Acute Kidney Injury

Use KDIGO criteria: increase in serum creatinine of at least 0.3 mg/dL within 48 hours; increase to at least 1.5 times baseline within 7 days; or urine output below 0.5 mL/kg/h for at least 6 hours. AKI may be nonoliguric. Historical creatinine is essential; when no baseline exists, repeat testing and the clinical context are central to distinguishing AKI from chronic kidney disease. BMJ+1BMJAcute kidney injury - Diagnosis recommendations | BMJ Best PracticeScienceDirectKDOQI US Commentary on the 2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury

Assign the higher stage reached by serum creatinine or urine output. Worsening stage predicts greater mortality and kidney replacement therapy requirement. Creatinine may rise approximately 24 hours after injury, whereas oliguria can be an earlier but less reliably captured signal. BMJBMJAcute kidney injury - Diagnosis recommendations | BMJ Best Practice

Immediately assess hemodynamics, volume status, infection, exposure to nephrotoxins, medication changes, surgical or vascular events, rhabdomyolysis, and symptoms of urinary retention or upper-tract obstruction. Common drivers are sepsis, hypovolemia or hypotension, and nephrotoxins; prolonged hypoperfusion can progress to acute tubular injury. BMJ+1BMJAcute kidney injury - Diagnosis recommendations | BMJ Best PracticeBMJAcute kidney injury - Symptoms, diagnosis and treatment | BMJ Best Practice

Order serum creatinine, electrolytes including potassium, bicarbonate, urea, complete blood count, and targeted studies driven by the phenotype. Obtain an ECG promptly for substantial hyperkalemia or suspected electrical effects. If infection is possible, obtain cultures and initiate source-directed sepsis care without delaying stabilization. BMJ+1BMJAcute kidney injury - Management recommendationsBMJAcute kidney injury - Diagnosis recommendations | BMJ Best Practice

Perform urine dipstick testing for blood, protein, leukocyte esterase, nitrites, glucose, and specific gravity. Blood plus protein without urinary tract infection or catheter trauma should prompt concern for glomerular disease and early nephrology involvement; send urine culture when infection is plausible. Fresh urine microscopy can add value: granular casts support tubular injury, red-cell casts suggest glomerulonephritis or vasculitis, and oxalate crystals suggest ethylene glycol exposure. BMJBMJAcute kidney injury - Diagnosis recommendations | BMJ Best Practice

Supportive management is cause-directed: correct hypovolemia, treat sepsis, relieve obstruction, avoid recurrent kidney insults, and monitor volume status and electrolytes closely. Both under-resuscitation and positive fluid balance are harmful; fluid orders should be reassessed frequently rather than continued automatically. BMJ+1BMJAcute kidney injury - Management recommendationsThe LancetAcute kidney injury

For clinically hypovolemic adults, crystalloid is preferred. A practical approach is an initial 500 mL bolus over 15 minutes, followed by reassessment of blood pressure, pulse, capillary refill, jugular venous pressure, pulmonary findings, and urine output; smaller boluses may be appropriate in heart failure. Balanced crystalloids are generally preferred, although normal saline may be selected when hyperkalemia is confirmed or strongly suspected. BMJBMJAcute kidney injury - Management recommendations

Persistent severe hypotension after adequate volume resuscitation warrants critical care escalation and vasopressor support with continuous hemodynamic monitoring. A mean arterial pressure of at least 65 mm Hg is a reasonable initial target, individualized to baseline blood pressure and clinical context; norepinephrine is the usual first vasopressor. Do not use low-dose dopamine to treat AKI. BMJBMJAcute kidney injury - Management recommendations

Stop avoidable nephrotoxins and reassess all medications for renal clearance, current kidney function, and evolving volume status. NSAIDs, aminoglycosides, and iodinated contrast are common nephrotoxic exposures. In hypotension or dehydration, ACE inhibitors, angiotensin receptor blockers, diuretics, and other antihypertensives may worsen reduced filtration reserve and often require temporary withholding. BMJ+1BMJAcute kidney injury - Management recommendationsBMJAcute kidney injury - Diagnosis recommendations | BMJ Best Practice

Dose adjustment is required for drugs cleared by the kidneys; clinically important examples include insulin, opioids, digoxin, and gabapentin. Medication reconciliation should include over-the-counter agents, supplements, and recent antimicrobials. At discharge, document which chronic therapies were withheld, a plan for reintroduction, and follow-up creatinine and potassium testing. BMJBMJAcute kidney injury - Management recommendations

Use loop diuretics only to manage clear volume overload, including pulmonary edema, and not to convert oliguric AKI to nonoliguric AKI or accelerate recovery. Stop if there is no response and do not allow diuretic trials to delay definitive kidney support when overload is refractory. BMJBMJAcute kidney injury - Management recommendations

Hyperkalemia requires ECG assessment and cardiac monitoring when clinically significant. Immediate intravenous calcium provides membrane stabilization when severe hyperkalemia or ECG changes are present; insulin with glucose shifts potassium intracellularly, and nebulized beta-agonist can be adjunctive. These measures do not remove potassium; identify and reverse the cause, stop potassium-raising drugs, and arrange dialysis when hyperkalemia is refractory. BMJBMJAcute kidney injury - Management recommendations

Consider intravenous sodium bicarbonate for severe metabolic acidosis only with expert supervision because sodium load, volume overload, hypernatremia, and ionized hypocalcemia can complicate therapy. Refractory acidosis, especially with volume overload, should prompt kidney replacement therapy rather than repeated bicarbonate administration. BMJBMJAcute kidney injury - Management recommendations

Do not initiate kidney replacement therapy from an isolated creatinine, urea, or potassium value. The decision integrates biochemical trajectory, urine output, catabolic burden, fluid needs, reversible cause, organ dysfunction, and patient-centered goals. BMJBMJAcute kidney injury - Management recommendations

Urgently involve nephrology for stage 3 AKI, uncertain cause, suspected glomerulonephritis, vasculitis, tubulointerstitial nephritis, myeloma, transplant recipients, advanced pre-existing CKD, refractory complications, or anticipated kidney replacement therapy. Immediate critical care and nephrology involvement is appropriate for severe metabolic complications, hemodynamic instability, or multiorgan failure. BMJBMJAcute kidney injury - Management recommendations

Recovery should not be assumed from hospital discharge creatinine alone. AKI is associated with later CKD and cardiovascular morbidity; intensity of follow-up should reflect baseline kidney function, AKI severity, duration, recovery, proteinuria, and dialysis exposure. Health systems should measure whether indicated patients receive laboratory and clinical follow-up after hospitalization. Nature+1NatureAcute kidney injury | Nature Reviews Disease PrimersScienceDirectQuality of Care for Acute Kidney Disease: Current Knowledge Gaps and Future Directions

At discharge, communicate the AKI episode, likely cause, peak stage, discharge creatinine, medication changes, and a plan for kidney function and potassium reassessment. Current guidance supports kidney-function monitoring within 3 months after AKI, with longer surveillance for CKD risk. Oxford AcademicOxford AcademicTop ten tips to manage patients after acute kidney injury

In BigpAK-2, adults undergoing major surgery with clinical AKI risk factors and postoperative urinary TIMP-2 × IGFBP7 of at least 0.3 (ng/mL)²/1000 were randomized to usual care or a KDIGO-based prevention bundle. The bundle included advanced hemodynamic monitoring, individualized fluid responsiveness assessment, MAP target of at least 65 mm Hg, nephrotoxin and contrast avoidance, temporary ACE inhibitor or ARB interruption, and hyperglycemia prevention. The LancetThe LancetA preventive care strategy to reduce moderate or severe acute kidney injury after major surgery (BigpAK-2); a multinational, randomised clinical trial

Moderate or severe AKI within 72 hours occurred in 14.4% with the bundle versus 22.3% with usual care, with an odds ratio of 0.57 and number needed to treat of 12. The trial did not show differences in 90-day major adverse kidney events, dialysis, or mortality, and its population excluded advanced CKD and pre-existing AKI. This strategy is therefore best viewed as targeted perioperative risk management in settings with assay availability and implementation capacity. The LancetThe LancetA preventive care strategy to reduce moderate or severe acute kidney injury after major surgery (BigpAK-2); a multinational, randomised clinical trial