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Azotemia Clinical Presentation

  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Feb 12, 2016
 

History

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.

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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.

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Contributor Information and Disclosures
Author

Moro O Salifu, MD, MPH, FACP Associate Professor, Department of Internal Medicine, Chief, Division of Nephrology, Director of Nephrology Fellowship Program and Transplant Nephrology, State University of New York Downstate Medical Center

Moro O Salifu, MD, MPH, FACP is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Society of Transplantation, American Society of Diagnostic and Interventional Nephrology, American Medical Association, American Society for Artificial Internal Organs, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Onyekachi Ifudu, MD, MBBS Director of Inpatient Dialysis Services, Associate Professor, Department of Internal Medicine, State University of New York Health Science Center at Brooklyn

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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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.
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.
 
 
 
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