Effect of Fetal Number on Maternal Serum Uric Acid Concentration

Cohen, Shlomo B.; Kreiser, Doron; Erez, Izhar; Kogan, I. J.; Seidman, Daniel S.; Schiff, Eyal

doi:10.1055/s-2002-34470

Cited by 10 publications

(5 citation statements)

References 16 publications

(20 reference statements)

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“…A study found significantly higher mean uric acid concentrations at term in twin and triplet pregnancies compared with singletons (0.27, 0.30 and 0.22 mmol/L respectively). 12 The authors suggested that for clinical purposes, the upper limit of the uric acid cut-off concentrations at term should be adjusted using mean + 2 standard deviations as follows: 0.309, 0.428 and 0.452 mmol/L for singleton, twin and triplets, respectively. The changes in renal circulation and increased cell turnover have been suggested as the possible mechanisms leading to hyperuricaemia in these women; 13 Diurnal variation – a study reported that the mean serum uric acid value between 08:00 and 09:00 hours was higher than that observed between 17:00 and 18:00 hours.…”

Section: Factors Affecting Serum Uric Acid Levels In Pregnancymentioning

confidence: 99%

Uric acid: is it time to give up routine testing in management of pre-eclampsia?

Talaulikar

Shehata

2012

Obstet Med

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Ever since it was first linked with the pathophysiology of pre-eclampsia, uric acid has been a routine test requested by many care-givers managing pregnant women with hypertensive disease of pregnancy for almost 100 years. Existing evidence however suggests that it has no definitive role in prediction, diagnosis or management of pre-eclampsia. We argue against routine uric acid testing in pregnancies complicated by hypertension not only because it has become a fruitless academic exercise but also because ceasing its routine use will ensure cost-savings for the health services.

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Section: Factors Affecting Serum Uric Acid Levels In Pregnancymentioning

confidence: 99%

Uric acid: is it time to give up routine testing in management of pre-eclampsia?

Talaulikar

Shehata

2012

Obstet Med

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“…Adding to the controversy was the now outdated and disproven belief that the placenta did not contain xanthine dehydrogenase/oxidase activity (70). A recent review (66) has suggested that increased fetal and/or placental production may contribute to circulating uric acid based on the finding of elevated uric acid in multifetal gestations (71) and that purine metabolites are elevated in the umbilical cord blood specimens from newborns with clinical signs of intrauterine hypoxia during labor (72). Trophoblast shedding into the maternal circulation has also been proposed as a source of purine availability for breakdown (66).…”

Section: Renal Handling Of Uric Acid In Preeclampsiamentioning

confidence: 99%

Renal function during normal pregnancy and preeclampsia

Jeyabalan

Conrad²

2007

Front Biosci

124

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Glomerular filtration rate and renal plasma flow increase by 40 to 65 and 50 to 85%, respectively, during normal pregnancy in women. Studies using the gravid rat as a model have greatly enhanced our understanding of mechanisms underlying these remarkable changes in the renal circulation during gestation. Hyperfiltration is largely due to increased renal plasma flow, the latter attributable to profound reductions in both the renal afferent and efferent arteriolar resistances. The ovarian hormone, relaxin, mediates renal vasodilation during pregnancy. Relaxin increases vascular gelatinase activity, thereby converting big ET to ET(1-32), which leads to renal vasodilation, hyperfiltration and reduced myogenic reactivity of small renal arteries via the endothelial ET(B) receptor and nitric oxide. Serum concentration of uric acid falls during normal pregnancy as a consequence of increased GFR and/or reduced proximal tubular reabsorption. The elevated urinary excretion of protein during pregnancy is secondary to increased GFR, reduced proximal tubular reabsorption, and perhaps alteration in the electrostatic charge of the glomerular filter. Whether the tubular secretion of Tamm-Horsfall protein increases during normal pregnancy is uncertain. In most women with preeclampsia, renal plasma flow and glomerular filtration rate are at most only modestly decreased as a consequence of increased afferent arteriolar resistance and/or reduced ultrafiltration coefficient. Serum uric acid concentrations are increased mainly as a consequence of reduced renal clearance. Reduced GFR leads to decreased filtered load of uric acid, and plasma volume contraction contributes to increased proximal tubular reabsorption coupled to sodium. The increase in urinary protein excretion in preeclampsia occurs secondary to alterations in the size and/or charge selectivity of the glomerular filter, possible increases in glomerular capillary pressure, and compromise of proximal tubular reabsorption. The renal histologic lesion characteristic of preeclampsia is termed "glomerular endotheliosis". Recent evidence suggests that anti-angiogenic factors emanating from the placenta in preeclampsia contribute to glomerular endotheliosis, proteinuria, and hypertension during disease.

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“…In pregnancy, serum uric acid concentrations decrease during the first trimester by at least 25%, and return to normal levels between the second and third trimester of pregnancy [17]. It has been shown that maternal serum uric acid concentrations rise in multiple pregnancies [18][19][20][21], suggesting that the presence of fetus and/or placenta contributes to the increased production of uric acid. Preeclampsia is a pregnancy-specific disease, characterized by hypertension and proteinuria, which contributes substantially to the incidence of iatrogenic preterm deliveries with its sequelae.…”

Section: Introductionmentioning

confidence: 99%