History
The clinician must quickly establish if azotemia is acute or chronic and whether it is due to prerenal, intrarenal, or postrenal causes. This is vital in initiating treatment and in preventing progression. Clinical evaluation requires a thorough history, physical examination, and specific laboratory tests (including serologies, urinalysis, and, if indicated, radiologic studies and kidney biopsy; see Workup).
Patients with prerenal azotemia commonly have a history of one or more of the following:
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Diarrhea
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Vomiting
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Profound heat exhaustion
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Excessive sweat loss
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Concurrent illness that impairs the ability to eat and drink adequately
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Hemorrhage
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Liver disease
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Congestive heart failure
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Polyuria (eg, caused by lithium intoxication, diuretics, diabetes, or diabetes insipidus)
Patients with intrarenal azotemia may have a history of nocturia, polyuria, proteinuria, shock, and edema. They may have a personal or family history of congenital or systemic diseases, especially diabetes, hypertension, systemic lupus erythematosus (SLE), other collagen vascular diseases, hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, syphilis, multiple myeloma, or HIV infection.
Obtain a detailed medication history, looking for nephrotoxic medications (especially antibiotics, nonsteroidal anti-inflammatory drugs [NSAIDs], angiotensin-converting enzyme [ACE] inhibitors, diuretics, and herbal remedies), chemical exposure, and intravenous (IV) drug abuse (which increases risk for HIV, HBV, and HCV infections).
Patients with postrenal azotemia frequently have a history of renal colic, dysuria, frequency, hesitancy, urgency, incontinence, pelvic malignancy, irradiation, or benign prostatic hyperplasia.
Physical Examination
Physical examination should be detailed but should focus on signs that have a high diagnostic yield.
In suspected prerenal azotemia, look for the following:
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Tachycardia
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Orthostatic hypotension (systolic blood pressure drop greater than 20 mm Hg or diastolic drop greater than 10 mm Hg from supine to standing)
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Hypotension
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Signs of dehydration, including dry mucous membranes, loss of skin turgor, and loss of axillary sweat
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Signs of congestive heart failure
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Signs of hepatic insufficiency
In suspected intrarenal azotemia, look for hypertension and its end-organ effects, such as hypertensive retinopathy and left ventricular hypertrophy (apical impulse displaced lateral to midclavicular line), rash, joint swelling or tenderness, needle tracks, hearing abnormality, palpable kidneys, abdominal bruits, pericardial rub, and asterixis. The last 2 signs are suggestive of uremia. Patients with uremic pericarditis require immediate dialysis.
Postrenal azotemia (obstruction) is suggested by a palpable bladder that is dull to percussion and the presence of a rectal or pelvic mass on digital examination.
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Graph shows relation of glomerular filtration rate (GFR) to steady-state serum creatinine and blood urea nitrogen (BUN) levels. In early renal disease, substantial decline in GFR may lead to only slight elevation in serum creatinine. Elevation in serum creatinine is apparent only when GFR falls to about 70 mL/min.
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Diagnostic indices in azotemia. Although such indices are helpful, it is not necessary to perform all these tests on every patient. Comparison should always be made with patients' baseline values to identify trends consistent with increase or decrease in effective circulating volume. Use of some of these indices may be limited in certain clinical conditions, such as anemia (hematocrit), hypocalcemia (serum calcium), decreased muscle mass (serum creatinine), liver disease (blood urea nitrogen [BUN], total protein, and albumin), poor nutritional state (BUN, total protein, and albumin), and use of diuretics (urine sodium). Fractional excretion of urea and fractional excretion of trace lithium appear to be superior for assessing prerenal status in patients on diuretics.
