Higher biomarker-calibrated protein intake is not associated with impaired renal function in postmenopausal women.
ABSTRACT With aging, renal function tends to decline, as evidenced by reduced glomerular filtration rate. High-protein intake may further stress the kidneys by causing sustained hyperfiltration. To investigate whether dietary protein is associated with impaired renal function, we used data from 2 nested case-control studies within the Women's Health Initiative Observational Study (n = 2419). We estimated protein intake using a FFQ and estimated glomerular filtration rate (eGFR) from cystatin C. To account for the original study designs, inverse probability weights were applied. Self-reported energy and protein were calibrated using biomarkers of energy and protein intake. Associations between protein intake and renal function were estimated by weighted linear and logistic regression models. Average calibrated protein intake (mean ± SD) was 1.1 ± 0.2 g/(kg body weight·d).Twelve percent (n = 292) of women had impaired renal function. The odds of impaired renal function, defined as eGFR <60 mL/(min·1.73m(2)), was not associated with calibrated protein intake. When eGFR was modeled continuously, there was no association with calibrated protein when protein was expressed in absolute (g/d) or relative to energy (protein % energy/d), but protein relative to body weight [g/(kg body weight·d)] was associated with higher eGFR. There was no evidence for effect modification by age, BMI, or general health status. These data suggest higher protein intake is not associated with impaired renal function among postmenopausal women without a diagnosis of chronic kidney disease.
Article: Dietary protein restriction and the progression of chronic renal disease: what have all of the results of the MDRD study shown? Modification of Diet in Renal Disease Study group.[show abstract] [hide abstract]
ABSTRACT: The Modification of Diet in Renal Disease (MDRD) Study was the largest randomized clinical trial to test the hypothesis that protein restriction slows the progression of chronic renal disease. However, the primary results published in 1994 were not conclusive with regard to the efficacy of this intervention. Many physicians interpreted the failure of the MDRD Study to demonstrate a beneficial effect of protein restriction over a 2- to 3-yr period as proving that this therapy does not slow disease progression. The authors believe that this viewpoint is incorrect, and is the result of misinterpretation of inconclusive evidence as evidence in favor of the null hypothesis. Since then, numerous secondary analyses of the MDRD Study have been undertaken to clarify the effect of protein restriction on the rate of decline in GFR, urine protein excretion, and onset of end-stage renal disease. This review describes some of the principles of secondary analyses of randomized clinical trials, presents the results of these analyses from the MDRD Study, and compares them with results from other randomized clinical trials. Although these secondary results cannot be regarded as definitive, the authors conclude that the balance of evidence is more consistent with the hypothesis of a beneficial effect of protein restriction than with the contrary hypothesis of no beneficial effect. Until additional data become available, physicians must continue to make recommendations in the absence of conclusive results. The authors suggest that physicians incorporate the results of these secondary analyses into their interpretation of the findings of the MDRD Study.Journal of the American Society of Nephrology 12/1999; 10(11):2426-39. · 9.66 Impact Factor
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ABSTRACT: Recent trends in weight loss diets have led to a substantial increase in protein intake by individuals. As a result, the safety of habitually consuming dietary protein in excess of recommended intakes has been questioned. In particular, there is concern that high protein intake may promote renal damage by chronically increasing glomerular pressure and hyperfiltration. There is, however, a serious question as to whether there is significant evidence to support this relationship in healthy individuals. In fact, some studies suggest that hyperfiltration, the purported mechanism for renal damage, is a normal adaptative mechanism that occurs in response to several physiological conditions. This paper reviews the available evidence that increased dietary protein intake is a health concern in terms of the potential to initiate or promote renal disease. While protein restriction may be appropriate for treatment of existing kidney disease, we find no significant evidence for a detrimental effect of high protein intakes on kidney function in healthy persons after centuries of a high protein Western diet.Nutrition & Metabolism 10/2005; 2:25. · 2.88 Impact Factor