Uric Acid Stones Clinical Presentation
- Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD more...
History
When obtaining the history, attempt to identify factors associated with hyperuricosuria such as the following:
- Lesch-Nyhan syndrome
- Familial gout
- Uricosuric medications
- Renal insufficiency
- Malignancy
- Hemolysis
- Lead exposure
- Purine disorders
- Sarcoidosis
- Glycogen-storage disease type I
- Laxative abuse in females with anorexia nervosa[4]
- Rotavirus-associated gastroenteritis
Infants with urate crystalluria may have pink-to-orange areas in their diapers after urination. If Serratia marcescens is also present, the diaper may appear red.
Physical
Renal stones, particularly in the upper urinary tract, cause pain, costovertebral angle tenderness, or both. The manifestations of pain are expressed differently in infants than in teenagers. Hematuria is most often present. Fever, nausea, and vomiting occur. Urinary tract infection may be present.
- No physical findings are sensitive or specific for uric acid urolithiasis.
- Children with inherited disorders such as trisomy 21, glycogen-storage disease, or Lesch-Nyhan syndrome may have physical findings consistent with their inherited disease.
- Children with malignancy may have findings such as lymphadenopathy, hepatosplenomegaly, or paleness secondary to anemia.
- Tophi (urate deposits) may be present.
Causes
Uric acid stones are produced when the urinary uric acid concentration is increased secondary to overproduction, increased renal tubular urinary uric acid secretion, decreased renal tubular urinary uric acid reabsorption, decreased urinary water content, or increased hydrogen ion concentration.
Specific causes include the following purine enzyme defects, which lead to overproduction and increased urinary uric acid concentration:
- HGPRT deficiency
- PRPP synthetase overactivity
- Glucose-6-phosphatase deficiency
Other causes include increased nucleotide turnover secondary to cell death.
- Myeloproliferative and lymphoproliferative disorders
- Hemolytic anemia
- Cytotoxic drugs
Other causes include the following:
- Excessive dietary purine intake producing increased urinary uric acid concentration
- Hyperuricemia related to rotavirus gastroenteritis likely caused by tissue breakdown in the infected GI tract and dehydration in infants.[3, 2]
- Decreased glomerular filtration, renal tubular uric acid reabsorption, or both producing increased uric acid concentration in urine (eg, renal failure, acidosis, drugs, lead nephropathy)
- Dehydration produces decreased urine water content (ie, increased urine solute concentration) and increases urinary uric acid concentration.
Baldree LA, Stapleton FB. Uric acid metabolism in children. Pediatr Clin North Am. Apr 1990;37(2):391-418. [Medline].
Fujita T, Shimooka T, Teraoka Y, Sugita Y, Kaito H, Iijima K, et al. Acute renal failure due to obstructive uric acid stones associated with acute gastroenteritis. Pediatr Nephrol. Dec 2009;24(12):2467-9. [Medline].
Kaneko K, Shimo T, Hirabayashi M, Ito T, Okazaki H, Harada Y. Cause of uric acid stones in rotavirus-associated gastroenteritis. Pediatr Nephrol. Oct 2010;25(10):2187-8. [Medline].
Kato K, Sai S, Hirata T, et al. Two cases of ammonium acid urate urinary stones related to anorexia nervosa and laxative abuse. Hinyokika Kiyo.Mar. 2004;50(3):181-5. [Medline].
Sakhaee K, Maalouf NM. Metabolic syndrome and uric acid nephrolithiasis. Semin Nephrol. Mar 2008;28(2):174-80. [Medline].
Raj GV, Auge BK, Assimos D, Preminger GM. Metabolic abnormalities associated with renal calculi in patients with horseshoe kidneys. J Endourol. Mar 2004;18(2):157-61. [Medline].
Barrat TM, PG Duffy. Nephrocalcinosis and Urolithiasis. In: Pediatric Nephrology. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999:933-46.
Camron JS, F Moro. Gout, Uric Acid, and Purine Metabolism in Pediatric Nephrology. In: Pediatric Nephrology. Vol 7. 1993:105-18.
Johnson RJ, Kivlighn SD, Kim YG, et al. Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease. Am J Kidney Dis. Feb 1999;33(2):225-34. [Medline].
| Neonates* | Children | Adults | |||||||||
| 29-33 wk | 34-37 wk | 38-40 wk | 3-4 y | 5-9 y | 10-14 y | 40-44 y | |||||
| Male | Female | Male | Female | Male | Female | Male | Female | ||||
| Serum uric acid (mg/dL) | 7.71±2.65 | 6.04±2.19 | 5.19±1.57 | 3.45±1.01 | 3.44±0.8 | 3.63±1.04 | 3.71±0.92 | 4.28±1.19 | 4.09±1.2 | 5.134±1.25 | 4.25±1.1 |
| Uric acid excretion (mg/dL GFR†) | 4.8±2.23 | 2.81±0.93 | 1.69±0.84 | 0.34±0.11 | 0.403±0.095 | ||||||
| Uric acid excretion (mg/kg/d) | N/A | N/A | 19.6 | 13.5±3.75 (3 y) | 11.5±3.75 (7 y) | 9±3.75 (12 y) | 10 | ||||
| Fractional excretion of uric acid (%) | 61.24±12.21 | 44.52±15.23 | 38.19±13.61 | 12±3.75 (3 y) | 10±3 (7 y) | 7.6±3.75 (12 y) | 7±1.6 | ||||
| *Gestational ages † Glomerular filtration rate | |||||||||||
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