Evidence suggesting hyperoxaluria as a cause of nephrocalcinosis in phosphate-treated hypophosphataemic rickets

Reusz, György; Latta, Kay; Hoyer, Peter F.; Byrd, Dennis J.; Ehrich, H.H.; Brodehl, J.

doi:10.1016/0140-6736(90)91304-s

Cited by 45 publications

(17 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Finally, we have no explanation for our conflicting re sults with those of Reusz et al [11] concerning oral phos phate treatment and the alleged oxalate-induced nephro calcinosis in patients with hereditary hypophosphatémie rickets. Further clinical and experimental studies seem necessary to clarify these conflicting issues.…”

Section: Discussioncontrasting

confidence: 46%

“…Therefore, the treatment of these patients must be accur ately monitored to avoid nephrocalcinosis and deteriora tion of renal function [6][7][8][9], However, despite careful con trol of urinary calcium excretion, the danger of nephrocalci nosis in the treatment of hypophosphatemic vitamin-D-re-sistant rickets has lately been emphasized by ultrasonic tech niques [9,10]. Therefore, in order to investigate possible causative factors of nephrocalcinosis other than calcium, Reusz et al [11] measured urinary oxalate excretion in 12 vitamin-treated phosphate-supplemented X-linked hypo phosphatemia (XLH) patients. Six of them showed evidence of nephrocalcinosis on ultrasound.…”

Section: Hyperoxaluria Is Not a Cause Of Nephrocalcinosis In Phosphatmentioning

confidence: 99%

See 1 more Smart Citation

Hyperoxaluria Is Not a Cause of Nephrocalcinosis in Phosphate-Treated Patients with Hereditary Hypophosphatemic Rickets

Tieder

Blonder²,

Strauß³

et al. 1993

Nephron

View full text Add to dashboard Cite

The treatment of X-linked hypophosphatemia (XLH) consists of phosphate and vitamin D₃ derivatives. Transient hypercalciuria and hypercalcemia are well-known signs of vitamin D intoxication. Despite urinary calcium excretion control, the danger of nephrocalcinosis in treated patients has been emphasized. It has recently been suggested that hyperoxaluria might be a causative factor of nephrocalcinosis other than calcium in phosphate-treated XLH patients. We measured urinary oxalate and phosphate excretion in 12 patients with the syndrome of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) receiving only oral phosphates and in 5 XLH patients receiving both oral phosphates and vitamin D. No correlation was found between the dosage of phosphate supplements or urinary phosphate excretion and urinary oxalate excretion, in either group of patients. Nephrocalcinosis, presenting as hyperechogenicity of the medullary pyramids, was found in 2 of the 5 XLH patients and only in 2 HHRH patients who had been treated with excessive doses of vitamin D₂ and calcium, prior to the true diagnosis being established. We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods.

show abstract

Section: Discussioncontrasting

confidence: 46%

Section: Hyperoxaluria Is Not a Cause Of Nephrocalcinosis In Phosphatmentioning

confidence: 99%

Hyperoxaluria Is Not a Cause of Nephrocalcinosis in Phosphate-Treated Patients with Hereditary Hypophosphatemic Rickets

Tieder

Blonder²,

Strauß³

et al. 1993

Nephron

View full text Add to dashboard Cite

show abstract

“…In one study magnesium oxide showed good clinical effects [53]. The positive effect of oral phosphate has to be questioned; depending on the dosage oxalate resorption seems to be increased [49]. Long-term use of calciuretic diuretics like furosemide is harmful, and therefore thiazides are the diuretics of choice [51].…”

Section: Treatmentmentioning

confidence: 97%

Primary hyperoxaluria type I

1990

Self Cite

View full text Add to dashboard Cite

Primary hyperoxaluria type I is a metabolic disorder caused by the deficiency of the peroxisomal alanine:glyoxylate aminotransferase. The disease is inherited as an autosomal recessive trait. The clinical course is outlined based on data from 330 published cases. Diagnostic cornerstones are clinical parameters, urinary excretion of oxalate and glycolate, and the determination of enzyme activity in liver tissue. Principles of conservative treatment, e.g. volume load and pyridoxine substitution, are described as well as experience with different modes of dialysis and transplantation. Kidney transplantation is associated with a high rate of recurrence of the original disease despite excellent management resulting in many instances in early graft loss. Liver transplantation offers the possibility to correct the metabolic defect and to prevent the progression of crystal deposition in the body.

show abstract

“…The vitamin D deficiency is caused by decreased 25(OH)-vitamin D-1␣-hydroxylase activity (7)(8)(9)(10). Conventional therapy consists of oral administration of pharmacologic doses of vitamin D and phosphate, though hypercalciuria and nephrocalcinosis are frequent complications of such therapy (11)(12)(13)(14)(15). Nephrocalcinosis can lead to renal insufficiency and renal tubular acidosis (15).…”

mentioning

confidence: 99%

Correction of proximal tubule phosphate transport defect inHypmicein vivoandin vitrowith indomethacin

Baum

Loleh

Saini

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

X-linked hypophosphatemia is the most prevalent inherited form of rickets. In this disorder, rickets results from hyperphosphaturia and inappropriately normal levels of 1,25(OH) 2-vitamin D. Current therapy with oral phosphate and vitamin D improves the rickets, but has significant morbidity and does not significantly affect the short stature and hypophosphatemia. In the present study, we demonstrate that Hyp mice, which have a mutation homologous to that in patients with X-linked hypophosphatemia, have a 2-fold greater urinary prostaglandin E 2 (PGE2) excretion than C57͞B6 mice. To determine whether PGs were involved in the pathogenesis of this disorder, Hyp and C57͞B6 mice received i.p. injections with vehicle or indomethacin (1 mg͞kg of body weight twice daily for 4 days) and were studied Ϸ12 h after the last dose of indomethacin. In the Hyp mice, indomethacin treatment decreased the fractional excretion of phosphate from 13.0 ؎ 3.2% to 2.2 ؎ 1.1% (P < 0.05), and increased serum phosphate from 2.9 ؎ 0.2 mg͞dl to 4.1 ؎ 0.2 mg͞dl (P < 0.05). There was no effect of indomethacin in C57͞B6 mice. Indomethacin did not affect serum creatinine or inulin clearance, demonstrating that the normalization of urinary phosphate excretion was not caused by changes in glomerular filtration rate. Indomethacin treatment increased renal brush border membrane vesicle NaPi-2 protein abundance in Hyp mice to levels comparable to that of C57͞B6 mice, but had no effect in C57͞B6 mice. In vitro isolated perfused proximal tubule studies demonstrate directly that 10 ؊6 M bath indomethacin normalized the phosphate transport defect in Hyp mice but had no effect on C57͞B6 mice. In conclusion, there is dysregulation of renal PG metabolism in Hyp mice, and indomethacin treatment normalizes the urinary excretion of phosphate by a direct tubular effect.X-linked hypophosphatemia ͉ rickets ͉ sodium͞phosphate cotransporter NaPi-2

show abstract

Evidence suggesting hyperoxaluria as a cause of nephrocalcinosis in phosphate-treated hypophosphataemic rickets

Cited by 45 publications

References 15 publications

Hyperoxaluria Is Not a Cause of Nephrocalcinosis in Phosphate-Treated Patients with Hereditary Hypophosphatemic Rickets

Hyperoxaluria Is Not a Cause of Nephrocalcinosis in Phosphate-Treated Patients with Hereditary Hypophosphatemic Rickets

Primary hyperoxaluria type I

Correction of proximal tubule phosphate transport defect inHypmicein vivoandin vitrowith indomethacin

Contact Info

Product

Resources

About