Research Article| Volume 76, ISSUE 4, P632-640, October 1970

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Renal circulatory studies in young adults with sickle cell anemia

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      Renal hemodynamics were examined in young adult patients with sickle cell anemia (SS hemoglobin) during a stable period of their disease and compared with those of control subjects. There was no evidence of renal disease except for the concentrating defect, which was present in every patient studied. The previously described elevation in glomerular filtration rate (GFR) and in renal plasma flow (RPF) was confirmed in these patients, while total renal blood flow (RBF) was shown to be normal or moderately increased. The additional perfusion of blood through the kidney was demonstrated by an increase in cortical plasma flow (CPAH). The renal extraction of p-aminohippurate (EPAH) was normal or low in every patient studied. Insofar as EPAH represents the intrarenal distribution of blood between cortex and medulla, noncortical plasma flow (NCPF), including medullary blood flow (MBF), was either normal or increased. None of the patients had a decreased MBF as was previously believed. While the mechanism responsible for the increase in renal hemodynamics in patients with sickle cell anemia remains unknown, a causal relationship may exist between these circulatory changes in the renal medulla and the associated impairment in urinary concentration. These changes in the present study would seem to indicate that the renal concentrating defect has a functional basis in early life which may be caused, at least in part, by an increase in MBF.
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