Medical Management of Acute Kidney Injury (AKI)

1. General Principles

• Identify and reverse the underlying cause - volume depletion, obstruction, nephrotoxins
• Eliminate nephrotoxic agents - ACE inhibitors, ARBs, NSAIDs, aminoglycosides, contrast agents, chemotherapy, checkpoint inhibitors
• Optimize hemodynamics - maintain MAP >65 mmHg through volume resuscitation and vasopressors as needed
• Early nephrology consultation - improves outcomes in critically ill patients with AKI
• Adjust all drug doses for the degree of renal impairment (note: serum creatinine overestimates GFR in non-steady-state AKI)

Brenner and Rector's The Kidney - Harrison's Principles of Internal Medicine 22E

2. Management by AKI Category

A. Prerenal AKI

• Fluid resuscitation with isotonic crystalloid is the initial step. Balanced crystalloids (e.g., Lactated Ringer's, PlasmaLyte) are preferred over normal saline - randomized trials and meta-analyses show balanced crystalloids reduce major adverse kidney events compared with isotonic saline
• Colloids vs. crystalloids: Colloids (especially HES - hydroxyethyl starch) are associated with increased need for RRT and adverse outcomes; not recommended for routine resuscitation
• Blood transfusion for hemorrhagic hypovolemia with ongoing bleeding or dangerously low hemoglobin
• Correct the underlying cause - stop excessive diuresis, treat diarrhea/vomiting, address cardiac output

• Heart failure: Inotropes, preload/afterload reduction, mechanical circulatory support, invasive hemodynamic monitoring
• Hepatorenal syndrome (HRS): IV albumin (25-50 g, max 100 g/day) + vasoconstrictors (norepinephrine, terlipressin, or octreotide + midodrine). Rule out SBP by ascitic fluid analysis. Albumin prevents AKI in patients treated with antibiotics for SBP. Definitive treatment is liver transplantation
• Sepsis: Early antibiotics + rapid volume resuscitation targeting MAP >65 mmHg. EGDT targets (CVP 10-12 mmHg, ScvO2 >70%, urine output >0.5 mL/kg/hr) have not shown consistent benefit for AKI specifically across major trials (ProCESS, ARISE, PROMISe)

Brenner and Rector's The Kidney

B. Intrinsic AKI

Harrison's Principles of Internal Medicine 22E - Campbell-Walsh-Wein Urology

C. Postrenal AKI

• Urethral/bladder neck obstruction: transurethral or suprapubic catheter
• Ureteric obstruction: percutaneous nephrostomy tubes or cystoscopically placed ureteral stents
• After relief: expect a physiologic post-obstructive diuresis lasting days. About 5% of patients develop prolonged salt-wasting requiring IV fluid replacement to maintain blood pressure
• Urologic evaluation is needed for definitive management of the underlying cause

Brenner and Rector's The Kidney

3. Supportive Management of Metabolic Complications

Volume Overload

• Salt restriction (<1-2 g/day) and water restriction (<1 L/day)
• Loop diuretics: IV furosemide bolus (assess response in 60 min); if response achieved, dose every 6-8 hours OR continuous infusion (e.g., 10 mg/hr if patient responds to 60 mg bolus). Continuous infusions provide more consistent drug delivery
• Alternative loop diuretics: bumetanide, torsemide (higher potency, better oral bioavailability; torsemide has longer duration). Ethacrynic acid used in sulfonamide allergy (more ototoxic, harder to give IV)
• For loop diuretic resistance: add low-dose thiazide (metolazone 2.5-5 mg/day) - watch closely for hypokalemia and metabolic alkalosis
• High-dose loop diuretics equivalent to 200 mg furosemide IV bolus or 20 mg/hr continuous may be needed
• Ultrafiltration or dialysis if diuretics fail. Discontinue diuretics if no response at high doses (risk of ototoxicity)
• Response to diuretics is a favorable prognostic sign in AKI

Hyponatremia

• Restrict oral and IV free water intake
• Minimize hypotonic IV solutions and dextrose-containing fluids
• Hypertonic saline rarely needed; vasopressin antagonists generally not indicated

Hypernatremia

• Administer water, hypotonic saline, or hypotonic dextrose solutions

Hyperkalemia (most dangerous electrolyte disturbance)

Metabolic Acidosis

• Sodium bicarbonate if pH <7.2 or HCO3- <15 mmol/L
• Restrict dietary protein
• RRT for refractory cases

Hyperphosphatemia

• Dietary phosphate restriction
• Phosphate binders taken with meals: calcium acetate, sevelamer hydrochloride, lanthanum carbonate, aluminum hydroxide

Hypocalcemia

• Oral or IV replacement only if symptomatic (or if planning to give sodium bicarbonate)
• Use calcium carbonate or calcium gluconate

Hypermagnesemia

• Discontinue magnesium-containing antacids

Hyperuricemia

• Acute treatment usually not required except in tumor lysis syndrome (allopurinol or rasburicase)

Brenner and Rector's The Kidney - Harrison's Principles of Internal Medicine 22E

4. Nutrition

Brenner and Rector's The Kidney - Harrison's Principles of Internal Medicine 22E

5. Renal Replacement Therapy (RRT)

Absolute Indications

• Volume overload unresponsive to diuretics
• Persistent hyperkalemia despite medical therapy
• Severe metabolic acidosis unresponsive to bicarbonate
• Overt uremic symptoms: encephalopathy, pericarditis, uremic bleeding diathesis

Relative Indications

• Progressive azotemia without overt uremic symptoms
• Persistent oliguria

Timing

• Classic "late" threshold: BUN ~90-100 mg/dL based on older observational data
• Two large RCTs (AKIKI, IDEAL-ICU) comparing early vs. standard/delayed RRT initiation found no mortality benefit with early initiation, and early initiation was associated with more complications. Current evidence supports avoiding early prophylactic RRT in the absence of clear indications
• RRT does not hasten recovery of kidney function and may delay it

RRT Modalities

Dose of RRT

• Delivered dose of 20-25 mL/kg/hr for CRRT is recommended (KDIGO)
• Studies (ATN trial, RENAL trial) showed no benefit of higher-dose CRRT (35-40 mL/kg/hr) over standard dose

Brenner and Rector's The Kidney

6. Glycemic Control

• Normoglycemia maintenance (80-110 mg/dL with intensive insulin) showed reduced AKI rates in some single-center RCTs
• However, intensive insulin therapy carries risk of hypoglycemia; evidence remains controversial
• Standard approach: avoid both hyperglycemia and hypoglycemia

7. Prevention Strategies

Sources: Brenner and Rector's The Kidney, 2-Volume Set | Harrison's Principles of Internal Medicine 22E (2025) | Campbell-Walsh-Wein Urology

Specific Nursing Management of AKI

1. Nursing Assessment (Ongoing - Every Shift and PRN)

Renal/Fluid Assessment

• Urine output - hourly in critically ill patients (insert urinary catheter for accurate measurement). Oliguria = <0.5 mL/kg/hr. Anuria = <100 mL/day. Urine output responds faster than serum creatinine - if GFR suddenly drops to zero, urine output changes immediately while serum creatinine takes hours to rise
• Urine characteristics - colour (dark/concentrated = dehydration), clarity, odour, specific gravity (>1.030 = concentrated, dehydrated)
• Daily weight - same time each day, same scale, same clothing. Weight gain >0.5 kg/day = fluid retention (~1 kg ≈ 1 L retained fluid)
• Strict intake and output (I&O) - document all oral, IV, NG, and other inputs; all urine, drainage, stool, vomiting outputs
• Fluid balance calculation every 8-12 hours

Cardiovascular/Haemodynamic Assessment

• Vital signs: blood pressure, HR, MAP (target MAP >65 mmHg), orthostatic changes
• Signs of volume depletion: tachycardia, hypotension, poor skin turgor, dry mucous membranes, sunken eyes, low JVP
• Signs of fluid overload: hypertension, raised JVP/JVD, peripheral oedema (pedal, sacral), crackles on lung auscultation, S3/S4 gallop
• Continuous cardiac monitoring - electrolyte disturbances (hyperkalemia especially) cause life-threatening dysrhythmias

Respiratory Assessment

• Auscultate lungs: fine crackles = early pulmonary oedema; coarse crackles + dyspnoea = frank pulmonary oedema
• Respiratory rate, SpO2, work of breathing - fluid overload and metabolic acidosis drive respiratory compromise
• Kussmaul breathing (deep, laboured) = severe metabolic acidosis

Neurological Assessment

• Level of consciousness, orientation, confusion - altered LOC indicates fluid shifts, uraemia, electrolyte imbalance, or developing hypoxia
• Watch for uraemic encephalopathy: restlessness, asterixis (flapping tremor), confusion, seizures

Musculoskeletal/Skin

• Muscle cramps, weakness (hypokalaemia, hypocalcaemia, hyperkalaemia)
• Skin assessment: oedema grading (1+ to 4+), skin integrity, pruritus (uraemia)
• Uraemic frost (rare, severe) - white crystalline deposits on skin

Comprehensive Clinical Nephrology 7th Ed - American Nurse Journal

2. Laboratory Monitoring (Know Your Trends)

NurseTogether - Brenner and Rector's The Kidney

3. Nursing Diagnoses (NANDA Framework)

4. Nursing Interventions by Problem

A. Fluid Volume Management

• Administer IV fluid replacement as prescribed (isotonic crystalloids preferred - balanced solutions over normal saline per current evidence)
• Encourage oral fluid intake during diuretic phase (AKI may worsen if hypovolemia is not corrected)
• Monitor for signs of hypovolemia every hour in critically ill patients
• Blood products if haemorrhagic

• Strict fluid restriction per orders (typically <1 L/day when overloaded)
• Sodium restriction <1-2 g/day
• Administer loop diuretics (furosemide IV) as ordered - assess response within 60 minutes of bolus
• Elevate head of bed 30-45 degrees if respiratory distress
• Apply supplemental oxygen if SpO2 falls
• Prepare for ultrafiltration/dialysis if diuretics fail
• Weigh patient daily - same time, same scale

• Insert urinary catheter for accurate hourly urine output measurement
• Keep strict I&O records; calculate balance every shift
• Position: elevate oedematous limbs to reduce dependent oedema

Campbell-Walsh-Wein Urology - NurseTogether

B. Electrolyte Management

• Administer IV/oral sodium bicarbonate as prescribed (target pH >7.2, HCO3- >15 mmol/L)
• Monitor respiratory rate (Kussmaul breathing is compensatory - do not suppress)
• Restrict dietary protein per dietary orders (reduces acid load)

• Give phosphate binders (calcium acetate, sevelamer) WITH meals - not before or after
• Teach patient why timing matters

• Replace only if symptomatic (cramps, tetany, positive Chvostek's/Trousseau's sign)
• Give IV calcium gluconate slowly (can cause bradycardia if given too fast)
• Note: do not give calcium if patient is on digoxin (risk of toxicity) or if hyperphosphataemia is severe

Harrison's Principles of Internal Medicine 22E - Brenner and Rector's The Kidney

C. Medication Safety and Dose Adjustment

• Review ALL medications daily for renal clearance - serum creatinine in non-steady-state AKI overestimates GFR, meaning drug accumulation is underestimated
• High-risk drugs requiring close monitoring: digoxin, aminoglycosides (vancomycin, gentamicin), metformin (must be withheld - risk of lactic acidosis), NSAIDs (contraindicated), lithium, enoxaparin/LMWH
• Monitor drug levels: vancomycin trough/AUC, gentamicin troughs, digoxin levels
• Hold nephrotoxic drugs and document notification of prescriber: ACE inhibitors, ARBs, NSAIDs, contrast agents
• Avoid potassium-sparing diuretics (spironolactone, amiloride) in hyperkalemia
• Report when new nephrotoxic drugs are ordered - question appropriateness

D. Nutrition

• Ensure diet orders are correctly implemented: low K+, low Na+, low phosphate, adequate calories (20-30 kcal/kg/day)
• Protein: 0.8-1.0 g/kg/day (non-dialysis), 1.0-1.5 g/kg/day (dialysis-requiring), up to 1.7 g/kg/day (CRRT)
• Preferred route: enteral (NGT if patient cannot eat)
• Monitor for anorexia, nausea, vomiting (uraemic symptoms reducing intake)
• Document dietary intake; report significant under-eating
• Monitor serum albumin, pre-albumin, BUN, glucose trends
• Avoid IV dextrose solutions that are hypotonic (contribute to hyponatraemia)

E. Infection Prevention (Critical in AKI)

• Strict aseptic technique for IV lines, urinary catheters, wound care
• Remove indwelling urinary catheter as soon as accurate output measurement is no longer needed - catheter-associated UTI is a leading cause of worsening AKI
• Daily assessment of all line insertion sites (redness, swelling, discharge)
• Monitor temperature, WBC, CRP trends
• Do not routinely give antibiotics prophylactically, but escalate early signs of infection
• Meticulous hand hygiene - enforce with all staff and visitors

F. Skin Integrity

• Assess pressure points every 2 hours (oedematous tissue is fragile and poorly perfused)
• Turn and reposition every 2 hours; use pressure-relieving mattress
• Keep skin clean and dry; apply emollients for pruritus
• Elevate oedematous limbs
• Avoid tape on oedematous skin - use hydrocolloid or foam alternatives
• For pruritus: avoid hot baths, use soap-free cleansers, administer antihistamines if prescribed

G. Continuous Renal Replacement Therapy (CRRT) Nursing

• Set up, prime, and troubleshoot CRRT circuits per unit protocol
• Monitor circuit pressures (transmembrane pressure, filter pressure drop) and troubleshoot alarms
• Maintain accurate hourly fluid balance records (net ultrafiltration rate as ordered)
• Monitor for circuit clotting - inspect filter for dark streaks; check anticoagulation (heparin or citrate) levels
• Replace electrolytes lost through ultrafiltration (phosphate, potassium, calcium, bicarbonate)
• Watch for citrate toxicity if regional citrate anticoagulation used: signs = hypocalcaemia (tingling, cramps), metabolic alkalosis; monitor ionised calcium every 4-6 hours
• Prevent hypothermia (CRRT circuits cause significant heat loss) - use warming blankets; check temperature hourly
• Weigh filter membranes per protocol to assess clotting burden
• Protect lines and access sites (femoral, internal jugular, subclavian dialysis catheters)

Brenner and Rector's The Kidney - American Nurse Journal

H. Psychosocial and Education

• Explain what AKI is in plain language - many patients are frightened by the term "kidney failure"
• Address anxiety about possible dialysis - explain it is often temporary in AKI, unlike in CKD
• Involve family in fluid restriction education (they may bring outside food/drinks)
• Teach patient and family to report new symptoms: decreased urine output, swelling, breathlessness, confusion
• Discharge education (for recovering patients):
  • Avoid NSAIDs and aminoglycosides
  • Stay well hydrated; avoid dehydration
  • Know their baseline creatinine for future reference
  • Identify and avoid triggers (contrast agents, nephrotoxic drugs)
  • Follow-up nephrology appointment for all patients with AKI - risk of progression to CKD

5. Summary: Nursing Priorities by Phase

6. Escalation - When to Call the Physician Immediately

• Urine output <0.5 mL/kg/hr for >2 consecutive hours despite fluid management
• Serum K+ >6.0 mmol/L or any ECG change (peaked T waves, wide QRS)
• pH <7.2 or HCO3- <12 mmol/L
• Sudden drop in SpO2 or development of pulmonary oedema
• New confusion, seizures, or asterixis (uraemic encephalopathy)
• No urine output (anuria) for >6 hours
• Haemodynamic instability: MAP <65 mmHg unresponsive to fluids

Sources: Brenner and Rector's The Kidney, 2-Volume Set | Harrison's Principles of Internal Medicine 22E | Comprehensive Clinical Nephrology 7th Ed | American Nurse - AKI: A Nursing Challenge | NurseTogether - AKI Nursing Diagnoses & Care Plans | Tintinalli's Emergency Medicine

Fluid Management in AKI: How Much to Give?

The Core Framework: 4 Phases of Fluid Management

Brenner and Rector's The Kidney

1. Hypovolaemic / Prerenal AKI - Give Fluids Actively

• Start with isotonic crystalloid IV - typically 250-500 mL boluses, then reassess
• Monitor response: HR, BP, MAP, urine output, JVP/CVP, lung sounds
• Continue replacing until signs of hypovolaemia resolve
• Then shift to maintenance fluids - matching output + insensible losses (~500 mL/day insensible)

• Balanced crystalloids preferred (Ringer's lactate, PlasmaLyte) over normal saline (0.9% NaCl)
• In one sequential ICU study, switching from high-chloride to low-chloride solutions reduced KDIGO stage 3 AKI from 14% to 8.4% and RRT use from 10% to 6.3%
• Normal saline (chloride 154 mmol/L vs plasma 98-106 mmol/L) causes hyperchloraemic metabolic acidosis and renal vasoconstriction
• Avoid hydroxyethyl starch - associated with >20% increased risk of RRT and higher mortality across multiple large RCTs
• Albumin vs crystalloid: outcomes are similar for most patients; albumin is not routinely preferred (except in hepatorenal syndrome/SBP)
• Avoid albumin in traumatic brain injury - associated with increased mortality

Brenner and Rector's The Kidney - Goldman-Cecil Medicine

2. Maintenance Fluid (Euvolaemic Patient with AKI)

• Replace what goes out: urine output + insensible losses + any other drainage/losses
• Insensible losses in a non-febrile patient ≈ 500 mL/day (respiratory + skin)
• Add ~2-3 mL/°C/day extra for each degree of fever above 37°C
• Oral intake counts - subtract oral fluid from IV fluid requirement
• If oliguric (urine output <400 mL/day): total daily fluid intake is often restricted to 500-700 mL + previous day's urine output

3. Fluid-Overloaded AKI - Restrict

• Restrict sodium <1-2 g/day
• Restrict water <1 L/day (in overloaded state)
• Give loop diuretics (if non-anuric) to mobilise fluid
• If diuretics fail: ultrafiltration or dialysis

Brenner and Rector's The Kidney - Harrison's Principles of Internal Medicine 22E

4. Cause-Specific Fluid Volumes

Rhabdomyolysis - Most Aggressive Resuscitation

• Initially up to 10 litres per day of IV fluid
• Goal urine output: 200-300 mL/hr (or 3-4 mL/kg/hr) to flush myoglobin from tubules
• Fluid of choice: isotonic saline (0.9% NaCl); consider adding sodium bicarbonate if urine pH <6.5 (to alkalinise urine and prevent myoglobin precipitation)
  • Protocol: alternate 1 L normal saline with 1 L of 5% dextrose/0.45% saline + 100 mmol bicarbonate (2 ampules)
• IV mannitol (50 mL of 20%, up to 120 g/day at 5 g/hr) may be added to maintain urine output - but only if diuresis >20 mL/hr is not established within hours; discontinue if no response
• In crush syndrome: begin aggressive fluid resuscitation before extrication if CK >15,000 U/L

Harrison's Principles of Internal Medicine 22E - Goldman-Cecil Medicine

Contrast-Associated AKI Prevention

• Isotonic saline 1-1.5 mL/kg/hr for at least 6 hours before contrast and 6-12 hours after
• Alternative emergency protocol if no time: 5 mL/kg bolus before the procedure
• Periprocedural IV hydration with 0.9% saline at 100 mL/hr for 12 hours before and 12 hours after contrast
• N-acetylcysteine: not recommended - no advantage over hydration alone

Brenner and Rector's The Kidney - Campbell-Walsh-Wein Urology - Roberts and Hedges' Clinical Procedures in Emergency Medicine

Tumour Lysis Syndrome

• Aggressive IV hydration (2-3 L/m² per day) to maintain urine output >80-100 mL/m²/hr
• Combined with allopurinol or rasburicase

Sepsis-Associated AKI

• 30 mL/kg IV crystalloid in the first 3 hours (Surviving Sepsis Campaign initial resuscitation bundle)
• Then fluid-guided by dynamic measures of preload responsiveness (pulse pressure variation, passive leg raise test, stroke volume variation)
• MAP target: >65 mmHg (add vasopressors - norepinephrine first-line - if not achieved with fluids)

5. How to Know Enough Is Enough - Response Targets

6. The Danger Zone: Fluid Overload in AKI

• Pulmonary oedema and respiratory failure
• Abdominal compartment syndrome (intra-abdominal pressure >12 mmHg) - which itself worsens AKI by compressing renal veins and reducing venous return
• Dilutional hyponatraemia
• Impaired wound healing, gut oedema
• Increased mortality (independently associated in observational studies)
• Can mask true AKI severity by diluting serum creatinine

Brenner and Rector's The Kidney

Summary in One Rule

Give fluid when the patient is under-filled. Stop when they are euvolaemic. Restrict when they are overloaded. The goal is euvolemia - not a fixed number of litres.

Harrison's Principles of Internal Medicine 22E | Brenner and Rector's The Kidney | Goldman-Cecil Medicine | Campbell-Walsh-Wein Urology