History
A detailed and accurate history is crucial for diagnosing acute kidney injury (AKI) and determining treatment. Distinguishing AKI from chronic kidney disease is important, yet making the distinction can be difficult; chronic kidney disease is itself an important risk factor for AKI. [42] A history of chronic symptoms—months of fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus—suggests chronic kidney disease. AKI can cause identical symptoms, but over a shorter course.
It is important to elicit a history of any of the following etiologic factors:
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Volume restriction (eg, low fluid intake, gastroenteritis)
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Nephrotoxic drug ingestion (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], aminoglycosides) [42]
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Exposure to iodinated contrast agents within the past week [42]
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Trauma or unaccustomed exertion
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Blood loss or transfusions
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Exposure to toxic substances, such as ethyl alcohol or ethylene glycol
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Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners
People with the following comorbid conditions are at a higher risk for developing AKI:
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Hypertension
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Chronic heart failure
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Diabetes
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Liver disease
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Multiple myeloma
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Chronic infection
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Myeloproliferative disorder
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Connective tissue disorders
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Autoimmune diseases
Urine output history can be useful. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.
Because of a decrease in functioning nephrons, even a trivial nephrotoxic insult may cause AKI to be superimposed on chronic renal insufficiency.
Acute kidney injury (AKI) has a long differential diagnosis. The history can help to classify the pathophysiology of AKI as prerenal, intrinsic renal, or postrenal failure, and it may suggest some specific etiologies.
Prerenal failure
Patients commonly present with symptoms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension. Ask about volume loss from vomiting, diarrhea, sweating, polyuria, or hemorrhage. Patients with advanced cardiac failure leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal dyspnea.
Elders with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI. Insensible fluid losses can result in severe hypovolemia in patients with restricted fluid access and should be suspected in elderly patients and in comatose or sedated patients.
Intrinsic renal failure
Patients can be divided into those with glomerular etiologies and those with tubular etiologies of AKI. Nephritic syndrome of hematuria, edema, and hypertension indicates a glomerular etiology for AKI. Query about prior throat or skin infections. Acute tubular necrosis (ATN) should be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.
A careful search for exposure to nephrotoxins should include a detailed list of all current medications and any recent radiologic examinations (ie, exposure to radiologic contrast agents). Pigment-induced AKI should be suspected in patients with possible rhabdomyolysis (muscular pain, recent coma, seizure, intoxication, excessive exercise, limb ischemia) or hemolysis (recent blood transfusion). Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and antibiotics.
Postrenal failure
Postrenal failure usually occurs in older men with prostatic obstruction and symptoms of urgency, frequency, and hesitancy. Patients may present with asymptomatic, high-grade urinary obstruction because of the chronicity of their symptoms. A history of prior gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to the level of obstruction.
Flank pain and hematuria should raise a concern about renal calculi or papillary necrosis as the source of urinary obstruction. Use of acyclovir, methotrexate, triamterene, indinavir, or sulfonamides implies the possibility that crystals of these medications have caused tubular obstruction.
Physical Examination
Obtaining a thorough physical examination is extremely important when collecting evidence about the etiology of AKI. Clues may be found in any of the following:
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Skin
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Eyes
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Ears
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Cardiovascular system
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Abdomen
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Pulmonary system
Skin
Skin examination may reveal the following:
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Livido reticularis, digital ischemia, butterfly rash, palpable purpura - Systemic vasculitis
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Maculopapular rash - Allergic interstitial nephritis
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Track marks (ie, intravenous drug abuse) - Endocarditis
Petechiae, purpura, ecchymosis, and livedo reticularis provide clues to inflammatory and vascular causes of AK. Infectious diseases, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), and embolic phenomena can produce typical cutaneous changes.
Eyes and ears
Eye examination may reveal the following:
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Keratitis, iritis, uveitis, dry conjunctivae - Autoimmune vasculitis
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Jaundice - Liver diseases
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Band keratopathy (ie, hypercalcemia) - Multiple myeloma
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Signs of diabetes mellitus
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Signs of hypertension
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Atheroemboli - Retinopathy
Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis. Ocular palsy may indicate ethylene glycol poisoning or necrotizing vasculitis. Findings suggestive of severe hypertension, atheroembolic disease, and endocarditis may be observed on careful examination of the eyes.
Ear examination may reveal the following:
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Hearing loss - Alport disease and aminoglycoside toxicity
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Mucosal or cartilaginous ulcerations - Wegener granulomatosis
Cardiovascular system
The most important part of the physical examination is the assessment of cardiovascular and volume status. The physical examination must include the following:
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Pulse rate and blood pressure recordings measured in the supine and the standing position
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Close inspection of the jugulovenous pulse
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Careful examination of the heart and lungs, skin turgor, and mucous membranes
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Assessment for peripheral edema
Cardiovascular examination may reveal the following:
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Irregular rhythms (ie, atrial fibrillation) - Thromboemboli
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Murmurs - Endocarditis
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Pericardial friction rub - Uremic pericarditis
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Increased jugulovenous distention, rales, S 3 - Heart failure
In hospitalized patients, accurate daily records of fluid intake and urine output, as well as daily measurements of patient weight, are important. Hypovolemia leads to hypotension; however, hypotension may not necessarily indicate hypovolemia.
Severe heart failure may also cause hypotension. Although patients with heart failure may have low blood pressure, volume expansion is present and effective renal perfusion is poor, which can result in AKI.
Severe hypertension with renal failure suggests one of the following disorders:
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Renovascular disease
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Glomerulonephritis
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Vasculitis
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Atheroembolic disease
Abdomen
Abdominal examination may reveal the following:
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Pulsatile mass or bruit - Atheroemboli
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Abdominal or costovertebral angle tenderness - Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis
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Pelvic, rectal masses; prostatic hypertrophy; distended bladder – Urinary obstruction
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Limb ischemia, edema - Rhabdomyolysis
Abdominal examination findings can be useful in helping to detect obstruction at the bladder outlet as the cause of renal failure; such obstruction may be due to cancer or to an enlarged prostate.
The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return and result in AKI. The presence of an epigastric bruit suggests renal vascular hypertension, which may predispose to AKI.
Pulmonary system
Pulmonary examination may reveal the following:
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Rales - Goodpasture syndrome, granulomatosis with polyangiitis (Wegener granulomatosis)
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Hemoptysis - Wegener granulomatosis
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Pigmented, muddy brown, granular casts are visible in the urine sediment of a patient with acute tubular necrosis (400x magnification).
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Photomicrograph of a renal biopsy specimen shows renal medulla, which is composed mainly of renal tubules. Features suggesting acute tubular necrosis are the patchy or diffuse denudation of the renal tubular cells with loss of brush border (blue arrows); flattening of the renal tubular cells due to tubular dilation (orange arrows); intratubular cast formation (yellow arrows); and sloughing of cells, which is responsible for the formation of granular casts (red arrow). Finally, intratubular obstruction due to the denuded epithelium and cellular debris is evident (green arrow); note that the denuded tubular epithelial cells clump together because of rearrangement of intercellular adhesion molecules.
Tables
Stage |
GFR** Criteria |
Urine Output Criteria |
Probability |
Risk |
SCreat† increased × 1.5 or GFR decreased >25% |
UO‡< 0.5 mL/kg/h × 6 h |
High sensitivity (Risk >Injury >Failure) |
Injury |
SCreat increased × 2 or GFR decreased >50% |
UO < 0.5 mL/kg/h × 12 h |
|
Failure |
SCreat increased × 3 or GFR decreased 75% or SCreat ≥4 mg/dL; acute rise ≥0.5 mg/dL |
UO < 0.3 mL/kg/h × 24 h (oliguria) or anuria × 12 h |
|
Loss |
Persistent acute renal failure: complete loss of kidney function >4 wk |
High specificity |
|
ESKD* |
Complete loss of kidney function >3 mo |
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*ESKD—end-stage kidney disease; **GFR—glomerular filtration rate; †SCreat—serum creatinine; ‡UO—urine output Note: Patients can be classified by GFR criteria and/or UO criteria. The criteria that support the most severe classification should be used. The superimposition of acute on chronic failure is indicated with the designation RIFLE-FC; failure is present in such cases even if the increase in SCreat is less than 3-fold, provided that the new SCreat is greater than 4.0 mg/dL (350 µmol/L) and results from an acute increase of at least 0.5 mg/dL (44 µmol/L). |
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Stage |
Serum Creatinine Criteria |
Urine Output Criteria |
1 |
Increase of ≥0.3 mg/dL (≥26.4 µmol/L) or 1.5- to 2-fold increase from baseline |
< 0.5 mL/kg/h for >6 h |
2 |
>2-fold to 3-fold increase from baseline |
< 0.5 mL/kg/h for >12 h |
3* |
>3-fold increase from baseline, or increase of ≥ 4.0 mg/dL (≥35.4 µmol/L) with an acute increase of at least 0.5 mg/dL (44 µmol/L) |
< 0.3 mL/kg/h for 24 h or anuria for 12 h |
*Patients who receive renal replacement therapy (RRT) are considered to have met the criteria for stage 3 irrespective of the stage they are in at the time of RRT. |
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