ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0318

Uric Acid Crystallopathy Associated with Trimethoprim/Sulfamethoxazole (TMP/SMX) Use in a Patient with Gout

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Qiu, Mengting, Harvard Medical School, Boston, Massachusetts, United States
  • Tang, Mengyao, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Mount, David B., Brigham and Women's Hospital, Boston, Massachusetts, United States
Introduction

The commonly used antibiotic trimethoprim/sulfamethoxazole (TMP/SMX) is known to cause AKI. AKI induced by TMP/SMX can occur through various mechanisms, such as acute interstitial nephritis, crystalluria, acute tubular necrosis, and “pseudo”-AKI due to inhibition of proximal tubular secretory organic cation transporters by TMP. Here, we present a patient with a history of gout found to have AKI secondary to uric acid crystallopathy in the setting of TMP/SMX treatment.

Case Description

A 69-year-old male with a history of gout, heart transplant, and CKD3a secondary to calcineurin inhibitor toxicity was initiated on inpatient TMP/SMX treatment for Pneumocystis jirovecii pneumonia (PJP), with starting dose of 15mg/kg/day orally. 3 days later, creatinine was 3.2 mg/dL, from baseline of 1.6 mg/dL; cystatin C was 4.1 mg/L with an eGFR of 12. Urinalysis revealed pH of 5 and 4+ uric acid crystals. Serum uric acid level was 11.7 mg/dL, with an elevated fractional excretion of uric acid at 17%. Of note, the patient had been off urate-lowering therapy since heart transplant, and had had 3 gout flares in the 6 months prior to presentation. Because TMP/SMX is the preferred treatment for PJP, it was continued. He was given IV bicarbonate to alkalinize his urine; uric acid crystals were no longer present on repeat UA the next day. He was also given rasburicase, which lowered serum uric acid to <0.4 mg/dL. Creatinine began to downtrend 1 week after rasburicase therapy, reaching baseline levels about 3 weeks later, while still on TMP/SMX.

Discussion

Uric acid crystallopathy, uricosuria, and hypouricemia associated with SMX and/or TMP have been previously reported in the literature. It is hypothesized that SMX may inhibit uric acid reabsorption in the proximal tubule, increasing fractional excretion. TMP has also been shown to be uricosuric. Studies to determine whether SMX and TMP inhibit heterologously-expressed urate transporters are ongoing. Patients with a history of gout and a high baseline serum uric acid level may be at higher risk of kidney injury from uric acid crystallopathy when administered TMP/SMX. Thus, it seems appropriate to check serum uric acid levels before initiating TMP/SMX therapy in patients with gout. If serum uric acid level is elevated, concomitant urate-lowering therapy may be renoprotective.