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Education & Practice Online First, published on August 28, 2017 as 10.1136/archdischild-2017-313123 Epilogue
A boy with fever, cough and gross haematuria Giorgio Cozzi, Massimo Maschio, Gabriele Poillucci, Marco Pennesi, Egidio Barbi Abstract
A 5 year-old boy presented with 2-days of fever and cough. On examination, he had mild dyspnoea and chest pain, with crackles and hypoventilation at the right lung base. Blood tests showed: WBC 39.1×109/L; N 28.9×109/L; Hb 11.3gr/dL; PLT 375×109/L; CRP 28.7mg/ dL; ESR 41mm/h. Chest x-ray confirmed a pulmonary consolidation in the right lower lobe (figure 1), with an associated pleural effusion. Bacterial pneumonia was diagnosed and intravenous ceftriaxone 100mg/kg/die was started. The following day, he developed palpebral oedema and his urine became tea coloured. His blood pressure was 126/82mmHg (>99th percentile).1 Serum creatinine rose from 0.45mg/dl to 1.09mg/dl (39.8µmol/L – 93.4µmol/L) and C3 was 9mg/dl (n.r. 90-180mg/dl). Urinalysis re-
vealed gross hematuria and 3+ proteinuria, with microscopicy showing dysmorphic red blood cells with casts. Ultrasounds showed enlarged kidneys with increased echogenicity.
A 5-year-old boy presented with 2 days of fever and cough. On examination, he had mild dyspnoea and chest pain, with crackles and hypoventilation at the right lung base. Blood tests showed white blood cells of 39.1×109/L, neutrophils of 28.9×109/L, haemoglobin of 11.3 g/dL, platelets of 375×109/L, c-reactive protein of 28.7 mg/dL and erythrocyte sedimentation rate of 41 mm/hour. Chest X-ray confirmed a pulmonary consolidation in the right lower lobe (figure 1), with an associated pleural effusion. Bacterial pneumonia was diagnosed and intravenous ceftriaxone 100 mg/kg/ day was started. The following day, he developed palpebral oedema and his urine became tea-coloured. His blood pressure was 126/82 mm Hg (>99th percentile).1 Serum creatinine rose from 0.45 mg/dL to 1.09 mg/dL (39.8–93.4 µmol/L) and C3 was 9 mg/dL (normal range 90–180 mg/dL). Urinalysis revealed gross haematuria
Figure 1 Pulmonary consolidation in the right lower lobe, with consensual pleural effusion. Cozzi G, et al. Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/archdischild-2017-313123
1
Copyright Article author (or their employer) 2017. Produced by BMJ Publishing Group Ltd under licence.
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Epilogue and 3+ proteinuria, with microscopy showing dysmorphic red blood cells with casts. Ultrasounds showed enlarged kidneys with increased echogenicity. Question 1 Which of the following is the most likely diagnosis?
A. IgA nephropathy B. Haemolytic uraemic syndrome C. Acute glomerulonephritis associated to Streptococcus pneumoniae lung infection D. Acute glomerulonephritis with pulmonary oedema
Question 2 Which of the following pathogens more frequently cause APIGN in children?
A. B. C. D.
Streptococcus pneumoniae Mycoplasma pneumoniae Streptococcus pyogenes Adenovirus
Question 3 How should this patient be treated? Answers are on page 02. ANSWERS TO THE QUESTIONS ON PAGE 01. Answer to question 1 The clinical picture suggests acute nephritic syndrome secondary to pneumonia, with features suggesting a pneumococcal aetiology. Acute postinfectious glomerulonephritis (APIGN) is the most common cause of acute glomerular disease in children, primarily affecting children aged 3–12 years.2 3 The most common clinical presentation is nephritic syndrome, with haematuria, oedema, increased blood pressure and hypocomplementaemia C3. Pneumonia is rarely associated with APIGN.3 IgA nephropathy is a common cause of gross haematuria related to infections, but it is not associated with low serum C3 levels and it rarely leads to increased blood pressure and raised creatinine. Haemolytic uraemic syndrome should be suspected when haemolytic anaemia, thrombocytopaenia and acute renal failure are present. Pulmonary oedema in patients with acute glomerulonephritis may mimic pneumonia.5 Answer to question 2 Streptococcus pyogenes is the most common cause of APIGN in childhood, although other bacterial, viral and fungal pathogens have been associated with APIGN, including cases of APIGN following S. pneumoniae infection.4 6–8 Immunofluorescence suggests that antigens cause complement activation, with glomerular immune-complex deposition, manifesting in glomerulonephritis.9 Typically, the interval between the primary pneumococcal infection and APIGN is approximately 24–48 hours, in contrast to the average interval for APIGN from S. pyogenes (1–2 2
weeks for associated pharyngitis and 3–6 weeks for skin infections).6 High serum titres of antistreptolysin O (ASOT) were frequently reported in children with APIGN associated with S. pneumoniae, and ASOT is poor in distinguishing between S. pyogenes-related and S. pneumoniae-related APIGN.4 6 Answer to question 3 APIGN associated to S. pneumoniae is usually self-limiting, and acute kidney injury (AKI), when present, is mild and reversible.2 7 Persistent renal failure in the acute phase or persistent proteinuria in the subsequent months is predictive of a worse outcome.10 Supportive therapy helps to limit hypertension, including salt and water restriction, and diuretic and calcium channel blockers administration may be useful. ACE inhibitors (ACEIs) should be avoided in patients with AKI, particularly with diuretics, to avoid hyperkalaemia and worsening of AKI. After the acute phase, ACEIs are a suitable and usually a well-tolerated option.11 Antibiotic therapy limits the spread of nephritogenic pathogens, but does not affect the progression of glomerulonephritis. Amoxicillin 100 mg/kg for 7–10 days is the recommended treatment for uncomplicated pneumonia, while intravenous ampicillin or ceftriaxone is usually used in hospitalised children, along with vancomycin and pleural drainage in case of significant pleural effusions. Patient outcome His urine pneumococcal antigen test was positive, and his renal function normalised in 4 days, with C3 levels normalising by 1 month. He continued antihypertensive therapy with low-dose ACEI for 3 months, and an isolated microscopic haematuria persisted for 5 months and then resolved. Giorgio Cozzi, Massimo Maschio, Gabriele Poillucci, Marco Pennesi, Egidio Barbi Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy Correspondence to Dr Giorgio Cozzi, Institute for Maternal and Child Health IRCCS Burlo Garofolo, Via dell’Istria 65/1, Trieste 34137, Italy; giorgiocozzi@ gmail.com Contributors GC, MM, GP, MP, EB contributed equally to the manuscript. Competing interests None declared. Patient consent Parental/guardian consent obtained. Provenance and peer review Not commissioned; externally peer reviewed. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
To cite Cozzi G, Maschio M, Poillucci G, et al. Arch Dis Child Educ Pract Ed Published Online First: [please include Day Month Year]. doi:10.1136/ archdischild-2017-313123 Received 31 March 2017
Cozzi G, et al. Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/archdischild-2017-313123
Downloaded from http://ep.bmj.com/ on August 28, 2017 - Published by group.bmj.com
Epilogue Accepted 13 June 2017 Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/ archdischild-2017-313123
References 1 Neuhauser HK, Thamm M, Ellert U, et al. Blood pressure percentiles by age and height from nonoverweight children and adolescents in Germany. Pediatrics 2011;127:e978–88. 2 Dagan R, Cleper R, Davidovits M, et al. Post-Infectious Glomerulonephritis in Pediatric Patients over Two Decades: Severity-Associated Features. Isr Med Assoc J 2016;18:336–40. 3 Gunasekaran K, Krishnamurthy S, Mahadevan S, et al. Clinical Characteristics and Outcome of Post-Infectious Glomerulonephritis in Children in Southern India: A Prospective Study. Indian J Pediatr 2015;82:896–903. 4 Carceller Lechon F, de la Torre Espì M, Porto Abal R, et al. Acuteglomerulonephritis associated with pneumonia: a review of three case. Pediatr Nephrol 2010;25:161–4.
5 Chiu CY, Huang YC, Wong KS, et al. Poststreptococcal glomerulonephritis with pulmonary edema presenting as respiratory distress. Pediatr Nephrol 2004;19:1237–40. 6 Phillips J, Palmer A, Baliga R. Glomerulonephritis associated with acute pneumococcal pneumonia: a case report. Pediatr Nephrol 2005;20:1494–5. 7 Hibino S, Hoshino A, Fujii T, et al. Post-streptococcal acute glomerulonephritis associated with pneumococcal infection. Pediatr Int 2013;55:e136–8. 8 Ismail IH, Zainudin Z, Othman N. Pneumococcal glomerulonephritis in a healthy child: a case report and literature review. Singapore Med J 2014;55:e69–72. 9 Hyman LR, Jenis EH, Hill GS, et al. Alternative C3 pathway activiation in pneumococcal glomerulonephritis. Am J Med 1975;58:810–4. 10 Zhong J, Yang HC, Fogo AB. A perspective on chronic kidney disease progression. Am J Physiol Renal Physiol 2017;312:F375–84. 11 Misurac J, Nichols KR, Wilson AC. Pharmacologic Management of Pediatric Hypertension. Pediatric Drugs 2016;18:31–43.
Cozzi G, et al. Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/archdischild-2017-313123
3
Downloaded from http://ep.bmj.com/ on August 28, 2017 - Published by group.bmj.com
A boy with fever, cough and gross haematuria Giorgio Cozzi, Massimo Maschio, Gabriele Poillucci, Marco Pennesi and Egidio Barbi Arch Dis Child Educ Pract Ed published online August 28, 2017
Updated information and services can be found at: http://ep.bmj.com/content/early/2017/08/28/archdischild-2017-313123
These include:
References
This article cites 11 articles, 2 of which you can access for free at: http://ep.bmj.com/content/early/2017/08/28/archdischild-2017-313123 #BIBL
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Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
Education & Practice Online First, published on August 28, 2017 as 10.1136/archdischild-2017-313123 Epilogue
A boy with fever, cough and gross haematuria Giorgio Cozzi, Massimo Maschio, Gabriele Poillucci, Marco Pennesi, Egidio Barbi Abstract
A 5 year-old boy presented with 2-days of fever and cough. On examination, he had mild dyspnoea and chest pain, with crackles and hypoventilation at the right lung base. Blood tests showed: WBC 39.1×109/L; N 28.9×109/L; Hb 11.3gr/dL; PLT 375×109/L; CRP 28.7mg/ dL; ESR 41mm/h. Chest x-ray confirmed a pulmonary consolidation in the right lower lobe (figure 1), with an associated pleural effusion. Bacterial pneumonia was diagnosed and intravenous ceftriaxone 100mg/kg/die was started. The following day, he developed palpebral oedema and his urine became tea coloured. His blood pressure was 126/82mmHg (>99th percentile).1 Serum creatinine rose from 0.45mg/dl to 1.09mg/dl (39.8µmol/L – 93.4µmol/L) and C3 was 9mg/dl (n.r. 90-180mg/dl). Urinalysis re-
vealed gross hematuria and 3+ proteinuria, with microscopicy showing dysmorphic red blood cells with casts. Ultrasounds showed enlarged kidneys with increased echogenicity.
A 5-year-old boy presented with 2 days of fever and cough. On examination, he had mild dyspnoea and chest pain, with crackles and hypoventilation at the right lung base. Blood tests showed white blood cells of 39.1×109/L, neutrophils of 28.9×109/L, haemoglobin of 11.3 g/dL, platelets of 375×109/L, c-reactive protein of 28.7 mg/dL and erythrocyte sedimentation rate of 41 mm/hour. Chest X-ray confirmed a pulmonary consolidation in the right lower lobe (figure 1), with an associated pleural effusion. Bacterial pneumonia was diagnosed and intravenous ceftriaxone 100 mg/kg/ day was started. The following day, he developed palpebral oedema and his urine became tea-coloured. His blood pressure was 126/82 mm Hg (>99th percentile).1 Serum creatinine rose from 0.45 mg/dL to 1.09 mg/dL (39.8–93.4 µmol/L) and C3 was 9 mg/dL (normal range 90–180 mg/dL). Urinalysis revealed gross haematuria
Figure 1 Pulmonary consolidation in the right lower lobe, with consensual pleural effusion. Cozzi G, et al. Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/archdischild-2017-313123
1
Copyright Article author (or their employer) 2017. Produced by BMJ Publishing Group Ltd under licence.
Downloaded from http://ep.bmj.com/ on August 28, 2017 - Published by group.bmj.com
Epilogue and 3+ proteinuria, with microscopy showing dysmorphic red blood cells with casts. Ultrasounds showed enlarged kidneys with increased echogenicity. Question 1 Which of the following is the most likely diagnosis?
A. IgA nephropathy B. Haemolytic uraemic syndrome C. Acute glomerulonephritis associated to Streptococcus pneumoniae lung infection D. Acute glomerulonephritis with pulmonary oedema
Question 2 Which of the following pathogens more frequently cause APIGN in children?
A. B. C. D.
Streptococcus pneumoniae Mycoplasma pneumoniae Streptococcus pyogenes Adenovirus
Question 3 How should this patient be treated? Answers are on page 02. ANSWERS TO THE QUESTIONS ON PAGE 01. Answer to question 1 The clinical picture suggests acute nephritic syndrome secondary to pneumonia, with features suggesting a pneumococcal aetiology. Acute postinfectious glomerulonephritis (APIGN) is the most common cause of acute glomerular disease in children, primarily affecting children aged 3–12 years.2 3 The most common clinical presentation is nephritic syndrome, with haematuria, oedema, increased blood pressure and hypocomplementaemia C3. Pneumonia is rarely associated with APIGN.3 IgA nephropathy is a common cause of gross haematuria related to infections, but it is not associated with low serum C3 levels and it rarely leads to increased blood pressure and raised creatinine. Haemolytic uraemic syndrome should be suspected when haemolytic anaemia, thrombocytopaenia and acute renal failure are present. Pulmonary oedema in patients with acute glomerulonephritis may mimic pneumonia.5 Answer to question 2 Streptococcus pyogenes is the most common cause of APIGN in childhood, although other bacterial, viral and fungal pathogens have been associated with APIGN, including cases of APIGN following S. pneumoniae infection.4 6–8 Immunofluorescence suggests that antigens cause complement activation, with glomerular immune-complex deposition, manifesting in glomerulonephritis.9 Typically, the interval between the primary pneumococcal infection and APIGN is approximately 24–48 hours, in contrast to the average interval for APIGN from S. pyogenes (1–2 2
weeks for associated pharyngitis and 3–6 weeks for skin infections).6 High serum titres of antistreptolysin O (ASOT) were frequently reported in children with APIGN associated with S. pneumoniae, and ASOT is poor in distinguishing between S. pyogenes-related and S. pneumoniae-related APIGN.4 6 Answer to question 3 APIGN associated to S. pneumoniae is usually self-limiting, and acute kidney injury (AKI), when present, is mild and reversible.2 7 Persistent renal failure in the acute phase or persistent proteinuria in the subsequent months is predictive of a worse outcome.10 Supportive therapy helps to limit hypertension, including salt and water restriction, and diuretic and calcium channel blockers administration may be useful. ACE inhibitors (ACEIs) should be avoided in patients with AKI, particularly with diuretics, to avoid hyperkalaemia and worsening of AKI. After the acute phase, ACEIs are a suitable and usually a well-tolerated option.11 Antibiotic therapy limits the spread of nephritogenic pathogens, but does not affect the progression of glomerulonephritis. Amoxicillin 100 mg/kg for 7–10 days is the recommended treatment for uncomplicated pneumonia, while intravenous ampicillin or ceftriaxone is usually used in hospitalised children, along with vancomycin and pleural drainage in case of significant pleural effusions. Patient outcome His urine pneumococcal antigen test was positive, and his renal function normalised in 4 days, with C3 levels normalising by 1 month. He continued antihypertensive therapy with low-dose ACEI for 3 months, and an isolated microscopic haematuria persisted for 5 months and then resolved. Giorgio Cozzi, Massimo Maschio, Gabriele Poillucci, Marco Pennesi, Egidio Barbi Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy Correspondence to Dr Giorgio Cozzi, Institute for Maternal and Child Health IRCCS Burlo Garofolo, Via dell’Istria 65/1, Trieste 34137, Italy; giorgiocozzi@ gmail.com Contributors GC, MM, GP, MP, EB contributed equally to the manuscript. Competing interests None declared. Patient consent Parental/guardian consent obtained. Provenance and peer review Not commissioned; externally peer reviewed. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
To cite Cozzi G, Maschio M, Poillucci G, et al. Arch Dis Child Educ Pract Ed Published Online First: [please include Day Month Year]. doi:10.1136/ archdischild-2017-313123 Received 31 March 2017
Cozzi G, et al. Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/archdischild-2017-313123
Downloaded from http://ep.bmj.com/ on August 28, 2017 - Published by group.bmj.com
Epilogue Accepted 13 June 2017 Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/ archdischild-2017-313123
References 1 Neuhauser HK, Thamm M, Ellert U, et al. Blood pressure percentiles by age and height from nonoverweight children and adolescents in Germany. Pediatrics 2011;127:e978–88. 2 Dagan R, Cleper R, Davidovits M, et al. Post-Infectious Glomerulonephritis in Pediatric Patients over Two Decades: Severity-Associated Features. Isr Med Assoc J 2016;18:336–40. 3 Gunasekaran K, Krishnamurthy S, Mahadevan S, et al. Clinical Characteristics and Outcome of Post-Infectious Glomerulonephritis in Children in Southern India: A Prospective Study. Indian J Pediatr 2015;82:896–903. 4 Carceller Lechon F, de la Torre Espì M, Porto Abal R, et al. Acuteglomerulonephritis associated with pneumonia: a review of three case. Pediatr Nephrol 2010;25:161–4.
5 Chiu CY, Huang YC, Wong KS, et al. Poststreptococcal glomerulonephritis with pulmonary edema presenting as respiratory distress. Pediatr Nephrol 2004;19:1237–40. 6 Phillips J, Palmer A, Baliga R. Glomerulonephritis associated with acute pneumococcal pneumonia: a case report. Pediatr Nephrol 2005;20:1494–5. 7 Hibino S, Hoshino A, Fujii T, et al. Post-streptococcal acute glomerulonephritis associated with pneumococcal infection. Pediatr Int 2013;55:e136–8. 8 Ismail IH, Zainudin Z, Othman N. Pneumococcal glomerulonephritis in a healthy child: a case report and literature review. Singapore Med J 2014;55:e69–72. 9 Hyman LR, Jenis EH, Hill GS, et al. Alternative C3 pathway activiation in pneumococcal glomerulonephritis. Am J Med 1975;58:810–4. 10 Zhong J, Yang HC, Fogo AB. A perspective on chronic kidney disease progression. Am J Physiol Renal Physiol 2017;312:F375–84. 11 Misurac J, Nichols KR, Wilson AC. Pharmacologic Management of Pediatric Hypertension. Pediatric Drugs 2016;18:31–43.
Cozzi G, et al. Arch Dis Child Educ Pract Ed 2017;0:1–3. doi:10.1136/archdischild-2017-313123
3
Downloaded from http://ep.bmj.com/ on August 28, 2017 - Published by group.bmj.com
A boy with fever, cough and gross haematuria Giorgio Cozzi, Massimo Maschio, Gabriele Poillucci, Marco Pennesi and Egidio Barbi Arch Dis Child Educ Pract Ed published online August 28, 2017
Updated information and services can be found at: http://ep.bmj.com/content/early/2017/08/28/archdischild-2017-313123
These include:
References
This article cites 11 articles, 2 of which you can access for free at: http://ep.bmj.com/content/early/2017/08/28/archdischild-2017-313123 #BIBL
Email alerting service
Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
