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Acute Tubular Necrosis Clinical Presentation

  • Author: Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Dec 21, 2015
 

History

The patient’s history is very important in the diagnosis of acute tubular necrosis (ATN). It frequently reveals recent hypotension, sepsis, muscle necrosis, or volume depletion, as well as exposure to nephrotoxic agents. Patients with rhabdomyolysis present with severe muscle pains and generalized soreness.

ATN is more likely to occur in patients with a history of recent surgery, sepsis, or hypovolemia. The history is also important in establishing risk factors for the development of ATN.

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Physical Examination

Physical examination findings may be unremarkable because acute kidney injury (AKI) is often found incidentally on routine laboratory studies (ie, elevated blood urea nitrogen [BUN] and creatinine levels). However, if symptoms are present, they may include a pericardial friction rub, asterixis, and/or excoriation marks related to uremic pruritus. Hypertension or edema may be noted.

Otherwise, the physical examination findings are more likely to reflect the underlying disease process. For example, in a patient with rhabdomyolysis, physical examination may disclose tender “doughy” muscles, with significant edema of the involved extremities. In severe cases, compartmental compression syndromes, particularly characterized by neurovascular compromise, may occur.

The 2011 UKRA AKI guidelines state that physiological observation should be performed for all patients with AKI to find early signs of physiological deterioration that may require a rise in the level of care.[3]

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Complications of Acute Tubular Necrosis

Complications of ATN include fluid and electrolyte imbalances, uremia, infections, and anemia. Specific imbalances vary with the phase of illness; during oliguria, salt and water retention often leads to hypertension, edema, and heart failure. The polyuric phase of ATN may lead to hypovolemia and create a setting for prerenal azotemia and perpetuation of ATN.

Altered fluid and electrolyte balance

Clearly, the maintenance of fluid and electrolyte balance is critical. Hyperkalemia can be associated with life-threatening cardiac arrhythmias (eg, ventricular tachycardia or fibrillation, complete heart block, bradycardia, asystole). Arrhythmias have been reported in up to 30% of patients. On electrocardiography (ECG), hyperkalemia manifests as peaked T waves, prolonged PR interval, P wave flattening, and a widened QRS complex.

In addition to these worrisome cardiac effects, hyperkalemia can also lead to neuromuscular dysfunction and, potentially, respiratory failure. Hyperkalemia can be treated with glucose and insulin, binding resins, or, if necessary, dialysis.

Hyponatremia causes concern because of its effects on the central nervous system. In general, correction of hyponatremia should be of sufficient rapidity and magnitude as to reverse the manifestations of hypotonicity, but not be so rapid or large as to potentiate the risk of osmotic demyelination. The most recent published guidelines on treatment of hyponatremia recommend rates of correction of serum sodium ranging from 8 to 12 mmol/L per 24 h.[6] Go to Hyponatremia for complete information on this topic.

Other electrolyte disturbances include hyperphosphatemia, hypocalcemia, and hypermagnesemia. Hypocalcemia may be secondary to both deposition of calcium phosphate and reduced levels of 1,25-dihydroxyvitamin D. It is usually asymptomatic, but hypocalcemia may result in nonspecific ECG changes, muscle cramps, or seizures.

In rhabdomyolysis, hypocalcemia results from deposition of calcium in the injured muscle. Such deposited calcium is eventually released back into the circulation during the recovery phase, thereby accounting for transient hypercalcemia. For this reason, calcium administration is generally not recommended for hypocalcemia during the acute phase of rhabdomyolysis, unless the patient is symptomatic.

The 2011 UKRA guidelines recommend administering 0.9% sodium chloride and sodium bicarbonate for intravenous volume expansion in patients at risk of developing AKI secondary to rhabdomyolysis.[3] Metabolic acidosis may occur. It may be treated with bicarbonate or dialysis as well.

Uremia

Uremia results from the accumulation of nitrogenous waste. It is a potentially life-threatening complication associated with AKI. This may manifest as pericardial disease, gastrointestinal symptoms (ie, nausea, vomiting, cramping), and/or neurologic symptoms (ie, lethargy, confusion, asterixis, seizures). Platelet dysfunction is common and can lead to life-threatening hemorrhage.

Infections

Aggressive treatment of infections is prudent. Infections remain the leading cause of morbidity and mortality and can occur in 30-70% of patients with AKI. Infections are more likely in these patients because of an impaired immune system (eg, uremia, inappropriate use of antibiotics) and because of increased use of indwelling catheters and intravenous needles.

Anemia

Anemia may develop from many possible causes. Erythropoiesis is reduced in AKI. Patients with ATN-related uremia may have platelet dysfunction and subsequent hemorrhage leading to anemia. In addition, volume overload may lead to hemodilution, and red cell survival time may be decreased. Anemia can be corrected with blood transfusions.

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Contributor Information and Disclosures
Author

Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF Clinical Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Research Director, Internal Medicine Training Program, Advocate Christ Medical Center; Consulting Staff, Associates in Nephrology, SC

Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF is a member of the following medical societies: American Heart Association, American Medical Association, American Society of Hypertension, American Society of Nephrology, Chicago Medical Society, Illinois State Medical Society, National Kidney Foundation, Society of General Internal Medicine

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Otsuka, Mallinckrodt, ZS Pharma<br/>Author for: UpToDate, ACP Smart Medicine.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation

Disclosure: Received ownership interest/medical directorship from South Shore DaVita Dialysis Center for other; Received ownership/medical directorship from Space City Dialysis /American Renal Associates for same; Received ownership interest from US Renal Care for other.

Brent Kelly, MD Assistant Professor, Department of Dermatology, University of Texas Medical Branch, Galveston, Texas

Brent Kelly, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association

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.

F John Gennari, MD Associate Chair for Academic Affairs, Robert F and Genevieve B Patrick Professor, Department of Medicine, University of Vermont College of Medicine

F John Gennari, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society of Nephrology, and International Society of Nephrology

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 Salary Employment

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A photomicrograph of renal biopsy shows renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells is observed, suggesting acute tubular necrosis (ATN) as the cause of acute kidney injury (AKI).
Acute tubular necrosis (ATN). Flattening of the renal tubule cells due to tubular dilation.
Acute tubular necrosis. Intratubular cast formation.
Acute tubular necrosis. Intratubular obstruction due to the denuded epithelium and cellular debris. Note that the denuded tubular epithelial cells clump together due to rearrangement of intercellular adhesion molecules (ICAM).
Sloughing of cells, which is responsible for the formation of granular casts, a feature of acute tubular necrosis (ATN).
Table. Laboratory Findings Used to Differentiate Prerenal Azotemia From ATN
Finding Prerenal Azotemia ATN and/or Intrinsic Renal Disease
Urine osmolarity



(mOsm/kg)



>500 < 350
Urine sodium



(mmol/d)



< 20 >40
Fractional excretion of sodium (FENa)



(%)



< 1 >2
Fractional excretion of urea



(%)



< 35 >50
Urine sediment Bland and/or nonspecific May show muddy brown granular casts
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