Hypouricemia or hypouricaemia is a level of
uric acid in
blood serum that is below normal. In humans, the normal range of this blood component has a lower threshold set variously in the range of 2 mg/dL to 4 mg/dL, while the upper threshold is 530 μmol/L (6 mg/dL) for women and 619 μmol/L (7 mg/dL) for men.[1] Hypouricemia usually is benign and sometimes is a
sign of a medical condition.
Hypouricemia is often
benign and not a medical condition, but it is a useful medical sign. It is known occasionally to result in a decreased ability to concentrate urine due to decreased hypertonicity of the
renal medulla, and may contribute to
hypotension when other risk factors are present. Hypotonicity of the
renal medulla is considered normal in the fetus and in infants due to hypouricemia caused by low protein intake. [6] Hypouricemia is usually due to drugs and toxic agents, sometimes to diet or genetics, and, rarely, suggests an underlying medical condition.[citation needed]
Hypouricemia is common in
vegetarians and
vegans due to the low
purine content of most vegetarian diets.[9] Vegetarian diet has been found to result in mean serum uric acid values as low as 239
μmol/
L (2.7 mg/dL).[10] While a vegetarian diet is typically seen as beneficial with respect to conditions such as
gout,[10] it may be associated with some other health conditions.[citation needed]
Transient hypouricemia sometimes is produced by
total parenteral nutrition.[11] Paradoxically, total parenteral nutrition may produce hypouricemia followed shortly by acute gout, a condition normally associated with hyperuricemia.[12][13] The reasons for this are unclear.
Genetics
Two kinds of
genetic mutations are known to cause hypouricemia: mutations causing
xanthine oxidase deficiency, which reduces the production of uric acid; and mutations causing abnormal kidney function that increases the excretion of uric acid. Collectively known as familial renal hypouricemia, the latter mutations are of two types, involving defects of presecretory and postsecretory reabsorption.[citation needed]
A genetic mutation in
Dalmatian dogs causes hypouricemia due to a kidney defect that interferes with reabsorption of uric acid. A similar mutation has been reported in a human brother and sister.[14]
In humans, loss-of-function mutations in the gene
URAT1 are associated with presecretory reabsorption defects.[15][16][17]
Medical conditions
Medical conditions that can cause hypouricemia include:
Uric acid clearance should also be performed, increase in clearance points to proximal tubular defects in the kidney, normal or reduced clearance points to a defect in xanthine oxidase.[citation needed]
Treatment
Idiopathic hypouricemia usually requires no treatment. In some cases, hypouricemia is a
medical sign of an underlying condition that does require treatment. For example, if hypouricemia reflects high excretion of uric acid into the urine (
hyperuricosuria) with its risk of uric acid
nephrolithiasis, the hyperuricosuria may require treatment.[20]
In one study, hypouricemia was found in 4.8% of hospitalized women and 6.5% of hospitalized men. (The definition was less than 0.14 mmol/L for women and less than 0.20 mmol/L in men.) [21]
^Mima A, Ichida K, Matsubara T, Kanamori H, Inui E, Tanaka M, Manabe Y, Iehara N, Tanaka Y, Yanagita M, Yoshioka A, Arai H, Kawamura M, Usami K, Hosoya T, Kita T, Fukatsu A (December 2008). "Acute Renal Failure After Exercise in a Japanese Sumo Wrestler With Renal Hypouricemia". Am. J. Med. Sci. 336 (6): 512–514.
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^Siener R, Hesse A (2003). "The effect of a vegetarian and different omnivorous diets on urinary risk factors for uric acid stone formation". Eur J Nutr. 42 (6): 332–7.
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^
abSzeto YT, Kwok TC, Benzie IF (October 2004). "Effects of a long-term vegetarian diet on biomarkers of antioxidant status and cardiovascular disease risk". Nutrition. 20 (10): 863–6.
doi:
10.1016/j.nut.2004.06.006.
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^Moyer RA, John DS (April 2003). "Acute gout precipitated by total parenteral nutrition". J. Rheumatol. 30 (4): 849–50.
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^Derus CL, Levinson DJ, Bowman B, Bengoa JM, Sitrin MD (October 1987). "Altered fractional excretion of uric acid during total parenteral nutrition". J. Rheumatol. 14 (5): 978–81.
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^Greene ML, Marcus R, Aurbach GD, Kazam ES, Seegmiller JE (September 1972). "Hypouricemia due to isolated renal tubular defect. Dalmatian dog mutation in man". Am. J. Med. 53 (3): 361–7.
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^Ichida K, Hosoyamada M, Kamatani N, Kamitsuji S, Hisatome I, Shibasaki T, Hosoya T (September 2008). "Age and origin of the G774A mutation in SLC22A12 causing renal hypouricemia in Japanese". Clin. Genet. 74 (3): 243–51.
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^Takahashi T, Tsuchida S, Oyamada T, Ohno T, Miyashita M, Saito S, Komatsu K, Takashina K, Takada G (May 2005). "Recurrent URAT1 gene mutations and prevalence of renal hypouricemia in Japanese". Pediatr. Nephrol. 20 (5): 576–8.
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