Resumo Introdução: A microbiota intestinal está envolvida na geração de toxinas urêmicas presentes nos pacientes com doença renal crônica (DRC) em hemodiálise (HD) como indoxil sulfato (IS), formado a partir da fermentação do aminoácido triptofano. Objetivo: Avaliar a ingestão de triptofano alimentar pelos pacientes renais crônicos em HD e sua possível relação com os níveis plasmáticos de IS. Métodos: Participaram do estudo 46 pacientes com DRC em programa regular de HD (56,5% homens; 52,7 ± 10,3 anos; 63 (32,2-118,2) meses em HD; IMC 25,6 ± 4,9kg/m2. A ingestão de triptofano foi avaliada por meio do recordatório alimentar de 24 (R-24h) realizado em três diferentes dias. Exames bioquímicos de rotina, bem como a avaliação antropométrica foram avaliados. Os níveis plasmáticos de IS foram determinados por cromatografia líquida de alto desempenho (HPLC) com detecção fluorescente e as concentrações plasmáticas de interleucina-6 (IL-6) pelo método imunoenzimático (ELISA, Enzyme Linked Immunosorbent Assay). Resultados: A ingestão média de triptofano estava dentro do recomendado, já os níveis plasmáticos de IS (35,0 ± 11,9mg/L) estavam elevados, porém de acordo com os valores da EUTox para indivíduos urêmicos. Não houve correlação entre a ingestão de triptofano e os níveis plasmáticos de IS. Contudo, houve correlação positiva entre ingestão de proteína e triptofano e variáveis que avaliam massa magra e, além disso, os níveis IS foram positivamente associados com os de IL-6 (r = 0,6: p = 0,01). Conclusão: O presente estudo sugere que a ingestão alimentar de triptofano pode não ser um fator determinante dos níveis de IS. No entanto, sugere que o intestino pode ter importante papel na inflamação sistêmica presente nos pacientes com DRC.

Abstract Introduction: Gut microbiota is involved in generation of uremic toxins in chronic kidney disease (CKD) patients on hemodialysis (HD), like indoxyl sulfate (IS) that is originated from tryptophan amino acid fermentation. Objective: To evaluate the tryptophan intake by chronic renal failure patients on HD and its possible relationship with IS plasma levels. Methods: Participated of the study 46 patients with CKD on HD regular program (56.5% men; 52.7 ± 10.3 years; 63 (32.2-118.2) months on HD; BMI 25.6 ± 4.9 kg/m2). The tryptophan intake was evaluated by a 24-hours dietary recall (R-24h) performed on 3 different days. Routine biochemical tests and anthropometric measurements were evaluated. IS plasma levels were determined by High Performance Liquid Chromatography (HPLC) with fluorescent detection and the interleukin-6 (IL-6) plasma levels by immunoenzymatic method (ELISA, Enzyme Linked Immunosorbent Assay). Results: The average of tryptophan intake was according to recommendation, but IS plasma levels (35.0 ± 11.9 mg/L) were elevated, however according to the EUTox values for uremic individuals. There was no correlation between the tryptophan intake and IS plasma levels. However, there was positive correlation between protein intake and tryptophan and variables used to evaluate lean body mass, and moreover, IS levels were positively associated with IL-6 (r = 0.6: p = 0.01). Conclusion: The present study suggests that tryptophan dietary intake may not be a determinant factor to IS levels. However, it suggests that gut microbiota may play an important role in systemic inflammation in patients with CKD.

Background: Chronic kidney disease (CKD) patients often have gastrointestinal symptoms which may result in malnutrition and a negative impact on their quality of life. Modulation of the gut microbiota can be a strategy to promote host health and homeostasis. Case report: The authors present a case of chronic diarrhea in a hemodialysis (HD) patient with an unknown etiology. After about one year and several failed interventions, synbiotic therapy was performed. The diarrhea episodes ceased after three months of daily supplementation and both biochemical and nutritional parameters improved. Synbyotic therapy promoted clinical benefits in this patient. Discussion: Therefore, this simple therapy may be a promising alternative in CKD and it should be tested in larger studies.

Introducción: los pacientes con enfermedad renal crónica (ERC) a menudo tienen síntomas gastrointestinales que pueden provocar desnutrición y un impacto negativo en su calidad de vida. La modulación de la microbiota intestinal puede ser una estrategia para promover la salud del huésped y la homeostasis. Caso clínico: los autores presentan un caso de diarrea crónica de etiología desconocida en un paciente en hemodiálisis (HD). Después de varias intervenciones fallidas durante un año, se realizó el tratamiento simbiótico. Los episodios de diarrea cesaron después de tres meses de la suplementación diaria y ambos parámetros bioquímicos y nutricionales mejoraron. La terapia con simbióticos promovió beneficios clínicos para este paciente. Discusión: por lo tanto, esta sencilla terapia puede ser una alternativa prometedora en la ERC y debe ser probada en estudios más amplios.

Introduction: Fructose intake has increased dramatically in consequence of the consumption of fructose-based sweetened foods and beverages. Research suggests that high fructose intake has a strong association with uric acid (UA) levels and worse prognosis of chronic kidney disease (CKD). Objective: The aim of this study was to investigate the influence of fructose intake on plasma UA levels in nondialysis-dependent CKD patients. Methods: Fifty-two patients on stages 3-5 (64.2 ± 9.6 years, 24 men, glomerular filtration rate of 30.5 ± 10.3ml/ min) were divided into two groups: high fructose intake (>50g/d, n=29, 61.7 ± 9.3years) and low fructose intake (<50g/d, n=23, 65.8 ± 9.7years). Blood samples were collected to determine lipid profile and plasma levels of UA, inflammatory (interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP)) and cardiovascular markers (monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)). The energy, protein and fructose intake was estimated using 3-day 24-hour food recall. Results: High fructose intake was observed in 55.8% of patients and the mean UA levels were 7.7 ± 1.3 and 6.2 ± 1.6mg/dl in patients with high and low fructose intake, respectively (p<0.05). According to the regression analysis, fructose intake was the only variable able to affect the AU levels (ß=0.42, p=0.016) after adjustment for gender, BMI, energy and protein intake, cardiovascular markers and lipid profile. Conclusions: These findings support a potential role for fructose in hyperuricemia in these patients.

Introducción: El consumo de fructosa ha aumentado dramáticamente en consecuencia del consumo de alimentos y bebidas azucaradas a base de fructosa. Pesquisas sugieren que el alto consumo de fructosa tiene una fuerte asociación con niveles de ácido úrico (AU) y empeora el pronóstico de la enfermedad renal crónica (ERC). Objetivo: El objetivo de este estudio fue investigar la influencia del consumo de fructosa en los niveles plasmáticos de ácido úrico en pacientes con ERC que no son dependiente de diálisis. Métodos: Cincuenta y dos pacientes en fases 3-5 (64,2±9,6 años, 24 hombres, tasa de filtración glomerular de 30,5±10,3ml/min) se dividieron en dos grupos: alto consumo de fructosa (>50g/día, n=29, 61,7±9,3 años) y bajo consumo de fructosa (<50g/día, n=23, 65,8±9,7 años). Muestras de sangre fueron recogidas para determinación del perfil lipídico y niveles plasmáticos de AU, citocinas inflamatorias (interleucina-6 (IL-6), factor de necrosis tumoral-α (TNF-α), proteína C-reactiva (CRP)), y marcadores cardiovasculares (proteína quimiotáctica de monocitos-1 (MCP-1), molécula de adhesión inter-celular-1 (ICAM-1) y molécula de adhesión vascular-1 (VCAM-1)). El consumo de energía, proteína y fructosa fue estimulado utilizando 3 días de recordatorio alimentar de 24 horas. Resultados: El alto consumo de fructosa fue observado en el 55,8% de los pacientes y los niveles medios de AU fueron 7,7±1,3 y 6,2±1,6mg/dl en pacientes con alto y bajo consumo de fructosa, respectivamente (p<0,05). De acuerdo con el análisis de regresión, el consumo de fructosa fue la única variable capaz de afectar los niveles de AU (b=0,42, p=0,016) después del ajuste para el género, composición corporal, energía y proteína, marcadores cardiovasculares y el perfil lipídico. Conclusiones: Estos resultados apoyan un papel potencial de la fructosa ocasionando la hiperuricemia en estos pacientes.