Immunohistochemical and serological evidence for the role of streptococcal proteinase in acute post-streptococcal glomerulonephritis.

BACKGROUND: We have previously demonstrated the preferential secretion of streptococcal proteinase or streptococcal pyrogenic exotoxin B (SPEB) by nephritic strains of Group A streptococci isolated from the skin or throat of patients with acute poststreptococcal glomerulonephritis (APSGN). METHODS: To further explore the possible role of SPEB in APSGN, we performed ELISA studies to detect anti-SPEB antibodies in the sera of patients with APSGN, acute rheumatic fever (ARF), scarlet fever (SF) and normal children. Using ELISA, anti-SPEB titers on acute and convalescent APSGN sera were measured to determine immunity to APSGN. We also performed immunofluorescence studies on APSGN and non-APSGN kidney biopsies to probe for the presence and localization of SPEB. RESULTS: Our data show that anti-SPEB antibodies are present in APSGN sera and antibody titers are significantly higher than in ARF, SF and normal sera. Anti-SPEB titers tend to rise acutely and decrease with time but do not reach baseline after one year. When kidney biopsies were probed with rabbit anti-SPEB antibody, 12 of 18 (67%) of the APSGN cases were positive while only 4 of 25 (16%) of the non-APSGN cases were positive. CONCLUSIONS: In summary, we were able to demonstrate unique reactivity to SPEB in human sera and kidney biopsies of APSGN suggesting a significant role of this toxin in the pathogenesis of acute post-streptococcal glomerulonephritis.

Cardiopulmonary recirculation in dialysis. An underrecognized phenomenon.

Access recirculation can be determined by measuring blood temperature or blood water concentration in the dialyzer inlet after injecting a bolus of cold saline into the venous line. In patients with access recirculation, some of the cooled venous blood re-enters the blood inlet line soon after injection, resulting in a sharp transient drop in its temperature. There is also a prompt increase in blood water concentration at the dialyzer blood inlet caused by the dilution effect of the recirculated saline. In this study, data are reported on four patients studied under conditions where no access recirculation could occur because blood was returned to a second access or into a central vein. In these patients, transient cooling of the blood in the dialyzer inlet and a transient hemodilution after venous line injection of cold saline was still observed. These observations can be explained by passage of the injected saline through the heart and pulmonary blood vessels and return of a portion of the cooled blood to the vascular access, bypassing the systemic capillary microcirculation. This "cardiopulmonary recirculation" can cause dilution of urea in dialyzer inlet blood, with resulting errors in urea kinetic modeling and in computing access recirculation.