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Persistent non-gastrointestinal metabolic acidosis in pediatric HIV-1 infection
Rana Chakraborty1, Constancia S Uy, James M Oleske
1Department of Child Health, St. George's Hospital and Medical School, London UK.
Insights
Non-gastrointestinal acidosis, including high anion gap and renal tubular types, affects 17% of HIV-infected children. These conditions are linked to growth failure and specific antibiotic prophylaxis in advanced HIV disease.
Area of Science:
- Pediatric Nephrology
- Infectious Diseases
- HIV Medicine
Background:
- Metabolic acidosis is a potential complication in children with Human Immunodeficiency Virus type 1 (HIV-1) infection.
- Understanding the types and clinical associations of acidosis is crucial for managing pediatric HIV patients.
Purpose of the Study:
- To determine the incidence of non-gastrointestinal renal tubular acidosis and high anion gap acidosis in HIV-1-infected children.
- To identify clinical parameters associated with these acidosis types.
Main Methods:
- Retrospective review of 202 HIV-1-infected children to identify metabolic acidosis.
- Prospective analysis of serum and urine chemistries for persistent non-gastrointestinal acidosis.
- Calculation of serum anion gap (SAG) and urine anion gap (UAG).
Main Results:
- Persistent acidosis was observed in 17% of children (34/202).
- Elevated SAG acidosis occurred in 47% (16/34), and distal renal tubular acidosis in 53% (18/34).
- Acidosis was associated with Pneumocystis carinii pneumonia prophylaxis, shorter height, and more advanced HIV disease (CDC C3 classification).
Conclusions:
- High anion gap acidosis and renal tubular acidosis are prevalent in HIV-infected children with advanced disease.
- These conditions may contribute to growth failure and are potentially linked to sulfur/sulfone-containing antibiotic prophylaxis.
- HIV infection and its treatments may cause renal tubular damage, warranting further investigation into the causes of elevated SAG acidosis.
Objectives:
To determine the incidence and to identify the clinical parameters associated with non-gastrointestinal renal tubular and high anion gap acidosis in a cohort of HIV-1-infected children.
Methods:
Records of 202 HIV-1-infected children were reviewed to identify patients with metabolic acidosis. Serum and urine chemistries of those children with persistent non-gastrointestinal acidosis were then studied prospectively. Serum and urinary anion gaps (SAG and UAG) were calculated. Those with acidosis (group 1) were compared with children without acidosis (group 2). Associations were determined with Pediatric HIV classification, height, weight, antiretroviral therapy, and Pneumocystis carinii pneumonia prophylaxis.
Results:
Persistent acidosis was noted in 34 out of 202 children (17%): 16 out of 34 (47%, group 1A) had elevated SAG acidosis, and 18 out of 34 (53%) had normal SAG acidosis with a positive UAG (distal renal tubular) acidosis (group 1B). Those with acidifying defects more often received P. carinii pneumonia prophylaxis (P = 0.02 and 0.01 for groups 1 and 1A, respectively) independently of HIV-1 classification. This group was shorter in height than group 2 (P = 0.007). Differences in weight were not significant (P = 0.1). However, acidotic subjects were more immunocompromised than those in group 2 (multivariate P < 0.001 for HIV classification C3).
Conclusions:
Elevated SAG acidosis and renal tubular acidosis are not uncommon among HIV-infected children with advanced disease. These disorders may be associated with height growth failure and prophylaxis with sulfur/sulfone containing antibiotics. HIV infection and/or its associated therapies may cause renal tubular damage. The causes of elevated SAG acidosis require further investigation.