Acute Kidney Injury in Pediatric Patients
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Acute Kidney Injury in Pediatric Patients: Diagnosis and Management in the Emergency Department

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Table of Contents
 
About This Issue

Pediatric acute kidney injury is a condition that is underdiagnosed among children seen in the emergency department, and it has been associated with significant morbidity and mortality, including increased risk for chronic kidney disease. The most common etiologies in pediatric patients are now known to be due to hypovolemia, sepsis, shock, and cardiac dysfunction. This issue compares 3 classification systems for the diagnosis and staging of acute kidney injury and reviews the etiologies that lead to kidney injury in children. The management of pediatric acute kidney injury focuses on identifying patients at high risk, monitoring intravascular volume status, avoiding nephrotoxic medication exposure, and involving a pediatric nephrologist once acute kidney injury is diagnosed.

Table of Contents
  1. Abstract
  2. Case Presentations
  3. Introduction
  4. Critical Appraisal of the Literature
  5. Classification of the Stages of Acute Kidney Injury
    1. RIFLE/pRIFLE Criteria
  6. Etiology and Pathophysiology
    1. Prerenal Acute Kidney Injury
    2. Intrinsic Acute Kidney Injury
      1. Intrinsic Acute Kidney Injury Caused by Nephrotoxin Exposure
        • Nonsteroidal Anti-inflammatory Drugs
        • Acetaminophen
        • Contrast-Induced Nephropathy
      2. Intrinsic Acute Kidney Injury Caused by Vascular Damage
        • Hemolytic Uremic Syndrome
        • Rhabdomyolysis
      3. Intrinsic Acute Kidney Injury Caused by Glomerular Damage
    3. Postrenal Acute Kidney Injury
  7. Differential Diagnosis
  8. Prehospital Care
  9. Emergency Department Evaluation
    1. History
    2. Physical Examination
  10. Diagnostic Studies
    1. Laboratory Studies
      1. Serum Creatinine
      2. Metabolic Panel and Additional Serum Testing
      3. Urinalysis
      4. Other Laboratory Studies
    2. Imaging Studies
  11. Prevention and Treatment
    1. Fluid Resuscitation
    2. Vasopressors and Inotropes
    3. Mannitol and Loop Diuretics
    4. Alkali Therapy
    5. Intravenous Fluids
      1. Prevention of Contrast-Induced Nephropathy
      2. Treatment of Electrolyte Derangements
    6. Renal Replacement Therapy
    7. Nephrology Consultation
  12. Special Circumstances
    1. Trauma
    2. Children With Special Needs
    3. Children With Solitary Functioning Kidneys
    4. Patients Who Have Had a Kidney Transplant
  13. Controversies and Cutting Edge
    1. Biomarkers for Diagnosis of Acute Kidney Injury
    2. Novel Therapies for Acute Kidney Injury
  14. Disposition
  15. Summary
  16. Risk Management Pitfalls in Pediatric Patients With Acute Kidney Injury
  17. Time- and Cost-Effective Strategies
  18. Case Conclusions
  19. Clinical Pathway for Management of Pediatric Patients With Suspected Acute Kidney Injury
  20. Tables and Figures
    1. Table 1. Comparison of the Current Classification Systems for Acute Kidney Injury
    2. Table 2. Etiology and Pathophysiology of Acute Kidney Injury
    3. Table 3. Commonly Used Medications With Potential for Nephrotoxicity
    4. Table 4. Reference Values for Creatinine Based on Age
    5. Figure 1. Analysis of Kidney Perfusion
    6. Figure 2. Ultrasound Imaging of Kidneys
  21. References

Abstract

Pediatric acute kidney injury is a condition that is underdiagnosed among children seen in the emergency department, and it has been associated with significant morbidity and mortality, including increased risk for chronic kidney disease. The most common etiologies in pediatric patients are now known to be due to hypovolemia, sepsis, shock, and cardiac dysfunction. This issue compares 3 classification systems for the diagnosis and staging of acute kidney injury and reviews the etiologies that lead to kidney injury in children. The management of pediatric acute kidney injury focuses on identifying patients at high risk, monitoring intravascular volume status, avoiding nephrotoxic medication exposure, and involving a pediatric nephrologist once acute kidney injury is diagnosed.

Case Presentation

An otherwise-healthy 3-year-old girl presents to the ED. According to the child’s mother, her daughter has been vomiting after meals for 3 days and has had 5 episodes of nonbloody, liquid diarrhea today. The mother also states that the girl drank only 4 oz of juice and 4 oz of water yesterday and would only drink half as much today. The girl has urinated only once today. She is afebrile, with a heart rate of 145 beats/min and a blood pressure of 80/30 mm Hg. On examination, the girl appears tired, has dry mucous membranes, and a capillary refill time of 3 seconds. She has diffuse abdominal tenderness but no costovertebral angle tenderness and no rash.

In the next room, a 16-year-old adolescent boy who was diagnosed with osteosarcoma 4 months ago and recently underwent treatment with cisplatin has presented with 1 day of diffuse abdominal and back pain associated with nausea, vomiting, and a decrease in oral intake and urine output.

Which historical or physical examination findings in these patients would warrant an evaluation for acute kidney injury? Which laboratory tests or imaging would be most useful in the diagnosis of these patients? How should the risk of kidney injury affect your medical management of these patients?

Introduction

Acute kidney injury (AKI) refers to a sudden loss of kidney function resulting in a decline in the glomerular filtration rate (GFR) and a reduced capacity to excrete nitrogenous waste and regulate extracellular volume and electrolytes. AKI is an increasing problem in children as the medical care being administered becomes increasingly complex. An initial report of hospitalization data revealed an AKI diagnosis in 3.9 per 1000 hospitalized patients; however, the true incidence may be higher, as most diagnostic criteria rely on knowledge of a patient's baseline creatinine level.1-4 While the incidence of AKI is higher among children who are hospitalized or in the intensive care unit (ICU), the incidence among children presenting to the emergency department (ED) is unclear.5 In one surveillance study, only 18.5% of pediatric patients who had AKI during hospitalization were diagnosed in the ED, with the majority developing AKI after admission.6

The true incidence of pediatric AKI (pAKI) is partly unknown due to the lack of consensus regarding the definition of pAKI and the lack of prospective data. However, available studies suggest that pAKI is slightly more prevalent among boys than girls (1.3:1) and among black patients as compared with other races.1 Previously, the most common causes of pAKI in hospitalized patients were thought to be hemolytic uremic syndrome, glomerulonephritis, and primary renal pathology. More recent data have identified sepsis, surgery for congenital heart disease involving cardiopulmonary bypass, nephrotoxic drug exposure, and oncologic illness as having the highest association with pAKI.7 With these other associated disease processes, pAKI diagnosis and management may be overlooked in the ED setting.

Beyond the potentially worsening acute clinical processes taking place, pAKI may also be a risk factor for chronic kidney disease (CKD),3 which affects 26 million Americans and is responsible for over $40 billion of Medicare payments annually.8 Previously, AKI was thought to be a transient and reversible process; however, animal studies have shown that episodes of AKI can cause a permanent reduction in peritubular capillaries, predisposing a patient to further renal hypoxia, inflammation, and eventually fibrosis.9 In a retrospective meta-analysis of 346 pediatric patients, Greenberg et al demonstrated a high rate of proteinuria, hypertension, decreased GFR, and mortality after pAKI; however, the primary studies in this systemic review were small and lacked control groups.Pediatric emergency clinicians may have an opportunity to provide immediate treatment for pAKI, and, in doing so, may mitigate potential long-term effects.

This issue of Pediatric Emergency Medicine Practice focuses on the recently constructed definitions of AKI, the array of diagnoses that are associated with its development, and the management of these patients in the ED setting.

Critical Appraisal of the Literature

The available literature on pAKI and its management was reviewed in PubMed using the search terms acute kidney injury, acute kidney injury management, acute renal failure, kidney failure, renal insufficiency, renal vein thrombosis, prerenal failure, and obstructive renal failure. The search was limited to studies of patients from birth to age 18. Abstracts were reviewed for relevance to the topic, and cited articles within the search results were also considered. Articles that primarily focused on neonatal intensive care or cardiac surgery patient populations were excluded.

The current literature on pAKI includes few high-powered prospective controlled trials, with a greater volume of retrospective data, case reports, and adult studies. Many of the existing pediatric studies are limited by small sample size and a primary focus on ICU patients or those requiring dialysis.10 The greatest limitation is the lack of a single unified classification system; prior to 2004, over 30 definitions of AKI existed in the literature, making cohort analyses virtually impossible.11

Risk Management Pitfalls in Pediatric Patients With Acute Kidney Injury

1. “The rise in creatinine was minimal and the patient was classified in the Risk category of AKI. There was no need to consult nephrology, since this category does not lead to any longterm consequences.”

AKI is not a static process, but can progress throughout the course of a patient’s illness based on the etiology and the management they receive. Thus, AKI in a patient who is in the Risk stage that is not caught early could continue to progress to worsening stages, particularly if the patient has a serious illness, such as sepsis. When AKI is identified, a nephrology consult should be considered, as all patients may be at risk for long-term consequences and should have follow-up even when ”recovered.”

2. “I checked that patient’s creatinine, and the result was within the normal range, so I ruled out AKI.”

While the creatinine level is typically used as a screening tool to diagnose AKI, it is not always a reliable indicator in children. This is due to the relatively low levels of creatinine in children as compared to adults, and the wide range of normal values for different age groups. Since many children do not have baseline values of creatinine available as a reference point, it is  difficult to assess the degree of change based on a measurement at a single point in time.

3. “Muscle aches associated with viral infections are a benign symptom and are not associated with AKI.”

While myalgias are a common complaint associated with viral infections, emergency clinicians should consider viral myositis in their differential as well. In this case, muscle breakdown could lead to rhabdomyolysis and cause AKI. Other causes of rhabdomyolysis include exertion and traumatic crush injuries.

4. “Mannitol is an osmotic diuretic. It improves a patient’s urine output, and, thus, renal function. That’s why it is the best treatment option for AKI.”

While osmotic diuresis facilitated by mannitol can correct a patient’s oliguria, there is no evidence to support the use of mannitol in the prevention or management of AKI. In fact, the administration of mannitol may worsen AKI by causing or worsening nephropathy. This is also true of other diuretics, which should only be used in the setting of volume overload.

5. “Since I didn’t have a baseline creatinine value to compare to my current creatinine level, I ordered a renal ultrasound to determine whether AKI is present.”

Renal ultrasonography is considered the first diagnostic imaging modality of choice for AKI; however, it cannot identify whether AKI is present. In patients with CKD, small kidney size may be noted on ultrasound and may be an indication that the elevated creatinine is not from an acute process. Similarly, in postrenal AKI, the ultrasound may demonstrate hydronephrosis as a cause of elevated creatinine. However, in patients with intrinsic renal disease, the ultrasound may be normal or show enlarged, echogenic kidneys, but this does not distinguish between acute and chronic disease.

6. “The patient’s creatinine did not increase much compared to a prior value in her medical record, so she cannot have AKI.”

Although a rise in creatinine is used in all of the classification systems to define AKI, it is not the most sensitive or reliable test. Creatinine may not rise until up to 50% of the patient’s glomerular filtration is lost, and may not increase during the first 24 to 48 hours of disease, thus delaying the ability of this test to identify patients with AKI.

7. “The patient with AKI was tolerating oral fluids, so I did not consider the need for expedited volume repletion with IV fluids.”

While oral rehydration is often the first-line choice for management of mild dehydration in children, it may be insufficient in the setting of AKI. Moderate-to-severe dehydration, elevated creatinine levels, and decreased urine output should prompt the provider to consider IV fluid replacement therapy. Prompt administration of IV isotonic fluids may improve renal perfusion and lessen further kidney damage. Urine output should be monitored carefully in this setting.

8. “Ibuprofen is a benign medication, and its use in patients is always appropriate.”

Ibuprofen is a commonly administered medication to address pain and/or fever. However, ibuprofen can also cause AKI. The history should include questions regarding a patient’s previous use of ibuprofen, as this is an identifiable risk factor for AKI. The use of ibuprofen should be avoided if it is unnecessary, particularly in a dehydrated patient. After controlling for the degree of dehydration, ibuprofen exposure increased the risk of AKI more than 2-fold in this setting, and concomitant use of ibuprofen and acetaminophen further increased the risk of developing AKI. Therefore, ibuprofen use should be avoided in any child suffering from acute gastroenteritis or other illnesses that may predispose them to hypovolemia.

9. “The urinalysis was negative, so there was no evidence of kidney injury.”

Similar to creatinine, a urinalysis may provide helpful information about the kidneys and their function; however, it is not a useful screening test for AKI. Nonetheless, positive findings on urinalysis may be helpful in the differential diagnosis. The presence of leukocyte esterase or nitrites may indicate a urinary tract infection. The presence of hematuria may indicate nephritis, urolithiasis, trauma, viral cystitis, or myoglobinuria from rhabdomyolysis. The presence of red cell casts is diagnostic of glomerulonephritis. Persistent proteinuria may be an indicator of nephrotic syndrome, tubulointerstitial disease, or glomerular disease, whereas transient proteinuria may have a more benign etiology. The combination of hematuria and proteinuria should suggest a renal disease such as Alport syndrome, membranoproliferative glomerulonephritis, or IgA nephropathy.

10. “There was no evidence of kidney involvement because there was no abdominal pain, back pain, or costovertebral angle tenderness on examination.”

A high degree of suspicion is needed to diagnose AKI in children. There may be no indication from the history or physical examination that a renal problem is present. Pain is often not a presenting sign. Emergency clinicians must consider the risk of AKI when managing other acute problems in children such as dehydration, infection, trauma, drug intoxication, and medication administration.

Tables and Figures

Table 1. Comparison of the Current Classification Systems for Acute Kidney Injury

References

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study is included in bold type following the references, where available. The most informative references cited in this paper, as determined by the authors, are noted by an asterisk (*) next to the number of the reference.

  1. * Sutherland SM, Ji J, Sheikhi FH, et al. AKI in hospitalized children: epidemiology and clinical associations in a national cohort. Clin J Am Soc Nephrol. 2013;8(10):1661-1669. (Cross-sectional analysis; 2,644,263 children)
  2. Vachvanichsanong P, Dissaneewate P, Lim A, et al. Childhood acute renal failure: 22-year experience in a university hospital in southern Thailand. Pediatrics. 2006;118(3):e786-e791. (Retrospective; 311 children)
  3. Askenazi DJ, Feig DI, Graham NM, et al. 3-5 year longitudinal follow-up of pediatric patients after acute renal failure. Kidney Int. 2006;69(1):184-189. (Retrospective; 174 children)
  4. Greenberg JH, Coca S, Parikh CR. Long-term risk of chronic kidney disease and mortality in children after acute kidney injury: a systematic review. BMC Nephrol. 2014;15:184. (Retrospective; 346 patients)
  5. Kaddourah A, Basu RK, Bagshaw SM, et al. Epidemiology of acute kidney injury in critically ill children and young adults. N Engl J Med. 2017;376(1):11-20. (Prospective observational study; 4984 patients)
  6. de Rovetto CR, Mora JA, Alexandre Cardona S, et al. Acute kidney injury applying pRIFLE scale in children of Hospital Universitario del Valle in Cali, Colombia: clinical features, management and evolution. Colomb Med (Cali). 2012;43(3):200-205. (Case series; 27 children)
  7. Ball EF, Kara T. Epidemiology and outcome of acute kidney injury in New Zealand children. J Paediatr Child Health. 2008;44(11):642-646. (Retrospective; 226 children)
  8. National Institute of Diabetes and Digestive and Kidney Diseases (U.S.), USRDS Coordinating Center. U.S. renal data system. Annual data report, researcher’s guide, reference tables, ADR slides. Ann Arbor, MI: National Institute of Diabetes and Digestive and Kidney Diseases, U.S. Renal Data System Coordinating Center. (Government report)
  9. Basile DP, Donohoe DL, Roethe K, et al. Chronic renal hypoxia after acute ischemic injury: effects of L-arginine on hypoxia and secondary damage. Am J Physiol Renal Physiol. 2003;284(2):F338-F348. (Animal study)
  10. *Goldstein SL. Acute kidney injury in children and its potential consequences in adulthood. Blood Purif. 2012;33(1-3):131-137. (Review)
  11. Akcan-Arikan A, Zappitelli M, Loftis LL, et al. Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney Int. 2007;71(10):1028-1035. (Prospective; 150 children)
  12. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8(4):R204-R212. (Consensus)
  13. Van Biesen W, Vanholder R, Lameire N. Defining acute renal failure: RIFLE and beyond. Clin J Am Soc Nephrol. 2006;1(6):1314-1319. (Review)
  14. * Plotz FB, Bouma AB, van Wijk JA, et al. Pediatric acute kidney injury in the ICU: an independent evaluation of pRIFLE criteria. Intensive Care Med. 2008;34(9):1713-1717. (Retrospective; 103 children)
  15. Palmieri T, Lavrentieva A, Greenhalgh D. An assessment of acute kidney injury with modified RIFLE criteria in pediatric patients with severe burns. Intensive Care Med. 2009;35(12):2125-2129. (Retrospective; 123 children)
  16. Bailey D, Phan V, Litalien C, et al. Risk factors of acute renal failure in critically ill children: a prospective descriptive epidemiological study. Pediatr Crit Care Med. 2007;8(1):29-35. (Prospective; 1047 children)
  17. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. (Report)
  18. Kellum JA, Lameire N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care. 2013;17(1):204. (Report)
  19. Sutherland SM, Byrnes JJ, Kothari M, et al. AKI in hospitalized children: comparing the pRIFLE, AKIN, and KDIGO definitions. Clin J Am Soc Nephrol. 2015;10(4):554-561. (Retrospective review; 14,795 pediatric hospitalizations)
  20. Askenazi D. Evaluation and management of critically ill children with acute kidney injury. Curr Opin Pediatr. 2011;23(2):201-207. (Review)
  21. Bridi RA, Balbi AL, Neves PM, et al. Acute kidney injury after massive attack of Africanised bees. BMJ Case Rep. 2014;2014. (Case report)
  22. Toth R, Breuer T, Cserep Z, et al. Acute kidney injury is associated with higher morbidity and resource utilization in pediatric patients undergoing heart surgery. Ann Thorac Surg. 2012;93(6):1984-1990. (Retrospective; 1510 children)
  23. Bresolin N, Bianchini AP, Haas CA. Pediatric acute kidney injury assessed by pRIFLE as a prognostic factor in the intensive care unit. Pediatr Nephrol. 2013;28(3):485-492. (Prospective cohort study; 126 children)
  24. Askenazi DJ, Ambalavanan N, Goldstein SL. Acute kidney injury in critically ill newborns: what do we know? What do we need to learn? Pediatr Nephrol. 2009;24(2):265-274. (Review)
  25. Langenberg C, Wan L, Egi M, et al. Renal blood flow in experimental septic acute renal failure. Kidney Int. 2006;69(11):1996-2002. (Animal study)
  26. Bagshaw SM, Lapinsky S, Dial S, et al. Acute kidney injury in septic shock: clinical outcomes and impact of duration of hypotension prior to initiation of antimicrobial therapy. Intensive Care Med. 2009;35(5):871-881. (Retrospective; 4532 adults)
  27. El-Achkar TM, Hosein M, Dagher PC. Pathways of renal injury in systemic gram-negative sepsis. Eur J Clin Invest. 2008;38 Suppl 2:39-44. (Review)
  28. Agraharkar M, Nerenstone S, Palmisano J, et al. Carboplatin-related hematuria and acute renal failure. Am J Kidney Dis. 1998;32(5):E5. (Case report)
  29. Luciano RL, Perazella MA. Nephrotoxic effects of designer drugs: synthetic is not better! Nat Rev Nephrol. 2014;10(6):314-324. (Review)
  30. * Moffett BS, Goldstein SL. Acute kidney injury and increasing nephrotoxic-medication exposure in noncritically-ill children. Clin J Am Soc Nephrol. 2011;6(4):856-863. (Retrospective; 1660 children)
  31. *Goldstein SL, Kirkendall E, Nguyen H, et al. Electronic health record identification of nephrotoxin exposure and associated acute kidney injury. Pediatrics. 2013;132(3):e756-e767. (Prospective quality improvement study; 21,807 children)
  32. Buck ML, Norwood VF. Ketorolac-induced acute renal failure in a previously healthy adolescent. Pediatrics. 1996;98(2 Pt 1):294-296. (Case report)
  33. Seyberth HW, Leonhardt A, Tonshoff B, et al. Prostanoids in paediatric kidney diseases. Pediatr Nephrol. 1991;5(5):639-649. (Review)
  34. Misurac JM, Knoderer CA, Leiser JD, et al. Nonsteroidal anti-inflammatory drugs are an important cause of acute kidney injury in children. J Pediatr. 2013;162(6):1153-1159, 1159.e1. (Retrospective study; 1015 patients)
  35. * Balestracci A, Ezquer M, Elmo ME, et al. Ibuprofen-associated acute kidney injury in dehydrated children with acute gastroenteritis. Pediatr Nephrol. 2015. (Prospective cohort study; 105 children)
  36. Ito T, Watanabe S, Tsuruga K, et al. Severe intrinsic acute kidney injury associated with therapeutic doses of acetaminophen. Pediatr Int. 2015;57(2):e53-e55. (Case report)
  37. Lorz C, Justo P, Sanz A, et al. Paracetamol-induced renal tubular injury: a role for ER stress. J Am Soc Nephrol. 2004;15(2):380-389. (Laboratory experiment)
  38. * Yue Z, Jiang P, Sun H, et al. Association between an excess risk of acute kidney injury and concomitant use of ibuprofen and acetaminophen in children, retrospective analysis of a spontaneous reporting system. Eur J Clin Pharmacol. 2014;70(4):479-482. (Retrospective analysis; 47,803 children)
  39. Kagan A, Sheikh-Hamad D. Contrast-induced kidney injury: focus on modifiable risk factors and prophylactic strategies. Clin Cardiol. 2010;33(2):62-66. (Review)
  40. Kanbay M, Covic A, Coca SG, et al. Sodium bicarbonate for the prevention of contrast-induced nephropathy: a meta-analysis of 17 randomized trials. Int Urol Nephrol. 2009;41(3):617-627. (Meta-analysis of 17 randomized controlled trials; 2448 patients)
  41. Andreoli SP. Acute kidney injury in children. Ped Nephrol. 2009;24(2): 253-263. (Review)
  42. Cheung V, Trachtman H. Hemolytic uremic syndrome: toxins, vessels, and inflammation. Front Med (Lausanne). 2014;1:42. (Review)
  43. Ake JA, Jelacic S, Ciol MA, et al. Relative nephroprotection during Escherichia coli O157:H7 infections: association with intravenous volume expansion. Pediatrics. 2005;115(6):e673-e680. (Prospective cohort study; 29 children)
  44. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72. (Review)
  45. Mannix R, Tan ML, Wright R, et al. Acute pediatric rhabdomyolysis: causes and rates of renal failure. Pediatrics. 2006;118(5):2119-2125. (Retrospective; 210 children)
  46. Grunau BE, Pourvali R, Wiens MO, et al. Characteristics and thirty-day outcomes of emergency department patients with elevated creatine kinase. Acad Emerg Med. 2014;21(6):631-636. (Retrospective; 400 patients)
  47. Delaney KA, Givens ML, Vohra RB. Use of RIFLE criteria to predict the severity and prognosis of acute kidney injury in emergency department patients with rhabdomyolysis. J Emerg Med. 2012;42(5):521-528. (Retrospective; 135 adults)
  48. Talving P, Karamanos E, Skiada D, et al. Relationship of creatine kinase elevation and acute kidney injury in pediatric trauma patients. J Trauma Acute Care Surg. 2013;74(3):912-916. (Retrospective; 521 children)
  49. Turner ME, Weinstein J, Kher K. Acute renal failure secondary to pyelonephritis. Pediatrics. 1996;97(5):742-743. (Case report)
  50. Gearhart JP, Herzberg GZ, Jeffs RD. Childhood urolithiasis: experiences and advances. Pediatrics. 1991;87(4):445-450. (Review)
  51. Milliner DS, Murphy ME. Urolithiasis in pediatric patients. Mayo Clin Proc. 1993;68(3):241-248. (Retrospective; 221 children)
  52. Coward RJ, Peters CJ, Duffy PG, et al. Epidemiology of paediatric renal stone disease in the UK. Arch Dis Child. 2003;88(11):962-965. (Retrospective; 121 children)
  53. VanDervoort K, Wiesen J, Frank R, et al. Urolithiasis in pediatric patients: a single center study of incidence, clinical presentation and outcome. J Urol. 2007;177(6):2300-2305. (Retrospective; 188 children)
  54. Howard SC, Kaplan SD, Razzouk BI, et al. Urolithiasis in pediatric patients with acute lymphoblastic leukemia. Leukemia. 2003;17(3):541-546. (Retrospective; 2095 children)
  55. Uthup S, Binitha R, Geetha S, et al. A follow-up study of children with posterior urethral valve. Indian J Nephrol. 2010;20(2):72-75. (Follow-up study; 30 children)
  56.  Chugh KS, Malik N, Uberoi HS, et al. Renal vein thrombosis in nephrotic syndrome--a prospective study and review. Postgrad Med J. 1981;57(671):566-570. (Prospective study; 44 patients)
  57. Markowitz GS, Brignol F, Burns ER, et al. Renal vein thrombosis treated with thrombolytic therapy: case report and brief review. Am J Kidney Dis. 1995;25(5):801-806. (Case report)
  58. Berkovich GY, Ramchandani P, Preate DL Jr, et al. Renal vein thrombosis after martial arts trauma. J Trauma. 2001;50(1):144-145. (Case report)
  59. Mintz G, Acevedo-Vazquez E, Gutierrez-Espinosa G, et al. Renal vein thrombosis and inferior vena cava thrombosis in systemic lupus erythematosus. Frequency and risk factors. Arthritis Rheum. 1984;27(5):539-544. (Prospective study; 43 patients)

  60. Ellis D. Recurrent renal vein thrombosis and renal failure associated with antithrombin-III deficiency. Pediatr Nephrol. 1992;6(2):131-134. (Case report)
  61. Wolak T, Rogachev B, Tovbin D, et al. Renal vein thrombosis as a presenting symptom of multiple genetic pro-coagulant defects. Nephrol Dial Transplant. 2005;20(4):827-829. (Case report)
  62. Bernie JE, Friedel WE, Fernandez R, et al. Left renal vein thrombosis treated conservatively. J Urol. 1972;107(4):517-520. (Case report)
  63. Carmody JB, Charlton JR. Short-term gestation, long-term risk: prematurity and chronic kidney disease. Pediatrics. 2013;131(6):1168-1179. (Review)
  64. Singhal N, Saha A. Bedside biomarkers in pediatric cardio renal injuries in emergency. Int J Crit Illn Inj Sci. 2014;4(3):238-246. (Review)
  65. Lagos-Arevalo P, Palijan A, Vertullo L, et al. Cystatin C in acute kidney injury diagnosis: early biomarker or alternative to serum creatinine? Pediatr Nephrol. 2015;30(4):665-676. (Prospective cohort study; 160 children)
  66. The Johns Hopkins Hospital. The Harriet Lane Handbook: A Manual for Pediatric House Officers. 18th ed. Philadelphia: Elsevier Mosby; 2003. (Textbook)
  67. Dobrin RS, Larsen CD, Holliday MA. The critically ill child: acute renal failure. Pediatrics. 1971;48(2):286-293. (Review)
  68. Hellman RN, Decker BS, Murray M. Elevated serum creatinine and a normal urinalysis: a short differential diagnosis in the etiology of renal failure. Ren Fail. 2006;28(5):389-394. (Retrospective study; 515 patients)
  69. Schinstock CA, Semret MH, Wagner SJ, et al. Urinalysis is more specific and urinary neutrophil gelatinase-associated lipocalin is more sensitive for early detection of acute kidney injury. Nephrol Dial Transplant. 2013;28(5):1175-1185. (Prospective observational; 488 patients)
  70. Alavi-Moghaddam M, Safari S, Najafi I, et al. Accuracy of urine dipstick in the detection of patients at risk for crush-induced rhabdomyolysis and acute kidney injury. Eur J Emerg Med. 2012;19(5):329-332. (Retrospective, multicenter cohort study; 1821 patients)
  71. * Faubel S, Patel NU, Lockhart ME, et al. Renal relevant radiology: use of ultrasonography in patients with AKI. Clin J Am Soc Nephrol. 2014;9(2):382-394. (Review)
  72. Chen L, Hsiao A, Langhan M, et al. Use of bedside ultrasound to assess degree of dehydration in children with gastroenteritis. Acad Emerg Med. 2010;17(10):1042-1047. (Prospective observational study; 112 children)
  73. Lin SM, Huang CD, Lin HC, et al. A modified goal-directed protocol improves clinical outcomes in intensive care unit patients with septic shock: a randomized controlled trial. Shock. 2006;26(6):551-557. (Prospective radomized controlled study; 224 patients)
  74. Spandorfer PR, Alessandrini EA, Joffe MD, et al. Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial. Pediatrics. 2005;115(2):295-301. (Prospective randomized controlled study; 73 children)
  75. Selewski DT, Symons JM. Acute kidney injury. Pediatr Rev. 2014;35(1):30-41. (Retrospective; 96 infants)
  76. Stapleton FB, Strother DR, Roy S 3rd, et al. Acute renal failure at onset of therapy for advanced stage Burkitt lymphoma and B cell acute lymphoblastic lymphoma. Pediatrics. 1988;82(6):863-869. (Retrospective; 40 patients)
  77. Bellomo R, Chapman M, Finfer S, et al. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000;356(9248):2139-2143. (Randomized controlled trial; 328 patients)
  78. Solomon R, Werner C, Mann D, et al. Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994;331(21):1416-1420. (Prospective observational study; 78 patients)
  79. Homsi E, Barreiro MF, Orlando JM, et al. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Ren Fail. 1997;19(2):283-288. (Retrospective; 24 patients)
  80. Kodner CM, Kudrimoti A. Diagnosis and management of acute interstitial nephritis. Am Fam Physician. 2003;67(12):2527-2534. (Review)
  81. Viswanathan G, Gilbert S. The cardiorenal syndrome: making the connection. Int J Nephrol. 2011;2011:283137. (Review)
  82. Sinert R, Doty CI. Update: prevention of contrast-induced nephropathy in the emergency department. Ann Emerg Med. 2009;54(1):e1-e5. (Review)
  83. Subramaniam RM, Suarez-Cuervo C, Wilson RF, et al. Effectiveness of prevention strategies for contrast-induced nephropathy: a systematic review and meta-analysis. Ann Intern Med. 2016;164(6):406-416. (Meta-analysis)
  84. Traub SJ, Mitchell AM, Jones AE, et al. N-acetylcysteine plus intravenous fluids versus intravenous fluids alone to prevent contrast-induced nephropathy in emergency computed tomography. Ann Emerg Med. 2013;62(5):511-520.e5. (Randomized controlled trial; 359 patients)
  85. Flynn JT. Choice of dialysis modality for management of pediatric acute renal failure. Pediatr Nephrol. 2002;17(1):61-69. (Review)
  86. Stein JP, Kaji DM, Eastham J, et al. Blunt renal trauma in the pediatric population: indications for radiographic evaluation. Urology. 1994;44(3):406-410. (Retrospective; 48 children)
  87. Westland R, Kurvers RA, van Wijk JA, et al. Risk factors for renal injury in children with a solitary functioning kidney. Pediatrics. 2013;131(2):e478-e485. (Prospective observational; 407 children)
  88. Mehrotra A, Rose C, Pannu N, et al. Incidence and consequences of acute kidney injury in kidney transplant recipients. Am J Kidney Dis. 2012;59(4):558-565. (Retrospective cohort study, 3066 patients)
  89. Panek R, Tennankore KK, Kiberd BA. Incidence, etiology, and significance of acute kidney injury in the early post-kidney transplant period. Clin Transplant. 2016;30(1):66-70. (Retrospective study; 334 patients)
  90. Nakamura M, Seki G, Iwadoh K, et al. Acute kidney injury as defined by the RIFLE criteria is a risk factor for kidney transplant graft failure. Clin Transplant. 2012;26(4):520-528. (Retrospective study, 289 patients)
  91. Du Y, Zappitelli M, Mian A, et al. Urinary biomarkers to detect acute kidney injury in the pediatric emergency center. Pediatr Nephrol. 2011;26(2):267-274. (Prospective cohort study; 252 children)
  92. Devarajan P. Neutrophil gelatinase-associated lipocalin: a promising biomarker for human acute kidney injury. Biomark Med. 2010;4(2):265-280. (Review)
  93. Singer E, Marko L, Paragas N, et al. Neutrophil gelatinase-associated lipocalin: pathophysiology and clinical applications. Acta Physiol (Oxf). 2013;207(4):663-672. (Review)
  94. Schmidt-Ott KM. Neutrophil gelatinase-associated lipocalin as a biomarker of acute kidney injury--where do we stand today? Nephrol Dial Transplant. 2011;26(3):762-764. (Review)
  95. Mishra J, Dent C, Tarabishi R, et al. Neutrophil gelatinase-associated lipocalin (NGAL) as a biomarker for acute renal injury after cardiac surgery. Lancet. 2005;365(9466):1231-1238. (Prospective study; 71 children)
  96. Parikh CR, Devarajan P, Zappitelli M, et al. Postoperative biomarkers predict acute kidney injury and poor outcomes after pediatric cardiac surgery. J Am Soc Nephrol. 2011;22(9):1737-1747. (Prospective multicenter cohort study; 311 children)
  97. Hall IE, Yarlagadda SG, Coca SG, et al. IL-18 and urinary NGAL predict dialysis and graft recovery after kidney transplantation. J Am Soc Nephrol. 2010;21(1):189-197. (Prospective multicenter cohort study; 91 patients)
  98. Ichimura T, Hung CC, Yang SA, et al. Kidney injury molecule-1: a tissue and urinary biomarker for nephrotoxicant-induced renal injury. Am J Physiol Renal Physiol. 2004;286(3):F552-F563. (Animal study)
  99. Vanmassenhove J, Vanholder R, Nagler E, et al. Urinary and serum biomarkers for the diagnosis of acute kidney injury: an in-depth review of the literature. Nephrol Dial Transplant. 2013;28(2):254-273. (Meta-analysis)
  100. Nejat M, Pickering JW, Walker RJ, et al. Rapid detection of acute kidney injury by plasma cystatin C in the intensive care unit. Nephrol Dial Transplant. 2010;25(10):3283-3289. (Prospective; 442 patients)
  101. Andreucci M, Faga T, Pisani A, et al. The ischemic/nephrotoxic acute kidney injury and the use of renal biomarkers in clinical practice. Eur J Intern Med. 2017;39:1-8. (Review)
  102. Chindarkar NS, Chawla LS, Straseski JA, et al. Reference intervals of urinary acute kidney injury (AKI) markers [IGFBP7][TIMP2] in apparently healthy subjects and chronic comorbid subjects without AKI. Clin Chim Acta. 2016;452:32-37. (Retrospective study; 372 patients)
  103. Moffett BS, Mott AR, Nelson DP, et al. Renal effects of fenoldopam in critically ill pediatric patients: a retrospective review. Pediatr Crit Care Med. 2008;9(4):403-406. (Retrospective analysis; 13 children)
  104. Ricci Z, Luciano R, Favia I, et al. High-dose fenoldopam reduces postoperative neutrophil gelatinase-associated lipocaline and cystatin C levels in pediatric cardiac surgery. Crit Care. 2011;15(3):R160. (Randomized controlled trial; 80 patients)
  105. Bove T, Zangrillo A, Guarracino F, et al. Effect of fenoldopam on use of renal replacement therapy among patients with acute kidney injury after cardiac surgery: a randomized clinical trial. JAMA. 2014;312(21):2244-2253. (Randomized controlled trial; 667 patients)
  106. Jefferies JL, Price JF, Denfield SW, et al. Safety and efficacy of nesiritide in pediatric heart failure. J Card Fail. 2007;13(7):541-548. (Retrospective; 63 children)
  107. Liu J, Xie Y, He F, et al. Recombinant brain natriuretic peptide for the prevention of contrast-induced nephropathy in patients with chronic kidney disease undergoing nonemergent percutaneous coronary intervention or coronary angiography: a randomized controlled trial. Biomed Res Int. 2016;2016:5985327. (Randomized controlled trial; 218 patients)
  108. Nickolas TL, O’Rourke MJ, Yang J, et al. Sensitivity and specificity of a single emergency department measurement of urinary neutrophil gelatinase-associated lipocalin for diagnosing acute kidney injury. Ann Intern Med. 2008;148(11):810-819. (Prospective cohort study; 635 patients)
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Publication Information
Authors

Daniel Mohrer, MD; Melissa Langhan, MD, MHS

Publication Date

May 2, 2017

CME Expiration Date

June 2, 2020

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