Abstract:
Chronic kidney diseases (CKD) caused by acute kidney injury (AKI) results rapid and reversible loss in renal
function. A real-time, highly accurate, and sensitive acute kidney injury biomarker is urgently required in order
to keep these patients alive and prevent end stage renal disease and related complications that include hypertension,
fluid and electrolyte retention, metabolic acidosis, anemia, stroke etc. This study was designed to
develop a specific and sensitive model for the early identification of renal damage in male albino rats. Using a
single intraperitoneal dose of cisplatin (10 mg/kg body weight) to the rats, the various duration-dependent
nephrotoxic activities were compared using multiple physiological, biochemical, genomic, and histopathological
markers. We looked into when renal dysfunction would start occurring after receiving a single high dose of
cisplatin while blood urea nitrogen (BUN) and serum creatinine (sCr) remained normal. Following a single
cisplatin injection, various measurements were taken in plasma, urine, and/or kidney tissues of rats euthanized
on days 1, 2, 3, 5, and 7. When the urine kidney injury molecule (KIM-1), interleukine 18 (IL-18), nephrin,
neutrophil gelatinase-associated lipocalin (NGAL) and serum cystatin C (Cys C) levels are greatly raised on day 3
after cisplatin treatment, BUN and sCr levels remain normal. Nephrotoxicity of cisplatin is also indicated by the
upregulated mRNA expression of KIM-1, IL-18, Cys C, and NGAL and downregulated expression of nephrin in
kidney tissue at very initial stage. Protein expression of KIM-1, IL-18 and NGAL level of kidney tissues was
upregulated indicated confirmatory results done by western blot. Utilising an array of kidney impairment indicators
has emerged as an earlier, more effective, and more reliable technique to diagnose AKI when compared
to the most sophisticated signs now available.
