Can dehydration lead to acute kidney injury?

Can Dehydration Lead to Acute Kidney Injury?

Yes, dehydration is a well-established cause of acute kidney injury (AKI) and represents one of the most common and preventable mechanisms of kidney damage in clinical practice. 1

Mechanisms of Dehydration-Induced AKI

Dehydration causes AKI through multiple pathophysiological pathways:

• Volume depletion (hypovolaemia) reduces renal perfusion pressure, directly impairing glomerular filtration and leading to acute tubular injury 1
• Hemoconcentration increases blood viscosity and alters red blood cell properties, further compromising renal microcirculation 2
• Activation of vasopressin, aldose reductase-fructokinase pathway, and chronic hyperuricemia contribute to kidney damage, particularly with recurrent dehydration 3
• Inflammation-related pathways overlap between dehydration and kidney injury, with elevated interleukin-6 and C-reactive protein predicting subsequent AKI 4

High-Risk Clinical Contexts

Certain populations and clinical scenarios dramatically increase the risk of dehydration-induced AKI:

• Elderly patients, those with atherosclerosis, heart failure, or baseline chronic kidney disease are at highest risk 5
• Patients taking RAAS inhibitors (ACE inhibitors, ARBs), diuretics, NSAIDs, or SGLT2 inhibitors have blocked compensatory mechanisms that normally protect kidney perfusion during hypovolemia 1, 5
• COVID-19 patients commonly present with dehydration on admission and experience increased insensible fluid losses from fever and tachypnea 1
• Agricultural workers and athletes experiencing recurrent heat exposure, physical exertion, and dehydration are at risk for both acute and chronic kidney disease 4, 6
• Patients with diabetes taking metformin or SGLT2 inhibitors should stop these medications during dehydration to prevent lactic acidosis and AKI 1

Clinical Evidence and Biomarkers

Recent research demonstrates that even mild prolonged dehydration can trigger AKI biomarkers:

• Prolonged mild hypohydration (24 hours of fluid deprivation) significantly increased urinary [IGFBP7·TIMP-2], an FDA-approved AKI biomarker, in healthy young adults 7
• Urine osmolality ≥952 mosmol/kgH₂O and urine specific gravity ≥1.025 demonstrated excellent ability to discriminate positive AKI risk following dehydration 7
• Baseline dehydration, reduced urine uromodulin, and elevated inflammatory markers predicted subsequent AKI in agricultural workers 4

Prevention and Management

Ensuring adequate hydration is essential in preventing and treating AKI, but fluid administration must be guided by hemodynamic assessment: 1

• For patients without shock, confusion, or swallowing difficulty, oral rehydration with any available rehydration drink or potable water should be initiated immediately 1
• 4% to 9% carbohydrate-electrolyte drinks are preferred over plain water for exertional dehydration 1
• Intravenous fluid administration should be based on repeated assessment of fluid status and dynamic tests of fluid responsiveness, not empiric boluses 1
• Avoid indiscriminate fluid administration in patients with established AKI, as inappropriate attempts to "reverse" AKI can lead to fluid overload and worsen kidney function 1

Critical Medication Management

During dehydration, specific medications must be temporarily discontinued to prevent AKI:

• Stop metformin due to risk of lactic acidosis and monitor renal function carefully 1
• Stop SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin) due to risk of dehydration, diabetic ketoacidosis, and AKI 1
• Consider temporary discontinuation of RAAS inhibitors and diuretics in patients with chronic kidney disease experiencing dehydration, with monitoring of serum creatinine and potassium 5
• Monitor GLP-1 receptor agonists closely as dehydration can lead to serious illness; encourage adequate fluid intake 1

Monitoring Requirements

Patients at risk for or with dehydration-induced AKI require specific monitoring:

• Measure serum urea, creatinine, and electrolytes at least every 48 hours or more frequently if clinically indicated 1
• Assess fluid status by clinical examination (peripheral perfusion, capillary refill, pulse rate, blood pressure, postural hypotension) and fluid balance daily 1
• Monitor urine output, with oliguria representing a warning sign but having multiple etiologies beyond hypovolemia 1
• Use early warning scores (NEWS2) for patients with deteriorating clinical condition 1

Common Pitfalls to Avoid

• Do not assume oliguria always indicates hypovolemia requiring fluid boluses – oliguria has multiple etiologies and inappropriate fluid administration can create a vicious cycle of fluid overload worsening kidney function 1
• Do not use the outdated term "pre-renal AKI" as it is often misinterpreted as "hypovolemic" and encourages indiscriminate fluid administration 1
• Do not continue nephrotoxic medications during dehydration without careful risk-benefit assessment and monitoring 1
• Do not overlook recurrent mild dehydration as a risk factor for chronic kidney disease progression, particularly in vulnerable populations 3, 4