The comparability of oxalate excretion and oxalate:creatinine ratio in the investigation of primary hyperoxaluria: review of data from a referral centre

Clifford-Mobley, Oliver; Tims, Christopher; Rumsby, Gill

doi:10.1177/0004563214529937

Cited by 23 publications

(17 citation statements)

References 29 publications

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“…Normal values considered as 100–460 μmol/day/1.73 m 2 of oxalate excretion. (Adequate collection was estimated via measuring 24 h creatinine of 0.1–0.2 mmol/kg/day) [9]. In cases of persistent hyperoxaluria, urine was also sent for glycolate: creatinine ratio as well as measurement of L-glycerate.…”

Section: Methodsmentioning

confidence: 99%

Epidemiology of paediatric renal stone disease: a 22-year single centre experience in the UK

et al. 2017

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BackgroundWhilst still rare, the incidence of paediatric stone disease is increasing in developed countries and it is important to evaluate the aetiology. We set up a dedicated renal stone service for children combining medical and surgical expertise in 1993 and now have a large case series of children to investigate the epidemiology.MethodsA retrospective hospital note review of children presenting with kidney stones during the last 22 years (1993–2015) was conducted. All patients had a comprehensive infective and metabolic screen and were classified as metabolic, infective or idiopathic stone disease.ResultsFive hundred eleven patients (322 male) were reviewed. The median age of presentation was 4.4y for males (1 m-16.6y) and 7.3y (1–18.5y) for females with a median height and weight on the 25th centile for male and on 10th and 25th for female, respectively. One hundred seventy five (34%) had an underlying metabolic abnormality, 112 (22%) had infective stones and 224 (44%) were classified as idiopathic.Of the 175 patients with a metabolic abnormality: 91 (52%) had hypercalciuria (76 persistent and 15 transient), 37 (21%) hyperoxaluria, 38 (22%) cystinuria, 3 (2%) abnormalities in the purine metabolism and the remainder other metabolic abnormalities. Bilateral stones occurred in 27% of the metabolic group compared to 16% in the non-metabolic group (OR 0.2, p < 0.05). Urinary tract infection was a common complication (27%) in the metabolic group.ConclusionsIn this paper, we present the largest cohort of paediatric stone disease reported from a developed country giving details on both, clinical and laboratory data. We show that in the majority of the patients there is an identifiable underlying metabolic and/or infective aetiology emphasizing the importance of a full work up to provide adequate treatment and prevent recurrence. Moreover, we show that stone disease in children, in contrast to the adult population, does not seem to be associated with obesity, as children have a weight below average at presentation.

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Section: Methodsmentioning

confidence: 99%

Epidemiology of paediatric renal stone disease: a 22-year single centre experience in the UK

et al. 2017

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“…This is because they are less susceptible to episodic variations in excretion related to factors such as time of day and food intake (42,50,81) that can potentially skew the interpretation of spot samples. Indeed, comparisons of these two measures have demonstrated that the oxalate-to-creatinine ratio in spot urine samples cannot directly substitute for a 24-h collection as part of a metabolic evaluation (11,43,62).…”

Section: Conflicting Phenotypical Characteristics Of the Sat-1-ko Mouse Modelmentioning

confidence: 99%

Absence of the sulfate transporter SAT-1 has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia

Whittamore

Stephens

Hatch

2019

American Journal of Physiology-Gastrointestinal and Liver Physi

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The anion exchanger SAT-1 [sulfate anion transporter 1 (Slc26a1)] is considered an important regulator of oxalate and sulfate homeostasis, but the mechanistic basis of these critical roles remain undetermined. Previously, characterization of the SAT-1-knockout (KO) mouse suggested that the loss of SAT-1-mediated oxalate secretion by the intestine was responsible for the hyperoxaluria, hyperoxalemia, and calcium oxalate urolithiasis reportedly displayed by this model. To test this hypothesis, we compared the transepithelial fluxes of 14C-oxalate, 35[Formula: see text], and 36Cl− across isolated, short-circuited segments of the distal ileum, cecum, and distal colon from wild-type (WT) and SAT-1-KO mice. The absence of SAT-1 did not impact the transport of these anions by any part of the intestine examined. Additionally, SAT-1-KO mice were neither hyperoxaluric nor hyperoxalemic. Instead, 24-h urinary oxalate excretion was almost 50% lower than in WT mice. With no contribution from the intestine, we suggest that this may reflect the loss of SAT-1-mediated oxalate efflux from the liver. SAT-1-KO mice were, however, profoundly hyposulfatemic, even though there were no changes to intestinal sulfate handling, and the renal clearances of sulfate and creatinine indicated diminished rates of sulfate reabsorption by the proximal tubule. Aside from this distinct sulfate phenotype, we were unable to reproduce the hyperoxaluria, hyperoxalemia, and urolithiasis of the original SAT-1-KO model. In conclusion, oxalate and sulfate transport by the intestine were not dependent on SAT-1, and we found no evidence supporting the long-standing hypothesis that intestinal SAT-1 contributes to oxalate and sulfate homeostasis. NEW & NOTEWORTHY SAT-1 is a membrane-bound transport protein expressed in the intestine, liver, and kidney, where it is widely considered essential for the excretion of oxalate, a potentially toxic waste metabolite. Previously, calcium oxalate kidney stone formation by the SAT-1-knockout mouse generated the hypothesis that SAT-1 has a major role in oxalate excretion via the intestine. We definitively tested this proposal and found no evidence for SAT-1 as an intestinal anion transporter contributing to oxalate homeostasis.

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“…16 Outcomes in PH3 are thought to be more favourable, 17 and only one case of PH3 has been reported to have ESRF. 18 However, the level of hyperoxaluria in PH3 overlaps with PH1 and PH2, 19 so the natural history may not yet be clearly defined for this relatively newly described disease. Prevalence estimates from public whole exome sequencing in the USA give a figure of $7 per million for PH3, 18 which is much higher than the reported prevalence of PH1 ($1 per million in Europe 20 ) or PH2.…”

Section: Introductionmentioning

confidence: 99%

Simultaneous analysis of urinary metabolites for preliminary identification of primary hyperoxaluria

2015

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The comparability of oxalate excretion and oxalate:creatinine ratio in the investigation of primary hyperoxaluria: review of data from a referral centre

Cited by 23 publications

References 29 publications

Epidemiology of paediatric renal stone disease: a 22-year single centre experience in the UK

Epidemiology of paediatric renal stone disease: a 22-year single centre experience in the UK

Absence of the sulfate transporter SAT-1 has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia

Simultaneous analysis of urinary metabolites for preliminary identification of primary hyperoxaluria

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