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Azotemia Treatment & Management

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

Pharmacologic and Supportive Therapy

Prerenal azotemia

If volume depletion is due to free water loss, the serum sodium is often elevated by 10 mEq/L from baseline. The amount of fluid replacement in liters—that is, the free water deficit—can be estimated from serum sodium (mg/dL) and patient weight (kg) as follows:

[(Na/140) – 1] × 0.5 × weight

The volume of fluid to be administered is equal to the sum of the free-water deficit and daily maintenance fluids. Fifty percent of this total volume should be administered in the first 24 hours, and a new calculation should be performed at 24 hours based on new laboratory results.

Maintenance fluid can be roughly estimated at 1.5-2 L/day; however, it can also be estimated from caloric intake since 1 kCal requires 1 mL of water in the metabolic process. Normal caloric intake is about 30 Kcal/kg (low catabolic state requires < 30 kCal/kg and high catabolic state requires >40 kCal/kg). A 70-Kg person at normal caloric intake requires 2100 Kcal/day or 2.1 L of fluid intake. This volume should be added to the free-water deficit and administered as noted above.

Alternatively, the total free water deficit is usually quite close to the sum of 50% free-water deficit and daily maintenance fluids. Therefore, for all practical purposes, the total free-water deficit can be administered intravenously in 24 hours.

The fluid to be administered should consist of hypotonic solutions such as 0.5% saline or 5% dextrose in water (D5W). Alert patients should be encouraged to drink as much free water as they can tolerate; 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 in the serum sodium. To prevent brain edema, the rate of decrease in serum sodium should be no more than 0.7 mEq/h (17 mEq/24 h). 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 that necessitates replacement with normal saline. Normal–anion gap metabolic acidosis occurring with diarrhea warrants infusion of bicarbonate in 0.5% normal saline.

Diuretic-induced volume depletion, especially in the elderly, manifests as dehydration, hyponatremia,[8] and, occasionally, hypokalemia. The treatment of choice consists of normal saline infusion and correction of hypokalemia.

Decreased cardiac output requires optimization of cardiac performance through careful use of diuretics, an angiotensin-converting enzyme (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. Because 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.

Reduced effective arterial volume due to systemic shunting can result from sepsis or liver failure. Severe edema, hyponatremia, and hypoalbuminemia often pose management problems. Decreased oncotic pressure, increased vascular permeability, and exaggerated salt and water retention shift the Starling forces toward formation of interstitial fluid. Effective treatment of sepsis with antibiotics and of hypotension with dopamine and norepinephrine is mandated. Crystalloid replacement can be tried, but it often leads to more edema.

In severely hypoalbuminemic patients, salt-poor albumin infusion may 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 hepatorenal syndrome (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, necessitating replacement therapy.

Intrarenal azotemia

Acute renal failure (acute kidney injury)

For ischemic or nephrotoxic acute tubular necrosis (ATN) due to shock (hypovolemic, cardiogenic, septic), the initial approach is to restore volume and pressure (with fluid replacement and vasopressors, respectively) and to withdraw any nephrotoxic drugs.[9] . If the patient becomes oliguric or anuric from shock, volume in the form of crystalloids should be aggressively administered as boluses (eg, 300 mL every 2 hours, rather than 150 mL every hour). Bolus infusion leads to acute intravascular volume expansion, release of atrial natriuretic peptide from the heart, increased renal blood flow, and natriuresis, all of which are favorable in recovery from ATN compared with slow intravenous hydration.

If at least 2 L of fluids has been administered in a relatively short period (approximately 12 hours) with no improvement in urine output, a trial of high-dose intravenous furosemide at 100-160 mg can be tried, prior to preparation for renal replacement. This approach, called “tank and blast” in shock, is clinically useful but almost no evidence supports it. In one small study, hemodynamic and renal support with a continuous infusion of noradrenaline (0.06-0.12 microg/kg/min) and furosemide (10-30 mg/hr) induced polyuria and reversed acute tubular necrosis to nonoliguric acute renal failure in 11 of 14 cancer patients who had severe sepsis and multiorgan dysfunction syndrome.[10] If the patient does not respond within 6 hours of this approach, dialysis or continuous renal replacement therapy should be considered as soon as possible.

If the patient responds by restoration of urine output to greater than 30 mL/h, continue on the appropriate amounts of intravenous fluids, vasopressors, and as-needed diuretics to keep the patient at the desired fluid balance (negative, positive, or match intake to output).

This approach is not indicated in nonshock patients with AKI. Nonshock patients with AKI require maintenance fluids, if needed, and avoidance of nephrotoxicity.

In both scenarios, early initiation of renal replacement therapy if azotemia sets in has a better prognosis than late initiation.

Albumin can be administered in combination with high-dose furosemide to enhance the diuretic effect of furosemide. The use of albumin in this context is not for volume expansion; rather, it allows more furosemide to be bound to albumin for delivery to the organic anion transporter in the kidney, thereby enabling more furosemide to enter the tubule than would otherwise do so.

Although this approach is widely used, research on the combination of albumin and a loop diuretic has principally studied its use for improving diuretic-resistant edema in patients with nephrotic syndrome.[11] Other therapies that have not been conclusively shown to be beneficial are 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 a maintenance fluid, owing to salt wasting during this phase, and to allow the patient to lose excess water retained while the patient was oliguric. Hypokalemia may result from the saline diuresis, and potassium should be replaced. Recovery is marked by the return of blood urea nitrogen (BUN) and creatinine levels to near-baseline values.

Acute interstitial nephritis is managed by withdrawing the offending nephrotoxin, avoiding 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/day and tapering over 6 weeks) or IV pulse methylprednisolone (1 g for 3 days) in severe cases may be considered. If the patient is a poor candidate for biopsy but the diagnosis is strongly suspected, therapy should be started.

Contrast-induced azotemia, which typically becomes evident 3-5 days after exposure, is best prevented by adequate hydration with half-normal saline at 1 mL/kg/h 12 hours before contrast administration 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 for preventionof contrast-induced azotemia are still being debated.[12, 13, 14] A systematic review and meta-analysis of prevention strategies found that the greatest clinically and statistically significant reduction in contrast-induced nephropathy occurred with N-acetylcysteine in patients receiving low-osmolar contrast media (compared with IV saline) and with statins plus N-acetylcysteine (compared with N-acetlycysteine alone).[15]

Chronic kidney disease

It is important that patients with chronic kidney disease (CKD) be referred early to a nephrologist for the management of complications and for the transition to renal replacement therapy (ie, hemodialysis, peritoneal dialysis, and renal transplantation). There is some evidence that early referral of patients with CKD improves short-term outcome.

Disease progression can be slowed by means of various maneuvers, such as aggressive control of diabetes, hypertension, and proteinuria; dietary protein and phosphate restriction; and specific therapies for some of the glomerular diseases, such as lupus. Anemia, hyperphosphatemia, acidosis, and hypocalcemia should be aggressively managed before renal replacement therapy.

Postrenal azotemia

Relief of the obstruction is the mainstay of therapy for postrenal azotemia. 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 suggests obstructive uropathy, and the cause should be further investigated.

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Surgical Relief of Obstruction

If hydronephrosis is due to ureteral obstruction, unilateral or bilateral stenting or percutaneous nephrostomy is performed. Recovery of renal function takes 7-10 days, but renal function may be severely impaired, necessitating dialysis until such time as partial recovery is adequate for withdrawal of dialysis.

Up to 500-1000 mL/min of postobstructive polyuria can be seen with relief of obstruction. This is an appropriate response and represents an attempt to excrete the excess fluid accumulated 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 the patient is hypokalemic. Close monitoring is indicated to prevent hypotension and prerenal azotemia.

Matching the hourly urine output with IV replacement fluid is not recommended, because the excess water retained during the period of obstruction cannot be offloaded 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 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

References
  1. Delanaye P, Cohen EP. Formula-based estimates of the GFR: equations variable and uncertain. Nephron Clin Pract. 2008. 110(1):c48-53. [Medline].

  2. Eklof H, Bergqvist D, Hagg A, et al. Outcome after endovascular revascularization of atherosclerotic renal artery stenosis. Acta Radiol. 2009 Apr. 50(3):256-64. [Medline].

  3. Mindikoglu AL, Weir MR. Current concepts in the diagnosis and classification of renal dysfunction in cirrhosis. Am J Nephrol. 2013. 38(4):345-54. [Medline]. [Full Text].

  4. Carvounis CP, Nisar S, Guro-Razuman S. Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney Int. 2002 Dec. 62(6):2223-9. [Medline]. [Full Text].

  5. Faubel S, Patel NU, Lockhart ME, Cadnapaphornchai MA. Renal relevant radiology: use of ultrasonography in patients with AKI. Clin J Am Soc Nephrol. 2014 Feb. 9(2):382-94. [Medline]. [Full Text].

  6. Holmquist F, Hansson K, Pasquariello F, et al. Minimizing contrast medium doses to diagnose pulmonary embolism with 80-kVp multidetector computed tomography in azotemic patients. Acta Radiol. 2009 Mar. 50(2):181-93. [Medline].

  7. Sofocleous CT, Bahramipour P, Mele C, et al. Transvenous transjugular renal core biopsy with a redesigned biopsy set including a blunt-tipped needle. Cardiovasc Intervent Radiol. 2002 Mar-Apr. 25(2):155-7. [Medline].

  8. Fenske W, Stork S, Koschker AC, et al. Value of fractional uric acid excretion in differential diagnosis of hyponatremic patients on diuretics. J Clin Endocrinol Metab. 2008 Aug. 93(8):2991-7. [Medline].

  9. Liu KD, Matthay MA, Chertow GM. Evolving practices in critical care and potential implications for management of acute kidney injury. Clin J Am Soc Nephrol. 2006 Jul. 1(4):869-73. [Medline]. [Full Text].

  10. Zahorec R, Setvak D, Cintula D, Belovicova C, Blaskova A. Renal rescue therapy in early stage of severe sepsis: a case study approach. Bratisl Lek Listy. 2004. 105 (10-11):345-52. [Medline].

  11. Duffy M, Jain S, Harrell N, Kothari N, Reddi AS. Albumin and Furosemide Combination for Management of Edema in Nephrotic Syndrome: A Review of Clinical Studies. Cells. 2015 Oct 7. 4 (4):622-30. [Medline]. [Full Text].

  12. Marenzi G, Assanelli E, Marana I, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med. 2006 Jun 29. 354(26):2773-82. [Medline]. [Full Text].

  13. Recio-Mayoral A, Chaparro M, Prado B, et al. The reno-protective effect of hydration with sodium bicarbonate plus N-acetylcysteine in patients undergoing emergency percutaneous coronary intervention: the RENO Study. J Am Coll Cardiol. 2007 Mar 27. 49(12):1283-8. [Medline].

  14. Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000 Jul 20. 343(3):180-4. [Medline].

  15. Subramaniam RM, Suarez-Cuervo C, Wilson RF, Turban S, Zhang A, Sherrod C, et al. Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis. Ann Intern Med. 2016 Feb 2. [Medline].

 
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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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