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: PO0079

Roux-en-Y Gastric Bypass Is the Most Common Current Cause of Biopsy-Proven Oxalate Nephropathy

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Reddy, Swetha, Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Lieske, John C., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Keddis, Mira T., Mayo Clinic Arizona, Scottsdale, Arizona, United States
Background

The objective of this study was to analyze patient characteristics and outcomes of biopsy-proven oxalate nephropathy likely due to an enteric cause at a single large tertiary health system.

Methods

Cases of oxalate nephropathy were identified based on documented kidney biopsy findings between 2009-2019 in patients with an associated enteric process likely to cause fat malabsorption.

Results

A total of 30 cases were identified (mean age of 65.2±8.56 years; 18(60.0%) female) with a median follow-up of 5 months; Risk factors included: hypertension in 21(70%), diabetes in 14 (46.7%), chronic kidney disease (CKD) stage 3A or greater in 16(53.3%) and prior kidney stones in 6(20%). The most common enteric causes were Roux en Y gastric bypass (RYGB) in 17(56.7%), pancreatic insufficiency in 6(20%), inflammatory bowel disease in 4(13.3%), and recurrent C. difficile infection in 3(10%). At the time of diagnosis, acute kidney injury (AKI) stage II and stage III were present in 9 (30%) and 15 (50%) respectively, while 11(36.7%) required dialysis. Urinalysis revealed proteinuria in 16(55.2%), oxalate crystals in 10(33.3%), and hematuria in 9(31%). Median plasma oxalate at the time of biopsy was 18.3 [reference <2.0]) µmol/L in 26 patients and median 24 hour urine oxalate excretion was 53 (reference [9.7-40.5]) mg/24 hrs in 17 patients. RYGB patients had a higher plasma oxalate compared to patients with other enteric causes (median 24.6 vs 16.5 µmol/L, p=0.03). Renal biopsy and clinical outcomes are shown in table1 [table1]. Patients with acute tubular injury had greater number of tubules with calcium oxalate crystals by biopsy (median 19 vs 4), as did patients with CKD5 at last follow-up (20 vs 6). Features at the time of biopsy predictive of CKD5 at follow-up included AKI severity (p=0.002), dialysis at diagnosis (p=0.0008), and the presence of moderate to severe tubulointerstitial atrophy (p=0.001).

Conclusion

In this series RYGB was the most common enteric cause of biopsy-proven oxalate nephropathy. Severity of AKI at presentation and degree of tubulointerstitial fibrosis were both associated with worse renal outcome. The amount of renal crystal deposits at diagnosis associated with the short and long term renal injury.

Renal Histology (A) & Outcome (B)
(A) Acute tubular injury

Interstitial inflammation

Number of tubules with calcium oxalate crystals

Moderate to severe tubular atrophy
26 (86.6%)

21 (70%)

Median 19 (range 2, 40)

23 (76.7%)
(B) Renal recovery

CKD Stage 3

CKD Stage 4

CKD Stage 5

Dialysis

Kidney transplant
1 (3.33%)

5 (16.7%)

8 (26 %)

5 (16.7%)

10 (33.3%)

1(3.33%)