Background. Drug induced kidney disorder (DIKD) is a frequent adverse event which contributes to morbidity and even incapacitation. Toxic nephropathy also is one of the pathological syndromes or complications in acute alcohol poisoning (AAP). Recent years experience shows the insensitivity of serum creatinine to the early stages of kidney damage. NGAL has been shown as a preferred marker of acute kidney damage in a variety of clinical settings. However, no similar studies of serum NGAL have been performed in patients with toxic nephropathy. The presence of markers discovers the possibility of earlier detection, timely treatment and prevention of disease progression to chronic kidney disease (CKD), which can improve the patients prognosis.
Aims to study serum NGAL levels in patients with AAP and DIKD with clinically diagnosed nephropathy and without signs of kidney damage. The effect of glomerular filtration rate (GFR) on serum NGAL levels was studied.
Materials. This prospective cross-sectional study was conducted on the basis of the biochemical laboratory of the Karaganda Medical University in conjunction with the toxicological department of the Regional Medical Center (from January 2018 to October 2019). The study included 89 patients with AAP and 50 patients with DIKD. 25 healthy donors (control group) and 25 patients with CKD served as comparison groups. Serum NGAL levels were measured using a commercially available ELISA kit.
Results. We detected the increased serum NGAL level in both groups with drug-induced nephropathy and nephropathy, caused by AAP compared with the control group values (p 0.01). However, there were no significant differences in NGAL level, depending on the type of toxic nephropathy. After ranking the GFR, it was revealed that GFR did not affect the serum NGAL level (F = 2.21; p = 0.12) and its increase was observed both at reduced and increased GFR relative to the control group values (p 0.05).
Conclusions. The results of our study showed a multiple increase in the concentration of NGAL in serum not only in patients with toxic nephropathy, but also in patients with increased GFR, even in the absence of clinical and laboratory signs of impaired renal function.