Potassium dichromate (Cr) is a ubiquitous inorganic chemical reagent, most frequently employed as
an oxidizing agent in variety of laboratory and industrial settings and can result in nephrotoxicity. The
current study was done to explore the nephrotoxic effects of Cr with a specific focus on alterations
in renal aquaporins (AQPs) expression, renal water channel protein, providing insights into how
exposure to Cr may compromise renal water homeostasis in a dose-dependent pattern. Thirty-six
Wistar albino male rats were assigned into 3 groups evenly; control rats received only distilled water
daily, while Cr-Low and Cr-High groups received, 2.5 mg/kg bw, and 7.5 mg/kg bw of Cr i.p for 14 days,
respectively. Blood and kidney samples were obtained. Cr induced nephrotoxicity in the current study
in a dose-dependent manner, as exhibited by a remarkable deterioration of the renal parameters,
oxidative status, histopathological and ultrastructural changes. Renal function registered a significant
rise in urea and creatinine, as opposed to total protein and albumin, which decreased substantially. A
significant dose dependent rise in malondialdehyde (MDA) level as well as dwindle in the antioxidant
enzymes level. Furthermore, hematology divulged a notable reduction in hemoglobin concentration
(Hb%) while significant upsurge in white blood cells (WBCs) in exposed groups. In addition, our study
demonstrated that Cr, alters the expression level of AQP1 and AQP2 in renal tissue which are salutary
for detecting the renal damage early. On the other hand, Cr boosted the upregulation of kidney
injury molecule-1 (KIM-1) in kidney tissue confirming its disruption. Interestingly, gene expression of
KIM-1, AQP1 and AQP2’s in renal membrane correlates well with creatine level, reinforcing their role
as sensitive markers of tubular damage and reflect impaired tubular water handling. High exposure
produced a severe nephrotoxic profile, distinctly different from controls and far more pronounced than
the Cr-Low group.