AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Uric acid is the relatively water-insoluble end product of purine nucleotide metabolism. It poses a special problem for humans because of its limited solubility, particularly in the acidic environment of the distal nephron of the kidney. It is problematic because humans do not possess the enzyme uricase, which converts uric acid to the more soluble compound allantoin. Three forms of kidney disease have been attributed to excess uric acid: acute uric acid nephropathy, chronic urate nephropathy, and uric acid nephrolithiasis. These disorders share the common element of excess uric acid or urate deposition, although the clinical features vary.

Pathophysiology

Properties of uric acid

Uric acid is the final metabolite of endogenous and dietary purine nucleotide metabolism. It is the product of xanthine oxidase–catalyzed conversion of xanthine and hypoxanthine. It is a weak acid with a pKa of 5.75, and, at a physiologic pH of 7.40 in the extracellular compartment, 98% of uric acid is thus in the ionized form as urate. In the collecting tubules of the kidneys, where the pH can fall to 5.0, uric acid formation is favored.

The critical physical property of uric acid in the clinical setting is solubility. Uric acid is less soluble than urate; thus, an acidic environment decreases solubility. Plasma at a pH of 7.40 is saturated with urate at a concentration of 7 mg/dL. Because normal plasma levels of urate are 3-7 mg/dL for men and 2-6 mg/dL for women, the solubility limit apparently is approached under physiologic conditions. Of the uric acid produced daily, the biliary and gastrointestinal tracts excrete 30% and the kidney excretes 70%.

Renal handling of urate

Renal excretion of uric acid involves 4 pathways—filtration, reabsorption, secretion, and postsecretory reabsorption. Urate is freely filtered at the glomerulus. An active anion-exchange process in the early proximal convoluted tubule reabsorbs most of it. Most urinary uric acid appears to be derived from tubular secretion, possibly from the S2 segment of the proximal tubule. Overall, 98-100% of filtered urate is reabsorbed and 6-10% is secreted and ultimately appears in the final urine.

Several factors influence the renal handling of urate. Many medications can affect the renal transport of uric acid through effects of proximal tubular absorption and secretion. Extracellular volume expansion or contraction, respectively, enhances or reduces uric acid excretion through the paired movement of sodium; consequently, in cases of extracellular compartment depletion, urate excretion is diminished.

Physiologically, the major factors that affect urate excretion are the tubular fluid pH, tubular fluid flow rate, and renal blood flow. The first 2 factors primarily diminish uric acid and urate precipitation in the collecting ducts, while the third is important in urate secretion. In disorders such as sickle cell disease, hypertension, and eclampsia, hyperuricemia out of proportion to decreases in glomerular filtration are a result of decreased renal blood flow. Organic acids, such as lactic acid and ketoacids, also can impair the proximal secretion of uric acid.

Acute uric acid nephropathy

Overproduction of uric acid occurs primarily when tissue breakdown is accelerated. Acute uric acid nephropathy is the term applied to the development of acute oligoanuric renal failure caused by renal tubular obstruction by urate and uric acid crystals. This is observed almost exclusively in the setting of malignancy, especially leukemia and lymphoma, in which rapid cell turnover or cell lysis occurs from chemotherapeutic agents or radiation therapy.

The release of intracellular nucleotides leads to severe hyperuricemia. When urate is filtered at exceedingly high concentrations from the plasma and is further concentrated through the course of the tubular system with a progressively more acidic pH, uric acid precipitation and obstruction in the tubules, collecting ducts, and even pelves and ureters may result. In animal models of uric acid nephropathy, the precipitation of uric acid and urate occurs primarily in the collecting duct system and, to some extent, in the vasa recta.

Crystal deposition causes increased tubular pressure, increased intrarenal pressure, and extrinsic compression of the small-diameter renal venous network. This causes an increase in renal vascular resistance and a fall in renal blood flow. The elevated tubular pressure and decreased renal blood flow cause a decline in glomerular filtration and can result in acute renal failure.

Chronic urate nephropathy

A widely accepted belief is that overproduction of uric acid and hyperuricemia can cause acute kidney l failure; however, whether chronic hyperuricemia independently results in chronic interstitial nephritis and progressive kidney failure is less clear.

In patients with chronic hyperuricemia and gout, early studies revealed microtophi formation in the renal medullary interstitium. These deposits contained monosodium urate monohydrate and were surrounded by a giant cell reaction. Thus, the theory was that urate deposition triggers a foreign body reaction and leads to chronic inflammation and fibrosis. Chronic renal failure from this process was termed chronic uric acid nephropathy, or gouty nephropathy, and articles from the 1960s suggested that all patients with long-standing gout had gouty nephropathy. However, recently, the existence of a chronic urate nephropathy has been questioned.

In a study of 11,408 consecutive autopsies in Switzerland, only 37 revealed urate deposits in the kidney and only 3 of these cases had otherwise unexplained kidney failure. Investigators also found urate deposition in the kidneys of patients without gout, suggesting this finding is not specific for gout. In another study, a long-term follow-up evaluation of 524 subjects with gout, the authors concluded that deterioration of kidney function could not be ascribed to hyperuricemia and gout alone. They found that in general, the decline in kidney function could be attributed to other known causes of chronic renal failure, such as nephropathy not associated with uric acid, renal stones, aging, or hypertension. In summary, little compelling evidence exists that chronic hyperuricemia leads to chronic urate nephropathy.

However, there continues to be considerable interest and debate on the relationship between hyperuricemia, hypertension, and progressive kidney failure. A newer hypothesis proposes that hyperuricemia may cause impairment of renal autoregulation, leading to hypertension, microalbuminuria and overt albuminuria, and progressive kidney failure, and recent epidemiological studies in Japan support a link between hyperuricemia and progressive kidney disease. Uric acid-lowering with allopurinol has been proposed to retard the progression of chronic kidney disease and prevent end-stage renal disease, with at least one small prospective clinical trial claiming to demonstrate this. However, routine use of allopurinol in chronic kidney disease and asymptomatic hyperuricemia is still not yet considered to be the standard of care, primarily due to the risk and cost of therapy and the continued lack of compelling evidence in its favor.

There is a rare group of patients in which chronic hyperuricemia clearly leads to kidney failure. These are patients with a congenital absence of hypoxanthine-guanine phosphoribosyltransferase (HGPRT), also known as patients with Lesch-Nyhan syndrome. This is an X-linked disorder that results in mental retardation, involuntary movement, self-mutilation, gout, and early kidney failure. In these patients, chronic uric acid overproduction results in hyperuricemia and uricosuria. The incidence of chronic kidney disease is high in this group. These patients have both intratubular uric acid deposits and interstitial urate deposits.

Uric acid nephrolithiasis

Uric acid stones represent 5-10% of all renal calculi in the United States and also are a result of uric acid precipitation in the collecting system. Uric acid stones are related to uric acid exceeding its solubility in the urine, and, thus, patients with hyperuricosuria have an increased risk of uric acid nephrolithiasis. Urine oversaturation with uric acid and subsequent crystal formation is determined largely by urine pH. Individuals who form uric acid stones tend to excrete less ammonium, which contributes directly to low urine pH. In addition, persons with gout and those who form stones, in particular, have a reduced postprandial alkaline tide (alkaline urine pH).

Frequency

United States

The incidence rate of acute uric acid nephropathy is not known. However, some deterioration in renal function secondary to hyperuricemia has been estimated to occur in as many as 10% of patients with leukemia and lymphoma who have undergone intensive chemotherapy and radiation. With prophylactic therapy, the occurrence of renal failure requiring dialysis due to acute uric acid nephropathy now appears to be quite rare.

Although once thought to be common, the frequency of chronic urate nephropathy appears to be very rare based on newer studies; in fact, its very existence has come into question.

The incidence of all renal calculi is 124 cases per 100,000 population per year. The exact prevalence of uric acid calculi is unknown, but the prevalence of all renal calculi in the United States in men is 4-9% and in women is 1.7-4.1% and uric acid calculi account for 5-10% of all stones in the United States.

Uric acid stones are more common in patients with gout, and the chance of stone formation increases with increasing serum urate levels and urine excretion rates. In one series, 35% of patients with gout who had urine uric acid levels of 700-1100 mg/d had uric acid calculi, and the overall prevalence in those with primary gout is estimated at 22%. In a retrospective series, the incidence rate of stones in patients with newly diagnosed gout was 1 case per 114 patients per year.

International

Reported rates vary widely in other countries. In one report from Israel, 75% of all stones were uric acid calculi.

Mortality/Morbidity

• In the 30 cases of acute uric acid nephropathy reported before 1966, the mortality rate was 47%. Subsequent cases reported had a markedly reduced mortality rate, primarily because of the advent of better preventive management and dialysis therapy. In current practice, the prognosis for persons with acute renal failure from acute urate nephropathy is excellent.
• The morbidity of uric acid nephrolithiasis arises from the manifestations of stones, obstruction, and crystalluria and is often accompanied by dysuria and hematuria. Secondary bacteriuria and pyelonephritis can also occur. However, life-threatening complications are rare.

Race

• A number of different malignancies cause a predisposition to acute uric acid nephropathy, making demographics for this entity difficult to characterize.

Sex

• Uric acid nephrolithiasis occurs most frequently in those with underlying hyperuricemia or gout, which occurs in men more frequently than women by a male-to-female ratio of 4:1.
• In the United States, the prevalence rate is 4-9% in men and 1.7-4.1% in women.

Age

• Uric acid nephropathy has been well documented in the pediatric and adult populations. It may occur more often in pediatric patients because of the increased incidence of acute lymphoblastic leukemia and Burkitt lymphoma in this population.
• Uric acid nephrolithiasis occurs most frequently in those with underlying hyperuricemia or gout, which has a peak incidence in the fifth decade of life.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

• Acute uric acid nephropathy is usually observed in patients shortly after presentation for acute neoplastic disorders or within 1-2 days of initiation of chemotherapy.
• The most frequently observed symptoms are nausea, vomiting, lethargy, and seizures.
• A history consistent with chronic urate nephropathy is progressive renal failure in a patient with coexisting gout or uric acid nephrolithiasis and no other identifiable cause for renal failure.
• Hypertension is common, and pyelonephritis may complicate the presence of obstructing calculi.
• Uric acid nephrolithiasis should be considered in a patient with a history of gout who presents with flank pain, urinary frequency, and dysuria.
• Hematuria is also common. However, note that uric acid nephrolithiasis often precedes the onset of gouty arthritis in patients with both conditions.

Physical

• Occasionally, ureteral obstruction from uric acid sludge can cause severe flank pain, abdominal pain, and dysuria.
• Oliguria is the primary sign of the onset of urate nephropathy, with subsequent edema and congestive heart failure.
• The well-recognized clinical entity of various combinations of hyperuricemia, azotemia, hyperkalemia, hyperphosphatemia, lactic acidosis, and hypocalcemia is known as tumor lysis syndrome.
• The physical examination may reveal subcutaneous tophi or the typical arthritic changes of gout.
• Much debate exists on the incidence of chronic urate nephropathy, and other comorbidities such as diabetes or hypertension often better explain the renal insufficiency.

Causes

• Most cases of acute uric acid nephropathy occur during treatment for leukemia or lymphoma. Uric acid nephropathy is observed more commonly in persons with acute leukemias than in persons with chronic forms of the disease. It also has been described in association with other malignancies, such as metastatic breast carcinoma, bronchogenic carcinoma, and disseminated adenocarcinoma.
• Seizures or ischemic states can lead to extensive release of cell metabolites and consequent hyperuricemia.
• Hyperuricemic acute renal failure has also been reported during pregnancy-related preeclampsia or eclampsia and in the setting of cyclosporine use and renal transplantation.
• Chronic hyperuricemia and gout are the only causes of chronic urate nephropathy, if it exists as a clinical entity.
• The hereditary enzyme disorder HGRPT deficiency, which leads to overproduction of urate, is an indisputable cause of a chronic urate nephropathy leading to renal insufficiency, and several other rare diseases are in this category, such as the following:
• • Uric acid nephrolithiasis can be caused by any underlying disorder that causes hyperuricosuria. This includes all of the previously mentioned causes of acute uric acid nephropathy, such as malignancy, hypercatabolic states, and the hereditary enzyme deficiencies.
  • Uric acid stones develop in 20% of people with gout.
  • Acute diarrheal states may increase urine uric acid concentration through excessive water loss and dehydration, leading to stone formation.
  • Urine pH also tends to decrease with extracellular volume contraction, and gastrointestinal bicarbonate loss may contribute to the acidic urine, thus promoting stone formation.
  • Aspirin and probenecid augment uric acid secretion and may lead to stone formation, especially in people with purine-rich diets.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Establishing the diagnosis of acute uric acid nephropathy is sometimes complicated by the variety of nephrotoxic drugs, radiographic studies, and associated clinical problems often observed during the early presentation of malignancies. Dehydration, contrast nephropathy, and acute tubular necrosis caused by nephrotoxic drugs or sepsis-related renal failure must be considered in this high-risk population. Renal complications associated with malignancies that may result in the sudden cessation of kidney function include hypercalcemia; tumor infiltration of the kidneys, ureter, or bladder; and the monoclonal gammopathies, which may cause a myeloma-type kidney disorder. In addition, chemotherapeutic agents may produce nephropathy with a secondary elevation of urate levels. Other causes of elevated urate levels are preexisting renal failure and drugs, including diuretics, salicylates (<2 g/d), ethambutol, pyrazinamide, vitamin A, cyclosporine, and tacrolimus.

The differential diagnosis for chronic urate nephropathy includes alternative etiologies of chronic renal insufficiency, including diabetes, hypertension, atherosclerotic disease, or primary glomerular diseases.

Other metabolic stone diseases can mimic uric acid nephrolithiasis, and hyperuricosuria is a known risk factor for calcium stone formation.

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• Hyperuricemia is an important finding, with urate levels in the plasma often exceeding 15 mg/dL and peaks as high as 50 mg/dL. Progressive azotemia and hyperphosphatemia are other important findings.
• An increased serum lactate dehydrogenase level is suggestive of a large tumor burden and correlates with risk.
• Urinalysis results are usually bland.
• • Uric acid and sodium monourate crystals may be observed.
  • Although variable, urine uric acid levels may be as high as 150-200 mg/dL.

• A random ratio of urine uric acid to creatinine higher than 1 is also suggestive of acute uric acid nephropathy.
• A disproportionate elevation in serum uric acid levels can also be a diagnostic clue.
• Elevated serum and urinary uric acid levels correlate with the frequency of nephrolithiasis, and 50% of patients with serum uric acid levels greater than 13 mg/dL or urinary uric acid secretion higher than 1100 mg/d will form stones. Uric acid stones are radiolucent, and the urine uric acid crystals are reddish-orange. Urate crystals have several forms but tend to be needle-shaped or flat, square plates; both are strongly birefringent.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

• Acute uric acid nephropathy
• • Prior to the dialysis era, treatment of acute uric acid nephropathy was not very successful, with mortality rates approaching 50%. With the use of modern treatment, including prophylaxis and dialysis, uric acid nephropathy is rare. Additionally, when it does occur, the prognosis for the acute renal failure is excellent. Management without dialysis involves attempts to lower the plasma urate level and the urate concentration within the renal tubules.

  • The xanthine oxidase inhibitor allopurinol has been a milestone in the prevention of acute uric acid nephropathy. It blocks the conversion of hypoxanthine and xanthine to uric acid, resulting in both a reduction in serum uric acid concentration and urinary excretion of urates. However, urinary excretion of hypoxanthine and xanthine increases. Hypoxanthine is highly soluble and does not cause clinical problems. Xanthine is less soluble than uric acid and precipitated xanthine can be found in the urine of those taking allopurinol, but these precipitates do not correlate with renal failure. However, well-documented cases of xanthine nephropathy exist.

  • Allopurinol has been used extensively in the prevention of acute uric acid nephropathy in patients with malignancy who are undergoing chemotherapy, and considerable experience has been gained in patients with leukemia and lymphoma. The half-life of allopurinol is less than 2 hours, due to renal excretion and rapid conversion to its chief metabolite, oxypurinol. Oxypurinol is an active metabolite, and it reduces serum uric acid concentration and urine uric acid secretion half as much as allopurinol. Oxypurinol is eliminated solely by the kidney, with a half-life of approximately 24 hours. Its clearance correlates directly with creatinine clearance. The clinical effects of allopurinol are probably mediated by oxypurinol because the half-life of allopurinol is short.

  • For optimal prophylaxis of acute uric acid nephropathy, allopurinol should be administered at 48-72 hours or, preferably, 5 days before the initiation of cancer therapy. Uric acid nephropathy is relatively rare if this is accomplished.

  • The level of existing renal function must be considered when dosing the drug. In some instances, hyperuricemia and acute uric acid nephropathy cannot be avoided because of a large tumor burden, aggressive chemotherapy, and the inability to delay chemotherapy until allopurinol has lowered the serum uric acid concentration.

  • Allopurinol can lead to a life-threatening toxicity syndrome that is characterized by a diffuse desquamative skin rash, fever, hepatic dysfunction, eosinophilia, and worsening renal function of unknown etiology. Eighty percent of the patients reported to have this syndrome had preexisting renal insufficiency.

  • In patients with healthy renal function, a starting dose of 300-600 mg of allopurinol daily is safe and achieves therapeutic levels of oxypurinol, which is a serum concentration of 30-100 µmol/L.

  • Patients with end-stage renal disease achieve therapeutic levels after one 300- to 600-mg dose and maintain this level until the next dialysis, at which time the serum level will be reduced by 40%. Therefore, the maintenance dose must be reduced in patients with renal insufficiency to avoid accumulation of oxypurinol.

  • If the creatinine clearance is approximately 50-90 mL/min, the dose should be 200 mg/d, and for a creatinine clearance of 10-50 mL/min, the dose should be 100 mg every 2 days. In patients with a creatinine clearance less than 10 mL/min, the dose should be 100 mg every 3 days.

  • After hemodialysis, the patient should be supplemented with 50% of the allopurinol dose.

  • In pediatric patients older than 6 years, 300 mg of allopurinol daily is the usual dose. The dose is reduced to 150 mg/d in those younger than 6 years.

  • No adequate or well-controlled studies have been performed on the effect of the drug on the fetus in pregnant women.

  • In addition to the use of a xanthine oxidase inhibitor to prevent hyperuricemia, high tubular flow rates induced by large-volume fluid intake and solute and water diuresis also have a role in protecting the kidney from developing high concentrations of urate that will result in precipitation. Patients should be hydrated with 4-5 L of normal saline every 24 hours. If the patient is well hydrated and not maintaining the expected urine output, diuretics should be initiated. If the urine output remains low, adjust the fluid intake to match the output in order to avoid fluid overload.

  • Although lacking evidence confirming its role, urinary alkalinization, theoretically, should increase uric acid solubility. In animal studies, high tubular flow rates were the most important factor in preventing uric acid and urate crystallization, with urinary alkalinization playing only a minor role. The agent used was acetazolamide, and its protection also may have been from its diuretic effect. Sodium bicarbonate administration carries the inherent risks of severe metabolic alkalosis, increased risk of symptomatic hypocalcemia, and calcium phosphate precipitation, which, in itself, can cause acute renal failure. Therefore, bicarbonate therapy should be included in the prophylactic regimen only when attempting to correct hyperuricemia. If hyperuricemia is present prior to chemotherapy, bicarbonate should be added to intravenous fluids with the goal of maintaining the urine pH above 7.0. Once hyperuricemia has been corrected, bicarbonate therapy should be discontinued.

  • Occasionally, despite the use of allopurinol, diuretics, and urine alkalinization, patients progress to acute kidney failure. Dialysis assists in the management of acute uric acid nephropathy in 2 ways. First, it protects patients from the complications of kidney failure (eg, hyperkalemia, fluid overload, uremia). Cases of fatal hyperkalemia have been reported within hours of initiation of chemotherapy. Second, dialysis is an effective way to reduce the serum uric acid level. This is important because patients with uric acid nephropathy do not recover until their serum uric acid level is reduced. In this regard, hemodialysis is superior to peritoneal dialysis because hemodialysis has much higher uric acid clearance, approximately 90-150 mL/min, compared to 10-20 mL/min for peritoneal dialysis.

  • Once the serum uric acid level is reduced, usually after 1-4 dialysis sessions, recovery of kidney function is signaled by a brisk diuresis. As a rule, with each dialysis, the plasma urate level is reduced by 50% for each 4- to 6-hour dialysis session.

  • Rasburicase (Elitek) is a recently FDA-approved drug for the treatment of tumor lysis syndrome for the pediatric population only, although it is used in Europe for the adult and geriatric populations and is even considered the standard of care at some centers there. It is a recombinant urate oxidase enzyme that converts uric acid to allantoin. In theory, this has the added benefit of converting existing uric acid to a nonnephrotoxic metabolite in contrast to allopurinol, which prevents future formation of uric acid.
    • It is a costly medication, and judicious use is recommended, as there is no evidence that it is superior to standard therapy with allopurinol and bicarbonate.

    • The FDA-recommended dosing guidelines for pediatric patients are 0.15 mg/kg or 0.2 mg/kg IV daily for a maximum of 5 days. Adverse effects include rash, hemolysis, and methehemoglobinemia and occurred in less than 1% of patients in various clinical trials.

• Chronic urate nephropathy
• • Because of the lack of evidence that hyperuricemia in itself causes chronic nephropathy (except in the rare enzyme deficiencies previously mentioned), the current trend is to not treat hyperuricemia for the prevention of chronic nephropathy alone, although this topic remains under active study and debate.

  • The significant toxicity of allopurinol and the lifelong expense make this therapy unwarranted. The emphasis should be on controlling other risk factors for kidney failure, such as diabetes and hypertension.

• Uric acid nephrolithiasis
• • The goals of uric acid nephrolithiasis therapy are to reduce the existing stone size and to prevent the formation of new stones. These objectives are achieved by decreasing production of uric acid and increasing its solubility.

  • Curtailing dietary purine, chiefly in the form of animal protein, can substantially decrease uric acid production. Increasing fluid intake to maintain a urine output of 2-3 L/d can be achieved with minimal inconvenience. Ingestion of alkali in the form of bicarbonate or citrate at a dose of 0.5-1.5 mEq/kg/d with a goal of urine pH of 6.0-6.5 can be effective. If nocturnal urine pH falls, a single dose of 250 mg oral acetazolamide at bedtime is usually effective to maintain alkaline urine.

  • Allopurinol should be used if stones recur despite the above therapies, when the urine uric acid excretion is greater than 1000 mg/d, or if the patient has gout. Allopurinol is also indicated for dissolving or reducing the size of existing stones and when large, nonobstructing renal pelvic stones are too large to pass.

  • Extracorporeal shock wave lithotripsy can be tried for problem calculi, but the procedure is less efficacious for uric acid stones than for other types of stones.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Xanthine oxidase inhibitors

Used for prevention of acute uric acid nephropathy. Block the conversion of hypoxanthine and xanthine to uric acid, resulting in a reduction in both serum uric acid concentration and urinary excretion of urates. Used in the treatment of gouty arthritis.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Deterrence/Prevention:

• The xanthine oxidase inhibitor allopurinol has been a significant development in the prevention of acute uric acid nephropathy. Allopurinol has been used extensively in the prevention of acute uric acid nephropathy in patients with malignancy who are undergoing chemotherapy. Rasburicase is another FDA-approved option in the pediatric population in the United States.

Prognosis:

• Prior to the dialysis era, treatment of acute uric acid nephropathy was not very successful, with mortality rates approaching 50%. With the use of modern treatment, including prophylaxis and dialysis, uric acid nephropathy is rare. Additionally, when it does occur, the prognosis for acute kidney failure is excellent.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

• Conger JD. Acute uric acid nephropathy. Med Clin North Am. Jul 1990;74(4):859-71. [Medline].
• Dykman D, Simon EE. Hyperuricemia and uric acid nephropathy. Arch Intern Med. Jul 1987;147(7):1341-5. [Medline].
• Guest SS. Uric acid and the kidney. In: Nephrology Rounds 4. Snell Medical Communications; 2001:1-5.
• Iseki K, Ikemiya Y, Inoue T, Iseki C, Kinjo K, Takishita S. Significance of hyperuricemia as a risk factor for developing ESRD in a screened cohort. Am J Kidney Dis. Oct 2004;44(4):642-50. [Medline].
• Johnson RJ, Segal MS, Srinivas T, Ejaz A, Mu W, Roncal C. Essential hypertension, progressive renal disease, and uric acid: a pathogenetic link?. J Am Soc Nephrol. Jul 2005;16(7):1909-19. [Medline].
• Nickeleit V, Mihatsch MJ. Uric acid nephropathy and end-stage renal disease--review of a non-disease. Nephrol Dial Transplant. Sep 1997;12(9):1832-8. [Medline].
• Pea F. Pharmacology of drugs for hyperuricemia. Mechanisms, kinetics and interactions. Contrib Nephrol. 2005;147:35-46. [Medline].
• Ueng S. Rasburicase (Elitek): a novel agent for tumor lysis syndrome. Proc (Bayl Univ Med Cent). Jul 2005;18(3):275-9.

Article Last Updated: Feb 1, 2007