Acute kidney injury

1. Acute Kidney Injury
ABDULAZIZ TURKI BAGASI
SENIOR MEDICAL STUDENT
UMM AL-QURA UNIVERSITY

2. Objectives:
1. Definition
2. Clinical presentation and etiology.
3. Workup
4. Treatment of AKI.

3. Definition.
 AKI is defined as any of the following:
 Increase in SCr by ≥ 0.3 mg/dl within 48 hours.
 Increase in SCr by ≥ 50%.
 Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred
within the prior 7 days.
 Urine volume { 0.5 ml/kg/h for 6 hours.

4. RIFLE criteria

5. Etiology and presentation.
Pre-Renal Renal Post-Renal

9. Presentation
History
 The presentation will depend on the underlying cause and severity of AKI.
 Urine output history can be useful ,Oliguria generally favors AKI.

10. Important history points
 Volume restriction (eg, low fluid intake, gastroenteritis)
 Nephrotoxic drug ingestion (eg, [NSAIDs], aminoglycosides)
 Exposure to iodinated contrast agents within the past week
 Trauma or unaccustomed exertion
 Blood loss or transfusions
 Hypertension
 heart failure
 Diabetes
 Liver disease

11. Important history points
 Prerenal : symptoms related to hypovolemia and CHF, including thirst,
decreased urine output, dizziness, and orthostatic hypotension.
 Renal : symptoms related to glomerular or tubular disease , eg: hematuria,
edema .
 Postrenal : eg :prostatic obstruction and symptoms of urgency, frequency,
and hesitancy.

12. Physical Examination
 Skin
 Eyes
 Ears
 Cardiovascular system
 Abdomen
 Pulmonary system

13. Workup
 Blood tests : CBC, RFT (Cr, BUN), LFT, Electrolytes.
 Urinalysis : Dipstick, Microscopic examination and sediments .
 Urine chemistry :urine osmolality, FENA, Urine NA .
(to distinguish between different forms of AKI).
 Urine culture and sensitivities : if infection is suspected.
 Renal ultrasound : to rule out obstruction.
 Additional workup:
ECG, K, ABG, CT, Renal biopsy

14. Pre-renal vs Renal AKI

15. Treatment
 Pre-renal:
treat the underlying disorder, give NS, eliminate any offending agents (ACE
inhibitors, NSAIDs).
 Renal:
therapy is supportive, eliminate the cause/offending agent, If the patient is
oliguric, a trial of furosemide may help to increase urine flow, This improves
fluid balance
 Post-renal:
bladder catheter may be inserted to decompress the urinary tract, consider
urology consultation.

16. Indications of urgent dialysis

17. Case:

18. Answer :

19. Case :

20. Answer :

21. Case :A 50 year old alcoholic male presents with sepsis secondary to klebsiella
pneumonia. His background includes IHD, previous pneumonia,
hypercholesterolaemia and hypertension. Medications include: furosemide, enalapril,
aspirin, clopidogrel, co-amoxiclav (current) and simvastatin
He is treated with IV antibiotics and is managed on an ITU setting for 1 week
On step down to a medical ward routine bloods reveal:
Sodium 132
Potassium 5.0
Urea 24 (from 8)
Creatinine 390 (from 60)
Clinically he is mildly dry, with a BP 135/83, HR 90, he is catheterised with a U/O
35ml/hr

22. Which one of the following is the best management option?
 1)Switch to high dose IV furosemide, stop enalapril, give IV fluids to
maintain urine output, daily bloods
 2) Stop furosemide, stop enalapril, add in dopamine and maintain
adequate hydration to maintain urine output, daily bloods
 3) Stop furosemide, stop enalapril, adequate fluids to maintain urine
output, daily bloods
 4) Continue furosemide, stop enalapril, high dose corticosteroids and
continue adequate fluids to maintain urine output, daily bloods
 5) None of the above

23. Answer
 Answer: 3 (stop furosemide, stop enalapril, adequate fluids to maintain
urine output, daily bloods)This man has risk factors for AKI (hypertension
and dehydration) and is on various renotoxic medications including aspirin,
enalapril (ACE-I) and furosemide (loop diuretic).
 The key is to maintain hydration to keep urine output reasonable
(>0.5ml/kg/hr) while stopping as many renotoxic medications as possible.
 Fluids should be given and frusemide and enalapril stopped. He has a
history of ischaemic heart disease so stopping aspirin is not ideal. Daily
bloods to monitor response is advised.
 There is no evidence for dopamine (mentioned in option 2) or
hydrocortisone (mentioned in option 4).

24. THANK YOU
 Reference:
1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney
Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney
Injury. Kidney inter., Suppl. 2012; 2: 1–138.
2. Rahman, M., Western, C., Shad, O. F., Permanente, K., Smith, O. M. C.,
& Western, C. (2012). Acute Kidney Injury: A Guide to Diagnosis and
Management.
3. Emedicine-medscape.
4. Oxford Medical Education website.