We thus can conclude that the pathology in sickle cell nephropathy is not only confined to the lesions in the renal medulla. These medullary vascular lesions implicate changes in water and sodium handling which, however, are compensated for by changes in other segments of the nephron. Evidence arises that the latter is mediated by an increase in renal vasodilating prostaglandins. The characteristic lesion of the kidney in SCA thereby offers an interesting model to study renal function in general. The way in which abnormalities in renal medullary functions are counterbalanced in this disease can lead to insight in the water and salt handling in other kidney diseases as well.
CITATION STYLE
De Jong, P. E., & Van Eps, L. W. S. (1985). Sickle cell nephropathy: New insights into its pathophysiology. Kidney International. https://doi.org/10.1038/ki.1985.70
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