Quick Recap
Renal System, Protocol 1/7.
1. Definition — KDIGO Staging
AKI = rapid decline in renal function with decreased urine output and accumulation of nitrogenous waste. Incidence in ICU patients ~57% in one multicenter study, with sepsis the attributed cause in ~41% — AKI is common and an independent risk factor for increased in-hospital and long-term mortality, not merely a marker of severity.
KDIGO Staging (only ONE criterion — creatinine OR urine output — needs to be met to qualify for a stage):
Stage | Serum Creatinine | Urine Output |
1 | 1.5-1.9x baseline OR >=0.3 mg/dL increase | <0.5 mL/kg/h for 6-12h |
2 | 2.0-2.9x baseline | <0.5 mL/kg/h for >=12h |
3 | 3.0x baseline OR sCr >=4.0 mg/dL OR RRT initiation | <0.3 mL/kg/h for >=24h OR anuria >=12h |
Timeframe nuance: the 0.3 mg/dL absolute increase is assessed within 48h; the 1.5x-baseline relative increase is assessed within a 7-day window (updated from earlier criteria).
Urine output classification: nonoliguric (>400 mL/day), oliguric (<400 mL/day), anuric (<100 mL/day) — lower urine output correlates with more severe injury and worse outcomes; prognosis is also worse if RRT is required.
2. Etiology Framework — Prerenal, Intrinsic, Postrenal
This three-way classification is the central organizing principle for AKI workup and should drive the differential before any specific therapy is chosen.
Prerenal AKI
Renal parenchyma is preserved — decreased GFR is a PHYSIOLOGIC response to hypoperfusion (true or effective volume depletion). Causes: true volume depletion (hemorrhage, GI losses); decreased effective volume (decompensated HF/liver failure, nephrotic syndrome, anaphylaxis); renal vasoconstriction (hypercalcemia, calcineurin inhibitors); impaired autoregulation (NSAIDs, ACE-I/ARB); sustained IAP >20mmHg (abdominal compartment syndrome — see dedicated protocol).
Diagnosis: history of volume loss/poor intake, tachycardia/hypotension, dry mucous membranes, decreased skin turgor. Urine sodium <20 mmol/L, urine osmolality >500 mOsm/kg, BLAND urine sediment (no cells/crystals/casts) — reflects appropriate tubular sodium-avid response to hypoperfusion.
Management: rapidly correct the hypoperfusion cause — prolonged ischemia converts prerenal AKI into intrinsic tubular injury (ATN), so speed matters. Discontinue offending drugs immediately.
Intrinsic AKI
Injury AT the level of kidney parenchyma — subclassified as tubular, glomerular, vascular, or interstitial, distinguishable largely via urine sediment analysis.
Acute Tubular Necrosis (ATN) accounts for up to 90% of intrinsic AKI in critical care — from prolonged prerenal ischemia or nephrotoxins (endogenous: myoglobin; exogenous: aminoglycosides, certain chemotherapy). In the ICU, nephrotoxic insults are usually simultaneous/sequential — no single precipitating factor may be identifiable, making thorough history/medication review essential. Urine sediment: renal tubular epithelial cells (RTECs) and MUDDY BROWN GRANULAR CASTS in the majority — glomeruli/interstitium typically spared, so heavy proteinuria/hematuria are ABSENT (their presence should prompt reconsidering the diagnosis). No specific reversal therapy exists once ATN has occurred — management is supportive (RRT if needed), avoiding further nephrotoxic insults, appropriate drug dosing, ensuring adequate perfusion. ~75% of patients with previously normal baseline function recover renal function, if they survive the hospitalization — an important prognostic point for family counseling, though recovery can take days to months.
Glomerular/microvascular causes: less common in acute ICU settings. Suspect vasculitis with constitutional symptoms + active urinary sediment. Pulmonary-renal syndromes (GPA, Goodpasture disease) should be considered with SIMULTANEOUS respiratory + renal dysfunction — universally fatal if not recognized/treated promptly (see Diffuse Alveolar Hemorrhage protocol, Respiratory System, for full detail). Renal biopsy may be needed for definitive diagnosis; removal of the offending agent/treatment of underlying infection is mainstay therapy; corticosteroid role remains controversial, with cyclophosphamide/mycophenolate/other immunosuppressants used in steroid non-responders after 2-3 weeks.
Postrenal AKI
A VERY RARE cause of AKI in the ICU — impediment to urine outflow (structural/functional). Obstruction can be unilateral/bilateral, acute/chronic, partial/complete, intrarenal (crystals, casts) or extrarenal. Increased pressure conveyed proximally -> rising tubular pressure -> decreased glomerular hydraulic gradient -> decreased GFR, plus tubular dysfunction (decreased concentrating ability, distal RTA pattern). Renal ultrasound is the key screening test given the rarity but importance of not missing an easily-reversible obstructive cause.
3. Renal Failure Indices — Prerenal vs Intrinsic (Tubulointerstitial) Discrimination
Parameter | Prerenal | Renal (tubulointerstitial) |
Urine sediment | Bland | Broad, brownish granular casts, WBC casts |
Urine sodium | <10 mEq/L (or <20) | >20 mEq/L (or >20) |
Urine osmolality | >500 mOsm/L | <350 mOsm/L |
Fractional excretion of urea | <35% | >35% |
Fractional excretion of Na (FENa) | <1% | >2% |
Urine specific gravity | >1.020 | <1.010 |
FENa = (urine Na x plasma creatinine) / (plasma Na x urine creatinine) x 100 — fractional excretion of UREA is more reliable than FENa in patients recently exposed to diuretics (FENa becomes unreliable once diuretics have forced natriuresis regardless of the underlying volume status).
4. Hepatorenal Syndrome (HRS-AKI) — Cross-Reference Detail
Diagnostic criteria: cirrhosis with ascites; worsening renal function over days-weeks with sCr >=1.5 mg/dL; absence of intrinsic renal disease (proteinuria >500mg/day, hematuria >50 RBC/hpf, or structural abnormality on imaging all argue against HRS); absence of shock; absence of concurrent/recent nephrotoxic medication use; NO improvement after diuretic withdrawal + albumin expansion (1 g/kg/day, max 100g/day) for at least 2 days.
Subtypes: Type 1 (rapidly progressive, sCr doubles to >2.5 mg/dL in <2 weeks) vs Type 2 (moderate, slowly progressive, sCr 1.5-2.5 mg/dL, typically with refractory ascites).
Treatment: increase intravascular volume with albumin; increase MAP by 10mmHg with vasopressors (midodrine PO or IV norepinephrine); decrease splanchnic vasodilation with octreotide; terlipressin (synthetic vasopressin analog, splanchnic vasoconstrictor, US-approved 2022) has demonstrated renal function improvement — watch closely for respiratory failure, particularly in volume-overloaded patients. Liver transplantation is the only definitive treatment. RRT should primarily be reserved for patients whose liver function is expected to recover OR who are transplant candidates — not a default therapy in HRS without a clear endpoint. (See also Acute-on-Chronic Liver Failure protocol, GI & Hepatology System, for the fuller HRS-AKI staging/management algorithm.)
5. Cardiorenal Syndrome (Type 1) — Brief Note
Most frequently encountered cardiorenal syndrome type in the ICU: acute renal function alteration in the setting of congestive heart failure. Pathophysiology centers on RENAL VENOUS CONGESTION compromising GFR (not just reduced forward flow/cardiac output) — treatment should therefore target DECONGESTION (diuresis) rather than defaulting to fluid administration for "AKI," a genuine and common bedside trap. See Acute Heart Failure protocol (Cardiovascular System) for full decongestion strategy.
6. Fluid Resuscitation Choice — Nuanced, Evidence-Updated Guidance
Balanced crystalloid solutions offer NO significant clinical advantage over 0.9% saline per two large multicenter RCTs (BASICS and PLUS trials) — an important update against the blanket "always use balanced solutions" teaching that has become common.
Balanced solutions should be AVOIDED in traumatic brain injury (see TBI protocol, Neurology System).
Lactated Ringer's suggested for its anti-inflammatory effect in acute pancreatitis (see Acute Pancreatitis protocol).
Balanced solutions are safe/effective in hyperkalemia (despite containing some potassium, ~4 mEq) — 0.9% saline's acidity (pH 5.4) can cause hyperchloremic non-anion-gap acidosis, which itself drives extracellular potassium shift and can WORSEN hyperkalemia — an important, somewhat counterintuitive point given the reflexive instinct to avoid potassium-containing fluids in hyperkalemia.
Colloids: SAFE trial showed no difference between 4% albumin and saline for general resuscitation. Avoid albumin in head injury (see Acute Liver Failure/general neurotrauma principles). Evidence-based albumin indications remain limited to: second-line septic shock therapy (combined with crystalloid), HRS diagnosis/treatment, SBP treatment, and post-large-volume-paracentesis resuscitation.
Starch-containing solutions are associated with INCREASED MORTALITY and should be AVOIDED.
Hemorrhage-driven prerenal AKI: blood products in a balanced ratio, or whole blood (see Hypovolemic Shock protocol).
7. Investigations
Urinalysis with microscopy (sediment examination is highly valuable for classification), renal function panel with electrolytes, urine sodium, urine osmolality, urine specific gravity, ABG, ECG (hyperkalemia screening), renal ultrasound (postrenal obstruction screen), drug level monitoring (aminoglycosides, vancomycin, other nephrotoxins as applicable). NephroCheck (urinary biomarker test, TIMP-2 x IGFBP7): indicated in ICU patients >=21 years with cardiovascular/respiratory compromise in the prior 24h; positive result (>0.3) predicts high risk for moderate-severe AKI within 12 hours, prompting nephrology consultation and preventive strategy implementation (volume optimization, nephrotoxin avoidance) BEFORE creatinine rise is even apparent — a genuinely proactive, pre-emptive tool rather than a purely diagnostic one.
8. General Management Principles
Avoid nephrotoxic drugs; maintain renal perfusion with judicious fluids +/- vasopressors/inotropes (avoiding both under- and over-resuscitation, the latter risking further ischemic/congestive injury); adjust drug dosing to eCCL (assume GFR <10 while on RRT for dosing purposes); monitor/manage hyperkalemia medically (see Hyperkalemia protocol); severe acidosis can be treated with IV sodium bicarbonate with vigilance for fluid overload and hypocalcemia; early nutritional support (high-calorie enteral diet with adequate protein — do NOT restrict protein, consistent with the principle established across the Liver Failure protocols).
Monitoring: hourly I/O, daily weight, cumulative fluid overload calculation [(total fluid in − total fluid out in liters) / ICU admission weight in kg x 100%], continuous hemodynamic monitoring, electrolytes every 6h during active management, daily renal function panel.
9. Organ Support
See dedicated CRRT Indications protocol for full renal replacement therapy detail; fluid/electrolyte management per Sections 6/8; standard ICU supportive care for the underlying primary illness driving AKI.
10. Consultation Matrix
Consultation | Trigger | Timing |
Nephrology | NephroCheck positive, KDIGO stage 2-3, RRT consideration, diagnostic uncertainty (glomerular/vasculitic picture) | Early, proactive where possible |
Urology | Postrenal obstruction confirmed | Prompt once identified |
Hepatology | HRS-AKI | Immediate |
11. Monitoring Framework
Hourly I/O, daily weight/cumulative fluid balance, 6-hourly electrolytes, daily renal function panel, serial urine sediment/chemistry if diagnosis evolving, drug level monitoring for nephrotoxins in use.
12. Complications
Progression to RRT-dependence, hyperkalemia/arrhythmia, volume overload/pulmonary edema, metabolic acidosis, uremic complications (encephalopathy, pericarditis, bleeding diathesis) if severe/untreated, drug toxicity from inadequate dose adjustment. Prevention: early recognition/staging, nephrotoxin avoidance, appropriate fluid strategy, proactive NephroCheck-guided intervention where available. Rescue: RRT per indications (see dedicated protocol).
13. Escalation & De-escalation
Escalate: KDIGO stage progression, refractory hyperkalemia/acidosis/volume overload, uremic symptoms -> RRT initiation per dedicated protocol criteria.
De-escalate: improving urine output/creatinine trend, resolved precipitant -> wean/discontinue RRT if applicable, transition to standard monitoring, nephrology follow-up for recovery trajectory.
14. ICU Discharge Criteria
Stable or improving renal function, no ongoing RRT need (or established outpatient dialysis plan if non-recovering), electrolytes/acid-base stable, nephrotoxin exposure minimized/reconciled, nephrology follow-up arranged.
15. Documentation & Medicolegal Checklist
16. Key Guidelines
Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury. Kidney Int. 2012;(suppl 2):1-138.
17. Landmark Trials
BASICS and PLUS trials — balanced crystalloid vs saline, no significant advantage shown. SAFE trial — 4% albumin vs saline, no difference in general resuscitation. Salerno F, Gerbes A, Gines P, Wong F, Arroyo V. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut. 2007;56(9):1310-1318 (HRS diagnostic criteria).
18. Controversies
Balanced crystalloid vs saline preference has genuinely shifted with BASICS/PLUS trial data — the older "always balanced" teaching is being revised, and this protocol reflects that update rather than the historical default. Corticosteroid use in glomerulonephritis/vasculitis-associated AKI remains controversial despite some supportive observational data. Optimal RRT modality/timing continues to be debated (see dedicated CRRT protocol for full discussion).
19. References
- Cummings J, Vijayan A. Acute Kidney Injury. Washington Manual of Critical Care, 4th ed, 2025 (Ch. 47).
- Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int. 2012;(suppl 2):1-138.
- Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Lancet. 2012;380:756-766.
- Salerno F, Gerbes A, Gines P, Wong F, Arroyo V. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut. 2007;56(9):1310-1318.
- Janjanam A, Kesavan S. Multiorgan Failure (AKI section). ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 38).
See also: CRRT Indications (Renal System), Acute-on-Chronic Liver Failure (HRS-AKI detail), Acute Heart Failure (cardiorenal syndrome decongestion), Diffuse Alveolar Hemorrhage (pulmonary-renal syndrome).