A low purine diet may help lower uric acid levels in the body by reducing or eliminating foods high in purines. Purines are compounds found mainly in animal proteins that are broken down into uric acid. This diet is given to treat gout and Lesch-Nyhan syndrome, a rare genetic disorder caused by a purine metabolism enzyme deficiency. High uric acid levels can cause problems like kidney stones or gout, characterized by painful joint inflammation from urate crystals. While low purine diets are commonly used to manage these conditions, high-quality long-term studies on their effectiveness are still lacking.
A low purine diet may help lower uric acid levels in the body by reducing or eliminating foods high in purines. Purines are compounds found mainly in animal proteins that are broken down into uric acid. This diet is given to treat gout and Lesch-Nyhan syndrome, a rare genetic disorder caused by a purine metabolism enzyme deficiency. High uric acid levels can cause problems like kidney stones or gout, characterized by painful joint inflammation from urate crystals. While low purine diets are commonly used to manage these conditions, high-quality long-term studies on their effectiveness are still lacking.
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diet rendah purin untuk pasien hiperurisemia yang juga menderita chronic kidney disease (CKD)
A low purine diet may help lower uric acid levels in the body by reducing or eliminating foods high in purines. Purines are compounds found mainly in animal proteins that are broken down into uric acid. This diet is given to treat gout and Lesch-Nyhan syndrome, a rare genetic disorder caused by a purine metabolism enzyme deficiency. High uric acid levels can cause problems like kidney stones or gout, characterized by painful joint inflammation from urate crystals. While low purine diets are commonly used to manage these conditions, high-quality long-term studies on their effectiveness are still lacking.
A low purine diet may help lower uric acid levels in the body by reducing or eliminating foods high in purines. Purines are compounds found mainly in animal proteins that are broken down into uric acid. This diet is given to treat gout and Lesch-Nyhan syndrome, a rare genetic disorder caused by a purine metabolism enzyme deficiency. High uric acid levels can cause problems like kidney stones or gout, characterized by painful joint inflammation from urate crystals. While low purine diets are commonly used to manage these conditions, high-quality long-term studies on their effectiveness are still lacking.
Background Low purine diets may be helpful in lowering levels of uric acid in the body, and may involve reducing or eliminating foods with high concentrations of purines. A purine is a compound that is mainly found in animal protein and is metabolized to uric acid in the body, comprising about 15% of the body's uric acid. This diet is usually given to individuals with gout and Lesch-Nyhan Syndrome (a rare genetic disorder that occurs in 1/100,000 people). Uric acid is a substance resulting from the breakdown of purines, which are part of all human tissue and are found in many foods. Uric acid dissolves in the blood, passes through the kidneys, and is then eliminated in the urine. The buildup of this substance in the body may lead to problems, including kidney stones and gout. Gout (hyperuricemia) is a condition characterized by abnormally high blood levels of uric acid (urate). Urate crystals may form in joints, resulting in inflammation and pain. Urate crystals may also form in the kidney and urinary tract, resulting in kidney stones. This condition usually develops first in the joint of the big toe first. Common symptoms include inflammation, pain, redness, stiffness, swelling, and warm to the touch. Symptoms of gout may develop quickly and typically occur in only one joint at a time. Touching or moving the joint may be extremely painful. Gout was once thought of as a "rich man's disease" because only the wealthy could afford to eat salted meats, rich breads, and malted liquors on a regular basis. The prevalence of gout has increased in the last 50 years due to the tendency of contemporary people to ignore foods high in purine levels in favor of convenience and cost. Lesch-Nyhan syndrome (LNS) is a rare, inherited disorder that affects how the body builds and breaks down purines. It is caused by a deficiency of the enzyme called hypoxanthineguanine phosphoribosyltransferase (HPRT). LNS is characterized by increased blood and uric acid levels which may lead to gout-like swelling in the joints or renal dysfunction. Although a low purine diet is often adopted for the treatment of gout or Lesch-Nyhan syndrome, high-quality, long-term human trials dealing explicitly with the management of gout through a low purine diet alone are still lacking. Low purine diets may be helpful in lowering levels of uric acid in the body, and may involve reducing or eliminating foods with high concentrations of purines. A purine is a compound that is mainly found in animal protein and is metabolized to uric acid in the body, comprising about 15% of the body's uric acid. This diet is usually given to individuals with gout and Lesch-Nyhan Syndrome (a rare genetic disorder that occurs in 1/100,000 people).
Uric acid is a substance resulting from the breakdown of purines, which are part of all human tissue and are found in many foods. Uric acid dissolves in the blood, passes through the kidneys, and is then eliminated in the urine. The buildup of this substance in the body may lead to problems, including kidney stones and gout. Gout (hyperuricemia) is a condition characterized by abnormally high blood levels of uric acid (urate). Urate crystals may form in joints, resulting in inflammation and pain. Urate crystals may also form in the kidney and urinary tract, resulting in kidney stones. This condition usually develops first in the joint of the big toe first. Common symptoms include inflammation, pain, redness, stiffness, swelling, and warm to the touch. Symptoms of gout may develop quickly and typically occur in only one joint at a time. Touching or moving the joint may be extremely painful. Gout was once thought of as a "rich man's disease" because only the wealthy could afford to eat salted meats, rich breads, and malted liquors on a regular basis. The prevalence of gout has increased in the last 50 years due to the tendency of contemporary people to ignore foods high in purine levels in favor of convenience and cost. Lesch-Nyhan syndrome (LNS) is a rare, inherited disorder that affects how the body builds and breaks down purines. It is caused by a deficiency of the enzyme called hypoxanthineguanine phosphoribosyltransferase (HPRT). LNS is characterized by increased blood and uric acid levels which may lead to gout-like swelling in the joints or renal dysfunction. Although a low purine diet is often adopted for the treatment of gout or Lesch-Nyhan syndrome, high-quality, long-term human trials dealing explicitly with the management of gout through a low purine diet alone are still lacking. http://www.healthline.com/natstandardcontent/alt-low-purine-diet Hyperuricemia in CKD
Answers
Hyperuricemia, as defined as serum urate levels above 6.5 mg/dl, is particularly
common in chronic kidney disease, due to decreased uric acid clearance, and may increase the risk of acute arthritis, chronic tophaceus gout, uric acid nephrolithiasis and gouty nephropathy. In addition, high uric acid levels may precede the development of high blood pressure and cardiovascular disease, although its direct causal role is still a matter of lively debate. Consequently, no large consensus exists about whether treating asymptomatic hyperuricemia with uric acid-lowering agents might offer any renal or cardiovascular benefit in individuals with established chronic kidney disease. Both older and recent observational studies evaluating the causal role of uric acid in the development and progression of CKD have led to inconclusive or conflicting results. For instance, a 14% increase in the risk of kidney disease progression was demonstrated per each 1 mg/dL increase in uric acid levels in the Cardiovascular Health Study (Conchol, MB et al. Am J Kidney Dis. 2007; 50: 239247). On the other hand, when the MDRD study was examined, uric acid was not a predictor of CKD progression, as defined as the need for dialysis or transplantation, in patients with stage 3-4 CKD followed for 10 years (Madero, M et al. Am J Kidney Dis. 2009; 53: 796-803). Along the same line, uric acid levels did not predict CKD
progression in patients with mild to moderate CKD over 7 years of follow-up (Sturm G et al. Exp Gerontol. 2008; 43: 347-352). However, it is difficult to ascertain the pathogenic role of uric acid in the progression of CKD by evaluating epidemiological studies, as high uric acid levels are also strongly associated with obesity, hypertension, and diabetes. Thus, the potential independent association between uric acid and CKD progression although not necessarily causal given the epidemiological nature of the studies- is difficult to demonstrate in multivariate analyses. Additional data have been provided by both experimental studies and intervention trials. In 2001, the group of Richard Johnson revitalized the interest in the role of uric acid in renal disease by using a new experimental model, wherein hyperuricemic rats developed hypertension, afferent arteriole arteriolopathy, interstitial fibrosis glomerulosclerosis and albuminuria, independent of intrarenal deposition of uric crystals (Mazzali, M. Hypertension. 2001. 38: 1101-1106). The onset of both hypertension and tubulointerstitial injury was prevented by allopurinol, a xanthine oxidase inhibitor, or benziodarone, an uricosuric drug. To further investigate the role of uric acid in CKD progression, Kang and coauthors used a remnant kidney model (5/6 nephrectomy), demonstrating that even modest hyperuricemia greatly exacerbated CKD progression. While allopurinol blocked the renal functional and histological changes, benziodarone only partially improved renal changes, with minimal effects on the vasculature (Kang DH. J Am Soc Nephrol. 2002; 13: 2888-2897). Despite these encouraging findings, evidence from intervention studies evaluating the effect of uric acid lowering in CKD progression is scant. In a prospective randomized trial enrolling patients with CKD and hyperuricemia, allopurinol on top of usual therapy significantly reduced the risk of serum creatinine increase or ESRD (16 vs 46%) compared to controls (Siu YP et al. Am J Kidney Dis. 2006. 47: 51-59). Along the same line, in a recent post-hoc analysis of the RENAAL trial, the risk of renal events lowered by 6% per each 0.5 mg/dL reduction in uric acid levels during the first 6 months of the study, independent of other risk factors (MiaoY et al. Hypertension. 2011. 58: 2-7). The authors suggested that about one-fifth of the renoprotective effects of losartan could be attributed to its effect on uric acid levels. Finally, allopurinol therapy reduced CKD progression and cardiovascular events in patients with eGRF lower than 60 ml/min, compared to usual therapy alone (Goicoechea, M et al. Clin J Am Soc Nephrol. 2010. 5: 1388-1393). However, further and larger clinical trials are needed before suggesting a wide usage of hypouricemic drugs in CKD patients in daily clinical practice. This is particularly true in asymptomatic hyperuricemia, given the risk of serious or life-threatening adverse events, including Stevens-Johnson syndrome and toxic epidermal necrolysis (Fagugli R et al. Clinical Nephrology. 2008. 70: 523-526), that is even higher in some ethnic groups, such as Koreans and all persons of Han Chinese and Thai descent http://www.theisn.org/ask-the-experts/root/general-nephrology/hyperuricemia-in-ckd/itemid-622
