Dehydration, characterized by a deficit in total body water, significantly alters renal hemodynamics and biochemical markers of kidney function. When intravascular volume contracts, renal blood flow diminishes, triggering compensatory neurohormonal pathways such as the renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone (ADH) secretion. These responses prioritize intravascular volume restoration, directly altering standard kidney function tests. The primary laboratory biomarkers affected include: Blood Urea Nitrogen (BUN) and Serum Urea: Intravascular volume depletion slows tubular fluid flow, enhancing the passive reabsorption of urea into systemic circulation. Consequently, BUN levels rise sharply, reflecting pre-renal azotemia. Serum Creatinine: Creatinine elevation occurs due to a reduced glomerular filtration rate (GFR). However, unlike urea, creatinine reabsorption is minimal, making its initial increase less pronounced than that of BUN in early fluid deficit states. BUN-to-Creatinine Ratio: A BUN/Creatinine ratio exceeding 20:1 serves as a classic diagnostic hallmark of pre-renal azotemia caused by hypovolemia or dehydration, helping clinicians differentiate functional hypoperfusion from intrinsic renal tissue damage. Estimated Glomerular Filtration Rate (eGFR): Reduced hydrostatic pressure within glomerular capillaries leads to a transient drop in eGFR, which typically reverses upon adequate rehydration. Urinalysis and Electrolytes: Dehydration manifests as elevated urine specific gravity (>1.020) and high urine osmolality. Plasma sodium levels may also show hypernatremia secondary to hemoconcentration. Dehydration alters renal biomarkers primarily through hemodynamic adaptation rather than structural parenchymal damage. Recognizing these biochemical changes is essential for accurate clinical evaluation, preventing misdiagnosis, and instituting prompt fluid replacement to restore baseline renal function. Al-Mustaqbal University The First University in Iraq