Since Herrick's first reported case,1 sickle cell disease has become a well described clinical and pathologic entity. The usual renal manifestations are of minor importance until late in the disease. Traces of albumin or urobilin or a few casts are found in the urine in some cases; in others the urine is essentially normal.2
The lesions in the kidneys, as elsewhere, stem from the fundamental tendency of the abnormally shaped erythrocytes to become blocked up in the small arterioles and capillaries. Early in the disease, renal sections exhibit vascular stasis and congestion. Later, after multiple small thromboses and infarctions, the kidneys show more or less extensive fibrosis with deposition of blood pigments.2e As more and more glomeruli are destroyed, renal function deteriorates and there may be terminal uremia.3
We could find only one report in the literature in which gross hematuria was a prominent feature of
ABEL MS, BROWN CR. SICKLE CELL DISEASE WITH SEVERE HEMATURIA SIMULATING RENAL NEOPLASM. JAMA. 1948;136(9):624–625. doi:10.1001/jama.1948.72890260003008a
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