Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 22-05: Acute Kidney Injury + Key Features Download Section PDF Listen +++ +++ Essentials of Diagnosis ++ Rapid increase in serum creatinine Oliguria may be present Symptoms and signs depend on cause +++ General Considerations ++ Defined as an absolute increase in serum creatinine by ≥ 0.3 mg/dL within 48 hours or relative increase to at least 1.5 times baseline that is known or presumed to have occurred within 7 days Characterized as oliguric if urine production is < roughly 400–500 mL/day Clinically, characterized by an inability to maintain acid-base, fluid, and electrolyte balance and to excrete nitrogenous wastes The 2012 KDIGO Clinical Practice Guidelines for AKI describes three progressive stages based on the elevation in serum creatinine or decline in urinary output Stage 1: 1.5- to 1.9-fold increase in serum creatinine or a decline in urinary output to 0.5 mL/kg/h over 6–12 hours Stage 2: 2.0–2.9 increase in serum creatinine or a decline in urinary output to 0.5 mL/kg/h over > 12 hours Stage 3: 3.0-fold or greater increase in serum creatinine, an increase in serum creatinine to ≥ 4 mg/dL, or a decline in urinary output to < 0.3 mL/kg/h for ≥ 24 hours, anuria for ≥ 12 hours, or initiation of renal replacement therapy Serum creatinine concentration can typically increase by 1.0–1.5 mg/dL daily +++ Demographics ++ 5% of hospital admissions and 30% of ICU admissions have acute kidney injury 25% of hospitalized patients develop acute kidney injury + Clinical Findings Download Section PDF Listen +++ +++ Symptoms and Signs ++ Nausea, vomiting Malaise Hypertension Pericardial friction rub, effusions, and cardiac tamponade Ventricular tachycardia and other tachyarrhythmias Rales Abdominal pain and ileus Bleeding secondary to platelet dysfunction Encephalopathy, altered sensorium, asterixis, seizures Oliguria, defined as urinary output < 500 mL/day or < 20 mL/h +++ Differential Diagnosis +++ PRERENAL CAUSES ++ Dehydration Hemorrhage (eg, gastrointestinal bleeding) Heart failure Renal artery stenosis, including fibromuscular dysplasia Nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors +++ POSTRENAL CAUSES ++ Obstruction (eg, benign prostatic hyperplasia, bladder tumor) +++ INTRINSIC RENAL DISEASE ++ Acute tubular necrosis Toxins NSAIDs Antibiotics Intravenous contrast Plasma cell myeloma Rhabdomyolysis Hemolysis Chemotherapy Hyperuricemia Cyclosporine Ischemia (eg, prolonged prerenal insults) Acute glomerulonephritis Immune complex IgA nephropathy Endocarditis Systemic lupus erythematosus (SLE) Cryoglobulinemia Postinfectious Membranoproliferative Pauci-immune (ANCA-positive) Granulomatosis with polyangiitis Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome) Microscopic polyarteritis Antiglomerular basement membrane (anti-GBM) Goodpasture disease Anti-GBM glomerulonephritis Vascular Malignant hypertension Thrombotic thrombocytopenia purpura Atheroembolism Acute interstitial nephritis Drugs Beta-lactams Sulfa Diuretics NSAIDs Rifampin Phenytoin Allopurinol Infections Streptococcus Leptospirosis Cytomegalovirus Histoplasmosis Rocky Mountain spotted fever Immune SLE Sjögren syndrome Sarcoidosis Cryoglobulinemia + Diagnosis Download Section PDF Listen +++ +++ Laboratory Tests ++ Serum creatinine and BUN elevated BUN–creatinine ratio > 20:1 in prerenal and postrenal causes, and acute glomerulonephritis; < 20:1 in acute tubular necrosis and acute interstitial nephritis Hyperkalemia Anion gap metabolic acidosis Hyperphosphatemia Hypocalcemia Anemia Fractional excretion of sodium (FENa) can be useful in oliguric states: FENa = clearance of Na+/GFR = clearance of Na+/creatinine clearance FENa = (urineNa /serumNa)/(urineCr/ serumCr) × 100% FENa low (< 1%) in prerenal insults; high (> 1%) in acute tubular necrosis; variable in postrenal causes, acute interstitial nephritis, acute glomerulonephritis +++ Imaging Studies ++ Renal ultrasonography to exclude obstruction or other anatomic abnormalities; check renal size and echotexture CT or MRI if retroperitoneal fibrosis from tumor or radiation suspected +++ Diagnostic Procedures ++ ECG: peaked T waves, PR prolongation, and QRS widening in hyperkalemia, long QT interval with hypocalcemia + Treatment Download Section PDF Listen +++ +++ Therapeutic Procedures ++ Prerenal insults Treatment depends on cause Achieve euvolemia Monitor serum electrolytes Avoid nephrotoxic drugs Postrenal causes: relieve obstruction if present Place catheters or stents through an obstruction Catheterize bladder if hydroureter, hydronephrosis and enlarged bladder on ultrasonography Intrinsic renal disease: treat underlying cause (see Tubular Necrosis, Acute); hold offending agents Indications for hemodialysis, peritoneal dialysis: Uremic symptoms (eg, pericarditis, encephalopathy, or coagulopathy) Fluid overload unresponsive to diuresis Refractory hyperkalemia Severe metabolic acidosis (pH < 7.20) Neurologic symptoms (eg, seizures or neuropathy) + Outcome Download Section PDF Listen +++ +++ When to Refer ++ If a patient has signs of acute kidney injury that have not reversed over 1–2 weeks, but no signs of acute uremia, the patient can usually be referred to a nephrologist rather than admitted If a patient has signs of persistent urinary tract obstruction, the patient should be referred to a urologist +++ When to Admit ++ The patient should be admitted if there is sudden loss of kidney function resulting in abnormalities that cannot be handled expeditiously in an outpatient setting (eg, hyperkalemia, volume overload, uremia) or an acute intervention is needed, such as emergent urologic procedures or dialysis + References Download Section PDF Listen +++ + +Levey AS et al. Acute kidney injury. Ann Intern Med. 2017 Nov 7;167(9):ITC66–80. Erratum in: Ann Intern Med. 2018 Jan 2;168(1):84. [PubMed: 29114754] + +Malhotra R et al. Biomarkers for the early detection and prognosis of acute kidney injury. Clin J Am Soc Nephrol. 2017 Jan 6;12(1):149–73. [PubMed: 27827308] + +Ronco C et al. Acute kidney injury. Lancet. 2019 Nov 23;394(10212):1949–64. [PubMed: 31777389] + +Srisawat N et al. The role of biomarkers in acute kidney injury. Crit Care Clin. 2020 Jan;36(1):125–40. [PubMed: 31733675]