ABSTRACT
Hyperuricemia and gout, the clinical manifestation of monosodium urate crystal deposition, are common in patients with chronic kidney disease (CKD). Although the presence of CKD poses additional challenges in gout management, effective urate lowering is possible for most patients with CKD. Initial doses of urate-lowering therapy are lower than in the non-CKD population, whereas incremental dose escalation is guided by regular monitoring of serum urate levels to reach the target level of <6mg/dL (or <5mg/dL for patients with tophi). Management of gout flares with presently available agents can be more challenging due to potential nephrotoxicity and/or contraindications in the setting of other common comorbid conditions. At present, asymptomatic hyperuricemia is not an indication for urate-lowering therapy, though emerging data may support a potential renoprotective effect.
Subject(s)
Allopurinol/administration & dosage , Febuxostat/administration & dosage , Gout , Hyperuricemia , Renal Dialysis , Renal Insufficiency, Chronic , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Diet Therapy/methods , Disease Management , Gout/diagnosis , Gout/etiology , Gout/metabolism , Gout/therapy , Gout Suppressants/administration & dosage , Humans , Hyperuricemia/diagnosis , Hyperuricemia/drug therapy , Hyperuricemia/etiology , Hyperuricemia/metabolism , Male , Middle Aged , Renal Dialysis/adverse effects , Renal Dialysis/methods , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/diagnosis , Renal Insufficiency, Chronic/metabolism , Renal Insufficiency, Chronic/therapy , Symptom Flare Up , Treatment Outcome , Uric Acid/bloodABSTRACT
The excess of uric acid is recognized as a risk factor for diverse metabolic diseases which include gout, urolithiasis, type 2 diabetes, arterial hypertension as well as metabolic syndrome and cardiovascular disease. Current studies suggest that the exaggerated increment in fructose consumption, caused mainly by added suggars, is implicated in the high prevalence of hyperuricemia in the western population.The loss of uricase by mutation of its gene 15 million years ago in the large hominids, including man, has contributed to hyperuricemia, facilitated through the metabolism of fructose the formation of uric acid. It has been proposed that the elevation of uric acid in the remote past was an evolutionary benefit to intensify the lipogenic effects of fructose, allowing humans to survive periods of fruit shortages. However, today the high consumption of fructose and resultant hyperuricemia are a disadvantage, increasing the development of obesity and type 2 diabetes.
El exceso de ácido úrico es reconocido como un factor de riesgo para diversas enfermedades metabólicas, incluyendo: gota, urolitiasis, diabetes tipo 2, hipertensión arterial, síndrome metabólico y enfermedad cardiovascular. Estudios actuales sugieren que el incremento exagerado del consumo de fructosa, proveniente especialmente de los azúcares añadidos, está implicado en la alta prevalencia de hiperuricemia que muestra la población occidental. La pérdida de la uricasa por mutación de su gen hace 15 millones de años atrás en los grandes homínidos, incluyendo el hombre, ha contribuido a la hiperuricemia, facilitando a través del metabolismo de la fructosa la formación de ácido úrico. Se ha propuesto que la elevación del ácido úrico en épocas pasadas, fue una ventaja evolutiva al intensificar los efectos lipogénicos de la fructosa, permitiendo al ser humano sobrevivir en períodos de escasez de frutas. Sin embargo, hoy la alta ingesta de fructosa y su hiperuricemia resultante es una desventaja, promoviendo el desarrollo de obesidad y diabetes tipo 2.
ABSTRACT
The association between serum uric acid (SUA) and prehypertension was evaluated in a racially admixed sample of civil servants aged 35 to 74 years, enrolled (2008-2010) in the Brazilian Longitudinal Study of Health (ELSA-Brasil). Of the 15 105 patients who enrolled in the study, we analyzed 3412 after excluding those who reported previous cardiovascular diseases, diabetes, or hypertension; were heavy drinkers; or had a body mass index (BMI) ≥ 35 kg/m(2). Among the men, logistic regression, adjusted for age, race, income, birth weight, salt intake, insulin resistance, BMI, and renal function revealed odds ratios (ORs) and 95% confidence intervals (CIs) of prehypertension from the bottom quartile (referent) to the top quartile of SUA levels as follows: 0.84 (95% CI, 0.61-1.38), 0.97 (0.71-1.34) and 1.44 (1.04-2.0; P for trend .01). Analyzing for 1-standard deviation of change in SUA, the ORs were 1.19 (1.06-1.32). This association persisted in the subgroup analysis consisting of patients who were white, overweight, with a high salt intake but with normal renal function, and without metabolic syndrome. No association was found among women. In conclusion, SUA levels were associated with prehypertension among men.
Subject(s)
Blood Pressure , Hyperuricemia/epidemiology , Prehypertension/epidemiology , Uric Acid/blood , Adult , Age Factors , Aged , Biomarkers/blood , Brazil/epidemiology , Comorbidity , Female , Health Surveys , Humans , Hyperuricemia/blood , Hyperuricemia/diagnosis , Life Style , Logistic Models , Longitudinal Studies , Male , Middle Aged , Odds Ratio , Prehypertension/diagnosis , Prehypertension/physiopathology , Risk Factors , Sex FactorsABSTRACT
La gota es la artritis crónica más común en el anciano. Puede ser fácilmente diagnosticada por la presencia de cristales de urato monosódico al examen microscópico del líquido articular. Existen algunas diferencias clínicas entre la gota del adulto y la del anciano. El tratamiento es altamente efectivo pero puede ocasionar serias reacciones adversas si no se tiene en cuenta la comorbilidad de este grupo.
Gout is the most common chronic arthritis in older people that can lead to significant and severe disability. It can be easy diagnosed with the presence of crystals of urate monosodic in the articular fluid. The clinical stages of gout include asymptomatic hyperuricemia, intermittent gouty arthritis, intercritical period and chronic tophaceous gout. There are some differences necessary to recognize to avoid errors in the management. Treatment of acute gout involves the use of NSAIDs, colchicine, corticosteroids or corticotropin (adrenocorticotropic hormone). Profilactic treatment includes the use of allopurinol and uricosuric agents; but all of these drugs could cause serious reactions in the elderly.