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Sickle Cell Disease and NO

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Nitric Oxide and the Kidney

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Abstract

A wide spectrum of functional and anatomical abnormalities occurs in the kidneys of patients with sickle cell disease (SS). In children and young adults, with either SS or SA - sickle cell trait disease, there is a renal concentrating defect which is reversible with blood transfusion [1]. Beyond the age of 15 however, blood transfusions no longer correct the defect. Occlusion of the vasa recta by sickled red blood cells (RBC), leading to tubular atrophy, interstitial scarring, and microinfarcts is thought to underlie the progressive nature of the concentrating defect [12]. More subtle functional disturbances in tubular transport are common and include the inability to sustain a maximum [H+] gradient and impaired K* secretion unrelated to the renin/aldosterone axis [35]. The transport defects do not usually translate into clinically apparent electrolyte disturbances unless some intervening event tips the scales, such as sepsis, excess dietary potassium intake, or a potassium-sparing drug is prescribed [6].

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  1. Norman Bank
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  2. Suzette Y. Osei
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  3. Rexford S. Ahima
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Editors and Affiliations

  1. Department of Medicine, State University of New York, Stony Brook, NY, USA

    Michael S. Goligorsky

  2. Department of Pharmacology, Cornell University Medical College, New York, NY, USA

    Steven S. Gross

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Bank, N., Osei, S.Y., Ahima, R.S. (1997). Sickle Cell Disease and NO. In: Goligorsky, M.S., Gross, S.S. (eds) Nitric Oxide and the Kidney. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6039-5_20

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  • DOI: https://doi.org/10.1007/978-1-4615-6039-5_20

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