Abstract
Urinary neutrophil gelatinase-associated lipocalin (uNGAL) is known to predict the prolonged delayed graft function after kidney transplantation. We examined the relation of uNGAL with histological findings of acute tubular injury (ATI). Analyses were made in biopsies taken at 6 weeks, 3 months, and 6 months after kidney transplantation. uNGAL was measured in the spot urines, normalized to urinary creatinine excretion, and correlated to biopsy findings and clinical, laboratory, and demographic variables. Controls included healthy individuals, individuals after kidney donation and ICU patients with acute kidney failure. Renal transplant recipients without ATI did not display elevated uNGAL levels compared to the healthy controls. Transplant patients with ATI had a higher uNGAL excretion at 6 weeks than patients without ATI (27,435 versus 13,605 ng/g; P = 0.031). This increase in uNGAL was minor compared to ICU patients with acute renal failure (2.05 × 106 ng/g). Patients with repeated findings of ATI or severe ATI did not have higher urinary NGAL levels compared to those with only one ATI finding or moderate ATI. Female recipient gender and urinary tract infection were identified as potential confounders. uNGAL has a relation with histological signs of acute tubular injury. The usability of this biomarker in renal allograft recipients is limited because of the low sensitivity.
Highlights
Acute kidney injury early after transplantation may arise from the donor’s condition, prolonged cold ischemia time, and early posttransplant injuries like rejection and drug toxicity
In a previous study by Mishra et al with immunochemical staining of renal allografts, a correlation was established between an increased expression of neutrophil gelatinase-associated lipocalin (NGAL) and prolonged cold ischemia time, elevated serum creatinine levels, and dialysis requirement [5]
There was no significant difference in Urinary neutrophil gelatinase-associated lipocalin (uNGAL) excretion in transplanted patients versus healthy individuals with 1 kidney and healthy individuals with 2 kidneys (Figure 1)
Summary
Acute kidney injury early after transplantation may arise from the donor’s condition, prolonged cold ischemia time, and early posttransplant injuries like rejection and drug toxicity. A rise in serum creatinine already implies a significant amount of kidney damage, which limits its ability to detect impaired graft function at early stages. Novel biomarkers such as Kim-1, IL-18, and neutrophil gelatinase-associated lipocalin (NGAL) have been proven useful in detecting nontransplant acute kidney damage [2]. In a previous study by Mishra et al with immunochemical staining of renal allografts, a correlation was established between an increased expression of NGAL and prolonged cold ischemia time, elevated serum creatinine levels, and dialysis requirement [5]. We addressed the question whether urinary NGAL correlates with histologically confirmed acute tubular injury using protocol biopsies taken within the first six months after transplantation
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