caa a22 4500 469128534 CHVBK 20180323133157.0 cr unu---uuuuu 170328e19920901xx s 000 0 eng 10.1007/BF00573489 doi (NATIONALLICENCE)springer-10.1007/BF00573489 Reduced glomerular filtration rate and cardiovascular damage in diabetes: a key role for abnormal albuminuria [Elektronische Daten] [C. Mogensen, E. Damsgaard, A. Frøland, K. Hansen, S. Nielsen, M. Pedersen, A. Schmitz, L. Thuesen, R. Østerby] There is general agreement that a fall rate in glomerular filtration rate (GFR) is the principal endpoint in diabetics with renal disease, and that abnormal albuminuria (including microalbuminuria) is an important intermediate end-point. The relative roles of blood pressure (BP) elevation and abnormal albuminuria in the prediction and genesis of renal disease are a matter of debate, and are further analysed in this paper. New studies show that neither genetic predisposition to hypertension (parental BP) nor parental abnormal albuminuria can be used to predict renal disease in patients with type 1 (insulin-dependent) diabetes. However, parental predisposition to proteinuria seems to be important to certain types of patients with type 2 (non-insulin-dependent) diabetes. Cross-sectional as well as follow-up studies document that GFR is generally well preserved in microalbuminuria (in both type 1 and type 2 patients), while the transition to clinical proteinuria is associated with a decline in GFR. Thus, prevention of overt proteinuria is important in clinical trials in microalbuminuric patients. In type 1 diabetes clear ultrastructural changes have been documented with microalbuminuria and a good correlation between abnormal albuminuria and structural damage is seen. Structural damage in normo- and microalbuminuric patients correlates poorly with BP. New studies in type 1 diabetes document that microalbuminuria (but not elevated BP) predicts not only clinical diabetic nephropathy but also end-stage renal failure and mortality. In type 2 diabetes microalbuminuria is the strongest predictor of mortality, whereas BP elevation is not a predictor. Several studies now document that antihypertensive treatment, especially with inhibitors of angiotensin converting enzyme, is able to reverse or reduce abnormal albuminuria, even in non-hypertensive type 1 patients, and possibly preserve GFR. Therefore, microalbuminuria may be the main indicator for starting antihypertensive treatment in these patients. With respect to organ damage in the retina, abnormal albuminuria is an important indicator of the risk of severe diabetic retinopathy. BP elevation seems not to be an initiating factor, but rather aggravates established retinopathy. Left ventricular hypertrophy has a stronger correlation with BP elevation than normoalbuminuria, suggesting that left ventricular hypertrophy is at least partially a phenomenon secondary to elevated BP in diabetic patients with abnormal albuminuria. Generally, abnormal albuminuria is a strong indicator of cardiovascular renal damage in diabetic patients and in most organs is a stronger factor than elevated BP. Springer-Verlag, 1992 Abnormal albuminuria nationallicence ACE-inhibition nationallicence Hypertension nationallicence Microalbuminuria nationallicence Diabetic nephropathy nationallicence Mogensen C. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Damsgaard E. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Frøland A. Medical Department, Fredericia Sygehus, Fredericia, Denmark aut Hansen K. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Nielsen S. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Pedersen M. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Schmitz A. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Thuesen L. Department of Cardiology, Skejby Sygehus, University Hospital of Aarhus, Aarhus, Denmark aut Østerby R. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut Acta Diabetologica Springer-Verlag 29/3-4(1992-09-01), 201-213 0940-5429 29:3-4<201 1992 29 592 https://doi.org/10.1007/BF00573489 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00573489 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Mogensen C. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Damsgaard E. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Frøland A. Medical Department, Fredericia Sygehus, Fredericia, Denmark aut NATIONALLICENCE 700 1- Hansen K. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Nielsen S. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Pedersen M. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Schmitz A. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Thuesen L. Department of Cardiology, Skejby Sygehus, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 700 1- Østerby R. Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, University Hospital of Aarhus, Aarhus, Denmark aut NATIONALLICENCE 773 0- Acta Diabetologica Springer-Verlag 29/3-4(1992-09-01), 201-213 0940-5429 29:3-4<201 1992 29 592 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer