Azotemia Clinical Presentation

  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Dec 1, 2010
 

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. Tests include serologies, urinalysis, and, if indicated, radiologic studies and kidney biopsy.

  • Prerenal azotemia: History of diarrhea, vomiting, profound heat exhaustion, excessive sweat loss, concurrent illness that impairs patient's ability to eat and drink adequately, hemorrhage, liver disease, congestive heart failure, and polyuria (eg, caused by lithium intoxication, diuretics, diabetes, diabetes insipidus)
  • Intrarenal azotemia
    • History of nocturia, polyuria, proteinuria, shock, and edema
    • Personal or family history of congenital or systemic diseases, especially diabetes, hypertension, systemic lupus erythematosus, other collagen vascular diseases, hepatitis B (HBV), hepatitis C (HCV), syphilis, multiple myeloma, and AIDS
    • Detailed medication history (looking for nephrotoxic medications, especially antibiotics, NSAIDs, ACE inhibitors, diuretics, and herbal remedies), chemical exposure, and intravenous drug abuse (exposure to HIV, HBV, and HCV infections)
  • Postrenal azotemia: Renal colic, dysuria, frequency, hesitancy, urgency incontinence, pelvic malignancy or irradiation, and benign prostatic hypertrophy
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Physical

Physical examination should be detailed but focused on signs of high diagnostic yield.

  • Prerenal azotemia: Look for tachycardia; orthostatic hypotension (systolic BP drop of >20 mm Hg, diastolic BP drop of >10 mm Hg or more from the supine to standing position); 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.
  • 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 latter 2 signs are suggestive of uremia. The presence of uremic pericarditis requires immediate dialysis.
  • Postrenal azotemia: A palpable bladder that is dull to percussion and a rectal or pelvic mass on digital examination is suggestive of postrenal azotemia (obstruction).
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Causes

Causes are broadly classified as prerenal, intrarenal, and postrenal.

  • Prerenal azotemia
    • Prerenal azotemia occurs as a result of impaired renal blood flow or decreased perfusion resulting from decreased blood volume, decreased cardiac output (congestive heart failure), decreased systemic vascular resistance, decreased effective arterial volume from sepsis or hepatorenal syndrome, and renal artery abnormalities.
    • It may be superimposed on a background of chronic renal failure.
    • Iatrogenic causes of prerenal azotemia, such as excessive diuresis and treatment with ACE inhibitors, should be ruled out.
  • Intrarenal azotemia
    • Intrarenal azotemia occurs as a result of injury to the glomeruli, tubules, interstitium, or small vessels.
    • It may be acute oliguric, acute nonoliguric, or chronic.
    • The presence of systemic disease, nocturia, proteinuria, loss of urinary concentrating ability (low urine specific gravity), anemia, and hypocalcemia are suggestive of chronic intrarenal azotemia.
  • Postrenal azotemia
    • Postrenal azotemia occurs when an obstruction to urine flow is present.
    • It is observed in bilateral ureteral obstruction from tumors or stones, retroperitoneal fibrosis, neurogenic bladder, and bladder neck obstruction from prostatic hypertrophy or carcinoma and posterior urethral valves.
    • It may be superimposed on a background of chronic renal failure.
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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 Medical Association, American Society for Artificial Internal Organs, American Society of Diagnostic and Interventional Nephrology, American Society of Nephrology, American Society of Transplantation, and National Kidney Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Onyekachi Ifudu, MD  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.

Specialty Editor Board

Frank C Brosius III, MD  Nephrology Program Director, Professor of Internal Medicine and Physiology, Department of Internal Medicine, Division of Nephrology, University of Michigan School of Medicine

Frank C Brosius III, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Society of Nephrology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Abbott Grant/research funds Speaking and teaching; AMAG Honoraria Speaking and teaching; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching; Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology

Disclosure: Nothing to disclose.

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The graph shows the relationship of the glomerular filtration rate (GFR) to steady-state serum creatinine and blood urea nitrogen (BUN) levels. As shown in this figure, in early renal disease, substantial decline in GFR may lead to only a slight elevation in serum creatinine. Elevation in serum creatinine is apparent only when the GFR falls to about 70 mL/min.
Diagnostic Images in Azotemia: Although these indices are helpful, it is not necessary to perform all these tests on a particular patient. Comparison should always be made with the patients baseline values to identify trends consistent with increase or decrease in effective circulating volume. It should be noted that use of some of these indices may be limited in certain clinical conditions, such as in anemia (hematocrit), hypocalcemia (serum calcium), decreased mucle mass (serum creatinine), liver disease (BUN, total protein, albumin), poor nutritional state (BUN, total protein, albumin) and use of diuretics (urine Na). FEUrea and FELi appear to be better in assessing prerenal status in patients on diuretics.
 
 
 
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