North American experience with Low protein diet for Non-dialysis-dependent chronic kidney disease

Abstract

Whereas in many parts of the world a low protein diet (LPD, 0.6-0.8 g/kg/day) is routinely prescribed for the management of patients with non-dialysis-dependent chronic kidney disease (CKD), this practice is infrequent in North America. The historical underpinnings related to LPD in the USA including the non-conclusive results of the Modification of Diet in Renal Disease Study may have played a role. Overall trends to initiate dialysis earlier in the course of CKD in the US allowed less time for LPD prescription. The usual dietary intake in the US includes high dietary protein content, which is in sharp contradistinction to that of a LPD. The fear of engendering or worsening protein-energy wasting may be an important handicap as suggested by a pilot survey of US nephrologists; nevertheless, there is also potential interest and enthusiasm in gaining further insight regarding LPD's utility in both research and in practice. Racial/ethnic disparities in the US and patients' adherence are additional challenges. Adherence should be monitored by well-trained dietitians by means of both dietary assessment techniques and 24-h urine collections to estimate dietary protein intake using urinary urea nitrogen (UUN). While keto-analogues are not currently available in the USA, there are other oral nutritional supplements for the provision of high-biologic-value proteins along with dietary energy intake of 30-35 Cal/kg/day available. Different treatment strategies related to dietary intake may help circumvent the protein- energy wasting apprehension and offer novel conservative approaches for CKD management in North America.

Keywords: CKD; Dietary protein intake; Dietary restriction; Low protein diet; Nutritional management.

Fig. 1

Estimated DPI in the USA across gender, race, and age; normalized to protein in g/kgIBW/d, for adults in the USA depicted for (a) sex, (b) race or ethnicity, and (c) age group. Analysis of variance for each panel, p<0.0001. Per panel, pairwise comparisons with each reference (ref) group: *p<0.0001, †p<0.01. Adapted from secondary NHANES data analyses by Moore et al. (with permission) [7]

Fig. 2

Estimated DPI in the USA across gender, race, and age accounting for stages of CKD: normalized to protein in g/kgIBW/d, for adults in the USA depicted for (a) sex, (b) race or ethnicity, and (c) age group. No evidence of CKD (No CKD), stage 1 CKD (eGFR, ≥90ml/min with kidney damage), stage 2 CKD (eGFR 60–89ml/min with kidney damage), stage 3 CKD (eGFR 30–59ml/min), or stage 4 CKD (eGFR <30 ml/min without dialysis). Overall FANOVA for each panel, P<0.0001. Per panel, pairwise comparisons with each reference group: *P<0.0001, †P<0.05. Per panel, pairwise comparisons with each subgroup ((a) females at each stage of CKD compared with NoCKD and males at each stage of CKD compared with NoCKD; (b) NH black at each stage of CKD compared with NoCKD, Mexican American or Latino at each stage of CKD compared with NoCKD, and NH white at each stage of CKD compared with NoCKD; (c) 20–54-year-olds at each stage of CKD compared with NoCKD, 55–64-year-olds at each stage of CKD compared with NoCKD, 65–74-year-olds at each stage of CKD compared with NoCKD, and 75+-year-olds at each stage of CKD compared with NoCKD): ‡P<0.0001, §P<0.001, ||P<0.01, ¶P<0.05. Adapted from secondary NHANES data analyses by Moore et al. (with permission) [7]