TABLE I.

Pathophysiology of Albuminuria in Sickle Cell Disease

Proposed mechanisms	References
Hyperfiltration	[15–18]
Glomerular hypertension	[7,8,19,20]
Ischemia-reperfusion injury/oxidative stress	[21–24]
Decreased nitric oxide bioavailability due to hemolysis and/or increased levels of soluble fms-like tyrosine kinase-1	[25–29]
Chronic treatment with opioid analgesics	[30]