Erythrocytosis and nephrocalcinosis.
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Biomedical subjects
Publications and source records attributed to O Wrong.
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Distal renal tubular acidosis (dRTA) is not a single disease. The experimental forms of the syndrome are unsatisfactory as models of the naturally occurring disease, not least because they are seldom complicated by nephrocalcinosis, which is present in the majority of patients with spontaneous disease and contributes to the renal tubular defects found in the syndrome. Impairment of minimal urine pH, reduced urine carbon dioxide tension (PCO2) during passage of alkaline urine, and reduced urinary ammonium (NH4+) excretion, have all been advocated as essential criteria for the diagnosis of dRTA. Minimal urine pH, measured during metabolic acidosis, sulphate infusion, or after oral frusemide, is the yardstick against which other criteria should be assessed. A reduced urinary PCO2 is commonly found in dRTA but is not specific for the syndrome and may be accounted for by tubular defects other than those involving reduced distal hydrogen ion secretion. NH4+ excretion is reduced in most patients with renal acidosis whatever the nature of the underlying renal disease; this function is closely related to nephron mass, and is not specifically impaired in renal tubular disease.
Antibody to Tamm-Horsfall glycoprotein in the sera of patients with distal renal tubular acidosis (dRTA) was measured by radioimmunoassay, as well as in samples of normal human serum. Normal human serum contains small amounts of IgG capable of interacting with Tamm-Horsfall glycoprotein. Appropriate assays were carried out on antiserum raised in rabbits against human Tamm-Horsfall glycoprotein serially diluted with normal human serum. Corrections were applied for the presence of interfering substances in serum. The amounts of antibody found in samples of normal and patient sera were not significantly different, although some of the patients were diagnosed as having immune as opposed to familial dRTA. Studies of cell-mediated immunity to Tamm-Horsfall glycoprotein was found not to differentiate between the normal and patient samples. dRTA does not appear to be associated with immune responses to Tamm-Horsfall glycoprotein.
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All three of the major human nitrogenous waste products--urea,, creatinine, and uric acid--are significantly degraded by intestinal bacteria. The breakdown products of creatinine and uric acid are not fully known, but metabolites of these complex heterocyclic nitrogen compounds may well turn out to play a role in uremic toxicity. Urea degradation is almost certainly by way of ammonia, but the exact site of urea hydrolysis in the alimentary tract is not known, and it is uncertain whether urea is the major source of intestinal ammonia. Ammonia is absorbed from the colon predominantly in unionized form, and the bicarbonate ion secreted by the colonic mucosa plays an important role in facilitating this absorption.
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