Primary hyperoxaluria: A case report

Ankita Deshmukh, S. Nemade, Ramesh Kalshetty, A. Padmanabhan, N. Gadgil
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Abstract

Renal failure can occasionally be caused by oxalate nephropathy. Glyoxylate metabolism abnormalities and particular hepatic enzyme deficits are the causes of primary hyperoxaluria (PH). Increased intestinal absorption, an excessive diet or an increased intake of oxalate precursors can all result in secondary hyperoxaluria. A 13-month old male child with high blood creatinine, low sodium, low calcium levels, high uric acid and low urine specific gravity is the subject of this research. Medullary papillary calcification was detected using sonography (nephrocalcinosis). Calcium oxalate crystals, sparse lymphocytic infiltration and interstitial fibrosis were seen on a renal biopsy. The patient was put on peritoneal dialysis, progresses to anuria and expired due to renal failure.
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原发性高血氧症1例报告
草酸肾病有时可引起肾功能衰竭。乙醛酸代谢异常和特殊的肝酶缺陷是原发性高草酸尿(PH)的原因。肠道吸收增加,饮食过量或草酸前体摄入增加都可导致继发性高草酸尿。本研究的对象是一名13个月大、血肌酐高、钠、钙含量低、尿酸高、尿比重低的男婴。超声检查髓状乳头状钙化(肾钙化症)。肾活检可见草酸钙结晶、稀疏淋巴细胞浸润及间质纤维化。患者经腹膜透析,进展为无尿,因肾功能衰竭而死亡。
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