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R Preuss

Publications and source records attributed to R Preuss.

25 records · Page 2Linked to original sources
PubMed1991

[Beta 2-microglobulinuria in cytomegalovirus infections following kidney transplantation].

In a prospective study the occurrence of cytomegalovirus (CMV) infection was diagnosed by demonstrating CMV-immediate early antigen (IEA) in the blood in 13 out of 68 (19%) patients who had undergone renal transplantation (27 women, 41 men, mean age 46.3 [21-64] years). Twenty-four hour urine samples were collected at the same time for quantitative determination of selected marker proteins by immunoluminometric assays (IgG and transferrin as glomerular markers, alpha 1-microglobulin and beta 2-microglobulin as tubular markers). In all 13 confirmed cases of CMV infection there was an isolated rise in urinary beta 2-microglobulin excretion amounting to more than three times the normal. In 11 of the 13 cases the beta 2-microglobulinuria was noted before the CMV-IEA test became positive. This suggests that quantitative assay of beta 2-microglobulin in the urine may be of value in the early diagnosis of CMV infection--a matter of some prognostic importance--and may hence offer additional support for therapeutic decisions.

Adult↗
PubMed1975

Effect of D-penicillamine on lymphocyte function.

Lymphocyte stimulation by different stimulating agents was dose dependently inhibited by D-penicillamine (Metalcaptase-R). The influence of D-penicillamine on the lymphocyte metabolism after the stimulation was established, was time dependently reduced. After preincubation of lymphocytes with D-penicillamine the lymphocyte metabolism was dose dependently reduced. The inhibition of the mixed lymphocyte cultures was by far less extensive after preincubation of the stimulator cells than of the responder cells. HeLa-cells were dose dependently inhibited by D-penicillamine, too. From these results there is much to be said for the assumption that D-penicillamine acts at the level of the cell membrane. D-Penicillamine seems to affect "membrane dependent" metabolic processes rather than block antigenic or other immunologically relevant structures.

Adult↗