1. The patient is experiencing acute kidney injury (AKI) as evidenced by his elevated urea and creatinine levels, which were previously normal. 2. The underlying mechanism is likely pre-renal AKI caused by the nephrotoxic effects of the ACE inhibitor (Lisinopril) medication prescribed for his hypertension. ACE inhibitors can cause afferent arteriole vasoconstriction leading to reduced kidney perfusion and function. 3. Management includes discontinuing the ACE inhibitor, optimizing his blood pressure with another class of antihypertensive medication, and monitoring his kidney function and fluid status.

1. Acute Kidney Injury
Dr. Wail Eldukali

2. case
• 55 y old male visiting ER complaining of headache, he
was recently diagnosed to hypertensive and his
primary care physician prescribed for him Lisinopril tab
10 mg/ day, his general exam was normal , Bp 160/90
mmHg, PR 77b/m, cardiovascular and respiratory exam
were normal, you ordered routine investigation which
came , urea 55 mg/dl, createnine 1.8mg/dl, CBC,LFT,
RBS all were normal , he had routine investigations
which were normal 2 weeks ago
1. What is wrong with his lab?
2. What is underlying mechanism?
3. How to manage him?

3. AKI
• Previously known as acute renal failure
• there is a sudden and often reversible loss of
renal function, which develops over days or
weeks and is often accompanied by a
reduction in urine volume

4. Causes Of AKI

5. Pathophysiology of AKI
• pre-renal: when perfusion to the kidney is
reduced
• renal : when the primary insult affects the
kidney itself
• post-renal: when there is obstruction to urine
flow at any point from the tubule to the
urethra

6. Pre-renal AKI
• A reduction in perfusion reduces GFR
• If not corrected leads to kidney injury namely
acute tubular necrosis (ATN)
• Histologically, the kidney shows:
inflammatory changes, focal breaks in the tubular
basement membrane and interstitial edema
Dead tubular cells may also be shed into the
tubular lumen, leading to tubular obstruction.

7. Renal AKI
• Tubular damage is the dominant feature
• Profound alteration in renal microcirculation
• Nephrotoxic drugs can cause ATN or allergic
interstitial nephritis
• Other common cause is Glomerulonephritis

8. Post-renal
• Obstruction to the renal tract leads to
elevation of intraluminal ureteral pressure
transmitted to the nephrons after prolonged
obstruction, with a subsequent fall in GFR
• If obstruction not relieved leads to a drop in
renal flow via Thromoxane A2 & Angiotensin II
this leads to chronic kidney injury

9. Clinical Features
• Early recognition and intervention is
important in AKI
• In ER Check RFT, BP, Pulse, T
• Risk assessment for AKI
– Coexistent diseases DM, liver disease
– Nephrotoxic drug ACE I & NSAIDS
– Previous measurements of RFT is of great value
• If createnine found to be high (acute, acute on
chronic or sign of CKD

10. Pre-renal
• Look for signs of hypovolemia:
– low BP, Orthostatic hypotension
– Tachycardia, cold extremity
– Delayed capillary refill > 3s
• Look for signs of sepsis
• Uncorrected renal hypoperfusion causing pre-
renal azotaemia may progress to ATN.

11. Renal
• Patient GMN presents with hematuria and
proteinuria
• Clinical features of underlying diseases, e.g.
SLE
• History of ACE I , PPI, NSAIDS

12. Post-renal
• Examine to look for distended bladder
• USS to look for hydronephrosis
• Medical history of renal stones, malignancy,
and BPH
• History of urine retention

13. Categories Of AKI
• Various criteria have been proposed to classify
AKI and to help identify high-risk patients,
guide treatment and provide information
regarding prognosis
• The most commonly used are the KDIGO, AKIN
and RIFLE criteria.

15. Management
1. Hemodynamic status:
• Assess fluid status as this will determine fluid
prescription:
 If hypovolaemic: optimize systemic haemodynamic
status with fluid challenge and inotropic drugs if
necessary Once euvolaemic, match fluid intake to
urine output plus an additional 500 mL to cover
insensible losses
 If fluid-overloaded: prescribe diuretics (loop diuretics
at high dose will often be required); if the response is
unsatisfactory, dialysis may be required

16. 2-hyperkalemia And Acidosis
• Administer calcium resonium to stabilise
myocardium and glucose and insulin to correct
hyperkalaemia if K+ > 6.5 mmol/L as a holding
measure until a definitive method of removing
potassium is achieved (dialysis or restoration
of renal function)
• Consider administering sodium bicarbonate
(100 mmol) to correct acidosis if H+ is > 100
nmol/L (pH < 7.0)

17. Rest Of Management
• Discontinue potentially nephrotoxic drugs and
reduce doses of therapeutic drugs according to
level of renal function
• Ensure adequate nutritional support
• Consider proton pump inhibitors to reduce the
risk of upper gastrointestinal bleeding
• Screen for intercurrent infections and treat
promptly if present
• In case of urinary tract obstruction, drain lower or
upper urinary tract as necessary

18. Renal Placement Therapy
• Decision for RRT is made on individual basis
• Weighing risks versus benefits
• The two main options for RRT in AKI are
intermittent haemodialysis and CRRT
• Peritoneal dialysis is also an option if
haemodialysis is not available

19. RRT

20. Recovery From AKI

21. case
• 55 y old male visiting ER complaining of headache, he
was recently diagnosed to hypertensive and his
primary care physician prescribed for him Lisinopril tab
10 mg/ day, his general exam was normal , Bp 160/90
mmHg, PR 77b/m, cardiovascular and respiratory exam
were normal, you ordered routine investigation which
came , urea 55 mg/dl, createnine 1.8mg/dl, CBC,LFT,
RBS all were normal , he had routine investigations
which were normal 2 weeks ago
1. What is wrong with his lab?
2. What is underlying mechanism?
3. How to manage him?

22. Answers
1. AKI due nephrotoxic drug ACE I
2. ACI mediated glomerular afferent
vasoconstriction leading to decrease GFR
3. Optimize his high BP change to another class
of anti- hypertensive drug

23. Thank you