Urinary Neutrophil Gelatinase Associated Lipocalin (NGAL) for Early Diagnosis of Acute Kidney Injury in Renal Transplant Recipients

Abstract Background Acute kidney injury (AKI) is a key risk factor for chronic kidney disease in the general population, but has not been investigated in detail among renal transplant recipients (RTRs). We investigated the incidence, severity and risk factors for AKI following cardiac surgery among RTRs compared with non-RTRs with otherwise similar clinical characteristics. Methods We conducted a retrospective cohort study of RTRs (n = 83) and non-RTRs (n = 83) who underwent cardiac surgery at two major academic medical centers. Non-RTRs were matched 1:1 to RTRs by age, preoperative (preop) estimated glomerular filtration rate and type of cardiac surgery. We defined AKI according to Kidney Disease: Improving Global Outcomes criteria. Results RTRs had a higher rate of AKI following cardiac surgery compared with non-RTRs [46% versus 28%; adjusted odds ratio 2.77 (95% confidence interval 1.36–5.64)]. Among RTRs, deceased donor (DD) versus living donor (LD) status, as well as higher versus lower preop calcineurin inhibitor (CNI) trough levels, were associated with higher rates of AKI (57% versus 33% among DD-RTRs versus LD-RTRs; P = 0.047; 73% versus 36% among RTRs with higher versus lower CNI trough levels, P = 0.02). The combination of both risk factors (DD status and higher CNI trough level) had an additive effect (88% AKI incidence among patients with both risk factors versus 25% incidence among RTRs with neither risk factor, P = 0.004). Conclusions RTRs have a higher risk of AKI following cardiac surgery compared with non-RTRs with otherwise similar characteristics. Among RTRs, DD-RTRs and those with higher preop CNI trough levels are at the highest risk.

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Contrast-induced acute kidney injury in renal transplant recipients after cardiac catheterization

Clinical Nephrology ◽

10.5414/cnp71687 ◽

2009 ◽

Vol 71 (06) ◽

pp. 687-696 ◽

Cited By ~ 6

Author(s):

V. Agrawal ◽

A. Swami ◽

R. Kosuri ◽

M. AlSabbagh ◽

M. Agarwal ◽

...

Keyword(s):

Acute Kidney Injury ◽

Renal Transplant ◽

Cardiac Catheterization ◽

Kidney Injury ◽

Renal Transplant Recipients ◽

Transplant Recipients

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Neutrophil Gelatinase-Associated Lipocalin Is Not Associated with Tacrolimus-Induced Acute Kidney Injury in Liver Transplant Patients Who Received Mycophenolate Mofetil with Delayed Introduction of Tacrolimus

International Journal of Molecular Sciences ◽

10.3390/ijms20123103 ◽

2019 ◽

Vol 20 (12) ◽

pp. 3103 ◽

Cited By ~ 1

Author(s):

Mio Fukuda ◽

Kimitaka Suetsugu ◽

Soichiro Tajima ◽

Yurie Katsube ◽

Hiroyuki Watanabe ◽

...

Keyword(s):

Liver Transplantation ◽

Acute Kidney Injury ◽

Mycophenolate Mofetil ◽

Liver Transplant ◽

Kidney Injury ◽

Transplant Recipients ◽

Fatty Acid Binding ◽

Neutrophil Gelatinase Associated Lipocalin ◽

Neutrophil Gelatinase ◽

Liver Transplant Recipients

Tacrolimus is widely used as an immunosuppressant in liver transplantation, and tacrolimus-induced acute kidney injury (AKI) is a serious complication. The urinary neutrophil gelatinase-associated lipocalin (NGAL) level has been linked to tacrolimus-induced AKI in patients starting tacrolimus treatment the morning after liver transplantation. Here we tested this association using a different immunosuppression protocol: Mycophenolate mofetil administration beginning on Postoperative Day 1 and tacrolimus administration beginning on Postoperative Day 2 or 3. Urine samples were collected from 26 living donor liver transplant recipients before (Postoperative Day 1) and after (Postoperative Day 7 or 14) tacrolimus administration. NGAL levels were measured via enzyme-linked immunosorbent assays, as were those of three additional urinary biomarkers for kidney diseases: Monocyte chemotactic protein-1 (MCP-1), liver-type fatty acid-binding protein (L-FABP), and human epididymis secretory protein 4 (HE4). HE4 levels after tacrolimus administration were significantly higher in patients who developed AKI (n = 6) than in those who did not (n = 20), whereas NGAL, MCP-1, and L-FABP levels did not differ significantly before or after tacrolimus administration. These findings indicate that NGAL may not be a universal biomarker of AKI in tacrolimus-treated liver transplant recipients. To reduce the likelihood of tacrolimus-induced AKI, our immunosuppression protocol is recommended.

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