Renal vascular A antigen expression correlates to donor A1/A2 subtypes, whereas B individuals show one singular antigen pattern. From antigen perspective, A1 and B donors are a "major" and A2 individuals a "minor" antigen challenge in ABO-incompatible renal transplantation.

The observed frequencies in our study of patients with small vessel vasculitides were higher than those previously documented. We also showed a periodic fluctuation of the annual frequencies and a seasonal variation of symptom onset.

No clinical risk factors for recurrence of immunoglobulin A (IgA) nephropathy in kidney transplants have been defined. This is a single-centre retrospect analysis of recurrence in 104 first kidney transplant patients with biopsy-verified IgA nephropathy. Fifty patients had living donors. All but an identical twin were treated with cyclosporin A. The median follow-up time was 5 yr. Graft biopsies had been obtained from 35 grafts later than 6 months after transplantation, due to deteriorating graft function or gross proteinuria. Thirteen biopsies showed mesangial glomerulopathy proliferative in eleven cases with IgA deposits. Recurrence caused failure of six grafts. Eleven grafts with recurrence were from living donors (p = 0.005). No specific human leukocyte antigen (HLA) was identified as a risk factor. Known duration of original disease until end-stage renal failure was significantly shorter in patients with recurrence (median 5 yr, range 0-25 yr) compared with those without (median of 10 yr, range of 0-37 yr) (p = 0.015). Cumulative graft survival was not reduced in living versus cadaveric donor recipients.

and sheep (between 43 and 53 days: Stokes & Boda, 1968). With a similar method, using antibodies conjugated with peroxidase, Nakane (1970) demonstrated the ultrastructural localization of several pituitary hormones in the adult rat. There are no similar electron microscopic studies on fetal rats to be found in the literature.The content of hormones in the fetal pituitary has also been demonstrated in bio-assay or with radio-immune assay methods. By transplantation of fetal pituitaries or injection of pituitary extracts into immature hypophysectomized tadpoles, Enemar (1960b) demonstrated the debut of hormone activities in pituitaries of fetal mice. With this technique, growth-promoting activity was demonstrated at 17.5 days. By in vitro culture of pituitaries and peripheral organs, the presence of hormone in the fetal pituitary may be demonstrated. In this way, Tixier-Vidal (1958) demonstrated the presence of thyrothrophin in the fetal chicken on the 7th day of gestation. Direct demonstration of pituitary hormone content by radio-immune assay has been performed in the fetal rat by Birge et al. (1967), who reported that STH was not present until the 19th day, the concentration then being 0.2 microgram per pituitary. Studies like these may give information on the presence and quantity of trophic hormones in the fetal pituitary, but, as has been emphasized by Moore (1950), conclusions cannot be drawn concerning the ability of the individual pituitary cell to release its hormones in the intact organism.The vascularization of the fetal pituitary is, from a functional point of view, of great interest in two respects, namely, the possible existence of regulatory mechanisms in the fetus between the hypothalamus and the adenohypophysis and also between the adenohypophysis and other organs. The development of the hypophyseal vascular system was thoroughly investigated in the mouse by Enemar (1961), who demon¬ strated in the light microscope that the primary capillary plexus has already developed and has nerve connection in eminentia mediana at 15.5 days, and that a neurovascular communication of adult type is organized by the 17.5 day stage. The appearance of the corresponding neurovascular communication has not been demonstrated in the rat, as far as is known from the literature, but the primary plexus is supposed to be present at the 15.5 to 16.5 day stage (Enemar, 1961). From this stage onwards, the adenohypophysis may be under the influence of hypothalamic centres.

Pig kidneys were extracorporeally "ex vivo" connected to the circulation of two volunteer male dialysis patients (Breimer et al., this issue). The patients were pretreated by daily plasmapheresis for 3 consecutive days, which reduced the anti-pig lymphocytotoxic titer from 8 to 2 in the first patient and from 8 to 1 in the second patient. The anti-pig hemagglutinating titers were reduced from 32 to 4 in the first patient and from 2 to 1 in the second patient. No drugs, except heparin, were given. The perfusion lasted for 65 min in patient 1 and the experiment was terminated due to increased vascular resistance in the pig kidney. Ultrastructural investigation showed a picture similar to a hyperacute vascular rejection. Immunohistochemical studies showed a weak staining of IgM antibodies, but no IgG in the small arteries and glomeruli. The pig kidney of patient 2 was perfused for 15 min and the experiment terminated due to serious side effects of the patient. Light and electron microscopical investigation showed virtually no structural changes of the kidney tissue and immunostaining for human antibodies was negative. In both patients, serum samples collected 2-5 weeks postperfusion showed a strong anti-pig antibody titer rise (up to 512) which thereafter declined but stabilized on a higher level than before the experiment. The antibody response in the two patients was different. In patient 1, the major anti-pig antibodies directed to carbohydrate antigens were of IgG (IgG1 and IgG2 subclasses) type, while the IgM response was less prominent and virtually no IgA antibodies were produced. Despite the short duration of the perfusion in patient 2, a humoral immune response was seen that was mainly confined to the IgA immunoglobulin class (IgA1 subclass). Blood group glycospingolipid fractions, prepared from the contralateral kidney of the donor pigs, were used for immunostaining with patient serum samples. In both patients, the antibodies produced after the perfusion, mainly recognized the Galα1-3Gal epitope both as part of the "linear B" pentasaccharide but also on more complex carbohydrate structures. Patient 1 was HLA-immunized before the experiment due to a kidney allograft and had a panel reactivity of 85% before the perfusion. No change in the panel reactivity of HLA-antibodies was found after the perfusion experiments. Patient 2 had no HLA antibodies before and remained negative after the perfusion. Patient serum samples collected before and after the perfusion were tested for reactivity against human endothelial cell lines. No antibodies were generated.