Influence of nutrition on urinary oxalate and calcium in preterm and term infants

Höppe, Bernd; Hesse, Albrecht; Neuhaus, Thomas J.; Fanconi, Sergio; Blau, Nenad; Roth, B.; Leumann, Ernst

doi:10.1007/s004670050366

Cited by 26 publications

(31 citation statements)

References 29 publications

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“…Renal calcium excretion was elevated initially (10 mol/mol creatinine) but decreased to 0.77 mol/mol creatinine at 3 months of age (normal values for preterm infants: 0.57ϩ0.41 mol/mol creatinine 27 ). The decline of urinary calcium excretion was independent from indomethacin treatment.…”

Section: Figmentioning

confidence: 98%

Hypokalemic Salt-Losing Tubulopathy With Chronic Renal Failure and Sensorineural Deafness

Jeck

Reinalter

Henne³

et al. 2001

Pediatrics

107

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ABSTRACT.Objective. To characterize a rare inherited hypokalemic salt-losing tubulopathy with linkage to chromosome 1p31.Methods. We conducted a retrospective analysis of the clinical data for 7 patients in whom cosegregation of the disease with chromosome 1p31 had been demonstrated. In addition, in 1 kindred, prenatal diagnosis in the second child was established, allowing a prospective clinical evaluation.Results. Clinical presentation of the patients was homogeneous and included premature birth attributable to polyhydramnios, severe renal salt loss, normotensive hyperreninemia, hypokalemic alkalosis, and excessive hyperprostaglandin E-uria, which suggested the diagnosis of hyperprostaglandin E syndrome/antenatal Bartter syndrome. However, the response to indomethacin was only poor, accounting for a more severe variant of the disease. The patients invariably developed chronic renal failure. The majority had extreme growth retardation, and motor development was markedly delayed. In addition, all patients turned out to be deaf.Conclusion. The hypokalemic salt-losing tubulopathy with chronic renal failure and sensorineural deafness represents not only genetically but also clinically a disease entity distinct from hyperprostaglandin E syndrome/antenatal Bartter syndrome. A pleiotropic effect of a single gene defect is most likely causative for syndromic hearing loss. Pediatrics 2001;108(1). URL: http:// www.pediatrics.org/cgi/content/full/108/1/e5; tubulopathy, Bartter syndrome, polyhydramnios, renal failure, syndromic deafness, pleiotropic gene.ABBREVIATIONS. HPS/aBS, hyperprostaglandin E syndrome/ antenatal Bartter syndrome; TAL, thick ascending limb of Henle's loop; PGE 2 , prostaglandin E 2 ; NKCC2, furosemide-sensitive Na-K-2Cl cotransporter; ROMK, renal outer-medullary potassium channel; SND, sensorineural deafness; GFR, glomerular filtration rate; BERA, brainstem-evoked response audiometry; PPN, partial parenteral nutrition. I nherited salt-losing tubulopathies with hypokalemic alkalosis involve an overlapping set of renal tubular disorders that can be subdivided into at least 3 phenotypes: 1) classic Bartter syndrome, 2) Gitelman syndrome, and 3) hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS). 1,2 Whereas patients with classic Bartter syndrome and Gitelman syndrome typically present in early infancy and childhood or adolescence, manifestation of HPS/aBS occurs in utero and the neonatal course is severe. 3 The first clinical sign is maternal polyhydramnios caused by fetal polyuria, which regularly results in premature birth between 28 and 34 weeks of gestation. 4,5 Postnatally, affected infants present with the typical pattern of impaired tubular reabsorption in the thick ascending limb of Henle's loop (TAL), including salt wasting, isosthenuric or hyposthenuric polyuria, and hypercalciuria with subsequent medullary nephrocalcinosis. 6 -8 Characteristically, endogenous formation of prostaglandin E 2 (PGE 2 ) is stimulated markedly, resulting in additional aggravation of saluretic polyuri...

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Section: Figmentioning

confidence: 98%

Hypokalemic Salt-Losing Tubulopathy With Chronic Renal Failure and Sensorineural Deafness

Jeck

Reinalter

Henne³

et al. 2001

Pediatrics

107

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“…oxalate). Babies receiving parenteral nutrition have a higher oxalate and calcium but lower citrate excretion, contributing to higher calcium oxalate saturation [4]. Urine from premature babies inhibits calcium oxalate crystal agglomeration less well than that from babies born at term, increasing the risk of nephrocalcinosis and stone formation [3].…”

Section: Nephrolithiasis In Ex-premature Childrenmentioning

confidence: 99%

Aetiological Factors in Paediatric Urolithiasis

Hoff

2004

Nephron Clin Pract

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The aetiology of stones in children differs from that in adults. Young children, especially boys, are prone to infective stones, although this type of calculi is decreasing in frequency over time in prosperous countries. Two monogenic causes, cystinuria and hyperoxaluria, each account for 5–15% of paediatric stones. Increased factors for stone formation in children include prematurity, neurological problems, ketogenic diet and reconstructed or augmented bladders. Hypercalciuria is commonly found in paediatric stone formers, is usually idiopathic and is only rarely associated with hypercalcaemia. All children with stones should undergo a metabolic evaluation.

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“…Indeed, two recent studies have shown that oxalate excretion in premature neonates depends on the GA as well as the day of life [15,32]. This study is the first to our knowledge that examined urinary oxalate in two groups of preterm infants with different type of feeding for a longer duration than the 1st week of life.…”

Section: Discussionmentioning

confidence: 96%

“…Other risk factors are furosemide treatment [18], steroid treatment, very low BW and gestational age (GA) and complicated perinatal course [19,29,31]. Recent studies have shown that disturbances in the renal excretion of certain factors, which promote or inhibit stone formation, may lead to nephrocalcinosis [15,30]. Such factors are calcium, oxalate (lithogenics), citrate and magnesium (inhibitors) [14,30,32].…”

Section: Introductionmentioning

confidence: 97%

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Urinary lithogenic and inhibitory factors in preterm neonates receiving either total parenteral nutrition or milk formula

et al. 2003

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In preterm neonates on total parenteral nutrition, urinary oxalate -to-creatinine ratio (a potent lithogenic factor) was lower and urinary citrate -to-creatinine ratio (a lithoprotective factor) also lower than in formula fed neonates. The type of feeding (total parenteral nutrition or special preterm milk formula) seems to affect urinary oxalate and citrate but not calcium and magnesium in non-furosemide treated preterm infants during the first 3 weeks of life.

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Influence of nutrition on urinary oxalate and calcium in preterm and term infants

Cited by 26 publications

References 29 publications

Hypokalemic Salt-Losing Tubulopathy With Chronic Renal Failure and Sensorineural Deafness

Hypokalemic Salt-Losing Tubulopathy With Chronic Renal Failure and Sensorineural Deafness

Aetiological Factors in Paediatric Urolithiasis

Urinary lithogenic and inhibitory factors in preterm neonates receiving either total parenteral nutrition or milk formula

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