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Systemic Lupus Erythematosus and Latent Renal Tubular Dysfunction

W. H. TU, M.D., F.A.C.P.; and MARTIN A. SHEARN, M.D., F.A.C.P.
Ann Intern Med. 1967;67(1):100-109. doi:10.7326/0003-4819-67-1-100
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Renal tubular acidosis (1), an impairment of renal acid excretion out of proportion to reduction of glomerular filtration rate, has been described in a variety of clinical settings. Its characteristic clinical manifestations are hyperchloremic acidosis, an inability to excrete a highly acid urine, and impaired renal concentrating ability. It may be associated, in the primary form, with renal calculi, nephrocalcinosis, osteomalacia, and potassium depletion (2). Subclinical cases—either asymptomatic or lacking the laboratory findings of the overt cases of renal tubular acidosis—have been uncovered by an acid-loading test designed to detect acid excretion inappropriate to the induced metabolic acidosis (3, 4).


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