PubMed · 50606
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D Brancaccio, E Rivolta, G Rainoldi. 1975. [Glomerular proteinuria].. https://pubmed.ncbi.nlm.nih.gov/50606/
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BACKGROUND AND OBJECTIVE: Even though there are simple and cost-effective means for the early diagnosis of diabetic nephropathy, only a small proportion of diabetics in Germany is regularly tests for microalbuminuria. On the basis of evidence-based knowledge and of international guidelines the PROSIT project (proteinuria screening and intervention) aims to make good this deficiency in the German Federal Republic by introducing nephropathy screening and a structured intervention to improve blood sugar and blood pressure regulation, optimizing lipid metabolism and nutritional intake. It was the aim of this study to assess with a computer-aided diabetes model the clinical value and cost-effectiveness of such an intervention. PATIENTS AND METHODS: From data collected for 589 diabetics who participated in the PROSIT project, the short-time effects after one year on HbA1c, systolic blood pressure and lipid levels were obtained and cost-effectiveness compared with that of standard care. Life expectancy, life-time costs to be met by health insurance and event frequency of the diabetic nephropathy stages were calculated with a Markov model for type 2 diabetics. RESULTS: PROSIT improved individual life expectancy by 0.23 years with reduction of life-time costs by DM 9,772 (ca. $4,900). The cumulative incidence of microalbuminuria was lowered by 30.5%, that of terminal renal failure by 55.9%. Even after discounting the results (i.e. the inclusion of time preference for cost and benefit) and stepwise changes of all variables by +/- 10%, PROSIT remained the more cost-effective variant. CONCLUSION: From a health economy viewpoint PROSIT is superior to standard management. Early recognition of albuminuria and the introduction of a multifactorial treatment strategy make it possible to delay progression to terminal renal failure. In addition to its clinical benefits, prevention of dialysis and transplantation would reduce the annual savings of the health care system by several billion DM.
Diabetic nephropathy is a serious long-term complication of diabetes characterized by persistent albuminuria (> 300 mg/24 h or 200 micrograms/min) associated with a decline in GFR, increasing arterial blood pressure, and high risk of cardiovascular morbidity and mortality. Diabetic nephropathy has become the leading cause of end stage renal disease in Europe, USA and Japan. There is a great inter-individual variation in the deterioration in GFR explained by genetic and non-genetic progression promoters (risk factors for losing GFR). In particular arterial blood pressure, glycaemic control, and albuminuria act as non-genetic promoters of progression. These factors are potentially modifiable. Genetic promoters of progression have also been identified, mainly the angiotensin converting enzyme insertion/deletion polymorphism. Knowledge of progression promoters can identify patients with a poor prognosis and direct therapy against modifiable risk factors, in particular hypertension and hyperglycaemia.
We investigated whether the prevention of the development of diabetic nephropathy by angiotensin-converting enzyme inhibitors is associated with decreases in renal angiotensin-converting enzyme activity and/or blood pressure in diabetic mice. C57Bl/6 mice were injected with streptozotocin (200 mg/kg, i.v.) and randomized to receive either imidapril (1 and 5 mg/kg) or captopril (10 and 50 mg/kg) or vehicle by gavage for 28 days. Each assay was performed on 8-10 mice from each treatment. At 28 days after the start of drug treatment, imidapril and captopril significantly reduced blood pressure of the diabetic mice, and this effect of captopril was stronger than that of imidapril. On the other hand, inhibition of renal angiotensin-converting enzyme activity by imidapril was stronger than that by captopril. Imidapril and captopril dose-dependently inhibited urinary albumin excretion to similar extents, but they failed to inhibit the renal hypertrophy and elevation of creatinine clearance. Total renal angiotensin-converting enzyme activity was significantly reduced in diabetic mice, but immunohistochemical localization of angiotensin-converting enzyme was intensive in the vasculature and glomeruli of the diabetic kidney. In conclusion, both effects on blood pressure and angiotensin-converting enzyme activity may be involved in the prevention of development of diabetic nephropathy by imidapril and captopril in streptozotocin-induced diabetic mice. The data suggest that the degrees of contribution of their effects on blood pressure and renal angiotensin-converting enzyme activity to the inhibition of urinary albumin excretion may be different between the two angiotensin-converting enzyme inhibitors.