A hidden cause of oxalate nephropathy: a case report.

BACKGROUND: Oxalate nephropathy is a rare disorder that can result in acute kidney injury (AKI) and progresses to end-stage kidney disease (ESKD). The causes can be either primary or secondary. Primary hyperoxaluria includes a group of hereditary disorders with enzymatic defects in the glyoxylate pathway, resulting in decreased oxalate metabolism. Secondary hyperoxaluria, often overlooked can result from increased intestinal absorption, nutritional deficiencies, decreased fluid intake, impaired excretion, and increased dietary consumption of oxalate. CASE PRESENTATION: We present a Caucasian case of acute oxalate induced nephropathy associated with consumption of large quantities of green vegetables in a patient with chronic kidney disease (CKD). Imaging study showed no evidence of kidney stone, but a kidney biopsy revealed acute tubular injury, tubular atrophy, interstitial fibrosis, and dense tubular deposition of calcium oxalate crystals. Upon further questioning the patient, we learned that in the months prior to presentation, he had very significantly increased his consumption of green vegetables. Because of no clinical improvement, the patient was initiated and maintained on hemodialysis. CONCLUSION: This report illustrates a case of acute oxalate nephropathy in the setting of very high dietary consumption of oxalate-rich foods in a patient with advanced CKD. Special attention should be given to the secondary causes of hyperoxaluria in patients with predisposing conditions such as CKD.

Bupropion for treatment of interferon-induced depression.

OBJECTIVE: To report the effect of bupropion in a patient with interferon (IFN)-induced depression and review the use of antidepressants for treatment of depressive symptoms associated with IFN therapy. CASE SUMMARY: A 43-year-old white woman with chronic hepatitis C and severe IFN-induced depression was treated with sustained-release bupropion initiated at 150 mg/day for 7 days and 100 mg twice daily thereafter. The dosage was increased again, to 350 mg/day when depressive symptoms recurred. While receiving that dose and continuing IFN treatment, she reported significant improvement in her depressive symptoms without experiencing any adverse effects. DISCUSSION: There is limited evidence suggesting that IFNs decrease central serotonergic transmission. There are several published reports on the use of selective serotonin-reuptake inhibitors for the treatment of IFN-induced depression. However, controlled studies are needed to assess the efficacy of serotonergic and noradrenergic antidepressants in IFN-treated patients with depressive symptoms. CONCLUSIONS: Sustained-release bupropion might be of potential benefit in patients with interferon-induced depression.