians who first see these patients.

Discussion

• A delayed diagnosis of PSGN in such instances may progress to respiratory failure and lead to inappropriate therapeutic intervention such as thoracostomy.

• In this series, the diagnosis of PSGN associated with pulmonary edema was not established in three patients until 2–12 days after hospitalization.

Discussion

• In a previous report of 104 p’ts with acute glomerulonephritis, cardiomegaly was present in 2/3 of p’ts and alveolar pulmonary edema in 16%

• Cardiomegaly (CT ratio 0.55) in the acute stage was seen in 3 p’ts (50%), but when compared with the cardiac size in the convalescent stage, cardiomegaly was also evident in the other 3 p’ts.=>either volume overload or cardiac insult

Discussion

• It must be emphasized that the differential dx of pulmonary alveolar infiltrates should include infections, hemorrhage, or edema. In particular, the presence of bilateral pleural effusions, increased CT ratio, and prominent septal thickening => unlikely presentation for acute bacterial pneumonia.

Discussion• The Px of acute PSGN in children has been exc

ellent when treated adequately, but early mortality may be as high as 25% in elderly p’ts who have Cxs of pulmonary edema, the Tx is mainly appropriate diuresis

• The presentation of pulmonary edema complicating an underlying glomerular disease of PSGN is consistent with the “ pulmonary renal syndrome’, which indicates the coexistence of pulmonary and glomerular renal disease

Discussion

• Urinalysis and BP, should be an essential part of the work-up in any severely ill p’t who presents with pulmonary edema to investigate the possible coexistence of a glomerular renal disease.

• Children with a glomerular renal disease such as PSGN, who have sudden onset of dyspneic respirations, a CxR should be performed to make an early dx of the potentially life-threatening complication of pulmonary edema.

Pneumococcal nephritis• Previously mentioned in medical journals• Rarely mentioned recently• Title

– Acute nephritis and pulmonary alveolitis following pneumococcal pneumonia.• Source

– Archives of Internal Medicine. 138(5):806-8, 1978 May.• Abstract

– Acute glomerulonephritis developed in a man with pneumococcal pneumonia. Serum complement studies revealed decreased levels of C4, properdin, and C3. Renal immunofluorescence studies demonstrated pneumococcal antigen, C1q, C4, C3 proactivator, properdin, C3, IgG, and IgM. Circulating cryoglobulin contained pneumococcal antigen and antibody, C3, and immunoglobulins. Serial pneumococcal antigen and antibody levels did not display patterns that were characteristic of classical immune elimination, but the patterns may have been influenced by the reentry of antigen. A diffuse, pulmonary alveolitis also developed in the patient. Lung immunofluorescence studies revealed pneumococcal antigen, IgG, and C3 in alveolar walls and capillary basement membranes. The glomerulonephritis and alveolitis resolved after a prolonged course. These findings provide presumptive evidence for pneumococcal, immune complex glomerulonephritis with complement activation via both classical and alternative pathways and suggest an immunologic pathogenesis for the pulmonary alveolitis.

Urinary pneumococcal antigen Alone?

• Nasopharyngeal Carrier Contamination? – CID 2002:34 (1 April) • BRIEF REPORTS

Urinary pneumococcal antigen Alone?• Sensitivity and Specificity?

– Sen 95.8%, Spe 93% in bacremic group– ANNALS OF EMERGENCY MEDICINE 40:4 OCTOBER 2002

At least we’ve this figure• Pediatrics 2003;112:1279–1282

Thank you for your attention and comment!