The joint diabetic-renal clinic in clinical practice: 10 years of data from a District General Hospital.

BACKGROUND: Diabetic nephropathy is the leading cause of end-stage renal failure. Untreated, it causes continuous decline in glomerular function, worsening hypertension and a marked increase in cardiovascular risk. Joint diabetic-renal clinics were established to address these factors and prepare patients for renal replacement therapy. AIM: To determine whether our joint diabetic-renal clinic influenced progression of renal disease, and whether we were able to achieve targets from clinical trials and guidelines in routine practice. DESIGN: Retrospective review. METHODS: We collected data using clinical notes and electronic records for 130 patients attending the clinic over 10 years. RESULTS: Our patients had 62% type 2 and 38% type 1 diabetes. Mean duration of diabetes was 24 years for type 1 and 11 years for type 2 diabetes. At referral, 56% had evidence of vascular disease and 45%, proliferative retinopathy. Baseline median creatinine was 124 micromol/l. Significant improvements were made in systolic BP, diastolic BP and cholesterol (p < 0.001), compared to measurements at presentation. We analysed progression of renal disease by linear regression on 45 patients who had follow-up data for 3 years. Rate of decline of GFR was significantly reduced from 1.09 ml/min/month in the first year to 0.39 ml/min/month in the third year, (p < 0.004). DISCUSSION: Our findings suggest that the rate of deterioration of renal function can be reduced by aggressive management of risk factors. Joint diabetic-renal clinics appear to be useful in achieving targets in routine clinical practice.

Impaired beta cell glucose sensitivity and whole-body insulin sensitivity as predictors of hyperglycaemia in non-diabetic subjects.

AIMS/HYPOTHESIS: The aim of this prospective study was to investigate predictors of deteriorating glucose tolerance in subjects of British extraction. METHODS: A total of 156 non-diabetic subjects (86 with a family history of type 2 diabetes) underwent a 75-g OGTT and anthropometric assessment at baseline and 5 years later. Pancreatic beta cell function and whole-body insulin sensitivity were studied by model assessment. Subjects were classified as progressors if glucose tolerance moved one or more steps from normal, impaired fasting glucose, impaired glucose tolerance and diabetes over the follow-up period. RESULTS: At baseline, the progressors (n=22) had increased adiposity and a higher proportion of familial diabetes and abnormal glucose tolerance than non-progressors. Baseline pancreatic beta cell sensitivity to changes in glucose (p<0.02) and whole-body insulin sensitivity (p<0.0001) were decreased in the progressors. Logistic regression revealed that baseline and follow-up changes in beta cell glucose sensitivity and insulin sensitivity, rather than the classical clinical predictors (adiposity, familial diabetes and glucose levels), were the key independent predictors of progression (explaining over 50% of the progression). CONCLUSIONS/INTERPRETATION: Impaired pancreatic beta cell glucose sensing and whole-body insulin sensitivity predict progression to hyperglycaemia. Strikingly, these pathophysiological changes override the importance of the clinical risk factors and highlight potential metabolic targets for prevention strategies.