1. Management of
Acute Kidney Injury
Mohammed Ahmed

2. Outline
• Prevention of AKI
• Management principles
• Prerenal azotemia
• Hepatorenal syndrome
• Intrinsic AKI
• Post renal AKI
• Supportive measures
• prognosis

3. Prevention and treatment
Management of individuals with and at risk for
AKI varies according to the underlying cause but
common to all are several principles.

4. Management principles
Optimization of hemodynamics,
Correction of fluid and electrolyte imbalances,
Discontinuation of nephrotoxic medications,
Dose adjustment of administered medications,

5. Cont.…
Management of life-threatening complications,
Diagnosis and specific management of underlying
cause,
Renal replacement therapies.

6. prevention
• Being aware of patients who are at risk for AKI
 Elderly
 Diabetics
 Post Vascular Surgery
 CRF
 Multiple antibiotics

7. • Use of preventive measures
Cautious prescription of nephrotoxic drugs.
Aggressive hydration prior to chemotherapy, IV contrast,
etc.
Giving prophylactic allopurinol or rasburicase.
• Aggressive surveillance
 Close monitoring of urine output and RFT(BUN &Cr) for
inpatients.

8. Prerenal Azotemia
• Prerenal azotemia in its early stages can be
rapidly corrected by aggressive normalization
of effective arterial volume. This may involve:
Administering Volume
And/or
Optimization of cardiac function

9. Administering Volume
• The composition of replacement fluids should
be targeted to the type of fluid lost.
Severe acute blood loss  packed RBCs.
Less severe acute hemorrhage or plasma loss
in case of burn and pancreatitis Isotonic
saline(0.9%NaCl,154mM Na+).
Less severe hypovolemia 
hypotonic crystalloid(0.4%).

10. Optimizing cardiac function
Inotropic agents,
Preload- and afterload-reducing agents,
Antiarrhythmic drugs, and
Mechanical aids such as an intra
aortic balloon pump.

11. Cirrhosis and hepatorenal
syndrome
• The definitive treatment of the hepatorenal
syndrome is orthotopic liver transplantation.
• Bridge therapies that have shown promise
include terlipressin, combination therapy with
octreotide and midodrine and norepinephrine,
• All in combination with intravenous albumin (25–
50 mg per day, maximum 100 g/d).

12. Intrinsic AKI
• Management of ATN is usually supportive.
• Attempts to convert oliguric to nonoliguric AKI
may be attempted.(said to have prognostic
implications).

13. • AGN or vasculitis immunosuppressive agents
and/or plasmapheresis.
• Hypertensive renal emergency(malignant
nephrosclerosis) gradual lowering of BP.
• AIN discontinue medication.
• Scleroderma ACE inhibitors.
• Rhabdomyolysis forced alkaline diuresis.

15. Postrenal AKI
• Prompt recognition and relief of urinary tract
obstruction can prevent the development of
permanent structural damage.
• The site of obstruction defines the treatment
approach.
• Relief of obstruction is usually followed by an
appropriate diuresis for several days.

16. Supportive Measures
Volume Management
– Restrict fluid and sodium.
– Diuretics may be used to increase the urinary
flow rate.
– In severe cases of volume overload, furosemide
may be given as a bolus (200 mg) followed by an
intravenous drip (10–40 mg/h), with or without a
thiazide diuretic.

17. Electrolyte and Acid-Base
Abnormalities
• Hyperkalemia
– Immediate antagonism of the cardiac effects of
hyperkalemia.(10 ml of 10% calcium gluconate IV over
2-3 min. with cardiac monitoring).
– Rapid reduction in plasma K+ concentration by
redistribution into cells.(10 units of IV regular insulin
followed immediately by 50 mL of 50% dextrose).
– Β2-agonists,most commonly albuterol, are effective
should be given with insulin.
– Restricting dietary K+ intake.

18. • Metabolic Acidosis
– Not treated unless severe (pH<7.2) & serum
bicarbonate <15mmol/L.
– Acidosis can be treated with oral or intravenous
sodium bicarbonate.
– Monitor for complications of overcorrection like
metabolic alkalosis, hypocalcemia, hypokalemia,
and volume overload.

19. • Hyperphosphatemia
– limiting intestinal absorption of phosphate using
phosphate binders (calcium carbonate or
aluminum hydroxide).
– Dietary restriction.
• Hypocalcemia
– Does not usually require therapy unless
symptoms are present.

20. Malnutrition
– Protein intake should be around 1.2–1.4 g/kg
– 20–25% of daily calories should be provided by lipids.
– Glucose is usually administered in a 70% solution.
– The estimated energy requirements for patients with
AKI usually fall between 30 and 40 kcal/kg normal
body weight/day.
– Water-soluble vitamins should be supplemented, as
these are lost during RRT.

21. Anemia
• May necessitate blood transfusion if severe or if
recovery is delayed.
• Gastrointestinal prophylaxis with proton pump
inhibitors or histamine (H2) receptor blockers is
required.

22. Dialysis
Is indicated when medical management fails to
control(Refractory *)
– Volume overload *
– Hyperkalemia *
– Severe metabolic acidosis
– Severe complications of uremia i.e.
pericarditis, neuropathy, unexplained decline in mental status,
uremic bleeding.
– Overdose with a dialyzable drug/toxin.

23. • The timing of dialysis is still a matter of
debate.
• Many nephrologists initiate dialysis for AKI
empirically when the BUN exceeds 100 mg/dL
in patients without clinical signs of recovery of
kidney function.

24. Modes of RRT
Peritoneal dialysis
Hemodialysis
Hemofiltration
The choice of modality is often dictated by the
Available technology
and
Expertise of medical staff.

25. Hemodialysis
• The most common form of RRT for AKI.
• Employed intermittently (3-4hr/day,3-4*/wk.) or
continuously.
• Vascular access is through the femoral, internal
jugular, or subclavian veins.
• Can be done through convective ,diffusive
clearance or combination of two.
• One of its major complications is hypotension.

26. • The optimal dose of dialysis for AKI is not clear.
• Does not confer a demonstrable survival or renal
recovery advantage.
• Studies have failed to show that continuous
therapies are superior to intermittent therapies.
• CRRT is often preferred in patients with severe
hemodynamic instability, cerebral edema, or
significant volume overload.

27. prognosis
• Mortality of ARF remains around 50%.
• Prerenal azotemia, and postrenal azotemia
carry a better prognosis than most cases of
intrinsic AKI.
• Oliguric AKI, developing in a surgical setting or
in older patients, carries a higher mortality
than other forms of AKI.

28. summary
 AKI remains a medical challenge to clinicians and
researchers.
 Recognition of patients at risk,
 Institution of preventive measures,
 Aggressive surveillance, and
 Early treatment of AKI will be much more effective
than treatment of established AKI with RRT.

29. References
• Harrison’s Principles of Internal Medicine,18th
edition.
• Cecil Textbook of Internal Medicine,23rd edition.
• Current Nephrology and Hypertension 1st edition.
• UpToDate 17.3.

30. THANK YOU