Correspondence

Research Letter

Phosphorus Content of Popular Beverages

To evaluate the association between soft drinks (SDs) consumption and estimated glomerular filtration rate (eGFR) in a Mexican adult population.

We used data from the RenMex consortium (n = 2095) that included the Mexican Teachers Cohort Study (34–65 years), the Health Workers Cohort Study (18–90 years), and the Comitán Study (19–91 years). In this cross-sectional study, we assessed SDs consumption (cola and flavored soda) using a food frequency questionnaire (FFQ) and estimated eGFR using the CKD Epidemiology Collaboration equation. Quantile regression was used to assess the association between SDs consumption and eGFR with eGFR as a continuous variable. Multinomial logistic regression models were used for eGFR categories derived from quantile regression (mildly decreased eGFR, ≥72.9–87.9 mL/min/1.73 m² and moderately decreased eGFR, <72.9 mL/min/1.73 m²).

Mean age of study participants was 47.2 years, 67.5% were women, and 12.2% had diabetes. eGFR was <60 mL/min/1.73 m² in 3.7% of study participants. Mildly decreased eGFR was present in 14.8%, and moderately decreased eGFR was present in 10.1% of study participants. Quantile regression results showed that SDs consumption was associated with lower eGFR at the 10th, 25th, 50th and 75th percentile. Based on the final adjusted multinomial model, ≥7 servings/week was positively associated with moderately decreased eGFR relative to <1 serving/week (Relative Risk Ratio = 1.95; 95% CI: 1.07–3.57).

Our results suggest that higher SDs consumption is associated with lower eGFR. Encouraging healthy dietary choices should be part of the management and prevention of CKD.

Nutritional epidemiology seeks to understand nutritional determinants of disease in human populations using experimental and observational study designs. Though randomized controlled trials provide the strongest evidence of causality, the expense and difficulty of sustaining adherence to dietary interventions are substantial barriers to investigating dietary determinants of kidney disease. Therefore, nutritional epidemiology commonly employs observational study designs, particularly prospective cohort studies, to investigate long-term associations between dietary exposures and kidney disease. Due to the covarying nature and synergistic effects of dietary components, holistic characterizations of dietary exposures that simultaneously consider patterns of foods and nutrients regularly consumed are generally more relevant to disease etiology than single nutrients or foods. Dietary intakes have traditionally been self-reported and are subject to bias. Statistical methods including energy adjustment and regression calibration can reduce random and systematic measurement errors associated with self-reported diet. Novel approaches that assess diet more objectively are gaining popularity but have not yet fully replaced self-report and require refinement and validation in populations with chronic kidney disease. More accurate and frequent diet assessment in existing and future studies will yield evidence to better personalize dietary recommendations for the prevention and treatment of kidney disease.

The modern diet is closely linked to the consumption of processed foods, causing an increase in the intake of salt, simple sugars, phosphorus and added potassium. This excess intake is associated with an increased risk of obesity, diabetes, hypertension and chronic kidney disease (CKD). CKD, which according to data from the ENRICA study affects 15% of the population, magnifies its impact due to the higher prevalence of diabetes and hypertension and due to limitations in the management of sodium and phosphorus. The intake of these products far exceeds the established recommendations, assuming 72% of total sodium, 25%–35% of phosphorus, 12%–18% of potassium and exceeding 10% of the caloric intake in simple sugars. Measures are necessary to reduce their contribution through nutritional advice, labeling review, education campaigns on healthy habits, fees and institutional actions that involve food safety agencies, industry, distribution and scientific societies.

La alimentación moderna está estrechamente vinculada al consumo de alimentos procesados, originando un aumento en la ingesta de sal, azúcares simples, fósforo y potasio añadidos. Este aporte excesivo se asocia a un mayor riesgo de obesidad, diabetes, hipertensión y enfermedad renal crónica (ERC). La ERC, que según datos del estudio ENRICA afecta al 15% de la población, magnifica su repercusión por la mayor prevalencia de diabetes e hipertensión y por las limitaciones en el manejo del sodio y fósforo. La ingesta de estos productos supera ampliamente las recomendaciones establecidas, suponiendo un 72% del sodio total, un 25%–35% del fósforo, un 12%–18% de potasio y más del 10% del aporte calórico en azúcares simples. Son necesarias medidas para disminuir su aporte a través de consejo nutricional, revisión del etiquetado, campañas de educación en hábitos saludables, tasas y actuaciones institucionales que impliquen a las agencias de seguridad alimentaria, industria, distribución y sociedades científicas.

Summary: The kidneys are responsible for maintaining our bodies’ homeostasis through excretion, biodegradation, and synthesis of different hormones. Therefore, a decline in renal function often results in significant derangements in hormone levels. The most common metabolic and endocrine abnormalities seen in patients with chronic kidney disease include deficiencies in erythropoietin, calcitriol, triiodothyronine, testosterone, and estrogen. In addition, accumulation of hormones such as adiponectin, leptin, triglycerides, and prolactin also is seen. Subsequently, this can lead to the development of a wide range of clinical consequences including but not limited to anemia, hyperparathyroidism, insulin resistance, anorexia-cachexia, infertility, bone disorders, and cardiovascular diseases. These disorders can negatively affect the prognosis and quality of life of patients with chronic kidney disease, and, thus, early diagnosis, nutritional intervention, and pharmacologic treatment is imperative.

Race and ethnicity imprecisely align with genetic differences based on ancestral origin. Rather, they reflect a complex and interacting mix of social, cultural, and biological factors. While genetic differences clearly contribute to some racial and ethnic disparities, including those in chronic kidney disease (CKD), these disparities are also fueled by the clustering of negative social determinants of health, or social risks, in minority and socially disadvantaged populations. These social risks have clear and strong associations with both CKD and end-stage renal disease (ESRD) and contribute to the substantial disparities that exist in CKD and ESRD across racial, ethnic, and socioeconomic lines. This chapter reviews the socially constructed nature of race and ethnicity, discusses the substantial disparities that exist in CKD and ESRD populations across race, ethnicity, and social class, and describes the role that social risks play in the development of CKD and ESRD and in their disparate impact on low-income and racial/ethnic minority populations.

Elevated blood pressure (BP) is a major cause of preventable disease in the United States and around the world. It has been postulated that phosphorus intake may affect BP, with some studies suggesting a direct and others an inverse association.

We systematically reviewed the literature on the association of dietary phosphorus with BP in adults and performed a qualitative synthesis.

We included randomized and nonrandomized behavioral intervention and feeding studies (intervention studies) and prospective observational studies that measured dietary phosphorus intake or urinary phosphorus excretion and BP. We excluded studies of supplements, children, or individuals with major medical conditions. We searched PubMed, Embase, Cochrane Trials, and clinicaltrials.gov on 1 June, 2017 and 22 August, 2018. We assessed studies’ risk of bias in their assessment of phosphorus exposure and BP.

We reviewed 4759 publications and included 14 intervention studies (2497 participants), 3 prospective observational cohorts (17,795 participants), and 2 ongoing trials. No included intervention studies were designed specifically to achieve a phosphorus contrast. Two studies found a significant positive association of dietary phosphorus with systolic BP, 4 a significant inverse association, and 8 no significant association. Four studies found a significant inverse association with diastolic BP and 10 no significant associations. Two cohorts found lower risk of incident hypertension comparing the highest with the lowest quintiles of phosphorus intake and 1 found no significant difference: HR: 0.86 (95% CI: 0.75, 0.98); HR: 0.83 (95% CI: 0.68, 1.02); and HR: 0.75 (95% CI: 0.45, 1.27), respectively.

We found no consistent association between total dietary phosphorus intake and BP in adults in the published literature nor any randomized trials designed to examine this association. This trial was registered at www.crd.york.ac.uk/prospero/ as CRD42017062489.