Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.

1. Acute Kidney
Injury
ANOOP K R
M.B.B.S, M.D

2. Epidemiology
• 5–7% of acute care hospital admissions
• 30% of admissions to the intensive care unit
( mortality rates may exceed 50%.)
•India- community acquired, yet 90% being potentially
reversible
•Developed nations AKI is almost hospital-acquired occurringin
an ICU setting

3. TOP FIVE CAUSES OF AKI IN
INDIA
1.Diarrhoeal diseases.
2.Sepsis: Pregnancy related
septicaemia.
3. Acute Malaria- P.falciparum.
4. Drug induced.
5.HospitalAcquired.

5.  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.

6. Risk
Injury
Failure
Loss of function
End-Stage Renal disease
Rifle Criteria for
stratifying AKI

7. RIFLE
Strat
a

8. Classification
Patho-Physiological basis :
 I. Pre-renal
 II. Intrinsic
 III. Post-renal

9. Classification of AKI (ARF)
Acute Kidney Injury
Pre-renal Intrinsic Post-renal
Glomerular Interstitial VascularTubular
55% 40% 5%
85%10%<5% <5%

14. Oliguric Vis-à-vis Non- oliguric
AKI:
Non- Oliguric:
In hospital set-up, secondary Nephrotoxic
agents.
Non-oliguric has better prognosis than oliguric
one.

15. ICU vs. Non-ICU AKI:
 Non-ICU AKI, in which the kidney is
usually the only failed organ, with mortality
rates of up to 10%.
 ICU AKI is often associated with sepsis and
with non-renal multi-organ system failure),
with mortality rates of over 50%

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

17. Careful history is essential
Exposure to nephrotoxins and drugs
Anuria may indicate post-renal causes
Skin rashes may indicate allergic nephritis
Evidences of volume depletion: diarrhea, bleeding
Pelvic and per-rectal examination: look for evidence
of abortion
Ischemia or trauma to the legs or arms may indicate
rhabdomyolysis

18. More severe hypoperfusion may lead to
ischemic injury of renal parenchyma
and intrinsic renal AKI.
Thus, prerenal AKI and intrinsic renal
AKI due to ischemia are part of a
spectrum of manifestations of renal
hypoperfusion.

19. •Prerenal AKI can complicate any
disease that induces :
 hypovolemia,
low cardiac output,
systemic vasodilatation, or
 selective renal
vasoconstriction.

20. IV. NSAIDS- they reduce
affarent renal vasodilation
V. ACEIs and ARBs- limit renal
efferent vasoconstriction

21. 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.

22. A history of prostatic disease,
nephrolithiasis
Recent surgical or radiologic
procedures
Past and present use of medications
Family history of renal diseases

23. Lower Urinary tract obstruction: is
suggested by suprapubic or flank mass
or symptoms of bladder dysfunction
(e.g. hesitancy, urgency)

24.  Review all medications
•
•
Cause of AKI .
DoseAdjustment.
 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

25. Blood Tests
 CBC,
 BUN/creatinine,
 Electrolytes,
 Uric acid,
 PT/PTT,

26. Urine Analysis
 Volume
 Proteinuria
 Urinary Indices: FENA and Urinary Sodium
 Sediments

28. Radiologic studies
 Renal ultrasound (useful for obstructive
forms)
 Doppler (to assess renal blood flow)
 CT Scan
 Pyelography
 Nuclear Medicine Scans :
DMSA: anatomy.
DTPA and MAG3: renal function,
urinary excretion and upper tract outflow.

29. BUN/plasma creatinine ratio: the BUN/plasma
creatinine ratio is normal at 10-15:1 in ATN, but
may be greater than 20:1 in prerenal disease due
to the increase in the passive reabsorption of
urea that follows the enhanced proximal
transport of sodium and water. Thus, a high ratio
is highly suggestive of prerenal disease as long
as some other cause is not present. But this
criterion is not highly specific.

30. Fractional excretion of Na+: is ratio of urine-to-
plasma Na ratio to urine-to-plasma creatinine
expressed as a percentage [ (UNa/PNa)/(Ucr/Pcr
)X 100]. Value below 1% suggest prerenal
failure , and values above 1% suggestATN
• Serum K+ and other electrolytes

33. •Cystatin C
•Neutrophil gelatinase-associated
lipocalin(NGAL)
•Interleukin-18
•Kidney injury molecule-1
•N-acetyl-D-glucosaminidase.
Important Biomarkers:

34. 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

35. Kidney Injury Molecule-1
(KIM-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.

36. 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.

37. Complications
 Uremia
 Hypervolemia and Hypovolemia
 Hyponatremia
 Hyperkalemia
 Hyperphosphatemia and Hypocalcemia
 Bleeding
 Infections
 Cardiac Complications.
 Malnutrition

38. Treatment

39. General Isssues
1.Optimization of systemic and renal
hemodynamics through volume resuscitation and
judicious use of vasopressors
2.Elimination of nephrotoxic agents (e.g., ACE
inhibitors, ARBs, NSAIDs, aminoglycosides) if
possible
3.Initiation of renal replacement therapy when
indicated

40. Hyperkalemia: 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 % glucose plus Insulin
10 units IV
o Give potassium –binding ion exchange resin
o Dialysis: it medial therapy fails or the patient is very
toxic

41. Hyperphosphatemia is usually controlled by
restriction of dietary phosphate and by oral
aluminum hydroxide or calcium carbonate,
which reduce gastrointestinal absorption of
phosphate.
Hypocalcemia does not usually require
treatment.

42. Pre-Renal AKI
 Prevention and treatment of prerenal
azotemia requires optimization of renal
perfusion.
 Severe acute blood loss should be treated
with packed red blood cells.

43. FLUIDS
 KDIGO suggest using isotonic crystalloids 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 (e.g., a cirrhotic
patient with spontaneous peritonitis, or in burns).
 Colloids- Albumin is renoprotective and
Hyperoncotic starch shows nephro- toxicity.

44. Vasopressors
 The Work Group emphasized that
vasoactive agents should not be withheld
from patients with vasomotor shock over
concern for kidney perfusion.
 Indeed, 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.

45. 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. (1A)

46. Cirrhosis and Hepatorenal
Syndrome
Albumin may prevent AKI in those treated with
antibiotics for spontaneous bacterial peritonitis.
Bridge therapies that have shown promise include
terlipressin (a vasopressin analog), combination therapy
with octreotide (a somatostatin analog) and midodrine
(an α 1-adrenergic agonist), and norepinephrine, all in
combination with intravenous albumin (25–50 mg per
day, maximum 100 g/d).

47. Cardio-Renal Syndrome
 Optimization of cardiac function .
 May require use of inotropic agents, preload-
and afterload-reducing agents,antiarrhythmic
drugs, and mechanical aids such as an
intraaortic balloon pump.

48. Intrinsic Acute Kidney Injury

49. Diuretic
•Renoprotective : Potentially lessening ischemic injury.
•Can also be harmful, by worsening establishedAKI.
•No evidence of incidence reduction.
•KDIGO recommend not using diuretics to preventAKI.
(1B)
•KDIGO suggest not using diuretics to treat AKI, except in
the management of volume overload. (2C)
•Indicated only for management of fluid balance,

50. FENOLDOPAM
 Fenoldopam mesylate is a pure dopamine
type-1 receptor agonist
 Without systemic adrenergic stimulation.
 No conclusive studies available.
 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.

51. Rhabdomyolysis
•Aggressive volume repletion (may require 10 L of fluid
per day).
•Alkaline fluids are beneficial.
•Diuretics may be used if fluid repletion is adequate and
there is no urinary output.
• Dialysis.
•Focus on calcium and phosphate status because of
precipitation in damaged tissue.

52. Glomerulonephritis or Vasculitis
•May respond to immunosuppressive agents and/or
plasmapheresis .
•Allergic interstitial nephritis due to medications requires
discontinuation of the offending agent.
•Glucocorticoids have been used, but not tested in randomized
trials.
• AKI due to scleroderma (scleroderma renal crisis) should be
treated with ACE inhibitors.

53. Aminoglycoside Induced AKI
•KDIGO suggest not using aminoglycosides for the treatment
of infections unless no suitable, less nephro - toxic, therapeutic
alternatives are available.
•Avoid in high risk patients age more than 65 years, DM,
cases of septic shock.
•KDIGO suggests using single dose daily rather than multiple-
dose daily treatment regimens.
•It also suggest using topical or local applications of
aminoglycosides (e.g., respiratory aerosols, instilled antibiotic
beads), rather than i.v. application, when feasible .

54. AMPHOTERICIN B
NEPHROTOXICITY
•KDIGO suggest using lipid formulations of
amphotericin B rather than conventional formulations of
amphotericin B.
•KDIGO recommend using azole antifungal agents
and/or the echinocandins rather than conventional
amphotericin B, if equal therapeutic efficacy can be
assumed.
•Some studies indicate that the liposomal form of
amphotericin B is less nephrotoxic than amphotericin B
lipid complex or amphotericin B colloidal dispersion.

55. Postrenal
 Prompt relief of urinary tract obstruction.
 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.

56. Indications for Dialysis
 A – Acidosis
 E – Electrolyte disturb., usually
hyperkalemia
 I – Intoxications (lithium, ethylene glycol,
etc)
 O – Overload (volume overload)
 U – Uremia (symptoms, signs )

57. Modes Of Dialysis
 Hemodynamically stable- IHD
 Hemodynamically unstable
1. CRRT
2. PD
3. SLED (Slow Low-efficiency dialysis).

58. Prognosis
 Pre-renal and Post- renal better prognosis.
 Kidneys may recover even after dialysis
requiring AKI.
 10% of cases requiring dialysis develop
ckd.
 Die early even after kidney function
recovers completely.

59. Carry Home Message
 Diagnose early – Biomarkers have great
potential.
 Look for Aetiology.
 Prevent rather than treat.
 No role of low dose dopamine, diuretics in
prevention and treatment.
 Initiate RRT when indicated.

60. Thank You