This document defines acute kidney injury (AKI) and describes its classification, diagnosis, and management. AKI is an abrupt deterioration in kidney function that is usually reversible. It is classified using criteria like RIFLE, AKIN, and KDIGO that stage AKI based on changes in serum creatinine and urine output. Biomarkers like cystatin C and NGAL can help detect early AKI. Treatment involves fluid resuscitation, removing nephrotoxins, and initiating renal replacement therapy if needed. Outcomes depend on the underlying cause and range from complete recovery to end-stage renal disease.

1. ACUTE KIDNEY INJURY
DR. ARAVIND P.S.
MODERATOR – DR. MANOKARAN SIR

2. DEFINITION
• ACUTE KIDNEY INJURY has variably been defined
as an abrupt deterioration in parenchymal renal
function, which is usually but not invariably,
reversible over a period of days or weeks.

3. CLASSIFICATION
• RIFLE CLASSIFICATION - 2004
• AKIN CRITERIA - 2007
• KDIGO GUIDELINES - 2012

4. • BASED ON TWO MARKERS.
• SERUM CREATININE AND
URINARY OUTPUT.
3 graded staging
Risk, Injury and
Failure.
2 outcomes
Loss of kidney
function > 4wks .
End stage renal
disease > 3 months

5. AKIN CRITERIA
ACUTE usually reversible decline in renal function
• Rapid time course( < 48 hrs)
• Reduction of kidney function:
A) Rise in serum creatinine, defined by either:
absolute increase in serum creatinine of >0.3mg/dl( >26µmol/l)
% increase in serum creatinine of > 50%
B) Reduction in urine output
Defined as < 0.5ml/kg/hr for more than 6 hrs.

6. KDIGO GUIDELINES
• KDIGO guidelines are same as AKIN criteria .
• With GFR less than 35ml/m/1.73m2 was added as
stage 3 of AKI in pediatric patients.

7. STAGES OF AKI

8. ACUTE KIDNEY DISEASE
• Strict adherence to definitions of both AKI and CKD may miss
individuals with functional or structural abnormalities present for
< 3 months but may benefit from active intervention to restore kidney
function.
• For this reason KDIGO have proposed the term AKD to include not
only those with AKI ,but also those with GFR<60ml/min/1.73m for
less than 3 months or a decrease by ≥ 35% or an increase in s.cr
by>50% for < 3 months.

9. INCIDENCE
• Approximately 7% of all hospitalized patient ( 65% of ICU)
• 20% of acutely ill patient developed AKI.
• Incidence of AKI needing dialysis 200/pm/year .
• Pre renal and acute tubular necrosis (ATN) accounts for 75%
of the cases of AKI Mortality.
• 5-10% in uncomplicated AKI .
• 50-70% in AKI secondary to other organ failure, infections.
• > 50% in dialysis requiring AKI .

10. AETIOLOGY

11. DIAGNOSIS
• Detailed History
• Examination
• Investigation

12. INVESTIGATION
• COMPLETE BLOOD ANALYSIS :
• Hb% ↓ Haemolysis, GI bleeding
• ↑/ ↓ Total leucocyte count : infection
• ↓platelets and altered coagulation : DIC, thrombotic
microangiopathy .
• Pancytopenia : marrow infiltration, others malignancy
• Peripheral smear : fragmented RBC : s LDH
haptoglobulin, reticulocyte count.

13. URINE ANALYSIS

14. URINE ANALYSIS

15. BIOCHEMISTRY :
• Elevated Blood urea, S,creatinine ratio indicate
pre- renal AKI
• ↑ K: needed urgent management .
• Na :usually normal, ↓ in case of volume overload
and diuretics
• ↓HCO3 : metabolic acidosis

16. • LFT : ↓ albumin- imply proteinuria and GN
• ↑ billirubin : Hepato Renal syndrome,
• CALCIUM AND PHOSPHATES : ↑ Ca ++: Myeloma,
Sarcoidosis Malignancy
• CRP : for Infection/ Inflammation
• CK: Rhabdomyolysis
• URATE Tumour lysis / Pre-eclampsia
• LACTATE : to asses under perfusion and tissue Ischemia

17. DIPSTICK TEST: trace or no proteinuria with pre-
renal and post-renal AKI.
• Mild to moderate proteinuria with ATN and moderate
to severe proteinuria with glomerular diseases.
• RBCs and RBC casts in glomerular diseases
• Crystals, RBCs and WBCs in post-renal ARF.

18. • ULTRASONOGRAPHY: helps to see the presence of
two kidneys, for evaluating kidney size and shape,
and for detecting hydronephrosis or hydroureter.
• It also helps to see renal calculi, and renal vein
thrombosis.
• RETROGRADE PYELOGRAPHY: is done when
obstructive uropathy is suspected

19. OTHER BIOMARKERS
• Cystatin C
• Neutrophil gelatinase-associated lipocalin(NGAL)
• Interleukin-18
• Kidney injury molecule-1
• N-acetyl-D-glucosaminidase

20. CYSTATIN C
• Superior to serum creatinine, as a surrogate marker
of early and subtle changes of kidney function.
• It identifies kidney injury while creatinine levels
remain in the normal range.
• Allows detection of AKI, 24-48 hours earlier than
serum creatinine

21. KIDNEY INJURY MOLECULE -1
• KIM-1 is a type 1 trans-membrane glycoprotein .
• Served as a marker of severity of AKI .
• Can be used to predict adverse outcomes in
hospitalized patients better than conventionally used
severity markers.

22. Neutrophil gelatinase-associated
lipocalin(NGAL)
• NGAL is highly upregulated after inflammation and
kidney injury and can be detected in the plasma and
urine within 2 hours of cardiopulmonary bypass–
associated AKI.
• Considered equivalent to troponin in acute
coronary syndrome.

23. EVALUATION OF PATIENT WITH AKI

24. MANAGEMENT
• Optimization of systemic and renal hemodynamic
through volume resuscitation and judicious use of
vasopressors .
• Elimination of nephrotoxic agents (e.g., ACE
inhibitors, ARBs, NSAIDs, aminoglycosides) if
possible .
• Initiation of renal replacement therapy when
indicated.

25. DIETARY MEASURES
• Adequate nutritional support should be ensured.
• High protein intake should be avoided.
• Enteral/ parenteral nutrition may be required.
• Providing nutrition preferentially via the enteral
route in patients with AKI

26. NUTRITIONAL AND GLYCEMIC
CONTROL
• Insulin therapy targeting plasma glucose 110–149 mg/dl
• Total energy intake of 20–30 kcal/kg/d in patients with any stage
of AKI.
• 0.8–1.0 g/kg/d of protein in non catabolic AKI patients without
need for dialysis.
• 1.0–1.5 g/kg/d in patients with AKI on RRT and up to a
maximum of 1.7 g/kg/d in patients on CRRT and in hyper
catabolic patients.

27. FLUIDS
• KDIGO suggest using isotonic crystalloids in absence of
hemorrhagic shock rather than colloids (albumin or
starches) .
• Colloids may be chosen in some patients to avoid
excessive fluid administration in patients requiring large
volume resuscitation, or in specific patient subsets.
• Colloids- Albumin is renoprotective and Hyperoncotic
starch shows nephro- toxicity.

28. VASOPRESSORS
• The vasoactive agents should not be withheld from patients
with vasomotor shock over concern for kidney perfusion.
• The appropriate use of vasoactive agents can improve kidney
perfusion in volume-resuscitated patients with vasomotor shock.
• The use of dopamine was associated with a greater number of
adverse events than Nor-epinephrine.

29. LOW- DOSE DOPAMINE
• Its use has been abandoned by most
subsequent to negative results of various
studies .
• KDIGO recommends not using low-dose
dopamine to prevent or treat AKI.

30. TREATMENT FOR INTRINSIC AKI
DIURETICS
• Reno protective : Potentially lessening ischemic injury.
• Can also be harmful, by worsening established AKI.
• No evidence of incidence reduction.
• KDIGO recommend not using diuretics to prevent AKI.
• KDIGO suggest not using diuretics to treat AKI, except in the
management of volume overload.
• Indicated only for management of fluid balance, hyperkalemia, and
hypercalcemia.

31. FENODOLPAM
• Fenoldopam mesylate is a pure dopamine type-1 receptor
agonist Without systemic adrenergic stimulation.
• For critically ill patients with impaired renal function, a
continuous infusion of fenoldopam 0.1mg/kg/min
improves renal function when compared to low dose
dopamine.
• KDIGO suggest not using it to treat AKI.

32. ERYTHROPOIETIN
• Recent animal studies suggest a potential clinical benefit of
erythropoietin in AKI.
• The reno protective action of erythropoietin may be related to
pleomorphic properties including anti apoptotic and anti oxidative
effects, stimulation of cell proliferation, and stem cell mobilization.
• Although one recent RCT in the prevention of human AKI was
negative, the usefulness of erythropoietin in human AKI should be
further tested in RCTs.

33. GROWTH FACTOR
• IGF-1 is a peptide with renal vasodilatory,
mitogenic and anabolic properties.
• KDIGO Work Group recommends against its
use in patients with AKI.

34. POST- RENAL AKI
• Prompt relief of urinary tract obstruction by
catheterization in urethral obstruction, correction of
ureteric obstruction by ureteric stent or percutaneous
nephrostomy.
• Relief of obstruction is usually followed by an appropriate
diuresis and may require continued administration of
intravenous fluids and electrolytes for a period of time.

35. INDICATION FOR DIALYSIS
• A – Acidosis(PH < 7.25 mmol/l despite medical treatment
• I – Intoxications (lithium, ethylene glycol, etc)
• O – Overload (volume overload-pulmonary oedema)
• U – Uremia (urea> 180-210 mg/dl, cr> 6.78 mg/dl) &
complications(pericarditis)
• S- sepsis

36. MODES OF DIALYSIS
• Hemodynamically stable- IHD
• Hemodynamically unstable
1. CRRT
2. PD
3. SLED (Slow Low-efficiency dialysis).

37. COMPLICATIONS
• Hyperkalemia
• Pulmonary oedema
• Acidosis
• Uremia
• Other electrolyte disturbance such as
• Hyperphosphataemia and Hypocalcaemia

38. Risk factors of AKI
• Elderly
• Pre-existing renal disease
• Surgery, trauma, sepsis or myoglobinuria
• Diabetes Mellitus
• Volume depletion states
• LV dysfunction
• Nephrotoxic drugs

39. RECOVERY OF RENAL FUNCTION
• Quantifying the recovery of renal function is extremely
challenging.
• COMPLETE RECOVERY : defined as return to pre-
AKI renal function ,assessed as the GFR +/- 10% of
baseline.
• NON RECOVERY: defined as persistent requirement of
RRT.
• PARTIAL RECOVERY : defined as persistent
impairement in GFR but no requirement of RRT.

40. PROGNOSIS
• Pre-renal and Post- renal better prognosis.
• Kidneys may recover even after dialysis requiring
AKI.
• 10% of cases requiring dialysis develop CKD.
• Individuals may die early even after kidney function
recovers completely.

41. REFERENCES
• HARRISONS PRINCIPLE OF INTERNAL
MEDICINE
• ACUTE KIDNEY INJURY JOURNAL CCSAP 2017

42. THANK YOU