Khneizer Gebran, Al-Taee Ahmad, Mallick Meher S, Bastani Bahar
Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, Missouri, USA.
Saint Louis Nephrology Associates, Saint Louis, Missouri, USA.
J Nephropathol. 2017 Jul;6(3):126-129. doi: 10.15171/jnp.2017.21. Epub 2017 Feb 5.
Hyperoxaluria has been associated with nephrolithiasis as well as acute and chronic kidney disease. We present a case of end stage renal failure caused by excessive dietary oxalate intake in a dietary weight loss regimen.
A 51-year-old Caucasian male with the past medical history of type 2 diabetes mellitus, gout, hypertension and morbid obesity was referred to the primary care clinic after being found pale and easily fatigued. The patient had lost 36 kg over a 7-month period by implementing exercise and intense dietary measures that included 6 meals of spinach, kale, berries, and nuts. Physical examination revealed a blood pressure of 188/93 mm Hg with sunken eyes and dry mucus membranes. Laboratory workup was notable for blood urea nitrogen of 122 mg/dL, creatinine of 12 mg/dL, and estimated glomerular filtration rate (eGFR) of 4.4 mL/min/1.73m2. Patient denied any history of renal disease or renal stones, or taking herbal products, non-steroidal anti-inflammatory drugs, antifreeze (ethylene glycol), or any type of "diet pills." Family history was unremarkable for any renal diseases. After failing intravenous fluid resuscitation, patient was started on maintenance hemodialysis. Abdominal imaging was consistent with chronic renal parenchymal disease with no evidence of nephrolithiasis. Renal biopsy revealed numerous polarized oxalate crystal deposition and diabetic nephropathy class IIA. At this point the patient was instructed to adopt a low oxalate diet. A 24-hour urine collection was remarkable for pH 4.7, citrate <50 mg, and oxalate 46 mg. Importantly, serum oxalate level was undetectable. Repeat renal biopsy 5 months later while patient was still on maintenance hemodialysis revealed persistence of extensive oxalate crystal deposition. Patient has been referred for evaluation for renal transplantation.
Clinicians need to maintain a high index of suspicion for dietary hyperoxaluria as a potential etiology for acute or chronic kidney failure, particularly in patients pursuing intensive dietary weight loss intervention.
高草酸尿症与肾结石以及急慢性肾病有关。我们报告一例因在饮食减肥方案中过量摄入膳食草酸盐导致终末期肾衰竭的病例。
一名51岁的白种男性，有2型糖尿病、痛风、高血压和病态肥胖病史，在被发现面色苍白且易疲劳后转诊至初级保健诊所。该患者在7个月内通过实施运动和严格的饮食措施减重36公斤，这些饮食措施包括6餐菠菜、羽衣甘蓝、浆果和坚果。体格检查显示血压为188/93 mmHg，双眼凹陷，黏膜干燥。实验室检查结果显示血尿素氮为122 mg/dL，肌酐为12 mg/dL，估计肾小球滤过率（eGFR）为4.4 mL/min/1.73m²。患者否认有任何肾病或肾结石病史，也未服用草药产品、非甾体抗炎药、防冻液（乙二醇）或任何类型的“减肥药”。家族史中无任何肾病。在静脉补液复苏失败后，患者开始接受维持性血液透析。腹部影像学检查结果与慢性肾实质疾病相符，无肾结石证据。肾活检显示有大量偏振草酸盐晶体沉积和IIA类糖尿病肾病。此时，患者被告知采用低草酸盐饮食。24小时尿液收集结果显示pH值为4.7，柠檬酸盐<50 mg，草酸盐为46 mg。重要的是，血清草酸盐水平无法检测到。5个月后，患者仍在接受维持性血液透析时再次进行肾活检，结果显示广泛的草酸盐晶体沉积持续存在。患者已被转诊进行肾移植评估。
临床医生需要高度怀疑膳食高草酸尿症是急性或慢性肾衰竭的潜在病因，尤其是在进行强化饮食减肥干预的患者中。
