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W. H. Tu, MD; M. A. Shearn, MD
Kaiser Foundation Hospital Oakland, Calif

JAMA. 1970;212(10):1707.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

An acidification and concentration defect consistent with renal tubular acidosis has been reported in various disorders of immune activity, including Sjögren's syndrome (Ann Rheum Dis 27:27, 1968), systemic lupus erythematosus (Ann Intern Med 67:100, 1967), and renal homograft rejection (Amer J Med 42:284, 1967). In view of the fact that rheumatoid arthritis often has many clinical and serological features in common with these conditions, it appeared reasonable to expect that an acidification defect might also be found in rheumatoid arthritis. Because of this probability, we have looked for evidence of renal tubular acidosis by means of an acute ammonium chloride loading test (Quart J Med 28: 259, 1959) and a concentration test (Ann Intern Med 67:100, 1967) in a group of 17 patients with rheumatoid arthritis.

The group means for the rate of acid excretion per unit of creatinine clearance (titratable acid, 42µEq/ . . . [Full Text PDF of this Article]

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