Seiju Onodera

Sjögren's syndrome and renal tubular acidosis

Abstract Clinical studies were conducted in four cases of Sjogrens syndrome complicated by renal tubular acidosis (group I) and in ten cases of Sjogrens syndrome without this complication (group II). No differences between the two groups were noted in respect to the ages of the patients or the duration of the disease. Hyperglobulinemia and an increase in serum IgG were observed in three of the four cases in group I, but no difference was found in the degree of increase when comparing the two groups. No differences were observed between the two groups when compared using various serologic tests. Marked lymphocytic infiltration was noted in the biopsy specimens of the lacrimal and parotid glands. In the kidney biopsy specimens in three cases of group I lymphocytic infiltration interspersed with plasma cells was conspicuous in the interstitial tissues. No lymphocytic infiltration was noted in one case without hyperglobulinemia but a marked interstitial fibrosis was seen. No remarkable changes were seen in the renal biopsy tissue in four cases of group II. Accordingly hyperglobulinemia of itself does not appear to be the primary cause of renal tubular acidosis in Sjogrens syndrome. Renal changes appear to represent one of several systemic changes occurring in Sjogrens syndrome. Therefore renal tubular acidosis is probably an inherent result of the disease process responsible for the development of Sjogrens syndrome.

Passive hemagglutination and hemolysis tests for the detection of anti-DNA antibody.

Passive hemagglutination (PHA) and hemolysis (PHL) tests using chromium chloride-treated sheep red blood cells were developed to detect and measure the anti-DNA antibodies. Sonication of native DNA was found to prevent the incidence of non-specific agglutination. Sheep red cells were coated with double-stranded DNA (dsDNA) which had been sonicated and treated with nuclease S1 to digest the single-stranded regions in the DNA. The specificities for dsDNA-coated cells were checked by inhibition studies in PHA test and plaque assay. In clinical studies fairly close correlations were found between the antibodies to DNA and the activity of the disease in patients with systemic lupus erythematosus (SLE). Complement-fixing antibodies were detected in most of SLE patients with active lupus nephritis, but rarely in those in remission. Anticomplementary activity seemed to be negligible in PHL test. These tests are simple and may be useful to the diagnosis and the management of SLE.