Longitudinal Studies Of Gfr In Microalbuminuric Patients With Type Diabetes Figure

In type 1 diabetes a few small studies have assessed rates of decline of GFR in microalbuminuric patients. In 1991 Mathiesen showed that GFR remained static over 4 years in 23 normotensive patients who were not treated with antihypertensive agents [77]. An extension of this study showed that mean GFR declined from 129 to 119 ml/min/1.73m2 over 8 years but this failed to reach statistical significance for the group as a whole [20]. However, 8 patients progressing to macroalbuminuria did show a significant decline in GFR over the study period. The concept of AER progression being a determinant of a decline in GFR in microalbuminuric patients with type 1 diabetes is largely based on a 5 year study of 40 normotensive patients who did not receive antihypertensive therapy [78]. In 14/40 patients who progressed to macroalbuminuria the mean GFR decreased by 2.2 ± 3.8 ml/min/1.73m2 (p = 0.05) compared with a rise of 0.5 ±2.1 ml/min/1.73m2 (p = NS) in the 26 non-progressors. There was a significant difference in the rate of change of GFR between the two groups (p < 0.05). Progressors showed a higher mean arterial pressure of 103 versus 93 mmHg in non-progressors, and the mean rate of decline of GFR was related to baseline systolic blood pressure. In addition, the rate of increase of AER was related to overall glycaemic control, supporting a role for glycaemic control as an initiator of the nephropathic process.

Other studies of placebo treated normotensive patients with type 1 diabetes and microalbuminuria who did not receive anti-hypertensive therapy have usually not shown significant rates of decline of GFR over intervals of 2 to 3 years. In 1994 a study of 46 placebo treated normotensive, microalbuminuric patients over 2 years reported a non-significant trend for GFR to decline by 3

ml/min/1.73m2/year [23]. Twelve of the 46 patients developed macroalbuminuria but the rate of GFR change was not reported. In 1998 an Italian study of 34 placebo treated normotensive patients with type 1 diabetes and microalbuminuria showed no significant changes in GFR over 3 years [79]. In 2001, the Melbourne Diabetic Nephropathy Study Group reported the results of a study in normotensive patients with type 2 diabetes and microalbuminuria [22]. Seven placebo treated patients with an initial GFR of 90 ±7 ml/min/1.73 m2 showed a non-significant trend towards a decline in GFR of 1.3 ± 1.1 ml/min/1.73 m2/year over a mean duration of follow-up of 65 ±8 months.

Recent studies in hypertensive patients with microalbuminuria have not included an untreated or placebo treated control arm for ethical reasons. The rate of change of GFR may therefore reflect the level of blood pressure achieved as well as the type of antihypertensive therapy.

In 1994 a 2 year study in hypertensive patients with type 1 diabetes and microalbuminuria [80] showed a significant decline in GFR from baseline to 2 years during treatment with captopril (4.9 + 2.1 ml/min/1.73m2/year) or atenolol (3.7 + 1.6 ml/min/1.73m2/year). However, if the rate of decline of GFR was calculated from 6 months onwards it was no longer significant. A study in type 1 diabetic patients with hypertension and overt nephropathy had previously demonstrated a blunting of the rate of decline of GFR with increasing duration of antihypertensive therapy [18]. Further studies are required to determine if greater reductions in MAP are associated with reversal of the decline in GFR in hypertensive microalbuminuric patients with type 1 diabetes.

In summary, although cross-sectional studies have shown that GFR changes from hyperfiltration toward normofiltration when AER exceeds 50 ^g/min [15], this has been difficult to demonstrate in longitudinal studies. However, the recent studies by Mauer's group indicate that even normoalbuminuria does not always ensure against reduction of GFR in type 1 diabetes which is associated with renal ultrastructural changes typical of diabetic nephropathy [65].

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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