Key result
Children with sickle cell disease had significantly higher urinary ACE activity compared to healthy controls (median 0.01 vs 0.00 mU/mL·creatinine, p<0.001).
Why the study?
Sickle cell nephropathy begins in childhood, but there is little information regarding alterations in circulating and urinary ACE activity in children with SCD.
Are serum and urinary ACE 1 activities altered in children with sickle cell disease compared to healthy controls?
Cross-Sectional
Are serum and urinary ACE 1 activities altered in children with sickle cell disease compared to healthy controls?
Children with sickle cell disease exhibit elevated urinary ACE 1 activity despite normal serum levels, suggesting intrarenal renin-angiotensin-aldosterone system activation that may contribute to sickle cell nephropathy.
Higher urinary ACE in SCD children may flag early intrarenal RAAS activation; hypothesis-generating and should not yet change practice.
INTRODUCTION: Sickle cell nephropathy begins in childhood and presents early increases in glomerular filtration, which, over the long term, can lead to chronic renal failure. Several diseases have increased circulating and urinary angiotensin-converting enzyme (ACE) activity, but there is little information about changes in ACEs activity in children with sickle cell disease (SCD). OBJECTIVE: We examined circulating and urinary ACE 1 activity in children with SCD. METHODS: This cross-sectional study compared children who were carriers of SCD with children who comprised a control group (CG). Serum and urinary activities of ACE were evaluated, as were biochemical factors, urinary album/creatinine rates, and estimated glomerular filtration rate. RESULTS: Urinary ACE activity was significantly higher in patients with SCD than in healthy children (median 0.01; range 0.00-0.07 vs median 0.00; range 0.00-0.01 mU/mL·creatinine, p < 0.001. No significant difference in serum ACE activities between the SCD and CG groups was observed (median 32.25; range 16.2-59.3 vs median 40.9; range 18.0-53.4) mU/m`L·creatinine, p < 0.05. CONCLUSION: Our data revealed a high urinary ACE 1 activity, different than plasmatic level, in SCD patients suggesting a dissociation between the intrarenal and systemic RAAS. The increase of urinary ACE 1 activity in SCD patients suggests higher levels of Ang II with a predominance of classical RAAS axis, that can induce kidney damage.
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Hsien et al. (2021) conducted a cross-sectional in Sickle Cell Disease. Sickle Cell Disease vs. Healthy children was evaluated on Urinary ACE activity (mU/mL·creatinine) (p=<0.001). Children with sickle cell disease had significantly higher urinary ACE activity compared to healthy controls (median 0.01 vs 0.00 mU/mL·creatinine, p<0.001).
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