The role of formaldehyde (CH2O) in the pathogenesis of anti-N-like antibodies found in patients on chronic hemodialysis was investigated. In vitro studies were performed by incubating MM cells in varying concentrations of CH2O for variable time periods, corresponding to conditions that occur in dialysis. This MM cells acquired reactivity to anti-N antibody. The antigenic shift is felt to occur from the interaction of CH2O with the terminal N-acetylneuraminic acid (sialic acid) groups of M substance, resulting in the exposure to an altered-N antigen that is immunogenically active. Through a similar mechanism, CH2O may also directly modify N substance.
Previous studies suggested that renal H+ retention during adaptation to hypocapnia might be critically dependent upon concomitant Na and/or K excretion. To test this hypothesis, seven dogs were allowed to recover from hypocapnia while receiving a low electrolyte diet. Despite negligible changes in Na and K excretion, cum delta net acid excretion was --33 meq during adaptation and +44 meq during recovery. Consequently, plasma [HCO3] fell from 19.2 to 14.2 meq/liter in the former and rose from 13.8 to 19.7 meq/liter in the latter groups; these changes were virtually identical to those observed previously in animals maintained on normal electrolyte intakes. These adaptive changes in renal H+ output appeared to be balanced by parallel changes in phosphate excretion. When phosphate retention was prevented during adaptation with Na remaining available for excretion, retention of H+ was still clearly evident. When both phosphate retention and augmented cation excretion were prevented during adaptation, however, H+ retention was abolished. Nevertheless, plasma [HCO3] still fell from 20.9 to 16.2 meq/liter, a level far beyond that attributable to tissue buffering.
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