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      Tubular Peptide Hypermetabolism and Urinary Ammonia in Chronic Renal Failure in Man: A Maladaptive Response?

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          Abstract

          Excessive renal tubular peptide uptake and degradation reflecting hypercatabolism may be a maladaptive response in chronic renal failure (CRF). It may also offer an explanation for the increased ammoniagenesis, per surviving nephron, observed in CRF but as yet unexplained. Neither has been explored in man. We have shown in patients with normal renal function and heavy (>5.0 g/24 h) proteinuria that tubular catabolism of a technetium-labelled peptide marker, aprotinin, and urinary ammonia were increased compared to others with less proteinuria. We now measure tubular kinetics of aprotinin and urinary ammonia in 16 CRF patients with variable proteinuria. Metabolism and turnover of aprotinin and ammonia excretion were increased, corrected for glomerular filtration rate, to levels found in patients with normal function and heavy proteinuria.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1998
          July 1998
          22 June 1998
          : 79
          : 3
          : 306-311
          Affiliations
          a Regional Renal Unit and Departments of b Nuclear Medicine and c Clinical Chemistry, Royal Liverpool University Hospital, Liverpool, UK
          Article
          45054 Nephron 1998;79:306–311
          10.1159/000045054
          9678431
          © 1998 S. Karger AG, Basel

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          Page count
          Pages: 6
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          Self URI (application/pdf): https://www.karger.com/Article/Pdf/45054
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