Azotemia Clinical Presentation

Updated: Sep 19, 2018
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It is necessary to 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 diarrhea, vomiting, profound heat exhaustion, excessive sweat loss, concurrent illness that impairs their ability to eat and drink adequately, hemorrhage, liver disease, congestive heart failure, and 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. There may be a personal or family history of congenital or systemic diseases, especially diabetes, hypertension, systemic lupus erythematosus (SLE), other collagen vascular diseases, hepatitis B (HBV), hepatitis C (HCV), syphilis, multiple myeloma, and AIDS.

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 (associated with exposure to HIV, HBV, and HCV infections).

Patients with postrenal azotemia frequently have a history of renal colic, dysuria, frequency, hesitancy, urgency incontinence, pelvic malignancy or irradiation, or benign prostatic hypertrophy.


Physical Examination

Physical examination should be detailed but should focus on signs that have a high diagnostic yield.

In suspected prerenal azotemia, look for tachycardia; orthostatic hypotension (systolic blood pressure drop greater than 20 mm Hg or diastolic drop greater than 10 mm Hg from supine to standing); hypotension; signs of dehydration, including dry mucous membranes, loss of skin turgor, and loss of axillary sweat; and signs of congestive heart failure or 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. The presence of uremic pericarditis requires 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.