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Background/aims-Simultaneous pancreas and kidney transplantation (SPK) has become an important option in selected IDDM patients with end stage renal disease (ESRD). Successful SPK transplants are associated with long term normoglycaemic control and improved quality of life. However, debate still continues on the benefit to patients in terms of stabilisation or amelioration of diabetic retinopathy. The progression of diabetic retinopathy (DR) in a cohort of 20 SPK transplant patients is reported. Methods-All patients were reviewed postoperatively with corrected visual acuity, slit lamp examination, and fundal biomicroscopy. Preoperative data were collected retrospectively and DR was considered unstable if there had been a drop in Snellen acuity greater than three lines or a need for laser photocoagulation or vitrectomy in the 2 years preoperatively. Results-20 patients who received SPK transplants between March 1983 and April 1994 were reviewed (mean age 35.1 years; mean duration of IDDM = 24.6 years). 17 patients still had functioning grafts at a mean follow up of 5.1 years. Nine of these patients had unstable DR before transplantation. Of these, 89% (8/9) had stabilised DR following transplantation with only a single case requiring laser photocoagulation. Of the eight patients that had stable DR before transplantation all had stable DR following transplantation. 41% of cases (7/17) required cataract surgery during the follow up period. Conclusions-Advanced diabetic retinopathy is present in a high proportion of cases managed with SPK transplant as a consequence of the duration of IDDM and the presence of ESRD. More than 90% of cases have stable DR following transplant. (Br J Ophthalmol 2000;84:736-740)

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SUMMARY The realisation that circulating gastrin is heterogeneous necessitates a reappraisal of gastrin's role in the increased incidence of duodenal ulcer disease that occurs in chronic renal failure. Radioimmunoassays employing region-specific antisera have been used to examine renal and extrarenal factors controlling serum gastrin concentration in patients with chronic renal failure. The present study has shown that basal serum gastrin concentrations measured with a carboxyl-terminal specific antibody were significantly higher in eight patients with chronic renal failure treated by dietary restriction (388±196 pM) than in 14 patients with chronic renal failure treated by haemodialysis (28.7 ±4.6 pM). However, basal gastrin concentrations in both groups of patients were significantly higher than in 25 normal subjects (12.3 ±1.8 pM) and showed significant negative correlations with maximal gastric acid secretion (p < 00 1). Markedly raised basal gastrin concentrations were observed only in chronic renal failure patients who were also achlorhydric. Although the peak postprandial increment in big gastrin concentration in 1 1 chronic renal failure patients (34 0± 75 pM) was significantly greater (p <0.05) than in 25 normal subjects (19.5±46 pM), the little gastrin responses were not significantly different. In addition, clearance of exogenous little gastrin was similar in four chronic failure patients (clearance half time: 8 1 ±0-7 min) and four normal subjects (clearance half time: 6.5 ±1.2 min). These studies suggest that the human kidney is unimportant in the metabolism of little gastrin. As circulating little gastrin is six times more potent than big gastrin in stimulating acid secretion, these studies suggest that the raised gastrin concentrations observed in patients with chronic renal failure have little significance in terms of their increased incidence of duodenal ulcer disease.An increased incidence of duodenal ulcer disease, hyperchlorhydria,1 and hypergastrinaemia2 3 has been described in patients with chronic renal failure (CRF). However, it is unclear whether the hypergastrinaemia is causally related to either the hyperchlorhydria or the propensity for these patients to develop ulcers. Studies in the dog have demonstrated a significant arteriovenous difference in gastrin concentrations across the kidney4 and a decreased clearance of exogenous gastrin from the circulation after bilateral nephrectomy.5 As a result of these findings it has been assumed that the hypergastrinaemia observed in CRF patients is a reflection of altered metabolism. However, this supposition has not been confirmed by the direct measurement of the metabolic clearance of gastrin in patients with chronic renal failure.