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