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.
From the From the Department of Child Health, St. George's Hospital and Medical School, London UK, the aDepartment of Pediatrics, University of Medicine and Dentistry, New Jersey Medical School, Newark, New Jersey, and the bDepartment of Child Health, at Queen Mary's School of Medicine and Dentistry, Royal London Hospital, Luckes House, Stepney Way, Whitechapel, London, E1 1BB.
Requests for reprints to: Reprint requests to G. D. McSherry, Department of Pediatrics, MSB F570A, UMD-New Jersey Medical School, 185 S. Orange Ave, Newark NJ 07103, USA.
Correspondence to R. Chakraborty, Department of Child Health St George's Hospital and Medical School, Blackshaw Rd, Tooting, London SW17 0QT, UK.
Note: This work was presented at the meeting of the American Pediatric Society/Society for Pediatric Research. May 1999, San Francisco, California, USA.
Received: 21 February 2002; revised: 6 September 2002; accepted: 8 November 2002.