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Acute kidney Injury

This chart presents a summary of recognition and management of AKI – acute kidney injury ( previously known as renal failure ).Characterized by a decline in renal excretory function over 
hours or days that can result in failure to maintain fluid , electrolyte
 and acid-base homeostasis ( AKI )

Seen in about 13-22 % % of hospitalized patients AKI has replaced the concept of renal failure Higher incidence and mortality in ICU patients Associated with serious short- and long term complications Acute tubular necrosis ( ATN ) accounts for majority ( 45-70 % ) of cases of AKI Often asymptomatic and only diagnosed by lab tests

Rise in serum creatinine of 26 micromol / L or greater within 48 hrs 50 % or greater rise in serum creatinine known or presumed to have occurred within the past 7 days Fall in urine output to less than 0.5 ml /kg /hour for more than 6 hrs

pre-renalReduced renal perfusion eg 
hypovolemia
haemorrhage
sepsis
3rd spacing of fluids
over diuresus
heart failure
 Renal vasoconstriction eg
hypercalcemia
catecholamines
 Impaired renal autoregulation
NSAIDs
ACE-i / ARB
Cyclosporine
 Hepatorenal syndrome- unexplained and progressive ↑↑ in plasma creatinine in advanced liver dis renal- Acute tubular necrosis
Ischaemic and Toxic Rapidly progressive Gl-Nephritis Interstitial nephritis Vascular diseases
vasculitis
thrombosis
athero/ thromboembolism
dissection Drugs eg aminoglycosides
amphotericin B Contrast induced post renal- Retroperitoneal fibrosis Lymphoma Renal stones Pyonephrosis Blocked catheter Pelvic mass Enlarged prostate Cervical carcinoma Ascending urinary infection incl pyelopnephritis Urinary retention

Admit- Likely stage 3 AKI Obstructed infected kidney suspected No apparent cause of AKI Frail with co-morbidities Risk of Ur Tr obstuction eg
♦ prostate or bladder disease
♦ abd / pelvic cancer
♦ previous known hydronephrosis
♦ recurrent UTIs
♦ anuria
♦ single functioning kidney
♦ neurogenic bladder Sepsis Hypovolemia Suspected AKI related complications eg
♦ pul oedema
♦ uraemic encephalopathy
♦ pericarditis
♦ severe hyperkalemia ( moderate or severe )

discuss- Stage 4-5 CKD Serious secondary cause suspected eg glomerulonephritis , vasculitis Inadequate response to treatment AKI related complications suspected eg
♦ hyperkalemia
♦ hyperphosphataemia
♦ hyponatremia
♦ hypermagnesemia
♦ hypocalcemia
♦ metabolic acidosis
♦ elevated urea nitrogen
♦ vol overload
♦ uraemia
♦ CKD and ESRD Renal transplant

Management of AKI based on recommendations from CKS NHS available via 
https://cks.nice.org.uk/acute-kidney-injury#!scenarioRecommendation:1

References

  1.  CKS NHS Acute Kidney Injury
  2. Pathophysiology of Acute Kidney Injury Compr Physiol.2012 Apr; 2 (2) : 1303-1353
  3. KDIGO Clinical Practice guideline for Acute Kidney Injury Volume 2 Issue 1 march 2012
  4. Acute Kidney Injury : prevention , detection and management NICE Clinical guideline CG 169 August 2013
  5. Acute kidney injury : summary of NICE guidance BMJ 2013 ; 347:f4930
  6. Acute Kidney Injury Simon Lines and A Lewington Clinical Medicine 9 (3),273-277
  7. Acute Kidney Injury Medscape Biruh T Workeneh et al Updated Jan 13 2017
  8. Clinical Practice Guidelines Acute Kidney Injury UK Renal Association 5th Edition , 2011
  9. http://www.scottishpatientsafetyprogramme.scot.nhs.uk/programmes/primary-care/
medicine-sick-day-rules-card
  10. BMJ Best Practice Acute kidney injury
  11. Acute Kidney Injury ( AKI ) Sultan Chaudhary McMaster Pathophysiology
  12. Review AKI Pathophysiology via https://gpcpd.walesdeanery.org/index.php/pathophysiology-of-aki
  13. https://www.slideshare.net/snehasisghosh7792/pathophysiology-of-acute-kidney-injury

 

 

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