The Role of Lactic Acid in the Reduced Excretion of Uric Acid in Toxemia of Pregnancy *

Abstract

Wlhen Chesley and Williams demonstrated low uric acid excretion in toxemiiic patients,1 they noted that the reduction in renal urate clearance was relatively greater than the reduction in glomerular filtration rate (1). This relationship has been confirmed (2) and is striking when c-ompared with observations on urate excretion in normal slibjects and patients with renal disease. It is generally accepted that tunder normal circtumstances serum urate is completely filtered at the glomertulus and that 5 to 10 per cent of filtered turate appears in the urine (3) ; net tubular reabsorption accounts for the other 90 to 95 per cent. Coombs and co-workers (4), in a sttudy of subjects with various degrees of renal imiipairment, found that as glomerular filtration rate fell, a progressively larger portion of filtered urate was excreted in the urine, uric acid clearance increasing to over 20 per cent of glomerular filtration rate. In preeclamptic and eclamptic patients, althotugh glomerular filtration rate is reduced, the ratio of urate clearance to glomerular filtration rate is often lower than normal. Unless there is a redtuction in the filtrability of serum turate, explanation of the low ratio of uric acid clearance to glomiiertular filtra-*

Acid base balance in pre-eclamptic, hypertensive and diabetic pregnancies. Maternal blood and amniotic fluid studies

“…This concurs with a recent report in which it was found that the base deficit was increased in "severe" but not "moderate" PE s compared to normal pregnancy [17]. Blood lactate levels were reported to increase in PE [9]. HANDLER [9] proposed that impaired placental blood flow in severe PE causes the fetus to be more dependent on anaerobic metabolism and to produce more lactate.…”

“…Blood lactate levels were reported to increase in PE [9]. HANDLER [9] proposed that impaired placental blood flow in severe PE causes the fetus to be more dependent on anaerobic metabolism and to produce more lactate. Also, placental lactate production was reported to be augmented in severe PE [8].…”

“…9 Recourant au test des compaxaisons multiples de TUKEY, les differences statistiquement significatives entre les groupes se sont limitees ä un PO 2 du liquide amniotique plus eleve chez les parturientes avec hypertension chronique et a un pH sanguin plus bas chez les parturientes avec pre-eclampsie grave. Une anaiyse de regression multiple a ete appliquee au pH du liquide amniotique.…”

Uric Acid Production in Gout

“…The action of these drugs not only provides a model for a possible renal basis of hyperuricemia, but also suggests a new etiological classification of drug-induced secondary gout. Urate retention after muscular exercise and in toxemia of pregnancy has been attributed to the increased amounts of lactic acid produced under these circumstances (30,31). It is conceivable that other metabolites having similar urate-retaining properties could be endogenously produced and thereby induce a renal basis for hyperuricemia.…”

Organic acid excretion patterns in gout.

“…In man, it has also been found that the hyperuricaemia following physical exercise (Nichols, Miller, and Hiatt, 1951) and over-indulgence in alcohol (Lieber, Jones, Losowsky, and Davidson, 1962), and associated with glycogen storage disease (Howell, Ashton, and Wyngaarden, 1962), was related to elevated plasma levels of lactate. An inverse correlation between plasma lactate levels and urate clearance has been demonstrated (Michael, 1944;Yu and others, 1957;Handler, 1960). The administration of citrate, on the other hand, increases urate excretion, presumably by providing a source of energy for tubular transport of urate through increased delivery of substrate to the Krebs cycle (Yu and others, 1957).…”