Erythropoietin Resistant Anemia in An Infant with End Stage Renal Disease.

Only a few disorder cause severe nephrocalcinosis with end stage renal disease (ESRD) in infancy. Bartter syndrome and the primary hyperoxalurias (PH) are the main causes of severe nephrocalcinosis with ESRD in infancy period. Bartter syndrome was ruled out because of the absence of hyponatremic hyp...

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Publicado en:Turkiye Klinikleri Journal of Medical Sciences Vol. 31; no. 6; pp. 1607 - 1609
Autores principales: Yavascan, Önder, Alparslan, Caner, Anil, Murat, Bal, Alkan, Anil, Ayse Berna, Aksu, Nejat
Formato: case study Journal Article
Publicado: Turkiye Klinikleri Nov/Dec2011
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Nov/Dec2011
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        2011440578
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        atl: Erythropoietin Resistant Anemia in An Infant with End Stage Renal Disease.
      aug:
        au:
          Yavascan, Önder
          Alparslan, Caner
          Anil, Murat
          Bal, Alkan
          Anil, Ayse Berna
          Aksu, Nejat
      sug:
        subj:
          Anemia Complications
          Drug Resistance
          Erythropoietin Adverse Effects
          Renal Insufficiency Complications
          Infant
          Infant: 1-23 months
      ab: Only a few disorder cause severe nephrocalcinosis with end stage renal disease (ESRD) in infancy. Bartter syndrome and the primary hyperoxalurias (PH) are the main causes of severe nephrocalcinosis with ESRD in infancy period. Bartter syndrome was ruled out because of the absence of hyponatremic hypokalemic metabolic alkalosis and recurrent dehydration attacks in our patient. Urinary chloride level was normal. Furthermore, SLC12A1 and CLCNKB gene analyses showed no mutation. Therefore, the most likely etiology in this infant with ESRD was the primary hyperoxalurias. The primary hyperoxalurias are autosomal recessive and rare metabolic disorders resulting from deficiencies of the hepatic peroxisomal enzyme alanine-glyoxlate aminotransferase (PH-1) and the enzyme glyoxylate reductase/hydroxypyruvate reductase (PH-2) which cause excessive oxalate formation and calcium oxalate deposition in various organs.1,2 The most common type of primary hyperoxaluria is type 1. Diagnosis relies on detection of increased levels of oxalate in urine (N: < 0.5 mmol/l/1.73m2 per day) and either assay enzyme activity from liver biopsy or molecular genetic testing of associated gene. Liver biopsy is still considered as the gold standard, but it is an invasive process and bears some risks. Genetic analysis provides some additional non-diagnostic information.1,2 However, the diagnosis of PH-1 was mainly established on the basis of clinical and radiologic findings in our case. Urine oxalate level could not be measured on admission due to financial problems of the family, and then urine output abruptly decreased.
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      doctype:
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        Journal Article
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    language: Turkish
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