Many articles have reported on the associations between gout and chronic kidney disease (CKD) using data gathered from different portions of the National Health and Nutrition Examination Survey (NHANES).
Most recently, a group of investigators recently focused on the associations between CKD and gout using the NHANES data from 1988-1994 and 2007-2010 (Semin Arthritis Rheum 2013; published online ahead of print).
The former cohort included a total of 15,132 subjects, while the latter was composed of 10,814 subjects. Estimated glomerular filtration rate (eGFR) was negatively associated with age, albuminuria, serum uric acid, and prevalence of diabetes mellitus, hypertension, and hyperuricemia. Diuretic and gout medication use increased with lower eGFR. The prevalence of gout in the former cohort was 2.7% while the latter was 3.7%. The relationship between eGFR and albuminuria with gout and hyperuricemia were continuous.
Individuals in the lowest eGFR category had a threefold increased prevalence of gout, and every 10 mL/min/1.73m2 increase in eGFR correlated with a 10% reduced prevalence of gout. Macroalbuminuria correlated with a twofold increased prevalence of gout.
Gout is linked to kidney health because urate clearance occurs through the GLUT9 transporter in the proximal renal tubule (Curr Opin Rheumatol 2012;24:127-131). Increased gout risk can occur from genetic mutations in the SLC2A9 gene associated with the GLUT9 transporter, which not only transports urate but also glucose and fructose. URAT1 is another transporter specifically involved in uric acid transport in the kidney, but genetic mutations in GLUT9 produce more dramatic effects on urate absorption than URAT1.
Although research is still required to assess whether the relationship between hyperuricemia and gout with CKD is simply correlative or causative, dietitians working with CKD patients may often find themselves offering dietary guidance related to gout management. A range of dietary factors can promote gout. Exogenous purine intake can induce gout flares due to the metabolism of purines to uric acid (Adv Chronic Kidney Dis 2012;19:392-397). Most high-protein foods have increased levels of purines that may contribute to a gout flare.
A diet extremely high in protein and fat with very little carbohydrate intake may induce ketogenesis, which is known to be an inhibitor of uric acid excretion. Another inhibitor of uric acid excretion is elevated lactate levels, which can be induced by alcohol ingestion. Refined sugar also exacerbates the issue through the increase in dietary fructose. Fructose metabolism promotes the conversion of adenine molecules found in ATP to uric acid.
Many recommendations for gout management focus primarily on the reduction of purine intake. Both animal proteins and plant proteins from beans have moderate levels of purine content; typically the highest purine content foods are derived from organ meats.
Following the typical recommended dietary allowance for protein intake of 0.8g/kg bodyweight will most likely not provide excessive exogenous purine sources as to aggravate a gout flare. Regarding alcohol intake, beer is the most problematic for hyperuricemia because not only does the alcohol stimulate increased lactate levels, but unlike wine and harder liquors, beer has a significant guanosine content due to the yeast.
Wine intake would be the safest form of alcohol since it does not match the purine content of beer nor the alcohol content of liquors. Extreme ketogenic diets should be limited if patients exhibit hyperuricemia and gout flares, but low carbohydrate diets that do not promote high levels of ketosis appear to be safe when well monitored and are accompanied by weight loss.
Because most individuals consuming Western diets do not often exhibit extreme intakes of protein or alcohol that would significantly increase risk of hyperuricemia or gout, fructose intake may become a more important focus of intervention, assuming strong genetic factors have been assessed. Several studies have focused in particular on the intake of sugar sweetened beverages and serum uric acid levels.
The results at this time have found associations between sugar sweetened beverage intake and increased uric acid levels as well as increased uric acid levels and increased blood pressure, but the direct association of sugar sweetened beverages to blood pressure needs more evidence at this time (J Hum Hypertens 2012; published online ahead of print).
Analyzing this information in the context of CKD, a few conclusions may be deduced. Hyperuricemia has to be proven to be a causative factor in kidney decline, but the presence of hyperuricemia and gout is a risk factor for decline.
The foods that may increase risks of gout flares—namely very-high-protein diets, excessive alcohol primarily from beer, and excessive fructose intake—are also dietary factors that may promote further kidney decline in individuals with CKD stages 3-5. Excessive fructose intake may aggravate blood sugar control in diabetic individuals that may further promote kidney decline.
Thus, when working with CKD patients, uric acid levels should be assessed when deciding which dietary restrictions to prioritize.
No comments:
Post a Comment