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Impaired urinary acidification--its incidence in diseases with autoimmune features.

Summary: The function of renal tubular acidification in patients with rheumatoid arthritis, systemic lupus erythematosus, “autoimmune” liver diseases and Sjogren's disease, and in control groups comprising healthy subjects and patients with trauma or vascular disease was studied by measuring urinary pH over six hours after giving ammonium chloride, 0.1 g per kg of body weight. Hypercalcaemia, hyperkalemia and hypokalaemia were excluded in every case. There was no correlation between minimum urine pH reached and serum gamma globulin levels. There was significant impairment of ability to acidify urine in most of the groups of patients with autoimmune diseases, as compared with both control groups; and the control patients over sixty years of age acidified urine less well than did healthy subjects. The few renal biopsies available from patients with impaired acidification showed non-specific changes. It is suggested that autoimmune damage to renal tubules may account for defective urinary acidification in the disease groups studied, but an immunological mechanism specifically reactive with a component of renal tubular cells has not as yet been demonstrated.