ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: FR-PO179

Severity of Kidney Dysfunction in Obstructing Tubulopathy Is Associated with the Number of Renal Tubular Obstructing Foci by Light Microscopy

Session Information

  • AKI: Mechanisms
    October 25, 2024 | Location: Exhibit Hall, Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Zhang, Ping L., Corewell Health, Royal Oak, Michigan, United States
  • Kanaan, Hassan D., Corewell Health, Royal Oak, Michigan, United States
  • Li, Wei, Corewell Health, Royal Oak, Michigan, United States
Background

Etiologies of renal failure due to renal tubular injury may result from either ischemic/toxic injury of proximal tubules (ATN), variants of interstitial nephritis or obstructing tubulopathy by the luminal blocking of either monoclonal casts, uric acid or calcified deposits. We hypothesized that the serum creatinine (SCr) levels and the number of tubular obstructing deposits such as calcium oxalate deposits in proximal tubules, and uric acid or monoclonal cast depoists in distal tubules were correlated so that the pathologic identification of obstructing foci can be predictable for the extent of renal dysfunction.

Methods

Eight controls with mild to moderate acute tubular injury and 11 cases with calcium oxalate nephropathy (calcium group) were selected for the study. Other type of tubular obstructing diseases by uric acid and monoclonal casts were also evaluated. The patient’s SCr values were obtained from electronic medical records and the number of polarizable calcium oxalate crystal deposits in the lumina of proximal tubules seen on Hematoxylin & Eosin stained slides at 400x high power field were recorded for each biopsy. Umpired student T-test was used to compare the two groups. Linear regression analysis was used to correlate SCr and the number of calcium oxalate deposits.

Results

Mean ages were not significantly different between two groups (49 ± 8 years in controls and 64 ± 6 years in calcium group). SCr was significantly higher in the calcium group (5.97 ± 0.68 mg/dl*) than in the control group (2.59 ± 0.37 mg/dl). No calcium oxalate deposits were seen in any of the controls, but the number of calcium oxalate deposits ranged from 3 to 7 in the calcium group. In our study, there was a significant linear correlation between SCr and the number of calcium oxalte deposits /high power field, when all cases were taken together (r value = 0.783, p value = 0.0002*). Additional pilot data also showed the similar correlation between the SCr levels and either uric acid deposits or monoclonal cast foci.

Conclusion

Our data indicate that the severity of renal dysfunction in obstructing tubulopathy, calcium oxalate variant, was significantly linked to deposit foci seen microscopically. Identifying the foci of obstructing tubulopathy may be a simple but reliable microscopic method to correlate with patients’ SCr levels.

Funding

  • Clinical Revenue Support