The etiological relationship of infections to the diffuse form of acute and subacute nephritis is a problem which for many years has commanded attention, but has rarely received more than casuistic study.L6hlein (a) in 1907 described in detail the early lesions of the glomeruli in acute glomerular nephritis, as well as the subsequent changes that took place in the kidney during the subacute and chronic stages of the disease. Since a large proportion of his cases of acute and subacute nephritis occurred in patients suffering from various forms of infection, usually due to streptococci, he concluded that in the vast majority of cases acute glomerular nephritis was the direct result of streptococcus infection. Fahr (1912), somewhat later,pointed out the frequency with which acute glomerular nephritis was preceded or accompanied by infections particularly those due to streptococci, while Volhard and Fahr (1914) inflammation, it has been the idea of other observers (Schridde (1913)) that the diffuse lesions in the glomeruli are caused by the elimination of a toxin, produced by streptococci or by other bacteria in a focus of infection distant from the kidney.The demonstration by Dochez (1924) and by Dick and Dick (192 la) that a type of hemolytic streptococcus is the cause of scarlet fever adds fresh incentive to investigations on this problem, for the post scaratinal nephritis has always been considered as the prototype of the diffuse glomerular variety. The experiments, moreover, of Dick and Dick (1924b) on the elaboration of a filterable "toxin" by Streptococcus scarlatinae indicate still further methods which might be applicable to studies upon nephritis.It has seemed to us important to investigate two phases of the problem, first the relationship of acute infections to the onset of glomerular nephritis, and secondly the relation of infections to the progress of nephritis. If streptococcus infections of the upper respiratory tract, such as tonsillitis, sinusitis, etc., are directly responsible for the onset of glomerular nephritis, the progress of the disease might bear some relationship to the course of the infection. With the subsidence of the infection and disappearance of the infecting organism one might expect recovery from the nephritis, provided the kidney itself is not the seat of active bacterial growth; while progression of the nephritis to a subacute or chronic stage might be accompanied by persistence or exacerbations of the infection such as those of the upper respiratory tract, or at least by the continued presence of the infecting organism in these situations.With this idea in mind it has been possible to study forty cases of acute or subacute glomerular nephritis in young adults, and in twentyseven of these to follow the course of the disease with some care over a period varying from a few months to four years. Cases of focal nephritis occurring in bacterial endocarditis were excluded.The ages of the patients were as shown on page 4. Most patients were seen within a few days to a few weeks of th...

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IntroductionChronic intestinal failure is defined by the lack of absorption of micronutrients, macronutrients or water requiring intravenous support. The absorptive capacity of the gut is determined by length of gut present in continuity, enteric adaptation and speed of transit. Frequently patients require intravenous micronutrient support. Following intestinal transplant (ITx) the graft is able to absorb both micro and macronutrients such that parenteral nutrition (PN) is no longer required. We studied transplanted patients in a single centre to assess the absorption of micronutrients.MethodThis was a retrospective analysis of a prospective database. Results were taken from patients being assessed for ITx, then at 3 monthly intervals, and then yearly. Data are inclusive of results either side of the specified timepoint. Data were analysed on Prism using one-way ANOVA and Tukey multiple comparisons test. Data reported as mean ±95% confidence interval.Results34 patients received 35 transplants. Mean age was 41.9y (range 23–73). M/F: 22:14. Median follow up was 774d (range 16–3029). Indications included Crohn’s disease (7/36,19%), intra-abdominal desmoids (4/36,11%), visceral neuromyopathy (5/36,14%), vascular ischaemia (6/36,17%), radiation enteritis (2/36,6%), NET (1/34,3%), pseudomyxoma peritonii (6/36,17%) and other (5/36,13%). Zinc, folic acid, B12, Vitamin A and Vitamin D were significantly different using one way ANOVA: Zinc (p<0.0001) with significant Tukey for pre-ITx (16.9±1.07) vs. 12m (14.2±1.2,p<0.05), vs. 24m (13.5±1.5,p<0.05), vs. 36m (12.9±1.4,p<0.005) and vs. 48m (13.2±1.2,p<0.005); Folic acid (p=0.0006) with significant Tukey for pre-ITx (10.1±0.9) vs. 3m (6.6±1.0,p<0.05), vs. 6m (5.71±1.3,p<0.05); and between 3m vs. 24m (11.7±2.5,p<0.005) and 6m vs. 24m (p<0.005); B12 (p=0.0349) with significant Tukey for 6m (883.2±202.8) vs. 24m (555.8±121.3); Vitamin A (p<0.0001) with significant Tukey for pre-Tx (1.87±0.41) vs 3m (3.27±0.56,p<0.001), 3m vs. 24m (1.79±0.32,p<0.001) and vs. 48m (2.22±0.34,p<0.05), 6m (2.80±0.55) vs. 24m (p<0.05); Vitamin D (p=0.0469) without significant Tukey for any timepoints.ConclusionObserving micronutrient changes aids our understanding of transplanted graft function and nutritional intake. The reduction in zinc, folate and B12 is perhaps more physiological than clinically significant, as the levels were within the normal range and may reflect over-treatment when on PN, though it is interesting to observe folate rising back to a higher level after 6m. It is reassuring to observe that the ITx is not deleterious to micronutrient metabolism.Disclosure of InterestNone Declared

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