Abstract: SA-PO366
Nephrocalcinosis Secondary to Excessive Oxalate Ingestion
Session Information
- Genetic and Diagnostic Trainee Case Reports
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1300 Health Maintenance, Nutrition, and Metabolism
Authors
- Tang, Mengyao, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Cherian, Jerald, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Day, Matthew, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Harris, Raymond C., Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction
Deposition of calcium oxalate or calcium phosphate within the renal medulla can lead to nephrocalcinosis. This most often occurs in the setting of hypercalciuria with or without hypercalcemia, but in rare instances, may occur due to hyperoxaluria. In the majority of cases, nephrocalcinosis is asymptomatic without progression to end stage renal disease, unless the underlying cause is left untreated. We present a case of renal failure secondary to nephrocalcinosis in the setting of prolonged secondary hyperoxaluria.
Case Description
A 68 year-old male with well-controlled hypertension presented to the emergency department after routine lab work at a yearly primary care visit revealed potassium 6.1 mEq/L, BUN 103 mg/dL, and creatinine 12.3 mg/dL. Corrected serum calcium was 8.2 mg/dL and 25-hydroxy vitamin D was 46.1 ng/mL. Two years prior to presentation, creatinine was 0.9 mg/dL, but had risen to 2.36 mg/dL one year prior to presentation. Four years prior to presentation, the patient had started a new diet consisting mainly of green beans, turnip greens, and broccoli. Review of previous urinalyses showed multiple instances of calcium oxalate crystals in his urine. Renal ultrasound showed decreased renal size bilaterally, as well as, bilateral non-obstructing renal calculi. CT abdomen and pelvis demonstrated bilateral nephrocalcinosis, likely secondary to hyperoxaluria in the setting of prolonged excessive dietary oxalate intake. Despite conservative medical management including initiation of a low oxalate diet, the patient did not recover renal function and became dialysis dependent.
Discussion
Once nephrocalcinosis is diagnosed, it is imperative to determine the underlying cause as to guide management. If standard laboratory testing does not reveal a cause, such as hypercalcemia or renal tubular acidosis, there should be increased suspicion for hyperoxaluria. Although secondary hyperoxaluria is most often due to fat malabsorption, a careful dietary history should also be taken to evaluate for chronic ingestion of excessive amounts of oxalate (e.g. rhubarb, spinach, green beans, etc.) or oxalate precursors (e.g. vitamin C), as highlighted by this case. In patients with secondary hyperoxaluria, dietary oxalate intake should be minimized, while calcium and fluid intake should be liberalized. If treated promptly, renal function often recovers.