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Kidney Week

Abstract: PO0980

Cutaneous Oxalosis in a Patient on Peritoneal Dialysis

Session Information

  • Peritoneal Dialysis
    November 04, 2021 | Location: On-Demand, Virtual Only
    Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

  • 702 Dialysis: Home Dialysis and Peritoneal Dialysis

Authors

  • Torres Rodriguez, Stephanie, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Pyle, Hunter, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Rutherford, Audrey, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Dominguez, Arturo R., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Shastri, Shani, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction

Oxalosis is the systemic deposition of calcium oxalate in multiple tissues and can be of primary or secondary etiology. Skin manifestations due to secondary hyperoxaluria (SH) attributable to renal insufficiency are rare. We present a case of cutaneous oxalosis in a patient with end stage renal disease (ESRD) receiving peritoneal dialysis (PD).

Case Description

A 45-year-old female with ESRD due to lupus nephritis (LN) on PD for 11 years presented with hypertensive encephalopathy. Dermatological evaluation revealed pseudoreticular hyperpigmented patches overlying firm, non-tender, subcutaneous nodules and plaques on bilateral lower extremities (Figure 1) and upper arms and firm nodules overlying the joints of her hands (Figure 2). With history of lupus, cutaneous findings were concerning for dystrophic calcinosis cutis. Skin biopsy showed radially arranged yellow-brown rhomboid crystals in the subcutis and deep dermis surrounded by histiocytes consistent with cutaneous oxalosis (Figure 3). Additional history revealed daily intake of Vitamin C 1g for past year and no prior gastrointestinal surgeries or chronic diarrhea. Non-obstructive bilateral nephrolithiasis were seen on imaging in 2020 but absent previously.

Discussion

Absence of early-age nephrolithiasis, negative family history & renal biopsy findings are inconsistent with primary hyperoxaluria (PH). SH is a result of excessive oxalate accumulation from increased intake, increased reabsorption due to small bowel disease, or decreased excretion in renal failure (retention oxalosis). Although dialysis patients may have high serum oxalate, clinical calcifications are rare. We speculate vitamin C supplementation and ESRD status contributed to the production of these deposits in our patient. Ascorbic acid is metabolized to oxalate; in long term dialysis patients doses of 500 mg daily may raise plasma oxalate by 50% to 100%. Management includes lowering serum calcium and oxalate levels by eliminating Vitamin C supplements or reducing dose < 100 mg daily, limiting dietary oxalate, increasing dialysis clearance and lowering dialysate calcium concentration if needed.