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Renal function and injury in infants and young children with congenital heart disease
Jianyong Zheng1, Yong Yao, Ling Han
1Center for Cardiovascular Diseases, PLA Navy General Hospital, Beijing, People's Republic of China. windywarrior@hotmail.com
Insights
Congenital heart disease (CHD) in young children can cause kidney injury, particularly tubular damage in those with severe cyanosis. Glomerular damage was also observed in some severe cases.
Area of Science:
- Pediatric Nephrology
- Cardiovascular Research
- Biomarker Discovery
Background:
- Congenital heart disease (CHD) affects renal function in infants and children.
- Early identification of renal injury in pediatric CHD is crucial.
Purpose of the Study:
- To investigate renal function and injury in infants and young children with CHD.
- To assess kidney biomarkers in different CHD severity groups.
Main Methods:
- Prospective enrollment of 58 children with CHD (aged ≤3 years) and 20 controls.
- Categorization into acyanotic CHD, cyanotic CHD (high/low oxygen saturation), and normal control groups.
- Measurement of urinary microalbumin (MA), N-acetyl-ß-D-glucosaminidase (NAG), and α1-microglobulin (α1-MG) corrected by creatinine (UCr).
Main Results:
- Elevated urinary α1-MG/UCr levels were observed in CHD patients, highest in severe cyanosis (Group III).
- Higher urinary NAG/UCr levels were found in acyanotic (Group I) and severe cyanotic (Group III) CHD.
- Urinary MA/UCr levels were significantly higher in all CHD groups compared to controls.
- Glomerular damage indicators (α1-MG/(α1-MG+MA) <15%) were present in some patients with advanced heart failure or severe cyanosis.
Conclusions:
- Tubular renal injury is prevalent in infants and young children with CHD.
- Severe cyanosis in CHD is associated with the most prominent tubular injury.
- Glomerular injury can occur in a subset of pediatric CHD patients, particularly those with severe cyanosis or heart failure.
Background:
The aim of this study was to investigate renal function and injury in infants and young children with congenital heart disease (CHD).
Methods:
We prospectively enrolled 58 CHD children aged ≤3 years and 20 age-matched controls and divided these into four groups: Group I, acyanotic CHD (n = 24); Group II, cyanotic CHD with arterial oxygen saturation of >75 % (n = 20); Group III, cyanotic CHD with arterial oxygen saturation of ≤75 % (n = 14); Group IV, normal controls (n = 20). Urinary levels of microalbumin (MA), N-acetyl-ß-D-glucosaminidase (NAG), and α1-microglobulin (α1-MG) corrected by creatinine (UCr) were compared.
Results:
Children with CHD had elevated urinary α1-MG/UCr levels, with Group III children having the highest level. Groups I and III children had higher urinary NAG/UCr levels than those of Groups II and IV. Urinary MA/UCr levels in the three patient groups were comparable and significantly higher than that in the control group. A α1-MG × 100/ (α1-MG + MA) of <15 %, indicative of glomerular damage, was present in two patients in Group I and one in Group III, but none in Group II.
Conclusions:
Tubular injury can occur in CHD patients during infancy and early childhood. Among our patient cohort, it was most prominent in children with severe cyanosis. Glomerular injury was detected in some individuals with advanced heart failure or severe cyanosis.
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