1. Acute Kidney Injury
By:-
Dr Kailash Shah

2. Anatomy of the Kidney Approximately 1,200 ml of blood or 25 % of Cardiac Output flows through the kidney in one minute
The Nephron
The urine producing part of the kidney
Distal tubule
Collecting duct
Loop
of Henle
Peritubular
capillaries
Proximal tubule
Bowman’s
capsule
Glomerulus
Afferent arteriole (
wider )
There are one million Nephrons in each kidney
The efferent arteriole, which is narrower than the afferent arteriole, creating a hydrostatic pressure in glomerulus
Efferent arteriole
(narrow)

3. Function of kidney

4. Definition of AKI Kidney Disease Improving Global Outcomes (KDIGO) :
Increase in SCr by ≥0.3mg/dl ( 26.5lmol/l) within 48 hours;
Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days;
Urine volume < 0.5ml/kg/h for 6 hours.

5. Causes of AKI

6. Rifle Criteria for stratifying AKI
R isk
I njury
F ailure
L oss of function
E nd-Stage Renal disease

7. E nd-Stage Renal disease
R isk
Increase in Cr of X baseline or
urine output < 0.5 mL/kg/hr for more than 6 hours.
I njury
F ailure
L oss of function
E nd-Stage Renal disease
Acute dialysis quality initiative (ADQI)

8. R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for more than 6 hrs
I njury
increase in Cr 2-3 X baseline (loss of 50% of GFR) or
urine output < 0.5 mL/kg/hr for more than 12 hours.
F ailure
L oss of function
E nd-Stage Renal disease
Acute dialysis quality initiative (ADQI)

9. R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr % or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure
increase in Cr rises > 3X baseline Cr (loss of 75% of GFR) or
an increase in serum creatinine greater than 4 mg/dL, or
urine output < 0.3 mL/kg/hr for more than 24 hours or anuria for more than 12 hours.
L oss of function
E nd-Stage Renal disease
Acute dialysis quality initiative (ADQI)

10. R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr % or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours
L oss of function
persistent renal failure (i.e. need for dialysis) for more than 4 weeks.
E nd-Stage Renal disease
Acute dialysis quality initiative (ADQI)

11. R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr % or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours
L oss of function: Need for dialysis for more than 4 weeks
E nd-Stage Renal disease
persistent renal failure (i.e. need for dialysis) for more than 3 months.
Acute dialysis quality initiative (ADQI)

12. Diagnosis History and Physical examination: Pre-renal:
History: vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.
Examination : Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in prerenal azotemia

13. Post- Renal:
Colicky flank pain radiating to the groin suggests acute ureteric obstruction.
Nocturia and urinary frequency or hesitancy can be seen in prostatic disease.
Abdominal fullness and suprapubic pain can accompany massive bladder enlargement. Definitive diagnosis of obstruction requires radiologic investigations.

14. Review all medications
Cause of AKI .
Dose Adjustment.
Systemic vasculitis with Glomerulonephritis:
Palpable purpura
Pulmonary hemorrhage,
Sinusitis.
Atheroembolic
Livedo reticularis and other signs of emboli to the legs.
Rhabdomyolysis.
Signs of limb ischemia

15. Investigations Urea and creatinine: raised, compare to previous result
Electrolytes: if K>6mmol/l, treat urgently
Calcium and phosphate: low Ca and high PO4 indicate CKD
Albumin: low alb in sepsis
CBC: anemia may indicate CKD
Urinalysis: marked hematuria suggest glomerulonephritis or bladder/obstructive lesion
Urine microscopy: cast or dysmorphic red cells glomerulonephritis, leukocytes suggest infection

16. Usg: hydronephrosis +/- enlarged bladder in post renal obstruction, small kidney suggest CKD
Cultures: blood/urine
Chest x-ray: pul edema in fluid overload
Serology: HIV and hepatitis serology, if dialysis is needed
ECG: risk of cardiac disease

17. Management Goal of treatment: Minimize the degree of kidney insult
Reduce extrarenal complication
Restoration of renal function to pre AKI state

18. Preliminary measures
• Exclusion of reversible causes: Obstruction should be relived , infection should be treated
• Correction of prerenal factors: intravascular volume and cardiac performance should be optimized
Nephrotoxic drug should be avoided

19. Intrinsic ARF
Maintenance of urine output: Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form.
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses

20. Prerenal ARF:
• The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid.
• Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells, whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (e.g., burns, pancreatitis).

21. Postrenal ARF:
Management of postrenal ARF requires close collaboration between nephrologist, urologist, and radiologist.
• Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter, which provides temporary relief while the obstructing lesion, is identified and treated definitively. Similarly, ureteric obstruction may be treated initially by percutaneous catheterization of the dilated renal pelvis or ureter.

22. Fluid and electrolyte management :
Following correction of hypovolemia, total oral and intravenous fluid administration should be equal to daily sensible losses (via urine, stool, and NG tune or surgical drainage ) plus estimated insensible ( i.e. , respiratory and derma ) losses which usually equals 400 – 500 ml/day. Strict input output monitoring is important.

23. Hypervolemia: can usually be managed by restriction of salt and water intake and diuretics.
Metabolic acidosis: should be corrected when serum bicarbonate concentration falls below 15 mmol/L or arterial pH falls below 7.2.
More severe acidosis is corrected by oral or intravenous sodium bicarbonate.
Patients are monitored for complications of bicarbonate administration such as hypervolemia, metabolic alkalosis, hypocalcemia, and hypokalemia.

24. Hyperkalemia management:
cardiac and neurologic complications may occur if serum K+ level is > 6.5 mEq/L
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10% solution over 5
minutes
o Glucose solution 50 ml of 50 % dextrose plus Insulin
10 units IV
o Potassium –binding ion exchange resin
o Dialysis: it medial therapy fails or the patient is very
toxic

25. Indication of Emergency dialysis

26. Clinical course and prognosis
Morbidity and mortality: are affected by the presence of oliguria o GI bleeding, septicemia, metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients.
The mortality rate for oliguric patients is 50 % where as that of nonoliguric patients is only 26 %