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

Unité de diabétologie Service de Médecine B CHU 49033 Angers Cedex 01 France E-mail: BeBouhanick{at}chu-angers.fr

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/m²) 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 x 10⁴ Bq [⁵¹Cr]EDTA and corrected by 1.73 m² body surface area. Hyperfiltration was defined as a GFR >137 mLmin^-11.73 m^-2 (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 gkg body wt^-1d^-1; P = 0.032) and fat (1.70 ± 0.54 compared with 1.39 ± 0.44 gkg body wt^-1d^-1; 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 gkg body wt^-1d^-1; P = 0.30) and fat (1.25 ± 0.41 compared with 1.46 ± 0.47 gkg body wt^-1d^-1; 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 follow-up studies are required to strengthen this hypothesis further.

REFERENCES

1. Riley MD, Dwyer T. Microalbuminuria is positively associated with usual dietary saturated fat intake and negatively associated with usual dietary protein intake in people with insulin-dependent diabetes mellitus. Am J Clin Nutr 1998;67:50–7.[Abstract]
2. Brenner BM, Meyer TW, Hosteller TH. Dietary intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease. N Engl J Med 1982;307:652–9.[Medline]
3. Mogensen CE, Christensen CK. Predicting diabetic nephropathy in insulin-dependent patients. N Engl J Med 1984;311:89–93.[Abstract]
4. Rudberg S, Persson B, Dahlquist G. Increased glomerular filtration rate as a predictor of diabetic nephropathy: an 8-year prospective study. Kidney Int 1992;41:822–8.[Medline]
5. Bouhanick B, Suraniti S, Berrut G, et al. Relationship between fat intake and glomerular filtration rate in normotensive insulin-dependent diabetic patients. Diabete Metab 1995;21:168–72.[Medline]
6. Marre M, Hallab M, Roy J, et al. Glomerular hyperfiltration in type 1, type 2 and secondary diabetes. J Diabet Complications 1992;6:19–24.
7. Mogensen CE, Chachati A, Christensen CK, et al. Microalbuminuria: an early marker of renal involvement in diabetes. Uremia Invest 1985;9:85–96.[Medline]

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