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Everything about acute kidney injury according to harrison. Fluid management in a patient having AKI

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Acute Kidney Injury — Harrison's Principles of Internal Medicine, 22E (2025)

Definition

AKI is defined by impairment of kidney filtration and excretory function over days to weeks (generally within 7 days), resulting in retention of nitrogenous and other waste products.

KDIGO Criteria (any one of):

↑ serum creatinine (SCr) ≥0.3 mg/dL within 48 h, OR
↑ SCr ≥1.5× baseline over 7 days, OR
Urine output <0.5 mL/kg/h for >6 h

AKI is a clinical diagnosis, not a structural one — a patient may have AKI with or without parenchymal injury.

Staging (KDIGO — Table 321-1)

Stage	Serum Creatinine	Urine Output
1	1.5–1.9× baseline OR ≥0.3 mg/dL increase	<0.5 mL/kg/h for 6–12 h
2	2.0–2.9× baseline	<0.5 mL/kg/h for ≥12 h
3	≥3.0× baseline OR SCr ≥4.0 mg/dL OR initiation of RRT	<0.3 mL/kg/h for ≥24 h OR anuria ≥12 h

Epidemiology

Complicates 5–7% of acute-care admissions and up to 30% of ICU admissions
Incidence has grown >4-fold in the US since 1988; ~500 per 100,000/year — higher than stroke
Morbidity >50% in ICU patients
Increases risk of CKD progression and future cardiovascular disease

Classification & Pathophysiology

Prerenal AKI

Decreased perfusion pressure to glomerular capillaries or interference with filtration:

Volume depletion, heart failure, liver failure, sepsis
Vasoconstriction from: NSAIDs, contrast agents, vancomycin, cyclosporine/tacrolimus, cocaine, hemoglobin/myoglobin
Hypercalcemia and hypoxia are vasoconstrictive
Urinary sodium low (<1%), urine:plasma creatinine >40

Intrinsic Renal AKI

Acute Tubular Necrosis (ATN): Most common cause. Results from gram-negative sepsis, hemodynamic collapse, rhabdomyolysis, hemoglobinuria, drugs (NSAIDs, aminoglycosides, cisplatin, methotrexate)
Ischemia-associated: Outer medulla most vulnerable; S3 segment of proximal tubule depends on oxidative metabolism; reduced GFR from vasoconstriction, tubuloglomerular feedback activation, backleak of filtrate, tubular obstruction
Glomerulonephritis/Vasculitis: palpable purpura, pulmonary hemorrhage, sinusitis → consider systemic vasculitis
Allergic Interstitial Nephritis: due to medications; may show fever, rash, arthralgias (but absence doesn't exclude it)
Other causes: viral infections (SARS-CoV-2, hantavirus, dengue), contrast nephropathy, pigment nephropathy

Postrenal AKI

Complete obstruction → anuria; incomplete obstruction → polyuria + bland sediment
FENa usually >1–2%
Diagnosis: hydronephrosis on ultrasound or large urine volume with bladder catheterization

Postoperative AKI

Most common after cardiac surgery with CPB (especially combined valve + bypass), vascular procedures with aortic cross-clamping, major intraperitoneal procedures. Risk factors: pre-existing CKD, diabetes, CHF, older age.

Clinical Evaluation

History: Oliguria/anuria, recent medications (NSAIDs, ACE-i, ARBs, aminoglycosides, contrast), prostatic disease, pelvic malignancy, autoimmune disease

Exam signs of prerenal: Orthostatic hypotension, tachycardia, reduced JVP, decreased skin turgor, dry mucous membranes

Urine findings:

Complete anuria = complete obstruction, renal artery occlusion, overwhelming septic shock, severe ischemia/cortical necrosis, or severe GN
Oliguria (<400 mL/24h) = worse AKI
Mild proteinuria (<1 g/d) in ischemic/nephrotoxic AKI; heavy proteinuria suggests glomerular disease
Red/brown urine with persistent supernatant color → rhabdomyolysis or hemolysis

Complications

Complication	Notes
Hyperkalemia	Especially severe in rhabdomyolysis, hemolysis, tumor lysis syndrome; risk of fatal arrhythmias
Metabolic acidosis	Usually elevated anion gap; not treated unless pH <7.20 and HCO₃ <15 mmol/L
Hyperphosphatemia	Especially catabolic patients, rhabdomyolysis, tumor lysis
Hypocalcemia	From metastatic Ca-PO₄ deposition, vitamin D–PTH–FGF-23 axis derangements; paresthesias, carpopedal spasms, prolonged QT
Anemia & bleeding	Uremia → ↓ erythropoiesis + platelet dysfunction
Infections	Common precipitant and dreaded complication; impaired host immunity
Cardiac	Arrhythmias, pericarditis, pericardial effusion, volume overload
Malnutrition	AKI is a severely hypercatabolic state

FLUID MANAGEMENT IN AKI (Core Focus)

Prerenal AKI — Volume Resuscitation

Oliguria alone is NOT an indication for fluid — intravascular hypovolemia is the only indication
Fluid type should match the type of fluid lost:
- Severe acute blood loss → packed red blood cells
- Crystalloids are favored over colloids in general
- Hydroxyethyl starch is contraindicated (withdrawn due to increased AKI risk)
- Most used: 0.9% normal saline
- Buffered crystalloids (Ringer's lactate, Hartmann's, Plasma-Lyte) are alternatives

Choosing between saline vs. buffered crystalloid:

Situation	Preferred fluid
Hypernatremia	Buffered crystalloids (slightly hypotonic)
Metabolic alkalosis	0.9% saline
Metabolic acidosis	Bicarbonate-containing solution (D5W + 150 mEq NaHCO₃)
Hyperchloremic risk	Avoid excess 0.9% saline (causes hyperchloremic metabolic acidosis)

Hypervolemic AKI — Volume Overload Management

Salt and water restriction
Diuretics — may help avoid dialysis; no evidence that ↑ urine output improves AKI natural history, but may relieve volume overload
- Severe overload: furosemide 200 mg IV bolus, then 10–40 mg/h IV drip, ± thiazide diuretic
- In decompensated heart failure: stepped diuretic therapy > ultrafiltration for preserving renal function
Ultrafiltration — if diuretics fail
Dopamine (low-dose): Transiently increases salt/water excretion in prerenal states, but clinical trials show no benefit in intrinsic AKI; risks outweigh benefits (arrhythmias, bowel ischemia) — not recommended

Cardiac Function Optimization

May require inotropes, preload/afterload reducers, antiarrhythmics, or mechanical ventricular assist devices
Invasive hemodynamic monitoring may be necessary

Cirrhosis and Hepatorenal Syndrome

Fluid management is challenging due to difficulty assessing intravascular volume
IV fluid challenge may be both diagnostic and therapeutic
Excessive fluids → worsen ascites and pulmonary compromise
Rule out spontaneous bacterial peritonitis (cell count + culture of ascitic fluid)
Albumin prevents AKI in SBP patients treated with antibiotics
Bridge therapies: norepinephrine, terlipressin (vasopressin analogue), or octreotide + midodrine + IV albumin (25–50 g, max 100 g/d)
Definitive treatment: orthotopic liver transplantation

Rhabdomyolysis — Specific Fluid Protocol

Early and aggressive volume repletion is mandatory
May initially require up to 10 L/day
Alkaline fluids (75 mmol/L NaHCO₃ added to 0.45% saline) may prevent tubular injury and cast formation — but carry risk of worsening hypocalcemia
Diuretics if fluid repletion adequate but urine flow <200–300 mL/h target

Sepsis-Associated AKI

Fluid resuscitation + vasopressors to achieve blood pressure goals
Avoid nephrotoxic agents (aminoglycosides, contrast)
CRRT preferred over intermittent hemodialysis in septic shock (avoids dynamic volume shifts)

General Management Principles (Table 321-3)

Optimize hemodynamics — volume resuscitation + judicious vasopressors; maintain MAP >65 mmHg
Eliminate nephrotoxins — ACE-i, ARBs, NSAIDs, aminoglycosides, chemotherapy, checkpoint inhibitors
Nutrition — 20–30 kcal/kg/day total energy:
- Non-catabolic, no dialysis: 0.8–1.0 g/kg/day protein
- On dialysis: 1.0–1.5 g/kg/day protein
- Hypercatabolic on CRRT: up to 1.7 g/kg/day protein
- Enteral route preferred; trace elements and water-soluble vitamins supplemented in dialysis patients
Electrolyte/acid-base corrections (see complications table above)
Drug dose adjustment — remember SCr lags behind true GFR changes in AKI (non-steady state)
VTE prophylaxis — avoid LMWH and factor Xa inhibitors in severe AKI (unpredictable pharmacokinetics)
GI prophylaxis — PPI or H₂ blocker (note: PPIs themselves are associated with AKI from interstitial nephritis)

Dialysis Indications (RRT)

RRT indicated when medical management fails for:

Volume overload unresponsive to diuretics
Hyperkalemia refractory to medical therapy
Severe acidosis
Uremic complications — asterixis, pericardial rub/effusion, encephalopathy, uremic bleeding
Toxic ingestions

Early RRT in sepsis-associated AKI is not associated with improved outcomes — initiate only for standard indications. Late initiation also not superior — timing remains individualized.

CRRT vs. IHD:

CRRT preferred in hemodynamically unstable patients (septic shock) due to fewer intravascular volume shifts
IHD remains appropriate in stable patients

Source: Harrison's Principles of Internal Medicine, 22nd Edition (2025), Chapter 321 — Acute Kidney Injury (Sushrut S. Waikar, Joseph V. Bonventre), and Chapter 23 (Sepsis-associated AKI section)

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