Abstract: TH-PO969
Mercury in Natural Health Products as a Cause of Membranous Nephropathy
Session Information
- Glomerular Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Tanner, Stephen B., Baylor Scott and White, Temple, Texas, United States
- Sharma, Vivek, Baylor Scott and White, Temple, Texas, United States
- Idoux, John W., Baylor Scott and White, Temple, Texas, United States
Introduction
Membranous nephropathy (MN) is characterized by subepithelial deposits along the glomerular basement membrane and it is the most common cause of nephrotic syndrome in white adults (1, 2). 80% of cases are primary with antibodies to specific podocyte antigens, Phospholipase A2 Receptor (PLA2R) or thrombospondin type-1 domain-containing 7A (THSD7A). The remainder are secondary to a variety of causes including malignancy and drugs (2). Mercury is a cause of MN with exposures from skin-lightening creams and traditional medicines (1,3). An emerging concern is use of natural health products (NHPs) including vitamins, supplements, and herbal remedies. The composition of these products is not tightly regulated and some have been shown to contain mercury (4). We present a case of MN due to mercury intoxication related to use of NHPs.
Case Description
39-year-old white male with past medical history of depression presented with worsening bilateral lower extremity edema and abdominal distention over the past month. He was taking multiple herbal supplements daily for 6 months. He denied changes in urine output, use of non-steroidal anti-inflammatory drugs, illicit drugs, or alcohol. He reported eating fish 1 meal per month. On evaluation, He demonstrated anasarca. No other abnormalities noted on physical examination. Lab work demonstrated normal renal function, nephrotic range proteinura, hypoalbuminemia, and hyperlipidemia. Urine protein-to-creatinine ratio was elevated at 14.3 (ref 0.00 - 0.19). ANA, hepatitis B and C, C3, and C4 were normal. Heavy metal serum screen returned mercury of 22.1 ug/L (0.0 to 10.0 ug/L) and 24- hour urine mercury was >80 ug/L (0.0 - 5.0 ug/L). Renal biopsy was consistent with membranous nephropathy. PLA2R and THSD7A were negative. The offending agents were discontinued. He started on Cyclosporine A, Atorvastatin, and Apixaban. Cyclosporine A was weaned off quickly following final diagnosis. He continued on Atorvastatin and Apixaban for 12 weeks. By 12 weeks, all lab parameters returned to normal.
Discussion
Mercury-induced membranous nephropathy is a known, but rare entity that has been associated with skin-lightening creams, Chinese herbal medicines, and now NHPs. Our case highlights the necessity of through medication review to identify causes of nephrotic syndrome that may respond to simple measures such as discontinuation of offending drugs.