Abstract: FR-PO0849
Identification of Urinary Renal Tubular Epithelial Cell Casts in Proteinuric Glomerular Diseases
Session Information
- Glomerular Diseases: Practice and New Concepts Shaping Modern Care
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Tupil, Ajay, UQ Medicine, Brisbane, Queensland, Australia
- Bendersky, Maggie, UQ Medicine, Brisbane, Queensland, Australia
- Li, Irene J., UQ Medicine, Brisbane, Queensland, Australia
- Hunt-Tobey, Bridget, UQ Medicine, Brisbane, Queensland, Australia
- Shankar, Nithyapriya, UQ Medicine, Brisbane, Queensland, Australia
- Anzalone, Amy S., UQ Medicine, Brisbane, Queensland, Australia
- Yuen, Joanna, UQ Medicine, Brisbane, Queensland, Australia
- Punukollu, Pooja A., UQ Medicine, Brisbane, Queensland, Australia
- Asad, Maira, UQ Medicine, Brisbane, Queensland, Australia
- Velez, Juan Carlos Q., UQ Medicine, Brisbane, Queensland, Australia
- Varghese, Vipin, UQ Medicine, Brisbane, Queensland, Australia
Group or Team Name
- Ochsner Nephrology
Background
Identification of renal tubular epithelial cell (RTEC) casts (RTECC) by urinary sediment microscopy (uSEDI) is traditionally linked to acute kidney injury (AKI) due to acute tubular injury (ATI). However, in proteinuric states, pathological engulfing of filtered protein by RTEC may lead to disruption of their integrity and sloughing into the tubular lumen. Thus, we hypothesized that RTECC may be commonly detected in proteinuric glomerular diseases.
Methods
Utilizing a prospective observational cohort of patients seen for nephrology consultation who completed uSEDI over a 7-yr period, we examined the relationship between presence of RTECC and proteinuria or kidney disease etiology: ATI (ischemic, toxic), acute interstitial nephritis (AIN) or acute/chronic glomerulopathy (GlomP). Presence of >5% low power fields with RTECC was deemed positive. We excluded cases missing a urine protein-to-creatinine ratio (UPCR) and those with cirrhosis (hyperbilirubinemia is known to be associated with RTECC).
Results
542 patients [median age 63, 42% women] were included. Median sCr was 3.3 mg/dL. The most common etiologies of AKI were ATI (63%) and GlomP (17%). RTECC were identified in 171 (32%). Mean UPCR was significantly higher in those with RTECC (4.2 vs. 2.4 g/g. p<0.0001). In addition, the proportion of patients with RTECC was the highest in those with GlomP (105/208, 51%) compared to ATI (72/393, 18%) or AIN (4/24, 17%), p<0.0001 for chi-square. Within ATI, toxic ATI (n=45) was associated with higher frequency of RTECC compared to ischemic ATI (40% vs. 15%, p<0.0001).
Conclusion
RTECC are associated with greater degree of proteinuria and are often found in specimens of patients with glomerulopathies. Therefore, finding RTECC should not lead to premature adjudication to ATI as primary etiology of AKI, especially when proteinuria is overt. Moreover, RTECC are more common in toxic ATI than in ischemic ATI. This observation aligns with the previously known association of bile cast tubulopathy (a form of toxic ATI) and RTECC, likely reflecting that the mechanism of injury of toxic ATI differs from the ischemic type. In summary, RTECC may serve as “readout” of luminal exposure to an injurious factor, filtered protein or a tubulo-toxic molecule.