Abstract: SA-PO149
The Development of AKI After Acute Nephrons Loss: An Unexpected Journey
Session Information
- AKI: Epidemiology, Risk Factors, Prevention - III
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Trevisani, Francesco, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Di marco, Federico, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Dell'Antonio, Giacomo, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Pani, Antonello, AziendaOspedalieraG. Brotzu, Cagliari, Italy
- Larcher, Alessandro, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Capitanio, Umberto, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Bettiga, Arianna, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Porrini, Esteban, University Hospital of the Canary Island, La Laguna, Spain
- Salonia, Andrea, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Briganti, Alberto, IRCCS San Raffaele Scientific Institute, Milan, Italy
- Montorsi, Francesco, IRCCS San Raffaele Scientific Institute, Milan, Italy
Background
Acute Kidney Injury (AKI) following radical nephrectomy (RN) is associated with an increased risk of morbidity and mortality. Up to know it is impossible to understand the major predictor for AKI developement.
Methods
We collected prospectively clinical data of a group of 195 patients who underwent RN for renal masses. To evaluate the risk of AKI after surgery, serum-creatinine (sCr) values were collected before surgery (t0), 24h and 48h after the operation (t1 and t2), and at dismissal (tf). We calculated eGFR with aMDRD formula. According to RIFLE criteria, we defined the AKI onset with a ratio of sCr/sCr(t0) higher than 1.5. A pathological evaluation using the Remuzzi Score was carried out on the healthy renal parenchima based on glomerular global sclerosis, tubular atrophy, interstitial fibrosis and arterial narrowing.
Results
In our study a strong significative correlation (p <0.001) was found with the basal eGFR at t0. In fact, the lower was the basal sCr, the higher was the risk of AKI development. A lower variation of eGFR from t0 to tf was related with the presence of tubular atrophy (p<0.01) or interstitial fibrosis (p<0.05)
Conclusion
An eGFR higher than 70 ml/min could represent an unexpected predictive cutoff of AKI development after RN. There are two possible explanation: a better medical treatment of the CKD patients; a “non adequate compensatory function mechanisms” after acute nephron loss. In fact, in healthy pts, the hyperfiltration mechanism is not yet well established (as in CKD pts) so that RN results in an unexpected trauma for the remnant kidney who will take time to restore the renal function.
Temporal pattern of renal function according AKI onset