Microalbuminuria, glomerular filtration rate, and dietary fat and protein intakes in type 1 diabetes

Abstract

Dear Sir: We read with interest the cross-sectional study by Riley and Dwyer (1), who reported a positive association between microalbuminuria and dietary saturated fat intake and a negative association between microalbuminuria and dietary protein intake in people with type 1 diabetes. They also reminded us that protein intake might be involved in renal hyperfiltration preceding the loss of nephron units in type 1 diabetes (2). Glomerular hyperfiltration may be another early marker of diabetic nephropathy (3, 4). We previously studied the relation between dietary macronutrient intake and glomerular hyperfiltration in 110 patients with type 1 diabetes (5). The patients’ mean ( SD) age was 34.6 ∠ 11.2 y, their mean duration of diabetes was 13.9 ∠ 9.0 y, and their mean body mass index (in kg/m 2 ) was 22.9 ∠ 2.9. None had hypertension. Mean glycated hemoglobin was 8.3 ∠ 1.4%, or 0.083 ∠ 0.014 (normal: ≤ 5.6%, or ≤ 0.056). The glomerular filtration rate (GFR) was assessed by the plasma disappearance of 3.7 3 10 4 Bq [ 51 Cr]EDTA and corrected by 1.73 m 2 body surface area. Hyperfiltration was defined as a GFR > 137 mL · min 21 · 1.73 m 22 (mean value + 2 SDs of age-matched healthy subjects) (6). Food intake was recorded with a computer-assisted program (5). The distribution of dietary intake was similar to that observed by Riley and Dwyer (1): the percentage of energy from fat, protein, and carbohydrate, respectively, was 40.2 ∠ 7.2%, 18.2 ∠ 3.2%, and 41.6 ∠ 6.9%. Our cross-sectional study outlined a positive relation of both protein and fat intakes with GFR, indicating that subjects with type 1 diabetes with glomerular hyperfiltration ( n = 15) ingested higher amounts of protein (1.60 ∠ 37 compared with 1.38 ∠ 0.34 g · kg body wt 21 ·d 21 ; P = 0.032) and fat (1.70 ∠ 0.54 compared with 1.39 ∠ 0.44 g · kg body wt 21 ·d 21 ; P = 0.0022) than did patients with normofiltration, although total energy intake was not significantly different between the 2 groups. Saturated fat intake was significantly higher in the group with hyperfiltration ( P = 0.05), whereas no difference was found for polyunsaturated fat intake. Univariate regression analysis showed that GFR was positively related to both protein intake (r = 0.28, P = 0.003) and fat intake (r = 0.25, P = 0.007). In a stepwise multivariate regression analysis, fat intake was an independent determinant of GFR (F = 13.15, P ≤ 0.002), whereas protein intake no longer appeared to be so ( F = 1.36, P ≤ 0.08). No relation was found between dietary intakes and serum total cholesterol, HDL cholesterol, apolipoprotein A-I, apolipoprotein B, or serum triacylglycerol. Thus, we found an independent, positive relation between hyperfiltration and fat intake, suggesting that fat intake may play a role in the development of renal disease. Fifteen of the 110 patients had microalbuminuria (defined as a urinary albumin excretion rate of 30‐300 mg/24 h in ♢ 2 of 3 timed, overnight urine collections) (7). Protein (1.50 ∠ 0.45 compared with 1.40 ∠ 0.33 g · kg body wt 21 ·d 21 ; P = 0.30) and fat (1.25 ∠ 0.41 compared with 1.46 ∠ 0.47 g · kg body wt 21 ·d 21 ; P = 0.10) intakes were not significantly different between patients with microalbuminuria and patients with normoalbuminuria. However, the study was not designed as a case-control study with microalbuminuria as a selection criterion. The results from Riley and Dwyer (1) and our own study support the hypothesis that dietary fat intake may play a role in the development of nephropathy in patients with type 1 diabetes. Prospective followup studies are required to strengthen this hypothesis further.