Can dehydration cause Acute Kidney Injury (AKI)?

Does Dehydration Cause Acute Kidney Injury?

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

Mechanism of Dehydration-Induced AKI

Volume depletion (hypovolemia) directly reduces renal perfusion pressure, impairing glomerular filtration and leading to acute tubular injury. 1 The KDIGO guidelines explicitly list dehydration or volume depletion as a key susceptibility factor for AKI development. 2

Evidence Supporting the Causal Relationship

• Pediatric DKA studies demonstrate that true dehydration (measured by weight change) is directly associated with elevated serum creatinine levels on admission (p = 0.042), confirming the causal link between dehydration and AKI. 3
• Experimental human studies show that 24 hours of fluid deprivation in healthy young adults markedly increases urinary AKI biomarkers [IGFBP7·TIMP-2] from 0.2 to 1.9 (ng/mL)²/1,000 (p = 0.0011), demonstrating that even mild prolonged hypohydration can trigger kidney injury. 4
• Mechanistic research identifies three major pathways by which recurrent dehydration causes permanent kidney damage: vasopressin effects on the kidney, activation of the aldose reductase-fructokinase pathway, and chronic hyperuricemia. 5

High-Risk Clinical Scenarios

Patients on Specific Medications (Critical)

Patients taking RAAS inhibitors (ACE inhibitors, ARBs), diuretics, NSAIDs, or SGLT2 inhibitors have blocked compensatory mechanisms that normally protect kidney perfusion during hypovolemia, dramatically increasing AKI risk. 1

• Two case reports demonstrate complete acute renal failure in patients with mild baseline kidney impairment who developed dehydration while on RAAS inhibitors, with full recovery only after rehydration and medication discontinuation. 6
• The mechanism involves blockade of normal protective pathways that maintain kidney perfusion during hypovolemia. 6

Vulnerable Populations

• Elderly patients with atherosclerosis or heart failure 6
• Patients with pre-existing chronic kidney disease 6
• COVID-19 patients who commonly present with dehydration and experience increased insensible fluid losses from fever and tachypnea 1
• Children with diabetic ketoacidosis, where 19% meet KDIGO criteria for AKI on admission 3

Prevention and Management Strategy

Immediate Medication Management

Stop the following medications immediately during dehydration: 1

• Metformin - risk of lactic acidosis
• SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin) - risk of dehydration, diabetic ketoacidosis, and AKI
• RAAS inhibitors and diuretics - temporary discontinuation often necessary 6
• NSAIDs - block protective renal mechanisms 2

Hydration Approach

For patients without shock, confusion, or swallowing difficulty, initiate oral rehydration immediately with any available rehydration drink or potable water. 1 For exertional dehydration, 4-9% carbohydrate-electrolyte drinks are preferred over plain water. 1

For intravenous hydration: 1, 7

• Use isotonic crystalloids, preferably balanced solutions (lactated Ringer's) rather than 0.9% saline to prevent metabolic acidosis and hyperchloremia 7
• Base fluid administration on repeated assessment of fluid status and dynamic tests of fluid responsiveness, not empiric boluses 1
• Avoid synthetic colloids due to increased kidney dysfunction and mortality risk 7

Critical Monitoring Requirements

Measure serum urea, creatinine, and electrolytes at least every 48 hours or more frequently if clinically indicated. 1, 7 Assess fluid status by examining: 1

• Peripheral perfusion and capillary refill
• Pulse rate and blood pressure
• Postural hypotension
• Urine output (oliguria is a warning sign but has multiple etiologies) 2

Common Pitfalls to Avoid

Do not assume all oliguria indicates hypovolemia requiring fluid boluses - oliguria has multiple etiologies beyond hypovolemia, and inappropriate fluid administration can create a vicious cycle of fluid overload that worsens kidney function. 2, 1

Do not use the outdated term "pre-renal AKI" as it is often misinterpreted as "hypovolemic" and encourages indiscriminate fluid administration. 2

Avoid fluid over-resuscitation - in pediatric DKA, fluid over-resuscitation and hyperchloremia are associated with delayed kidney recovery (p < 0.001), representing potentially modifiable clinical variables. 3

Do not continue nephrotoxic medications during dehydration without careful risk-benefit assessment and monitoring. 2 Furosemide specifically can cause acute urinary retention and worsen dehydration, with reversible elevations of BUN associated with dehydration that should be avoided, particularly in patients with renal insufficiency. 8

Long-Term Implications

Recurrent dehydration may lead to chronic kidney disease through sustained activation of injury pathways, as evidenced by the epidemic of CKD in Central America where recurrent heat-associated dehydration is the major risk factor. 5 This emphasizes that dehydration-induced AKI is not always fully reversible and can have permanent consequences.