PDF(Pubmed)
Abstract：
The kidney is particularly vulnerable to toxins due to its abundant blood supply, active tubular reabsorption, and medullary interstitial concentration. Currently, calcium phosphate-induced and calcium oxalate-induced nephropathies are the most common crystalline nephropathies. Hyperoxaluria may lead to kidney stones and progressive kidney disease due to calcium oxalate deposition leading to oxalate nephropathy. Hyperoxaluria can be primary or secondary. Primary hyperoxaluria is an autosomal recessive disease that usually develops in childhood, whereas secondary hyperoxaluria is observed following excessive oxalate intake or reduced excretion, with no difference in age of onset. Oxalate nephropathy may be overlooked, and the diagnosis is often delayed or missed owning to the physician\'s inadequate awareness of its etiology and pathogenesis. Herein, we discuss the pathogenesis of hyperoxaluria with two case reports, and our report may be helpful to make appropriate treatment plans in clinical settings in the future.
We report two cases of acute kidney injury, which were considered to be due to oxalate nephropathy in the setting of purslane (portulaca oleracea) ingestion. The two patients were elderly and presented with oliguria, nausea, vomiting, and clinical manifestations of acute kidney injury requiring renal replacement therapy. One patient underwent an ultrasound-guided renal biopsy, which showed acute tubulointerstitial injury and partial tubular oxalate deposition. Both patients underwent hemodialysis and were discharged following improvement in creatinine levels.
Our report illustrates two cases of acute oxalate nephropathy in the setting of high dietary consumption of purslane. If a renal biopsy shows calcium oxalate crystals and acute tubular injury, oxalate nephropathy should be considered and the secondary causes of hyperoxaluria should be eliminated.
We report two cases of acute kidney injury, which were considered to be due to oxalate nephropathy in the setting of purslane (portulaca oleracea) ingestion. The two patients were elderly and presented with oliguria, nausea, vomiting, and clinical manifestations of acute kidney injury requiring renal replacement therapy. One patient underwent an ultrasound-guided renal biopsy, which showed acute tubulointerstitial injury and partial tubular oxalate deposition. Both patients underwent hemodialysis and were discharged following improvement in creatinine levels.
Our report illustrates two cases of acute oxalate nephropathy in the setting of high dietary consumption of purslane. If a renal biopsy shows calcium oxalate crystals and acute tubular injury, oxalate nephropathy should be considered and the secondary causes of hyperoxaluria should be eliminated.
摘要：
背景：由于血液供应丰富，肾脏特别容易受到毒素的影响，主动肾小管重吸收，和髓质间质浓度。目前,磷酸钙诱导和草酸钙诱导的肾病是最常见的结晶肾病。由于草酸钙沉积导致草酸盐肾病，高草酸血症可能导致肾结石和进行性肾脏疾病。高草酸尿可以是原发性或继发性的。原发性高草酸尿症是一种常染色体隐性疾病，通常在儿童时期发展，而继发性高草酸尿是在草酸盐摄入过多或排泄减少后观察到的，发病年龄没有差异。草酸盐肾病可能被忽视，由于医生对其病因和发病机制认识不足，诊断往往会延迟或错过。在这里，我们用两例病例报告讨论高草酸尿症的发病机制，我们的报告可能有助于将来在临床环境中制定适当的治疗计划.
方法：我们报告2例急性肾损伤，这被认为是由于马齿轮轴（马齿轮轴）摄入的草酸盐肾病。两名患者均为高龄,出现少尿,恶心,呕吐,需要肾脏替代治疗的急性肾损伤的临床表现。一名患者接受了超声引导下的肾活检,表现为急性肾小管间质损伤和部分肾小管草酸盐沉积。两名患者均接受了血液透析，并在肌酐水平改善后出院。
结论：我们的报告说明了2例急性草酸盐肾病在高饮食消耗的情况下。如果肾活检显示草酸钙晶体和急性肾小管损伤，应考虑草酸肾病，并应消除高草酸尿的继发原因。
方法：我们报告2例急性肾损伤，这被认为是由于马齿轮轴（马齿轮轴）摄入的草酸盐肾病。两名患者均为高龄,出现少尿,恶心,呕吐,需要肾脏替代治疗的急性肾损伤的临床表现。一名患者接受了超声引导下的肾活检,表现为急性肾小管间质损伤和部分肾小管草酸盐沉积。两名患者均接受了血液透析，并在肌酐水平改善后出院。
结论：我们的报告说明了2例急性草酸盐肾病在高饮食消耗的情况下。如果肾活检显示草酸钙晶体和急性肾小管损伤，应考虑草酸肾病，并应消除高草酸尿的继发原因。
