caa a22 4500 469128836 CHVBK 20180323133158.0 cr unu---uuuuu 170328e19920601xx s 000 0 eng 10.1007/BF00572545 doi (NATIONALLICENCE)springer-10.1007/BF00572545 Schmitz Anita Medical Department M., Aarhus Kommunehospital, DK-8000, Aarhus C., Denmark aut The kidney in non-insulin-dependent diabetes [Elektronische Daten] Studies on glomerular structure and function and the relationship between microalbuminuria and mortality [Anita Schmitz] Summary: Disabilities and mortality from cardiovascular causes are the most important clinical consequences of type 2 (non-insulin-dependent) diabetes, whereas endstage renal failure (ESRF), the eventual outcome of diabetic glomerulopathy, seems to be of a rather low frequency (3-8%). Nevertheless, due to the high prevalence of type 2 diabetes nephropathy is an important health care problem also in these patients. This was only recently realized, and former studies on kidney function and structure have been very sparse, in contrast to the well-described natural course in type 1 (insulin-dependent) diabetes from early hyperfunction to ESRF (30-40%). One of the issues of the present studies was therefore to describe kidney function in (Caucasian) type 2 diabetic patients, as well as to obtain quantitative measures of glomerular structure. Compared with type 1 diabetes both similarities and dissimilarities in function and morphology were seen. This led to a discussion of the potential pathogenetic role of glomerular hyperfunction and hypertrophy to the development of nephropathy, including the consequences of uninephrectomy. Microalbuminuria is an increased urinary albumin excretion, but below the level of clinical proteinuria (20-200 μg/min≈30-300 mg/24 h), and has during recent years been established as a main parameter in type 1 diabetes. Persisting microalbuminuria characterizes patients with ‘incipient' nephropathy that is those who will progress to overt nephropathy with a high probability. Consequently, intervention measures have been introduced that postpone yet do not prevent the deterioration of kidney function in patients with incipient nephropathy as in those with overt disease. The relations between kidney function, microalbuminuria and cardiovascular disease and mortality were therefore addressed in type 2 diabetic patients. The results of the present study may be summarized as follows: the structural lesions of diabetic glomerulopathy are similar in the two types of diabetes at least at the light microscopic level, but the natural course of diabetic nephropathy reveals itself differently. The incidence and prevalence of diabetic nephropathy is unsettled in type 2 diabetes, but approximately half the diabetic patients treated for ESRF are reported to have the type 2 variety. Progression of nephropathy appears, however, slower and less detrimental than in IDDM, at least in our part of the world. Deaths from uraemia are rather rare, and the ultimate prognosis depends primarily on cardiovascular complications. The characteristic sizeable renal hyperfunction seen in type 1 diabetes during at least a decade of insulin dependence is absent in type 2 diabetes. Overall both glomerular filtration rate (GFR), and kidney volume (KV) as well as glomerular volume (N·V,V0) are not increased, but with a few exceptions. In the newly diagnosed patient with type 2 diabetes poor control is associated with a modest relative hyperfunction and hypertrophy as well as an increased urinary excretion of albumin, with reversal during treatment. KV, but not GFR, was increased in patients with microalbuminuria. Morphometric studies demonstrate that the volume of open glomeruli shows a positive linear association with frequency of glomerular occlusion. These findings are compatible with the notion of compensatory hypertrophy. It has been put forward that hyperfiltration plays an improtant role in the development of diabetic nephropathy; a notion based primarily on investigations in experimental rats with renal ablation and/or diabetes, and supported by a few clinical studies. The potential pathogenetic role of hyperfiltration in the progression of chronic renal failure, and particularly in the initiation of diabetic nephropathy, is, however, still a matter of controversy. We found that long-lasting extensive hyperfunction in subjects with a single kidney (including 3 IDDM patients) is not harmful and diabetic glomerulopathy may develop without preceding clear hyperfiltration. These findings argue against hyperfiltration per se as the cause of diabetic nephropathy. Among patients with type 2 diabetes microalbuminuria is characterised by: 1) high frequency, 30-40%, 2) likelihood to express widespread vascular disease rather than being merely a sign of early nephropathy and 3) independent prediction of reduced survival with a high probability. Microalbuminuria as well as proteinuria may already be persistent from diagnosis. The pathogenetic relations between albuminuria on one hand and cardiovascular disease and death on the other are not properly understood. The increased mortality among type 2 diabetic patients with microalbuminuria is not explained by coexisting risk factors such as hypertension, lipid- and haemostatic disorders or hyperglycaemia. The latter seems not to influence macrovascular complications. The others may add to a milieu favouring advancing vascular disease and the cluster of putative risk factors worsen in patients with overt proteinuria. Insulin resistance may play a key role also prior to overt diabetes. The patient at risk is easily identified, whereas specific guidelines to intervention are so far only suggestive. Prospective studies are inconsistent and microalbuminuria/proteinuria is the only risk marker not disagreed upon. In the few available short-term intervention trials microalbuminuria was reduced during improvement of metabolic control and by antihypertensive therapy. Future studies directed towards the clarification of the potential benefits from these and other interventions are of high priority. Springer-Verlag, 1992 Type 2 diabetes nationallicence Kidney function nationallicence Glomerular morphology nationallicence Microalbuminuria nationallicence Risk factors nationallicence Acta Diabetologica Springer-Verlag 29/2(1992-06-01), 47-69 0940-5429 29:2<47 1992 29 592 https://doi.org/10.1007/BF00572545 text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00572545 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- Schmitz Anita Medical Department M., Aarhus Kommunehospital, DK-8000, Aarhus C., Denmark aut NATIONALLICENCE 773 0- Acta Diabetologica Springer-Verlag 29/2(1992-06-01), 47-69 0940-5429 29:2<47 1992 29 592 Metadata rights reserved Springer special CC-BY-NC licence nationallicence SWISSBIB 137701497 BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer