Acidosis increases magnesiuria in children with distal renal tubular acidosis

Ariceta, Gema; Vallo, Alfredo; Rodríguez‐Soriano, Juan

doi:10.1007/s00467-004-1609-7

Cited by 13 publications

(4 citation statements)

References 31 publications

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“…In our cohort of 24 patients, only 3 children developed small calculi and none of them needed an intervention. Moreover, urinary calcium excretion is increased in acidosis and decreases after the administration of alkali [7,8]. This makes it a good marker for adherence to and/or adequacy of treatment, but is no longer reliable after the administration of thiazide diuretics.…”

Section: Treatmentmentioning

confidence: 99%

Clinical and molecular aspects of distal renal tubular acidosis in children

et al. 2017

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Section: Treatmentmentioning

confidence: 99%

Clinical and molecular aspects of distal renal tubular acidosis in children

et al. 2017

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“…3, 6,13 In the presence of acidosis, there is increased in urinary calcium excretion which can lead to increased risk of nephrolithiasis/nephrocalcinosis, which usually decreases with the administration of alkali therapy. 14,15 In our cohort, hypercalciuria was seen in the majority of the cases (82.1%) with nephrocalcinosis in 78.6% of the cases. In children with long-standing metabolic acidosis, failure to thrive with features of rickets is a common clinical presentation secondary to bone mineralization.…”

Section: Discussionmentioning

confidence: 61%

Phenotype and Genotype Profile of Children with Primary Distal Renal Tubular Acidosis: A 10-Year Experience from a North Indian Teaching Institute

et al. 2021

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Primary distal renal tubular acidosis (dRTA) or Type 1 RTA in children is caused by a genetic defect (involved genes ATP6V0A4, ATP6V1B1, SLC4A1, FOXI1, or WDR72), which causes tubular transport defects characterized by an inability to appropriately acidify urine with resultant persistent hyperchloremic metabolic acidosis. Retrospective analysis of 28 children (14 males) under the age of 14 years with dRTA seen from 2010 to 2019 was reviewed, and detailed clinic records were analyzed. The clinical features, investigations, and response to treatment were recorded. The median age of the children at presentation was 30 months (range: 9.25–72 months), and the median age at onset of symptoms was 2 months. All the children had growth failure, polyuria, and polydipsia at presentation. Mean serum potassium, pH, bicarbonate, and anion gap at presentation was 2.3 ± 0.5 mmol/L, 7.22 ± 0.09, 13.28 ± 4.37 mmol/L, and 9.3 ± 2.18, respectively. Mean serum potassium, pH, bicarbonate at follow-up was 3.88 ± 0.6 mmol/L, 7.35 ± 0.06, and 20.13 ± 4.17 mmol/L, respectively. The median z-score for the weight for age and height for age at initial presentation was −4.77 (–7.68 to –3.74) and –4.21 (–5.42 to –2.37) and at follow-up was –3.35 (–5.29 to –1.55) and –3.84 (–5.36 to –1.63), respectively. Twenty-two (78.6%) children had medullary nephrocalcinosis. Four children had sensorineural hearing loss. Seven children had genetic testing done, and six had pathogenic or likely pathogenic variants in ATP6V1B1 and ATP6V0A4 gene. Children with dRTA have a guarded prognosis and ATP6V1B1 and ATP6V0A4 mutations are the most common implicated genetic defect in Indian children with distal RTA.

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“…Perbedaan ini dipengaruhi oleh kadar albumin, kompartemen cairan tubuh, dan pH tubuh bukan dari faktor usia. 25,26 Skor PRISM III rata-rata lebih rendah pada subyek dengan hipomagnesemia dibandingkan dengan normomagnesemia, serupa dengan penelitian Limaye dkk 4 tetapi berbeda dengan Kumar dkk 27 dan Munoz dkk. 24 Secara teori, mortalitas dan PRISM III pasien dengan hipomagnesemia lebih tinggi dibandingkan dengan normomagnesemia karena skor PRISM III yang tinggi menggambarkan mortalitas yang tinggi juga.…”

Section: Hasilunclassified

Pengaruh Hipomagnesemia Terhadap Mortalitas Pasien Anak di Ruang Rawat Intensif

Gratya¹,

Martuti²,

Salimo³

2017

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Latar belakang. Magnesium merupakan kation intraselular kedua terbanyak setelah kalium. Pasien dengan penyakit kritis yang dirawat di ruang rawat intensif memiliki risiko tinggi terjadinya hipomagnesemia. Pasien dengan hipomagnesemia memiliki mortalitas yang tinggi. Tujuan. Melakukan analisis pengaruh hipomagnesemia terhadap mortalitas pada pasien anak di ruang rawat intensif. Metode.Penelitian bersifat kohort prospektif dilakukan pada bulan Mei hingga Juli 2016 di PICU dan HCU RS Dr. Moewardi Surakarta. Subjek berjumlah 40 anak diambil secara konsekutif. Analisis statistik dilakukan dengan program SPSS 22.0 menggunakan uji chi square atau Fisher bila syarat uji chi square tidak terpenuhi, uji t independen bila sebaran data normal, atau uji Mann Whitney bila sebaran data tidak normal. Pengaruh faktor risiko dan mortalitas dianalisis dengan logistik regresi. Hasil. Di antara 40 anak terdapat 21 orang laki-laki, 26 dengan penyakit non bedah dan 18 anak gizi baik. Kejadian hipomagnesemia terdapat pada 5 dan 1 anak di antaranya meninggal. Hipomagnesemia tidak berhubungan dengan mortalitas (p=1,000; OR 1,00; IK95% 0,096-10.408). Faktor risiko yang berhubungan dengan mortalitas adalah jenis penyakit non bedah. Jenis kelamin, usia, status nutrisi dan jenis penyakit tidak berhubungan dengan mortalitas. Kesimpulan. Tidak terdapat pengaruh hipomagnesemia terhadap mortalitas. Faktor risiko yang berhubungan dengan mortalitas adalah jenis penyakit non bedah. Sari Pediatri 2016;18(4):308-13 Kata kunci: hipomagnesemia,mortalitas, PRISM III The Effect of Hypomagnesemia to Mortality of Children in Intensive Care UnitResa Gratya, Sri Martuti, Harsono Salimo Background. Magnesium is the second largest intracellular cation after potassium. Patients with critical illness in intensive care unit have a high risk of hypomagnesemia. Patient with hypomagnesemia has high incidence in mortality. Objective. To analyze the effects between hypomagnesemia and mortality as well as the mortality risk factors in critically ill children. Methods. Prospective cohort study was conducted between May and July 2016 at PICU and HCU Moewardi Hospital. Fourty children were enrolled consecutively. Data were analyzed with SPSS 22.0 statistical analizes chi square, logistic regression. Results. Of the 40 children, 21 were girls, 26 children with non-surgical type of disease and 18 chilren were malnourished. Hypomagnesemia presented in 5 children and 1 of them passed away. The risk factors associated with mortality were: PRISM III score ≥8, non surgical cases. Hypomagnesemia was not associated with mortality(p = 1.000; OR 1.00; 95% CI 0.096 to 10.408). Gender, age, nutritional status and type of disease were not associated with mortality. Conclusion. Hypomagnesemia were not associated with mortality in critically ill children. Hypomagnesemia occurred in 12.5% of children and PRISM III scores ≥8 was a risk factor for mortality. Sari Pediatri 2016;18(4):308-13

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Acidosis increases magnesiuria in children with distal renal tubular acidosis

Cited by 13 publications

References 31 publications

Clinical and molecular aspects of distal renal tubular acidosis in children

Clinical and molecular aspects of distal renal tubular acidosis in children

Phenotype and Genotype Profile of Children with Primary Distal Renal Tubular Acidosis: A 10-Year Experience from a North Indian Teaching Institute

Pengaruh Hipomagnesemia Terhadap Mortalitas Pasien Anak di Ruang Rawat Intensif

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