Progression of diabetic nephropathy from the stage of macroproteinuria with near-normal renal function until start of dialysis was compared in 16 patients with type I and 16 patients with type II diabetes mellitus. The mean creatinine clearance at the beginning of the study was 89 +/- 13 ml/min/1.73 m2 in patients with type I and 81 +/- 6 ml/min/1.73 m2 in those with type II diabetes. Dialysis was started after a mean interval of 77 (44-133) months, when creatinine clearance had decreased to 8 +/- 2 ml/min/1.73 m2 in type I diabetic patients. The respective figures for type II diabetic patients were 81 (40-124) months and 7 +/- 2 ml/min/1.73 m2. The mean rate of decrease in creatinine clearance was 1.05 +/- 0.45 ml/min/month in type I and 0.91 +/- 0.41 ml/min/month in type II diabetes. The mean rate of decrease was 1.46 +/- 0.30 ml/min/month in type I diabetic patients with a systolic BP > 160 mmHg versus 0.80 +/- 0.42 ml/min/month with < 160 mmHg (P < 0.01). In the type II diabetics the respective figures were 1.38 +/- 0.40 ml/min/month versus 0.78 +/- 0.15 ml/min/month (P < 0.01). During the observation period the prevalence of coronary heart disease increased from 6 to 50% in type I and from 31 to 87% in type II diabetes. In conclusion, the rate of progression of diabetic nephropathy during the predialytic phase is similar in type I and type II diabetes; BP adversely affects the rate of progression to the same extent in both groups.

The objective of the study was to evaluate differences in the perinatal complications and in the 3-year follow up of infants of diabetic mothers with and without diabetic nephropathy stage IV. We compared the fetal and maternal complications and the early postpartal development until 3 years after delivery in 10 children of nephropathic diabetic mothers and 30 children of diabetic mothers without nephropathy. The mean (+/-SD) birthweight of the infants of nephropathic women was 2,250 +/- 496 g versus 3,544 +/- 435 g in the women without nephoropathy (p < 0.01). Births were premature in six pregnancies (60%) of the nephrotic women but in none of the women without nephropathy (p < 0.01). Three infants (30%) of the women with nephropathy showed respiratory distress syndrome in contrast to two babies (6%) of the women without nephropathy. Pre-eclampsia or eclampsia occurred in 6 (60%) pregnant women with and in two women (6%) without diabetic nephropathy (p < 0.01). Nephrotic syndrome was observed in 7 nephrotic women (70%) in contrast to none women without nephropathy. Three years postpartum, six of the children (60%) of nephropathic women had a body weight < the 50th percentile but none of the children of the women without nephropathy did so (p < 0.01). In addition, the children of nephropathic mothers started to speak significantly later (15 +/- 3 versus 12 +/- 13 months postpartum, p < 0.05) and had infectious diseases more commonly (60% versus 6%, p < 0.01) than the children of women without nephropathy. It can be concluded that in pregnancies of diabetic women the birth weights of the infants are significantly smaller and the fetal as well as maternal complication-rates significantly higher than in those of women without nephropathy. Also 3 years after delivery, the body weight of the children of nephropathic diabetic women is significantly lower than that of children of diabetic women without nephropathy. Additionally, children of nephropathic women are retarded in terms of linguistic development and their resistance to infections is reduced.

The influence of pregnancy on the progression of diabetic nephropathy in diabetic women with pre-existing moderate renal insufficiency is a subject of considerable controversy in the literature. In four of five female patients with type I diabetes mellitus with pre-existing impaired renal function (creatinine clearance less than 80 ml/min), significant proteinuria (greater than 2 g/24 h urine) and hypertension we have found a further decline in renal function during pregnancy, with an increased deterioration rate of creatinine clearance in comparison to the time before and after pregnancy. The mean decline of the glomerular filtration rate was 1.8 ml/min per month during pregnancy and 1.4 ml/min per month postpartum until the start of dialysis treatment. The difference in the progression of diabetic nephropathy during and after pregnancy can be explained by increased hypertension during pregnancy, especially in the third trimester, despite an intensified antihypertensive therapy. The long-term effect of pregnancy on renal function in our patients was therefore an earlier requirement for renal replacement therapy than would have been expected without pregnancy.

Two hundred eleven patients with acute ischemic stroke, stage III or IV, received daily intravenous infusion of 500-1000 mL low-molecular dextran (dextran 40) over a period of 4 days. In 10 cases (4.7%) acute renal failure, associated with dextran infusion, could be observed; oligoanuria occurred after a mean time of 4 (3-6) days. The incidence of dextran-induced acute renal failure was significantly higher in patients with a preexisting reduction of glomerular filtration rate below 30 mL/min/1.73 m2 (p < 0.005). Five of the patients (50%) with acute renal failure died within 4-12 days after the hemodilution therapy with dextran 40; this high lethality was due to nonrenal complications.

In 6 male subjects the diurnal variation of urinary oxalic acid excretion was studied after ingestion of chocolate, a food stuff rich in oxalic acid. The ingestion of chocolate caused a striking but transient increase in urinary oxalic acid excretion due to its absorption in the upper gastrointestinal tract. The peak excretion rates occurred 2–4 h after the intake of the chocolate. The peak values were 235% of the fasting excretion rate in the trial with 50 g chocolate and 289% in the trial with 100 g chocolate and reached the amounts found in cases with primary hyperoxaluria. The administration of ranitidine had no influence on oxalic acid absorption. The transient hyperoxaluria observed seems to be an important factor for the formation of calcium oxalate calculi in patients on risk for stone disorders.

We present a 42 year old woman with autoimmune phenomena following breast augmentation, and remission after explantation.

Simultaneous pancreas-kidney transplantation (SPKT) has become the therapy of choice in patients with Type I (insulin-dependent) diabetes mellitus who have end-stage renal disease. During the last decade graft and patient survival have been improved, the 1-year pancreas graft survival rate is currently at 81 % for SPKT [1].Several studies have shown that diabetic retinopathy and peripheral neuropathy are positively influenced by pancreas transplantation [2,3]. A recent study also showed that pancreas transplantation in non-uraemic patients can reverse lesions of diabetic nephropathy, but this is not seen before 5 years of normoglycaemia [4]. Diabetologia (2000) Abstract Aims/hypothesis. The aim of the study was to examine the effect of pancreas-kidney transplantation on the progression of macrovascular diseases in Type I diabetic patients with end-stage renal disease.Methods. The progression of cerebrovascular disease, coronary heart disease and peripheral vascular disease in uraemic patients with Type I (insulin-dependent) diabetes mellitus and who had had simultaneous pancreas-kidney transplantation was compared with that of recipients of a kidney transplant alone. Between 1986 and 1998 a total of 11 uraemic diabetic patients received a simultaneous pancreaskidney transplantation and 10 diabetic patients a kidney transplant alone. All transplants functioned for at least 24 months, the mean observation period was 69 ± 37 compared with 70 ± 33 months in both patient groups. Macroangiopathic diseases were classified in four stages as described earlier.Results. In the group with simultaneous pancreas-kidney transplantation progression of cerebrovascular and coronary heart disease was observed in four patients (36 %) and progression of peripheral vascular disease in five subjects (45 %). In the cohort with kidney transplant alone four patients (40 %) showed progression of cerebrovascular and coronary heart disease and five progression of peripheral vascular disease (50 %); the difference is not significant. Mean values of HbA 1 c (5.8 ± 0.2 vs 7.5 ± 0.6 %, p < 0.001) and serum triglycerides (1.2 ± 0.4 vs 2.0 ± 1.0 mmol/l, p < 0.05) were significantly lower in the patients with pancreas-kidney transplantation than in the patient group with kidney transplant alone. Serum cholesterol concentrations and blood pressures were similar in both cohorts. Conclusion/interpretation. From our results we concluded that pancreas-kidney transplantation reduces risk factors for the development of macroangiopathy but fails to halt progression of macrovascular diseases similar to Type I diabetic patients with kidney transplant alone. [Diabetologia (2000) 43: 231±234]

Hemodialyzed diabetic cigarette smokers show higher fibrinogen and systolic blood pressure values, a higher incidence of myocardial infarctions, and their 5-year survival rate is significantly decreased when compared with nonsmoking patients on hemodialysis.