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Uric Acid Nephrolithiasis
Introduction
Uric acid nephrolithiasis, a form of kidney stone disease, results from the accumulation of uric acid crystals in the kidneys. These crystals can aggregate into stones, leading to painful and potentially recurrent urinary tract obstructions. This condition often correlates with elevated uric acid levels in the bloodstream, known as hyperuricemia. Almost two-thirds of all uric acid kidney stones can be dissolved by increasing urinary pH and volume and decreasing hyperuricosuria.
Nephrolithiasis is a frequent health problem in developed nations, with an estimated 2 to 5% of people affected at least once in their lifetimes worldwide. Numerous conditions increase susceptibility to nephrolithiasis, including genetic disorders, underlying metabolic processes, and dietary and environmental factors.[1][2][3][4] Medical conditions, such as metabolic syndrome, obesity, diabetes mellitus, gout, hypertension, and chronic renal failure, can be associated with uric acid nephrolithiasis.[5][6]
Swedish pharmacist C. Scheele first identified what we now call "uric acid" as the primary acidic component of bladder stones in 1776.[7] Renal and, specifically, bladder stones made of uric acid have historically inflicted immense pain and suffering. In the absence of modern interventions, the sole available treatment was high-risk surgery with significant mortality rates.[8] Sir Isaac Newton and Michelangelo are 2 of many prominent historical figures who had recurrent uric acid kidney stones.
Etiology
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Etiology
In humans, uric acid is the end product of purine metabolism. The 3 sources of purines are (1) cellular RNA from cell turnover, (2) metabolic hepatic synthesis, and (3) dietary intake of high-purine foods.
Purine digestion produces xanthine, which is converted to uric acid through the enzymatic action of xanthine oxidase. Xanthine oxidase inhibitors block the oxidation of xanthine to uric acid. Xanthine is much more soluble than uric acid; however, it can also cause stones and nephropathy at high levels. In most other mammals, aside from humans and higher primates, uric acid is metabolized by uricase to allantoin, which is highly soluble and does not have adverse clinical effects.[9]
Endogenous uric acid synthesis is relatively stable at about 300 mg-400 mg daily. The contribution of dietary sources can vary, but diet is responsible for 50% or less of total daily uric acid production. Total uric acid excreted daily on a typical Western diet is generally estimated at 10 mg/kg body weight.[10] However, dietary factors, such as a high purine diet, can substantially increase urinary uric acid excretion by 50% or more.[11]
The most significant risk factor for uric acid stones is acidic urine, often associated with low urinary ammonia levels. Hyperuricosuria and low urine volumes are also important risk factors. In addition to uric acid stones, hyperuricosuria also leads to increased calcium oxalate urolithiasis, the most common type of kidney stone, accounting for 70% to 80% of kidney stones.[12] The mechanisms by which this occurs are thought to be monosodium urate acting as a nidus for calcium salts to precipitate and removing mucopolysaccharides, which inhibit calcium oxalate precipitation.[7][13][7]
The etiology of uric acid stones can be classified as idiopathic, acquired or secondary, and congenital.[14][15] Idiopathic is the most common etiology associated with metabolic disorders. Idiopathic causes are as follows:
- Aciduria (low urinary pH) is due to higher acid production or inadequate available buffers
- Diabetes mellitus
- Metabolic syndrome
- Obesity
Acquired or secondary etiologies are less common than idiopathic. These are associated with low urinary pH and volume and hyperuricosuria. Acquired or secondary etiologies include the following:
- Gout associated with high serum uric acid levels resulting in hyperuricosuria
- Persistent diarrhea associated with irritable bowel syndrome, gastric bypass surgery, and ileostomy. Low urinary volume and hypocitraturia are observed and are often associated with bicarbonate losses.
- Cancer, eg, high cell turnover, especially during chemotherapy, causes necrosis of tumor cells and acute tumor lysis syndrome
- Dietary factors, especially high purine sources include organ meats (liver, kidney), poultry, fish (herring, trout, sardines), and red meat
- Medications such as probenecid and sulfinpyrazone, which block renal reabsorption of uric acid, and other uricosuric drugs including indomethacin, losartan, and salicylic acid
Congenital etiologies are uncommon and are associated with hyperuricosuria. Examples of congenital etiologies are listed below.
- Lesch-Nyhan syndrome
- Von-Gierke disease
- Collagen storage disease type I
- Hartnup disease
- Wilson disease
- Familial hypouricemic hyperuricosuria (also known as Renal uric acid leak) and URAT1 mutations [16][17]
- Sickle cell disease and other hemolytic anemias (due to high cell turnover) [18]
The incidence of uric acid stones has risen considerably in patients with metabolic syndrome, and clinically, most patients with uric acid stones have some degree of metabolic syndrome, impaired glucose tolerance, or overt diabetes.[4][15][19] Aciduria is the single most important factor in the development of uric acid stones, and the cause is thought to be due to diet-dependent and diet-independent causes, such as metabolic syndrome that tends to produce a net acid load. Another underlying factor is reduced hepatic ammonia synthesis.[20] This causes an increase in net acid excretion as ammonia is the most active urinary buffer over the pH spectrum of urine.[21]
Uric acid is much less soluble at a low urinary pH (5.5 or less), whereas solubility greatly increases at a higher urinary pH (especially at a pH of 6.5 or more).[20] Diurnal variations also play a role as the lowest urine production and lowest urinary pH both occur in the early morning; hence, the morning is when uric acid crystals are most likely to form.[10]
Gout and hyperuricemia are associated with uric acid uropathy in 15% to 25% of patients.[22][23][24][25] Under normal physiological conditions, uric acid is secreted 70% by the kidneys and 30% by the intestine, but this proportion can change with renal insufficiency.[7] Of note, in addition to uric acid nephrolithiasis, uric acid itself is nephrotoxic. It can cause acute kidney injury by stimulating renal vasoconstriction, increasing inflammatory mediators, injuring renal microvasculature, and impairing renal autoregulation.[26]
Epidemiology
Uric acid stones account for about 10% of all urinary stones in the United States and 5% to 40% of all stone cases globally.[27][28] In the United States, the overall lifetime risk for urinary stones in men is 10.6%, and for women, 7.6%. Most untreated patients suffer from periodic abdominal pain, urinary tract infections, and loss of kidney function, eventually leading to renal failure. The annual economic burden associated with all nephrolithiasis has risen from $1.3 billion in 1994 to $2 billion in 2000 despite treatment and patient care advancements.[9]
Uric acid calculi comprise 10% to 15% of all urinary tract stones, with the majority presenting in men, most frequently aged 60 to 65.[29] Obesity, hyperglycemia, metabolic syndrome, and high blood pressure are commonly associated with uric acid calculi in Western countries.[30]
The prevalence of uric acid uropathy varies with age, gender, and environmental factors. For example, people older than 65 were found to suffer from uric acid stones twice as often as younger patients. Males have traditionally been affected up to 3 times more than females, but this pattern is evolving as more women are now experiencing this disorder.[31][32] Patients who form uric acid stones tend to have a somewhat greater risk of recurrences and stone-related surgeries than patients with calcium urolithiasis.[33]
The formation of uric acid nephrolithiasis is exceptionally high among certain ethnic groups. For example, about 50% of ethnic Hmong patients (from Laos and Thailand) were found to be affected by uric acid stones, whereas among non-Hmong patients from the same country, the rate was only 10%.[34] In the Middle East, some regions report that uric acid comprises one-third of all urinary calculi.[35]
Most Asian countries have very low rates of uric acid stones, where the reported incidence is <1%.[36] However, there are a few exceptions, such as Okinawa, which has a relatively high incidence of uric acid stones, accounting for 15% of all urinary calculi produced on the island.[37] These differences are due to genetic, dietary, and climate-based factors.
Environmental factors also influence the frequency of uric acid disorders and stone formation, and it is thought to be much more common in dry, arid regions. One study showed that the prevalence of all nephrolithiasis was 9% among factory workers laboring in hot environmental conditions. In contrast, it was only 0.9% among people working the same job at standard room temperature.[38][34]
Pathophysiology
Factors related to the formation of uric acid stones include a persistently low urine pH, hypovolemia, and hyperuricosuria (defined as 24-hour urinary excretion of uric acid more than 750 mg/d in females and 800 mg/day in males).[37][39] Notably, these values derive from statistical analyses of numerous 24-hour urine tests from individuals without nephrolithiasis and not from supersaturation ratios, crystallization rates, or other sources. For most practical purposes, a serum urinary uric acid level of 800 mg/d is acceptable in most patients without aciduria or hyperuricemia. While being treated for high uric acid levels, the optimal level of urinary uric acid is less than 600 mg/d.[40]
Decreased Urinary pH
Almost all individuals with uric acid nephrolithiasis present with aciduria.[41][42] The decrease in urine pH forms uric acid stones by inducing changes in the dissolution of uric acid.[43][44] In other words, uric acid solubility is heavily dependent on pH. While aciduria with a pH less than 5.5 is insufficient to cause uric acid stones, uric acid stones are also unlikely to form when urine pH exceeds 6.5.[7]
Aciduria is usually caused by decreased ammonia production, as ammonia is the primary urinary buffer.[45] In the proximal convoluted tubule, insulin increases glutamine metabolism, producing ammonia (NH3) and then forming ammonium ions (NH4+) in the presence of free hydrogen. Metabolic syndrome, impaired glucose metabolism, and diabetes cause proximal renal tubular steatosis, lipotoxicity, and insulin resistance, resulting in aciduria. One mechanism by which this occurs is that steatosis in the proximal tubule cells directly inhibits Na/H exchanger 3 (NHE3), which is the principal regulator of ammonium excretion.[21][46][47][48] Insulin resistance at the NHE3 receptor is also a possible contributor to defective NH4+ secretion.[12] One study compared patients with known uric acid stones with a similar control group of patients without uric acid stones and found that at all BMI levels, patients with uric acid stones had more acidic urine and lower ammonia/net acid excretion when both groups were given the same diet.[49]
Decreased Urine Output
A decrease in urine output can cause concentrated urinary solutes and supersaturation, precipitating uric acid crystals.[50][51] The most common reason for hypovolemia is dehydration, but gastrointestinal disturbances such as Crohn disease, irritable bowel syndrome, and ileostomies can also cause hypovolemia. In addition, these can also be associated with loss of bicarbonate through diarrhea and hypocitraturia, which further contributes to metabolic acidosis and aciduria.[45]
Hyperuricosuria
The renal glomerulus almost completely filters uric acid, then mostly reabsorbed in the proximal convoluted tubule. About 10% of the filtered uric acid is ultimately excreted in the urine. High uric acid levels in the urine usually result from excess purine ingestion, usually in red meats, especially organ meats, certain kinds of fish, and alcohol.[7] More recently, high salt and fructose diets have been linked to increased aldose reductase activity, which increases intracellular uric acid production.[52]
Rare genetic disorders can also cause high urinary uric acid levels. Lesch-Nyan syndrome is a rare X-linked disorder characterized by choreoathetosis, retardation of motor development, dystonia, and self-mutilation. It is caused by mutations in the hypoxanthine-guanine phosphoribosyltransferase (HGPRT) pathway, which causes excess degradation of purines and high serum and urine uric acid levels.[53] Congenital renal hypouricemic hyperuricosuria is seen due to mutations in the URAT1 channel.[54][55][56] Other even less common variants are listed above.
Crystallization Inhibitors
Many components in urine suppress the crystallization of urate and thus inhibit urinary stone formation. The most significant is citrate, which increases urinary pH; hypocitraturia is seen in most nephrolithiasis.[57][58] Certain urinary macromolecules are especially effective in inhibiting crystal growth. These include uromodulin (also called Tamm-Horsfall protein), urinary prothrombin fragment 1, and chondroitin sulfate.[58]
Histopathology
One study analyzed papillary biopsies of 23 patients with uric acid stones and compared them with control patients and those with calcium oxalate stones. Patient biopsies from the uric acid cohort showed intraluminal crystals, and the majority also had some degree of calcium oxalate present. Compared to patients with calcium oxalate stones, patients with uric acid stones showed less interstitial inflammation and less basement membrane plaque.[59]
History and Physical
History
Patients with uric acid nephrolithiasis commonly exhibit associations with obesity, diabetes, impaired glucose tolerance, or metabolic syndrome, and in some cases, underlying gastrointestinal conditions like irritable bowel syndrome or Crohn disease. The typical presentation involves severe, colicky abdominal/back/groin pain with radiation. Gross hematuria, dark or brownish urine, and dysuria are frequently observed symptoms.
Physical Examination
Physical exam findings in uric acid nephrolithiasis may include costovertebral tenderness or gout symptoms, such as tophi, podagra, or painful joint swelling with redness. Additionally, assessing for flank tenderness and evaluating for other symptoms of acute kidney injury can aid in diagnosis.
Evaluation
Laboratory
A urine dipstick usually shows acidic urine and hematuria. Urine microscopy may show uric acid crystals, which are rhomboid or rosette in shape and are generally yellow or reddish brown.
A 24-hour urine collection should be done to evaluate the uric acid level, urine pH, citrate excretion, creatinine, and volume. Urine pH below 5.5 is usually seen with uric acid nephrolithiasis. Serum uric acid and a basic metabolic panel should also be performed.[60]
Plain Abdominal X-ray
A kidney, ureter, and bladder (KUB) x-ray is readily available and is often used initially to evaluate abdominal pain to rule out peritonitis. Uric acid stones are radiolucent, while calcium-based stones are radioopaque.
Ultrasonography
Ultrasonography is readily available, free from harmful ionizing radiation, and can be performed easily at the bedside. Ultrasonography aids in the diagnosis of kidney stones when they reach a specific size (>0.4 cm) and in identifying associated findings like hydronephrosis, changes in renal echogenicity, and other abnormalities in the renal structures. However, an ultrasound cannot differentiate hydronephrosis from ureteropelvic junction obstruction or the benign extrarenal pelvis. An ultrasound also cannot identify ureteral stones or differentiate uric acid from calcium stones. Ultrasonography can be used to measure the resistive index, which is elevated in the presence of any obstructive uropathy on the affected side.[61] Ultrasonography has an overall 45% sensitivity and 88% specificity in detecting kidney stones.[62]
The combination of a KUB and a renal ultrasound can be helpful in the diagnosis of renal stone disease, especially when a CT scan is unavailable. This combination has sometimes been called a "poor man's CT scan."
Noncontrast Computed Tomography
A noncontrast-enhanced computed tomography (CT) scan of the kidney is the standard imaging modality for diagnosing nephrolithiasis. Noncontrast CT is more precise and effective than KUB or ultrasound, and it can identify the size, density, and location of any kidney or ureteral stones. Associated deformities, even in the absence of uric acid stones, can be revealed with this imaging study.[63][64]
Pure uric acid stones typically have CT measurements of about 500 Hounsfield units, while calcium stones are about 900 Hounsfield units.[65] Patients with kidney stones who have a urinary pH of 5.5 or less and whose stones are about 500 Hounsfield units or less can reliably be diagnosed as having uric acid stones.[65] Noncontrast CT scan studies are preferred because the contrast obscures the visualization of the stone.
Treatment / Management
Management of uric acid kidney stones includes lifestyle changes, medical treatment focusing on decreasing uric acid production and excretion, and urinary alkalinization.[22] Overall, urinary alkalinization is considered the single most effective therapy. The goal is to achieve a urine pH of 6 to 6.5. For uric acid kidney stones, renal ultrasonography can be used for tracking as the calculi will not be visible on a KUB.
Dietary Interventions
The most important treatment for all nephrolithiasis is drinking at least 2 liters of water daily to increase urine volume.[40] A low intake of purine-rich foods and animal proteins is also recommended to reduce uric acid production in patients with uric acid nephrolithiasis. Orange juice and lemonade are sometimes recommended, but fructose also increases uric acid stone formation, so this must be considered.[66] Recommendations to reduce obesity, appropriate management of hypertension, and high blood sugar are also helpful in reducing the burden of uric acid kidney stones.(A1)
Medical Management [14]
- Urinary alkalinization helps dissolve and prevent uric acid stones. The goal is a urinary pH that is consistently above 6.5. Ultrasound and CT scans can be used to monitor the response to treatment. Potassium citrate is usually preferred, but sodium citrate and sodium bicarbonate can also be used. However, sodium-based alkalinizing agents tend to increase urinary calcium excretion and may promote the formation of calcium-based nephrolithiasis.[67]
- Potassium citrate: 15 to 30 mEq, 2 or 3 times daily
- Sodium bicarbonate: 500 to 1000 mg 3 times a daily
- Acetazolamide: 500 mg per day increases urinary pH by inhibiting urinary bicarbonate absorption, but it also lowers citrate excretion and can cause volume depletion
(A1)
- Xanthine oxidase inhibitors are used in patients with hyperuricemia or hyperuricosuria. Adjust as needed for optimal serum uric acid levels of 6 mg/dL or less and urinary levels of 600 mg/d or less.
- Allopurinol: 100 to 300 mg daily; usual dose is 300 mg
- Febuxostat: 40 to 80 mg daily (typically administered when the patient does not tolerate allopurinol). Use was limited in 2019 per the FDA due to an increased risk of cardiovascular death compared to allopurinol.[68][69]
- See the companion StatPearls reference articles "Hyperuricemia," "Allopurinol," and "Febuxostat."[70][71][72]
(B3)
- As noted above, primates and humans are among the few mammals without endogenous uricase, which converts uric acid to the inert molecule allantoin. In cases of hyperuricemia-induced stones, recombinant uricase (current formulations include pegloticase and rasburicase) is used when urate-lowering therapy does not achieve the goal of uric acid levels less than 6mg/dL. Although very effective, they are generally used as second-line after urate-lowering therapy because of cost, need for IV infusion, concern for infusion reactions, and potential cardiovascular side effects. The 2020 American College of Rheumatology guidelines recommend against using recombinant uricase as first-line therapy.[73]
- Pegloticase is derived from porcine uricase and was FDA-approved for the treatment of refractory gout in 2010. It requires a minimum of a 2-hour infusion every 2 weeks with an average number of treatments needed of 4, and the median duration of therapy is 3 months.
- Clinical trials of pegloticase revealed that 6.7% of patients experienced infusion reactions, with 0.4% meeting the criteria for anaphylactoid reactions. Patients who do not respond to pegloticase with lower uric acid levels often have developed high titers of anti-pegloticase antibodies.
- Rasburicase is also a recombinant uricase approved to prevent hyperuricemia related to tumor lysis syndrome. It is prescribed as once daily infusions for 5 days.
- Rasburicase has an FDA warning because of its association with anaphylaxis, methemoglobinemia, and hemolysis. The risk of anaphylaxis increases significantly after that first dose.[26][74]
- Rasburicase is contraindicated in pregnancy and patients with glucose-6-phosphate dehydrogenase deficiency (G6PD). Testing for G6PD deficiency is recommended in patients at high risk for carrying the gene responsible for the deficiency.[74]
(B2)
- Medical expulsive therapy is typically used for smaller stones. Selective alpha-blockers, such as tamsulosin, have been shown to help facilitate spontaneous stone passage. This benefit is most useful for smaller stones in the distal ureter. The overall benefit appears to facilitate spontaneous stone passage by about 30%.[75][76] (A1)
- A new experimental use of theobromine, an alkaloid molecule in the xanthine family that occurs naturally in the cocoa bean and dark chocolate, has been described. Theobromine is a potent inhibitor of uric acid crystallization and has been used clinically to treat hypertension.[77][78]
Surgical Management
Medical management is preferred to surgical because of the inherent solubility of uric acid stones in alkaline environments. Surgical management is used when medical treatment fails or when associated with severe urinary tract infection.[79][80] A urinary tract infection with a blocked kidney from a stone is a surgical emergency and should be addressed urgently. It may require emergent drainage by a double J stent placed cystoscopically or a percutaneous nephrostomy. See the companion StatPearls reference article on "Complicated Urinary Tract Infections."[81]
- Extracorporeal shock wave lithotripsy: for calcific and radio-opaque kidney stones less than 2 cm. Uric acid stones can also be treated but will need contrast (IV or injected via a retrograde ureteral catheter) to make the stones visible for targeting.
- Ureteroscopic stone laser fragmentation and retrieval: for kidney and ureteral stones less than 2 cm. See our companion StatPearls reference article on "Ureteroscopy."[82]
- Percutaneous nephrolithotomy: for larger kidney stones (>2 to 2.5 cm).
Differential Diagnosis
Uric acid nephrolithiasis has a clinical presentation identical to calcium-based nephrolithiasis. Other possible differential diagnoses include acute appendicitis, acute cholecystitis, pyelonephritis, biliary colic, constipation, ectopic pregnancy, hydronephrosis, intestinal obstruction, and pelvic inflammatory disease.
Pertinent Studies and Ongoing Trials
Three ongoing interventional clinical trials on uric acid nephrolithiasis are being conducted in the United States. These trials are researching the following:
- Renal uptake of fatty acids in patients with idiopathic uric acid nephrolithiasis
- Pathophysiology of uric acid nephrolithiasis
- Pathogenesis of uric acid nephrolithiasis and its role in pioglitazone and weight loss
Toxicity and Adverse Effect Management
Treatment with alkalinizing agents like sodium bicarbonate can increase sodium levels and cause fluid overload, which can be life-threatening in patients with high blood pressure, congestive cardiac failure, or liver cirrhosis. High sodium can also increase the risk of calcium oxalate calculi by promoting calcium and sodium excretion.[83] Adverse effects from sodium bicarbonate can be controlled with the simultaneous use of acetazolamide, which also increases urinary alkalinization.[84]
Potassium citrate is the most commonly used urinary alkalinizing agent but should be used cautiously in patients prone to hyperkalemia, such as those with chronic kidney disease. Potassium citrate may also be costly for those without insurance. A possible commercial alternative is LithoLyte, a citrate supplement and urinary alkalinizer. LithoLyte is composed of potassium citrate, magnesium citrate, and sodium bicarbonate. It can be ordered online and is available without a prescription as it is not classified as a medication.
Prognosis
Medical treatment for the dissolution of existing uric acid stones is very effective. The prognosis of uric acid nephrolithiasis is usually good if proper treatment is followed consistently. Recurrent uric acid nephrolithiasis can be prevented by adopting good dietary habits, avoiding dehydration, treating elevated serum and urinary uric acid levels, and correctly using alkalinizing agents.
Complications
Uric acid stones can be associated with complications such as urinary tract obstruction, leading to renal failure and sepsis. Treatment-related complications with extracorporeal shock wave lithotripsy include the need for retreatment, urinary tract infections, hematoma, and sepsis. Complications of ureteroscopy include stent pain, ureteral injury, retreatment, urinary tract infections, urinoma formation, and sepsis. Complications of percutaneous nephrolithotomy include sepsis, hematuria, retroperitoneal hematoma formation, blood loss, and the need for arterial embolization to control excessive bleeding.[60]
Consultations
Consultation with nephrology is warranted to determine treatment and prevention. Urology consultation may also be helpful depending on the size of the uric acid stone or if hydronephrosis is present. Persistent elevation of serum uric acid may also warrant a rheumatology consult.
Deterrence and Patient Education
Patients with uric acid calculi often exhibit clinical presentations similar to those with calcium stones. Nevertheless, uric acid calculi have a distinct mechanism of stone formation. Radiological diagnosis of uric acid stones is more intricate, and their management approaches differ significantly from other stone types.[45]
Patients should receive education on preventing uric acid nephrolithiasis, emphasizing the importance of maintaining adequate fluid intake and practicing dietary control. Adherence to medication administration also plays a vital role in managing uric acid nephrolithiasis.
Enhancing Healthcare Team Outcomes
In summary, uric acid nephrolithiasis is a growing problem that includes about 10% of all urinary calculi. This nephrolithiasis is associated with metabolic syndrome, obesity, and diabetes. High-purine diets tend to promote these stones. Presentation and initial treatment are similar to other urinary calculi.[85] Diagnosis is primarily by an abdominal CT scan, preferably without contrast. One can reliably diagnose uric acid stones if the urine pH exceeds 5.5 and the Hounsfield units are 500 or less. Pure uric acid calculi typically are not visible on plain abdominal KUB x-rays.
Most uric acid stones are formed under conditions of excessive aciduria rather than hyperuricosuria. Urinary alkalinization is used as a prophylactic treatment, and potassium citrate is typically used. Sodium bicarbonate, sodium citrate, and magnesium citrate can be substituted for alkalinization if potassium citrate is not tolerated well or is otherwise unacceptable due to hyperkalemia. Sufficient alkalinization can also dissolve existing stones, but urinary pH needs to be at least 6.1 and optimally at least 6.5 or more to achieve dissolution.
If hyperuricuria or hyperuricemia is found, allopurinol can be used with a target of less than 600 mg urinary uric acid per day or serum levels of less than 6 mg/dL. Allopurinol and febuxostat are xanthine oxidase inhibitors, which decrease the conversion of xanthine to uric acid.
Diagnosing and managing uric acid nephrolithiasis requires coordination among various healthcare professionals, including nephrologists, radiologists, urologists, primary care providers, nurses, dieticians, and pharmacists. In most cases, conservative treatment with uric acid–dissolving medications helps to resolve the nephrolithiasis. However, in the case of urinary obstructions and accompanying renal failure or infection, urology surgical help is required for further management. The prognosis is good in most cases, and patient recovery is rapid.
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