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Nephrology›Condition·Updated Jul 11, 2026·v1

Acute Kidney Injury

Acute kidney injury is a common, high-mortality syndrome defined by KDIGO criteria (SCr rise ≥0.3 mg/dL in 48 h, ≥1.5× baseline in 7 d, or UO <0.5 mL/kg/h for ≥6 h). Management focuses on hemodynamic optimization with balanced crystalloids, avoidance of nephrotoxins, electrolyte correction, and delayed initiation of RRT (safe in ~40% of patients). Long-term, all survivors require structured nephroprotection with RAS blockade and SGLT2 inhibitors to prevent CKD progression.

High Evidence647 references·2,663 words·11 min read·v1
Acute Kidney InjuryNephrologyAcute Renal FailureKDIGORenal Replacement TherapyAcute Tubular NecrosisSepsis-Associated AKIContrast NephropathyDrug-Induced Nephritis

Quick Reference

RxDrug of choiceFor acute volume resuscitation: balanced crystalloids (lactated Ringer's, Plasma-Lyte). For life-threatening hyperkalemia: calcium gluconate 1 g IV + insulin 10 U + dextrose 25 g IV + albuterol 10-20 mg. For long-term nephroprotection: [[ACE inhibitor]]/[[ARB]] (lisinopril 5-40 mg/day or losartan 25-100 mg/day) + [[SGLT2 inhibitor]] ([[empagliflozin]] 10 mg/day or [[dapagliflozin]] 10 mg/day) ± [[finerenone]] 10-20 mg/day in diabetic CKD.
AltAlternativesFor RRT modality: CRRT for shock, IHD for stable patients, PD for low-resource settings. For ICI-AKI: prednisone 0.5-1 mg/kg/day. For metabolic acidosis: sodium bicarbonate 50-100 mEq (reserved for pH<7.0 or AKIN 2-3). For sedation in S-AKI: consider dexmedetomidine.
⊘AvoidHydroxyethyl starches, NSAIDs (in CKD or volume depletion), iodinated contrast without appropriate prophylaxis, ACEi/ARB during acute hemodynamic instability, non-dihydropyridine CCBs (verapamil, diltiazem) in heart failure with AKI, and routine loop diuretics without fluid overload.
DxTest of choiceUrine microscopy with sediment examination (muddy brown granular casts for ATN, dysmorphic RBCs for GN) and renal ultrasound to exclude obstruction. FENa (or FEUrea if on diuretics) to differentiate prerenal vs intrinsic.
ScKey scoreKDIGO staging (creatinine and urine output). Mehran risk score for contrast-associated AKI. SPARK index for postoperative AKI.
→When to referAKI Stage ≥2, need for RRT, uncertain etiology, suspected glomerulonephritis or systemic vasculitis, AKI not improving after 1-2 weeks, all AKI survivors for structured post-discharge follow-up.
AKI is a high-mortality syndrome affecting >10% of inpatients. Diagnose with KDIGO criteria; manage with balanced crystalloids, avoidance of nephrotoxins, electrolyte correction, and delayed RRT strategy (start for AEIOU criteria or oliguria >72h). Long-term, all survivors require RAS blockade + SGLT2i ± finerenone to prevent CKD progression.
Acute kidney injury (AKI) is a clinical syndrome defined by an abrupt decline in kidney function, quantified by a rise in serum creatinine or fall in urine output per KDIGO criteria [2]. It affects up to 20% of inpatients and over 50% of ICU patients, independently doubling short-term mortality even at Stage 1 [2][3]. AKI accelerates progression to chronic kidney disease and end-stage kidney disease, making standardized detection and management a global priority [41][60].

Overview and Recommendations

Background

  • •Acute kidney injury (AKI) is a clinical syndrome defined by an abrupt decline in excretory function, quantified by the 2012 criteria: a rise in serum creatinine (SCr) ≥0.3 mg/dL within 48 hours, an increase ≥1.5× baseline within 7 days, or a fall in urine output (UO) <0.5 mL/kg/h for ≥6 hours. Three severity stages exist, with Stage 1 representing the threshold and Stage 3 representing a ≥200 % SCr rise or initiation of renal replacement therapy (RRT). The pathophysiology is categorized into prerenal (renal hypoperfusion with intact parenchyma), intrinsic renal (direct injury to tubules, glomeruli, interstitium, or vasculature), and postrenal (urinary tract obstruction).
  • •AKI is a global public health priority. It affects approximately 10-15 % of all hospitalized patients and over 50 % of ICU patients, with 1-2 million hospitalizations annually in China alone. Even Stage 1 AKI independently doubles short-term mortality. Survivors face a significantly increased risk of chronic kidney disease (CKD; HR 2.67), end-stage kidney disease (HR 4.81), and death (HR 1.80). The syndrome is not self-limited, maladaptive repair drives fibrosis and the AKI-to-CKD transition, making structured follow-up mandatory.
  • •The most common intrinsic form is (ATN), often due to ischemia, sepsis, or nephrotoxins. Sepsis-associated AKI (S-AKI) is the leading cause in critical illness, involving microvascular dysfunction, inflammation, and metabolic reprogramming. Drug-induced AKI is frequent, especially from combinations like plus , , aminoglycosides, and iodinated contrast. Postrenal AKI (5-10 % of cases) is usually reversible if obstruction is relieved within 24-48 hours.
  • •The pathogenesis converges on mitochondrial failure, cell death (ferroptosis, apoptosis, necroptosis), and dysregulated inflammation. In ischemia-reperfusion, proximal tubular cells shift to anaerobic metabolism, ATP depletion disables ion pumps, and reperfusion generates reactive oxygen species that trigger ferroptosis. In S-AKI, preserved global renal blood flow coexists with microvascular shunting and metabolic reprogramming. Maladaptive repair, G2/M cell-cycle arrest in tubular cells, promotes a pro-fibrotic secretory phenotype (TGF-β, CTGF), pericyte-to-myofibroblast transition, and interstitial fibrosis.
  • •Key susceptibility factors include pre-existing CKD (HR 8.8 for CKD after AKI), diabetes (HR 1.49), hypertension, aging, and nephrotoxic drug combinations. Avoidance of nephrotoxic pairs (e.g., vancomycin + piperacillin-tazobactam) and hemodynamic optimization are the most effective prevention strategies. The Four Pillars of long-term nephroprotection, RAS blockade, SGLT2 inhibitors, nonsteroidal MRAs, and GLP-1 receptor agonists, have replaced the legacy approach of watching and waiting.

Evaluation

  • •Suspect AKI in any hospitalized patient with oliguria (UO <0.5 mL/kg/h for ≥6 hours), unexplained rise in SCr, or predisposing conditions (sepsis, surgery, contrast exposure, nephrotoxic medications). Confirm AKI using criteria: SCr increase ≥0.3 mg/dL within 48 hours, ≥1.5× baseline within 7 days, or UO <0.5 mL/kg/h for ≥6 hours.
  • •Ask about symptoms: reduced urine volume (oliguria or anuria), foamy or tea-colored urine (suggests glomerulonephritis), dark brown urine (suggests pigment nephropathy from or hemolysis), flank or suprapubic pain (obstruction), and constitutional symptoms (fatigue, anorexia, nausea). Probe for fever, rash, arthralgias (acute interstitial nephritis) and review all medications: NSAIDs, ± , proton pump inhibitors, contrast, herbal remedies.
  • •Examine volume status: orthostatic hypotension indicates prerenal cause; peripheral edema and jugular venous distention suggest volume overload from intrinsic AKI or heart failure; palpable bladder suggests obstruction. Look for asterixis (liver flap) as a sign of uremia. Assess respiratory rate and oxygen saturation for pulmonary edema.
  • •Order a renal ultrasound immediately to exclude obstructive uropathy, hydronephrosis, stones, or masses. In critically ill patients, point-of-care ultrasound also assesses volume status and cardiac function. Avoid contrast-enhanced studies unless absolutely indicated.
  • •Perform urine microscopy on a fresh, clean-catch sample. Muddy brown granular casts and renal tubular epithelial cell casts are pathognomonic for (ATN). White blood cell casts and eosinophiluria suggest acute interstitial nephritis (AIN). Dysmorphic red blood cells and red cell casts indicate glomerulonephritis. Acellular sediment with hyaline casts suggests prerenal azotemia.
  • •Calculate the fractional excretion of sodium (FENa): FENa = (U[Na] × P[Cr]) / (P[Na] × U[Cr]) × 100. FENa <1 % has 90 % sensitivity and 82 % specificity for prerenal AKI. FENa >2 % suggests intrinsic ATN. In patients on diuretics, use FEUrea <35 % for prerenal (less affected by loop diuretics).
  • •Order serum chemistry: SCr, BUN, electrolytes (K+, Na+, Cl-, HCO3-), calcium, phosphate, uric acid, creatine kinase (if rhabdomyolysis suspected). Complete blood count with smear to look for schistocytes (thrombotic microangiopathy). Check LDH, haptoglobin, and ADAMTS13 if TMA is considered.
  • •Consider novel biomarkers: neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin C can detect tubular injury earlier than creatinine, but they are not yet incorporated into standard diagnostic criteria. Cystatin C-based eGFR may identify occult kidney dysfunction (eGFRcys >27 % lower than eGFRcr confers HR 2.6 for subsequent AKI).
  • •If cause remains unclear after urine sediment and FENa, order serologies: complement C3/C4, ANA, ANCA, anti-GBM, anti-streptolysin O, hepatitis B and C, HIV, serum and urine protein electrophoresis with free light chains, and cryoglobulins.
  • •Perform a renal biopsy if the cause remains uncertain, if glomerulonephritis or systemic vasculitis is suspected, or if AKI does not improve after 1-2 weeks of supportive care. Biopsy distinguishes ATN (tubular injury), AIN (interstitial inflammation), glomerulonephritis (crescents, endocapillary proliferation), TMA, or crystal nephropathy.
  • •Use validated risk scores for specific settings: the Mehran score for contrast-associated AKI after PCI (AUC ≈0.80); the SPARK index for postoperative AKI in noncardiac surgery (c-statistic 0.80). Machine-learning models show higher discrimination (pooled AUC 0.82) but are not yet widely implemented.
  • •Identify red flags requiring urgent RRT evaluation: respiratory distress with SpO₂ <90 % despite high-flow oxygen (consider intubation if FVC <15 mL/kg), hyperkalemia >6.5 mmol/L with ECG changes (peaked T waves, widened QRS), severe metabolic acidosis pH <7.15, uremic pericarditis (pericardial rub, chest pain), rapidly rising creatinine >3 mg/dL over 24-48 hours, or anuria >12 hours.

Management

  • •Initiate hemodynamic optimization: correct hypovolemia with balanced crystalloids ( or Plasma-Lyte) rather than 0.9 % saline to reduce the risk of hyperchloremic metabolic acidosis and subsequent AKI. Avoid hydroxyethyl starches, they increase AKI and RRT need.
  • •Once euvolemia is achieved, restrict daily fluid balance to ≤0.5 L positive after the first 24-48 hours. Use 20-80 mg IV (or continuous infusion 5-20 mg/h) only for pulmonary edema, do NOT use diuretics to convert oliguric to non-oliguric AKI. Early diuretic use in Stage 3 AKI is associated with higher mortality (HR 1.42).
  • •Manage life-threatening hyperkalemia (K⁺ >6.5 mmol/L or with ECG changes): immediately administer calcium gluconate 1 g IV over 2-3 minutes for cardiac membrane stabilization. Then give regular insulin 10 U IV plus 50 mL of 50 % dextrose, followed by nebulized albuterol 10-20 mg. Consider sodium bicarbonate 50 mEq IV if metabolic acidosis coexists. Monitor blood glucose hourly.
  • •For severe metabolic acidosis (pH <7.15-7.20): administer IV sodium bicarbonate 1-2 ampules (50-100 mEq) over 30-60 minutes, but reserve for pH <7.0 or for AKI Stage 2-3 (BICAR-ICU subgroup benefit). Routine bicarbonate use does not improve survival and may worsen intracellular acidosis.
  • •Discontinue all nephrotoxic medications: NSAIDs, aminoglycosides, IV contrast (if feasible), ACE inhibitors/ARBs during hemodynamic instability, and proton pump inhibitors (risk of AIN). Dose-adjust all renally cleared drugs to estimated GFR.
  • •For sepsis-associated AKI, follow Surviving Sepsis guidelines: early broad-spectrum antibiotics, norepinephrine as first-line vasopressor, and goal-directed resuscitation. Consider as the preferred sedative, a meta-analysis found it significantly reduced AKI incidence (P=0.004) compared with other sedatives.
  • •Initiate renal replacement therapy (RRT) emergently if any AEIOU criterion is present: Acidosis (pH <7.15 refractory), Electrolyte disturbance (K⁺ >6.5 refractory), Intoxication (dialyzable toxin), Overload (diuretic-resistant pulmonary edema), Uremia (pericarditis, encephalopathy, or bleeding).
  • •If no AEIOU criteria, adopt a delayed RRT strategy: monitor kidney function and volume status; initiate RRT if oliguria persists >72 hours or BUN exceeds 112 mg/dL. This approach avoids RRT in ~40 % of patients without increasing mortality (STARRT-AKI, AKIKI). Do NOT initiate RRT early without indications, accelerated strategies increase RRT dependence at 90 days (10.4 % vs 6.0 %). Do NOT delay beyond BUN >140 mg/dL (AKIKI 2 showed harm).
  • •Choose RRT modality based on hemodynamic stability: continuous RRT (CRRT) for unstable patients; intermittent hemodialysis (IHD) for stable patients; peritoneal dialysis in resource-limited settings. Deliver a dose of 20-25 mL/kg/h, higher intensity does not improve survival. Anticoagulate with regional citrate for CRRT if feasible (longer filter life, potential survival benefit in S-AKI).
  • •After achieving hemodynamic stability and resolving acute phase, initiate long-term nephroprotection. Start an (e.g., lisinopril 5-10 mg daily) or (e.g., losartan 25-50 mg daily) in all AKI survivors with UACR ≥30 mg/g or hypertension. Titrate to maximally tolerated dose. Expect a small haemodynamic SCr rise (≤30 %), do not discontinue. Monitor K⁺ and Cr at 1-2 weeks.
  • •Add an once eGFR ≥20 mL/min/1.73 m²: 10 mg daily or 10 mg daily. This reduces kidney disease progression by 37 % and AKI by 23 % (meta-analysis). Continue until dialysis or transplant. No dose adjustment required.
  • •In patients with diabetic kidney disease (eGFR 30-90, UACR 100-5000), add 10-20 mg daily (nonsteroidal MRA). The CONFIDENCE trial showed that adding finerenone to empagliflozin plus RAS blockade reduced UACR by 29 % more than either agent alone. Monitor K⁺.
  • •Consider a (e.g., 0.6-1.8 mg SC daily) in patients with obesity or atherosclerotic cardiovascular disease and persistent albuminuria despite RAS blockade, SGLT2i, and finerenone. Liraglutide reduced the composite renal outcome by 22 % (LEADER trial).
  • •For immune checkpoint inhibitor-associated AKI (ICI-AKI): hold the ICI, discontinue PPI/NSAIDs, and start 0.5-1 mg/kg/day tapered over 4-6 weeks. Renal recovery occurs in ~85 % of treated patients. Rechallenge with ICI after resolution is feasible but carries a 23 % risk of recurrence.
  • •Refer to nephrology for: AKI Stage ≥2, need for RRT, uncertain etiology, suspected glomerulonephritis or systemic vasculitis, AKI not improving after 1-2 weeks of supportive care, and all AKI survivors for post-discharge follow-up within 30 days (associated with improved survival).
  • •At discharge, measure eGFR and UACR at 3 months, then at least annually. Educate patients to avoid over-the-counter NSAIDs when febrile or volume-depleted, maintain hydration during intercurrent illness, and seek medical attention for oliguria or weight gain. Aggressively control blood pressure to <120 mmHg in high-risk patients (SPRINT).
  • •For acute tubulointerstitial nephritis (drug-induced, non-ICI): remove the offending drug. Consider prednisone 0.5-1 mg/kg/day started within 7 days of diagnosis to improve renal recovery. For lupus nephritis, use induction with or plus corticosteroids.
  • •Do NOT give routine iron chelation or mesenchymal stem cells for AKI, phase 2 trials showed no benefit. Do NOT restrict protein intake to <0.8 g/kg/day in the post-AKI period, higher protein (≥2.2 g/kg/day) in critically ill patients with AKI worsened outcomes. Do NOT use isotonic sodium bicarbonate or acetylcysteine for contrast-AKI prevention (PRESERVE trial showed no benefit).

Board Review — High Yield

  • •Muddy brown granular casts, Pathognomonic for acute tubular necrosis on urine sediment.
  • •FENa <1%, Indicates prerenal AKI (sensitivity 90%, specificity 82%). Use FEUrea <35% if patient on diuretics.
  • •KDIGO Stage 1, SCr rise ≥0.3 mg/dL in 48 h or ≥1.5× baseline in 7 d; independently doubles mortality.
  • •STARRT-AKI, Delayed RRT (wait for conventional indications or oliguria >72h) not inferior to early; ~40% avoid RRT.
  • •SGLT2 inhibitors, Reduce AKI risk by 23% and CKD progression by 37% (empagliflozin 10 mg, dapagliflozin 10 mg).
  • •Hyperkalemia management, Calcium gluconate (cardiac protection) → insulin+glucose → albuterol → consider bicarbonate.
  • •AEIOU mnemonic, Indications for emergent RRT: Acidosis, Electrolytes, Intoxication, Overload, Uremia.
  • •Balanced crystalloids preferred, 0.9% saline increases risk of hyperchloremic metabolic acidosis and AKI.
  • •BigpAK-2 trial, Biomarker-guided care bundle (hemodynamic monitoring, avoid nephrotoxins, normoglycemia) reduced moderate-to-severe AKI by 43% (NNT=12).
  • •PRESERVE trial, No benefit for sodium bicarbonate or acetylcysteine in preventing contrast-associated AKI.

Deep Dive — Evidence Details

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