Azotemia Treatment & Management

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

Medical Care

  • Prerenal azotemia
    • If volume depletion is due to free water loss, the serum sodium is often greater than 10 mEq/L. The amount of fluid replacement in liters (free water deficit) can be estimated from serum sodium (patients Na-140/140 X 0.5 X weight in kg). The free water deficit should be administered intravenously over 2-8 hours and should consist of hypotonic solutions, such as 0.5% NaCl or D5W. Alert patients should be encouraged to drink free water as much as tolerated; otherwise, free water can be administered via a nasogastric tube. Serum sodium should be measured every 6-8 hours, and fluid replacement should be adjusted to avoid a precipitous decline. The rate of decrease in serum sodium should be no more than 0.7 mEq/h (17 mEq/24 h) to avoid brain edema. Volume depletion due to blood loss requires IV saline and transfusion to maintain pressure (as well as interventions to halt further loss).
    • Diarrhea often causes isotonic volume loss requiring replacement with normal saline. Normal anion gap metabolic acidosis occurring with diarrhea requires bicarbonate in 0.5% normal saline infusion.
    • Diuretic induced volume depletion, especially in the elderly, manifests as dehydration, hyponatremia,[6] and, occasionally, hypokalemia. The treatment of choice is normal saline infusion and correction of hypokalemia.
    • Decreased cardiac output requires optimizing cardiac performance by careful use of diuretics, an ACE inhibitor, beta-blockers, nitrates, positive inotropic agents (including dobutamine), and, when indicated, specific therapy for the cause of impaired cardiac function. When ACE inhibitors are contraindicated because of hyperkalemia, the combination of nitrates and hydralazine offers an alternative. As these patients tend to have risk factors for macrovascular disease, the diagnosis of ischemic nephropathy or atheroembolic disease should be entertained when renal function continues to worsen despite optimization of cardiac function.
    • Decreased effective arterial volume due to systemic shunting can result from sepsis or liver failure (hepatorenal syndrome [HRS]). These patients often pose a management problem because of severe edema, hyponatremia, and hypoalbuminemia. Decreased oncotic pressure and increased vascular permeability, as well as exaggerated salt and water retention, shift the Starling forces toward formation of interstitial fluid. Effective treatment of sepsis with the appropriate antibiotics and hypotension with dopamine and norepinephrine is mandated. Crystalloid replacement can be tried, but it often leads to more edema.
    • For the severely hypoalbuminemic patient, salt-poor albumin infusion can be undertaken, but there is no conclusive evidence of benefit. Adequate nutrition and effective treatment of sepsis may improve oncotic pressure and normalize vascular permeability, thereby decreasing the systemic shunting. The net result is improved renal perfusion, decreased salt and water retention, improved output, and edema. In the HRS, the average survival is 1-2 weeks; however, there is evidence that the kidneys will recover with early liver transplantation. Occasionally, renal function is advanced, requiring replacement therapy.
  • Intrarenal azotemia
    • Acute renal failure (acute kidney injury)
      • Ischemic or nephrotoxic ATN
        • The initial approach is to restore pressure (with fluid replacement) and to withdraw nephrotoxic drugs. If oliguria persists, albumin in combination with high-dose furosemide should be tried. The use of albumin in this context allows more Lasix to be bound to albumin for delivery to the organic anion transporter in the kidney, thereby allowing more Lasix to enter the tubule than would otherwise enter it. The administration of albumin in this setting is not for volume expansion. Although this approach is widely used, there is no supporting evidence for it.
        • Other approaches that have no conclusive benefit include renal dose dopamine and synthetic atrial natriuretic peptide. The renal failure phase usually lasts 7-21 days if the primary insult can be corrected. Postischemic polyuria can be seen in the recovery phase and represents an attempt to excrete excess water and solute. Saline may be replaced (75% of output) as maintenance fluid because of salt wasting during this phase. Hypokalemia may result from the saline diuresis. However, matching the hourly output with intravenous replacement is not recommended. Recovery is marked by the return of BUN and creatinine levels to near baseline values.
      • Acute interstitial nephritis: Management is by withdrawal of the offending nephrotoxin, avoidance of further nephrotoxic exposure, and dehydration. The creatinine level begins to improve within 3-5 days. Renal biopsy may be indicated if renal failure is severe or azotemia is not improving. Once the diagnosis is confirmed, a trial of oral prednisone (starting at 1 mg/kg/d and tapering over 6 wk) or intravenous pulse methylprednisolone (1 g for 3 d) in severe cases can be considered. If the patient is a poor candidate for biopsy but the diagnosis is strongly suspected, therapy should be started.
      • Radiocontrast-induced azotemia: This becomes evident 3-5 days after exposure. It is best prevented with adequate hydration with half-normal saline at 1 mL/kg/h 12 hours prior to administration of contrast and the use of smaller amounts of contrast. Clearly explain the risks of such procedures to the patient. The benefits of N -acetylcysteine and sodium bicarbonate are still being debated.[7, 8, 9] Until further evidence is derived from clinical trials, there are no contraindications for using these agents to help prevent contrast-induced nephropathy.
    • Chronic kidney disease
      • It is important that patients with CKD be referred early to a nephrologist for the management of complications and for the transition to renal replacement therapy (ie, hemodialysis, peritoneal dialysis, renal transplantation). There is some evidence that early referral of patients with CKD improves short-term outcome.
      • Disease progression can be slowed by various maneuvers, such as aggressive control of diabetes, hypertension, and proteinuria, and dietary protein and phosphate restriction, as well as specific therapies for some of the glomerular diseases, such as lupus.
      • Anemia, hyperphosphatemia, acidosis, and hypocalcemia should be aggressively managed prior to renal replacement therapy.
  • Postrenal azotemia
    • Relief of the obstruction is the mainstay of therapy.
    • In anuria, bladder catheterization is mandatory to rule out bladder neck obstruction, whereas in progressive azotemia, catheterization should be done after the patient has voided to determine the postvoid residual volume. A postvoid residual volume of 100 mL or more is suggestive of obstructive uropathy, and the cause should be further investigated.
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Surgical Care

  • Unilateral or bilateral percutaneous nephrostomy
    • If hydronephrosis is due to ureteral obstruction, unilateral or bilateral stents or percutaneous nephrostomy is performed. Recovery of renal function takes 7-10 days, but renal function may be severely impaired, requiring dialysis until such time that partial recovery is adequate for withdrawal of dialysis.
    • Up to 500-1000 mL/min of postobstructive polyuria can be seen with relief of obstruction, which is appropriate and represents an attempt to excrete the excess fluid during the period of obstruction.
    • Because of salt wasting during this phase, dehydration and hypokalemia are likely. Thus, two thirds of the urine output should be replaced with half-normal saline and potassium chloride if hypokalemic. Close monitoring is indicated to prevent hypotension and prerenal azotemia.
    • Matching the hourly urine output with intravenous fluids is not recommended since excess water retention during the period of obstruction cannot be lost if hourly urine output is matched.
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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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