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High dietary phosphorus intake (P-In) and high acid loads may adversely affect kidney function. In animal models, excessive phosphorus intake causes renal injury, which, in humans, is also inducible by chronic metabolic acidosis. We thus examined whether habitually high P-In and endogenous acid production during childhood and adolescence may be early indicators of incipient renal inflammatory processes later in adulthood. P-In and acid-base status were longitudinally and exclusively determined by biomarker-based assessment in 277 healthy children, utilizing phosphate and net acid excretion (NAE) measurements in 24 h urine samples repeatedly collected between the ages of 3 and 17 years. Standard deviation scores (by sex and age) were calculated for anthropometric data and for the urinary biomarkers available within age range 3-17 years. Multivariable linear regression was used to analyze the relations of phosphate excretion and NAE with the adulthood outcome circulating interleukin-18 (IL-18), a marker of inflammation and kidney dysfunction. After adjusting for growth- and adulthood-related covariates and pro-inflammatory biomarkers to rule out confounding by non-renal inflammatory processes, regression models revealed a significant positive relationship of long-term NAE (p = 0.01), but not of long-term phosphate excretion with adult serum IL-18. Similar significant positive regression results were obtained after replacing NAE with 24 h urinary ammonium excretion as the exposition variable. Our results suggest that even moderate elevations in renal ammonia production, as caused by habitually higher acid loading during growth, may affect the intrarenal pro-inflammatory system in the long-term, known to be boosted by acidosis-induced raised ammoniagenesis.

Author(s): Danika Krupp [sup.1], Yifan Hua [sup.1], Jonas Esche [sup.1], Thomas Remer [sup.1] Author Affiliations: (1) DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study Center, Department of Nutritional Epidemiology, Institute [...], Background Overweight and higher BMI are known to be related to increased blood pressure (BP) and additionally associate with lowered urine pH values even at comparable total daily acid loading. Since a reduced urine pH level at a given total acid load indicates an impaired renal net acid excretion capacity (NAEC) and renal function also relates to BP, we hypothesized that NAEC may be one mediator of the body fat-BP association. Methods Ammonium, titratable acid, pH, creatinine, and urea were measured in 24-h urine samples among 9-15-year-old adolescents of the DONALD Study. NAEC was determined as residual of the body surface area-corrected net acid excretion on urine pH (NAEC1) or body surface area-corrected ammonium excretion on urine pH (NAEC2). Markers of body fatness were determined anthropometrically and systolic and diastolic BP sphygmomanometrically. Multilinear regressions were used to examine cross-sectionally the body fat-NAEC and prospectively the NAEC1-BP associations. Results All body fat parameters were inversely associated with both NAEC1 and NAEC2 among youth (P [less than or equal to] 0.01). In a separate prospective analyses, to check for possible mediation, higher adolescent NAEC1 was significantly associated with lower systolic BP in male adults only (P = 0.04), but this association was attenuated to a trend (P = 0.07) in multivariable-adjusted models. Conclusions Independent of systemic acid load, NAEC, i.e., the kidney's function to eliminate acids is reduced with higher body fatness, and may also contribute as a mediator in the body fatness-BP relation.

Author(s): Jonas Esche [sup.1], Danika Krupp [sup.1], Gert BM Mensink [sup.2], Thomas Remer [sup.1] Author Affiliations: (1) DONALD Study Center Dortmund, IEL - Nutritional Epidemiology, University of Bonn, Dortmund, Germany [...], Background/Objective Preliminary interventional data suggest that a reduction of dietary acid load raises renal uric acid excretion and decreases serum uric acid (SUA). In line with this, in a recent cross-sectional analysis of a representative adult population sample, a higher potential renal acid load (PRAL) was found to associate with higher SUA levels. Against this background, we re-examined the relationship of the body's acid load with SUA and hyperuricemia using nutrition-derived estimates of renal net acid excretion (NAE). Subjects/Methods Cross-sectional analyses were performed in n = 6894 participants (18-79 y) of the German Health Interview and Examination Survey for Adults (DEGS1). Two different approaches were used to estimate NAE, one based on the sum of food frequency questionnaire (FFQ)-derived PRAL and body-surface area-derived organic acids (eNAE.sub.PRAL+OA) and the other based on FFQ-derived protein and potassium intake ratios (eNAE.sub.Prot/K). The associations of eNAE.sub.PRAL+OA and eNAE.sub.Prot/K with SUA were analyzed in multiple linear regression models. Multiple logistic regressions were used to calculate odds ratios (OR) for hyperuricemia comparing higher (T3) and lower (T1) tertiles of the NAE estimates. Results After adjusting for relevant confounders, eNAE.sub.PRAL+OA (p = 0.0048) and eNAE.sub.Prot/K (p = 0.0023) were positively associated with SUA. In addition, participants with a higher eNAE.sub.PRAL+OA or eNAE.sub.Prot/K had higher ORs for having hyperuricemia (OR: 1.73, 95% CI: 1.24-2.40, OR: 1.51, 95% CI: 1.10-2.08, respectively). Conclusion The results substantiate findings of a previous analysis that dietary acid load is a potential influencing factor on SUA. This implicates that a lower dietary acid load may have beneficial effects on SUA.