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Pediatric Pyelonephritis

  • Author: Patrick B Hinfey, MD; Chief Editor: Russell W Steele, MD  more...
 
Updated: Sep 30, 2015
 

Background

Findings on nuclear renal scans suggest that the vast majority of infants and young children with febrile urinary tract infections (UTIs) have acute cases of pediatric pyelonephritis. Early recognition and prompt treatment of UTIs, which are relatively common infections in children, is important to prevent late sequelae, such as renal scarring, hypertension, and renal failure.[1] When assessing the pediatric patient with UTI, one may encounter few specific symptoms. Older children are most likely to have symptoms attributable to the urinary tract. (See Treatment and Medication.)

In the pediatric patient it may be difficult, and sometimes impossible, to differentiate pyelonephritis, an upper-tract infection, from cystitis, a lower-tract infection that is characterized by voiding-related symptoms with or without fever and often without other systemic signs. Febrile UTI should be assumed to be pyelonephritis and treated accordingly. (See History, Physical Examination, and Workup.)

Complications

Dehydration is the most common acute complication of pyelonephritis. Intravenous (IV) fluid replacement is necessary in severe cases. Acute pyelonephritis may lead to renal abscess formation. Long-term complications include renal parenchymal scarring,[2] hypertension, decreased renal function, and, in severe cases, renal failure. Renal scarring with long-term renal insufficiency is a significant concern.[3] (See Prognosis.)

Patient education

For patient education information, see Urinary Tract Infections.

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Etiology

UTIs are generally ascending in origin and caused by perineal contaminants, usually bowel flora. However, in neonates, infection is assumed to be hematogenous in origin rather than ascending. This feature may explain the nonspecific symptoms associated with UTI in these patients. After the neonatal period, bacteremia is generally not the source of infection; rather, UTI or pyelonephritis is the cause of the bacteremia.

Bacterial pathogens are the most common cause of pyelonephritis. Bacterial sources of pyelonephritis include the following:

  • Escherichia coli - This is by far the most common organism, causing more than 90% of all cases of acute pyelonephritis
  • Extended-spectrum beta-lactamase–producing E coli is becoming more frequent [4]
  • Klebsiella oxytoca and species
  • Proteus species
  • Enterococcus faecalis and species
  • Gram-positive organisms, including staphylococcal species and group B Streptococcus - These are rare causes of acute pyelonephritis

Risk factors

High-grade vesicoureteral reflux (VUR) may increase the risk for pyelonephritis, and VUR has been reported in as many as 33% of children with acute pyelonephritis. Congenital or acquired anomalies, including dysplasia, hypoplasia, and obstruction, increase the risk for UTI, VUR, and pyelonephritis. Even in the absence of urinary tract abnormalities, cystitis may result in VUR or worsen preexisting VUR and lead to pyelonephritis. VUR increases the risk for and size of renal cortical lesions, although clinically significant lesions can develop in the absence of VUR.

Delayed or incomplete voiding, as seen with neurogenic bladder, obstruction, or dysfunctional voiding increases the risk for urinary stasis and overgrowth of colonizing bacteria. Constipation may impair bladder emptying, leading to stasis and ascending infection.

Catheterization may increase the risk of introducing periurethral bacteria into the bladder. Clean intermittent catheterization leads to colonization of the bladder that might lead to pyelonephritis if stasis allows any infection to ascend.

Boys who are uncircumcised have a risk of UTI that is 2.2% higher than that of circumcised boys. The risk of acute pyelonephritis is not established.

Sexual activity may cause urethral inflammation, lead to bladder colonization, and increase the risk for acute pyelonephritis.

Familial inheritance of susceptibility to pyelonephritis may be related to chemokine receptor inheritance. Host genetic factors that promote inflammation contribute to renal scarring. Interleukin (IL)-8 and CXCR1 polymorphisms, ACE insertion/deletion (ACE I/D) gene polymorphism, and tumor necrosis factor-[alpha] polymorphism have been identified as potential mediators to tissue fibrosis and subsequent renal scarring following acute pyelonephritis.[5]

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Epidemiology

Occurrence in the United States

The prevalence of pyelonephritis varies by age and sex. About 60-65% of children with febrile UTIs have acute pyelonephritis, as defined by presence of abnormalities of the renal cortex on dimercaptosuccinic acid (DMSA) scan.[6] In general, 2.7-4.1% of children younger than 2 years who have fever also have UTI, even if another source is identified. UTI is present in 17% of white girls younger than 2 years with fever (temperature >39°C).

Race-, sex-, and age-related demographics

The prevalence of urinary infection is 5-fold greater in white children than in black children and 2-fold greater than in children of other races.

The prevalence of UTI in uncircumcised males is 8 times greater than it is in circumcised males in the first year of life. In addition, the incidence of UTI is higher in uncircumcised male infants than in female infants. After age 12 months, UTIs are more frequent in girls than in boys.

In neonates, infection is generally hematogenous in origin. Girls younger than 11 years have a 3-5% risk of infection. For boys younger than 11 years, the risk is 1%. Febrile infants are more likely (6-8%) to have UTI as a source of fever than they are to be bacteremic (< 1%).[7] Children aged 1-5 years have a 3-fold increased risk of acute pyelonephritis on DMSA scanning compared with infants, whereas children older than 5 years have a 4.5-fold greater risk of acute pyelonephritis when evaluated for febrile UTI.

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Prognosis

Most cases of pyelonephritis respond readily to antibiotic treatment without further sequelae. Permanent renal scars develop in 18-24% of children after acute pyelonephritis. Treatment within 5-7 days from the onset significantly reduces the formation of renal scars.

For patients with severe cases or chronic infections, appropriate treatment, imaging, and follow-up help to prevent long-term sequelae.

VUR often resolves without permanent damage. Recurrent pyelonephritis in the setting of VUR may be an indication for ureteral reimplantation.

Morbidity and mortality

Acute mortality is uncommon and is related to sepsis. Generalized bacteremia or sepsis may develop from pyelonephritis. In patients younger than 2 years with acute pyelonephritis, 8-10% have bacteremia.

Acute renal parenchymal injury occurs in 20-90% of children with acute pyelonephritis. About 40% of these children have long-term renal scarring, which may lead to hypertension and renal insufficiency. Risk factors for renal scarring include young age, treatment delay, infection by P-fimbriated E coli and VUR. Treatment of pyelonephritis within the first 5-7 days after onset is necessary to prevent renal damage.

Impaired renal tubular function and secondary pseudohypoaldosteronism may develop in infants with pyelonephritis. Infants may develop hyperkalemia and hyponatremia.

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Contributor Information and Disclosures
Author

Patrick B Hinfey, MD Emergency Medicine Residency Director, Department of Emergency Medicine, Newark Beth Israel Medical Center; Clinical Assistant Professor of Emergency Medicine, New York College of Osteopathic Medicine

Patrick B Hinfey, MD is a member of the following medical societies: American Academy of Emergency Medicine, Wilderness Medical Society, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Stephen C Aronoff, MD Waldo E Nelson Chair and Professor, Department of Pediatrics, Temple University School of Medicine

Stephen C Aronoff, MD is a member of the following medical societies: Pediatric Infectious Diseases Society and Society for Pediatric Research

Disclosure: Nothing to disclose.

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Andrea CS McCoy, MD Associate Professor of Pediatrics, Temple University School of Medicine; Chief Medical Officer, Jeanes Hospital

Andrea CS McCoy, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Application of low-risk criteria and approach for the febrile infant: A reasonable approach for treating febrile infants younger than 3 months who have a temperature of greater than 38°C.
 
 
 
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