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Acute Kidney Injury Clinical Presentation

  • Author: Biruh T Workeneh, MD, PhD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Oct 31, 2015
 

History

A detailed and accurate history is crucial for diagnosing acute kidney injury (AKI) and determining treatment. Distinguishing AKI from chronic kidney disease is important, yet making the distinction can be difficult; chronic kidney disease is itself an important risk factor for AKI.[30] A history of chronic symptoms—months of fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus—suggests chronic kidney disease. AKI can cause identical symptoms, but over a shorter course.

It is important to elicit a history of any of the following etiologic factors:

  • Volume restriction (eg, low fluid intake, gastroenteritis)
  • Nephrotoxic drug ingestion (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], aminoglycosides) [30]
  • Exposure to iodinated contrast agents within the past week [30]
  • Trauma or unaccustomed exertion
  • Blood loss or transfusions
  • Exposure to toxic substances, such as ethyl alcohol or ethylene glycol
  • Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners

People with the following comorbid conditions are at a higher risk for developing AKI:

  • Hypertension
  • Chronic heart failure
  • Diabetes
  • Liver disease
  • Obesity [31, 32, 33]
  • Multiple myeloma
  • Chronic infection
  • Myeloproliferative disorder
  • Connective tissue disorders
  • Autoimmune diseases

Urine output history can be useful. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.

Because of a decrease in functioning nephrons, even a trivial nephrotoxic insult may cause AKI to be superimposed on chronic renal insufficiency.

Acute kidney injury (AKI) has a long differential diagnosis. The history can help to classify the pathophysiology of AKI as prerenal, intrinsic renal, or postrenal failure, and it may suggest some specific etiologies.

Prerenal failure

Patients commonly present with symptoms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension. Ask about volume loss from vomiting, diarrhea, sweating, polyuria, or hemorrhage. Patients with advanced cardiac failure leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal dyspnea.

Elders with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI. Insensible fluid losses can result in severe hypovolemia in patients with restricted fluid access and should be suspected in elderly patients and in comatose or sedated patients.

Intrinsic renal failure

Patients can be divided into those with glomerular etiologies and those with tubular etiologies of AKI. Nephritic syndrome of hematuria, edema, and hypertension indicates a glomerular etiology for AKI. Query about prior throat or skin infections. Acute tubular necrosis (ATN) should be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.

A careful search for exposure to nephrotoxins should include a detailed list of all current medications and any recent radiologic examinations (ie, exposure to radiologic contrast agents). Pigment-induced AKI should be suspected in patients with possible rhabdomyolysis (muscular pain, recent coma, seizure, intoxication, excessive exercise, limb ischemia) or hemolysis (recent blood transfusion). Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and antibiotics.

Postrenal failure

Postrenal failure usually occurs in older men with prostatic obstruction and symptoms of urgency, frequency, and hesitancy. Patients may present with asymptomatic, high-grade urinary obstruction because of the chronicity of their symptoms. A history of prior gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to the level of obstruction.

Flank pain and hematuria should raise a concern about renal calculi or papillary necrosis as the source of urinary obstruction. Use of acyclovir, methotrexate, triamterene, indinavir, or sulfonamides implies the possibility that crystals of these medications have caused tubular obstruction.

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Physical Examination

Obtaining a thorough physical examination is extremely important when collecting evidence about the etiology of AKI. Clues may be found in any of the following:

  • Skin
  • Eyes
  • Ears
  • Cardiovascular system
  • Abdomen
  • Pulmonary system

Skin

Skin examination may reveal the following:

  • Livido reticularis, digital ischemia, butterfly rash, palpable purpura - Systemic vasculitis
  • Maculopapular rash - Allergic interstitial nephritis
  • Track marks (ie, intravenous drug abuse) - Endocarditis

Petechiae, purpura, ecchymosis, and livedo reticularis provide clues to inflammatory and vascular causes of AK. Infectious diseases, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), and embolic phenomena can produce typical cutaneous changes.

Eyes and ears

Eye examination may reveal the following:

  • Keratitis, iritis, uveitis, dry conjunctivae - Autoimmune vasculitis
  • Jaundice - Liver diseases
  • Band keratopathy (ie, hypercalcemia) - Multiple myeloma
  • Signs of diabetes mellitus
  • Signs of hypertension
  • Atheroemboli - Retinopathy

Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis. Ocular palsy may indicate ethylene glycol poisoning or necrotizing vasculitis. Findings suggestive of severe hypertension, atheroembolic disease, and endocarditis may be observed on careful examination of the eyes.

Ear examination may reveal the following:

  • Hearing loss - Alport disease and aminoglycoside toxicity
  • Mucosal or cartilaginous ulcerations - Wegener granulomatosis

Cardiovascular system

The most important part of the physical examination is the assessment of cardiovascular and volume status. The physical examination must include the following:

  • Pulse rate and blood pressure recordings measured in the supine and the standing position
  • Close inspection of the jugulovenous pulse
  • Careful examination of the heart and lungs, skin turgor, and mucous membranes
  • Assessment for peripheral edema

Cardiovascular examination may reveal the following:

  • Irregular rhythms (ie, atrial fibrillation) - Thromboemboli
  • Murmurs - Endocarditis
  • Pericardial friction rub - Uremic pericarditis
  • Increased jugulovenous distention, rales, S 3 - Heart failure

In hospitalized patients, accurate daily records of fluid intake and urine output, as well as daily measurements of patient weight, are important. Hypovolemia leads to hypotension; however, hypotension may not necessarily indicate hypovolemia.

Severe heart failure may also cause hypotension. Although patients with heart failure may have low blood pressure, volume expansion is present and effective renal perfusion is poor, which can result in AKI.

Severe hypertension with renal failure suggests one of the following disorders:

  • Renovascular disease
  • Glomerulonephritis
  • Vasculitis
  • Atheroembolic disease

Abdomen

Abdominal examination may reveal the following:

  • Pulsatile mass or bruit - Atheroemboli
  • Abdominal or costovertebral angle tenderness - Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis
  • Pelvic, rectal masses; prostatic hypertrophy; distended bladder – Urinary obstruction
  • Limb ischemia, edema - Rhabdomyolysis

Abdominal examination findings can be useful in helping to detect obstruction at the bladder outlet as the cause of renal failure; such obstruction may be due to cancer or to an enlarged prostate.

The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return and result in AKI. The presence of an epigastric bruit suggests renal vascular hypertension, which may predispose to AKI.

Pulmonary system

Pulmonary examination may reveal the following:

  • Rales - Goodpasture syndrome, Wegener granulomatosis
  • Hemoptysis - Wegener granulomatosis
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Contributor Information and Disclosures
Author

Biruh T Workeneh, MD, PhD FASN, Assistant Professor of Nephrology, Baylor College of Medicine

Biruh T Workeneh, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, Texas Medical Association

Disclosure: Nothing to disclose.

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.

Rajiv Gupta, MD Assistant Professor, Department of Medicine, Texas A&M Health Science Center College of Medicine; Consulting Staff, Veterans Affairs Medical Center

Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

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

Aruna Agraharkar, MD, FACP Consulting Staff, Department of Gerontology, Space Center Clinic

Aruna Agraharkar, MD, FACP is a member of the following medical societies: American Medical Assocation

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Laura Lyngby Mulloy, DO, FACP Professor of Medicine, Chief, Section of Nephrology, Hypertension, and Transplantation Medicine, Glover/Mealing Eminent Scholar Chair in Immunology, Medical College of Georgia

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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Photomicrograph of a renal biopsy specimen shows renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells with loss of brush border is observed, suggesting acute tubular necrosis as the cause of acute renal failure.
Flattening of the renal tubular cells due to tubular dilation.
Intratubular cast formation.
Intratubular obstruction due to the denuded epithelium and cellular debris. Note that the denuded tubular epithelial cells clump together because of rearrangement of intercellular adhesion molecules.
Sloughing of cells, which is responsible for the formation of granular casts, is a feature of acute tubular necrosis.
Table 1. RIFLE Classification System for Acute Kidney Injury
Stage GFR** Criteria Urine Output Criteria Probability
Risk SCreat increased × 1.5



or



GFR decreased >25%



UO < 0.5 mL/kg/h × 6 h High sensitivity (Risk >Injury >Failure)
Injury SCreat increased × 2



or



GFR decreased >50%



UO < 0.5 mL/kg/h × 12 h
Failure SCreat increased × 3



or



GFR decreased 75%



or



SCreat ≥4 mg/dL; acute rise ≥0.5 mg/dL



UO < 0.3 mL/kg/h × 24 h



(oliguria)



or



anuria × 12 h



Loss Persistent acute renal failure: complete loss of kidney function >4 wk High specificity
ESKD* Complete loss of kidney function >3 mo
*ESKD—end-stage kidney disease; **GFR—glomerular filtration rate; †SCreat—serum creatinine; ‡UO—urine output



Note: Patients can be classified by GFR criteria and/or UO criteria. The criteria that support the most severe classification should be used. The superimposition of acute on chronic failure is indicated with the designation RIFLE-FC; failure is present in such cases even if the increase in SCreat is less than 3-fold, provided that the new SCreat is greater than 4.0 mg/dL (350 µmol/L) and results from an acute increase of at least 0.5 mg/dL (44 µmol/L).



Table 2. Acute Kidney Injury Network Classification/Staging System for AKI [3]
Stage Serum Creatinine Criteria Urine Output Criteria
1 Increase of ≥0.3 mg/dL (≥26.4 µmol/L) or 1.5- to 2-fold increase from baseline < 0.5 mL/kg/h for >6 h
2 >2-fold to 3-fold increase from baseline < 0.5 mL/kg/h for >12 h
3* >3-fold increase from baseline, or increase of ≥ 4.0 mg/dL (≥35.4 µmol/L) with an acute increase of at least 0.5 mg/dL (44 µmol/L) < 0.3 mL/kg/h for 24 h or anuria for 12 h
*Patients who receive renal replacement therapy (RRT) are considered to have met the criteria for stage 3 irrespective of the stage they are in at the time of RRT.
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