Acute Kidney Injury (AKI) is characterized by a rapid and sustained decrease in renal function, with significant morbidity and mortality associated with it. Key aspects include its epidemiology, causes, and the emerging importance of biomarkers for early diagnosis. Management involves identifying causes, staging severity, and treating complications, while recent discussions highlight the lack of consensus on the most effective renal replacement therapy methods.

1. ACUTE KIDNEY INJURY
DR LALIT AGARWAL
CONS. NEPHROLOGIST

2. What is AKI?
An abrupt (within 7 days) &
sustained (>6 hours)
decrease in renal function/GFR
(usually reversible)
resulting in accumulation of waste
products
associated with increased morbidity and
mortality.

3. Epidemiology of AKI
Community acquired AKI 1%
Hospital acquired AKI 5-7%
ICU - AKI 5-25%
RRT in ICU for AKI 6%
Mortality in AKI with MSOF 50%
RRT 80%

4. Consensus Definition of AKI - KDIGO
• Increase in S.cr by ≥ 0.3 mg/dl within 48 hrs or
• Increase in S.cr to ≥ 1.5 times of baseline,
which is known or presumed to have occurred
within prior 7 days or
• Urine volume < 0.5 ml/kg/hr for 6 hours.
ADQI(RIFLE) -- AKIN-- KDIGO GROUP

5. Staging of AKI(KDIGO)
Stage Serum Creatinine Urine output
1 1.5-1.9 times baseline within 1 wk or
≥ 0.3 mg/dl increase within 48 hrs
<0.5ml/kg/h for
6-12 hrs
2 2.0-2.9 times baseline <0.5ml/kg/h for
≥ 12 hrs
3 3.0 times baseline or
increase in serum creat to ≥ 4.0 mg/dl or
initiation of RRT or
in patients < 18 yrs, decrease in eGFR to
<35ml/min per 1.73 m²)
<0.3ml/kg/h for
≥ 24 hrs or
Anuria for ≥ 12
hrs

6. KI
AKI
Lags behind the change in GFR

7. KDIGO-AKI definition refers to kidney
function, not damage.
• This late clinical diagnosis of KDIGO AKI has led
interest in biomarkers of kidney injury which result in
early diagnosis (1-2 DAYS BEFORE CREAT -subclinical
AKI) and help in taking preventive measures
• The most widely investigated markers are neutrophil
gelatinase-associated lipocalin (NGAL), kidney
injury molecule -1 (KIM-1). Others are LFABP, TIMP-
2,IGFBP7.
• Only NGAL and TIMP-2*IGFBP7 are available for
clinical use.
• Guidelines on how AKI biomarkers should be used
in clinical practice is lacking.

8. SPECTRUM OF KIDNEY INJURY

9. AKD – Acute kidney disease
• Acute kidney disease: a recent entity
• Acute kidney disease (AKD) defined as an
AKI episode that lasts longer than 7 days
but less than 90 days has recently been
proposed as a concept.
• It aims at closing the gap between AKI and
CKD (which requires 3 months to be
diagnosed).
• AKD uses the creatinine criteria of the
KDIGO definition.

10. Key causes of AKI
• Prerenal AKI
Functional or minimal cellular damage with
treatment rapid recovery
• Intrinsic AKI
Glomerular, Tubular , Interestitial and Vascular
• Postrenal AKI

11. COMMON CAUSES OF AKI IN ICU
• SEPSIS
• MAJOR SURGERY
• LOW CARDIAC OUTPUT
• HYPOVOLEMIA
• MEDICATIONS (20%)
• HEPATORENAL
SYNDROME
• TRAUMA
• CARDIOPULMONARY
BYPASS
• ABDOMINAL
COMPARTMENT
SYNDROME
• RHABDOMYOLYSIS
• OBSTRUCTION

12. Pathophysiology of AKI
• AKI : ATN (Ischemic / Nephrotoxic injury)
• ICU-AKI : Multifactorial(sepsis, decreased
perfusion & Nephrotoxic drugs)
• Decrease in GFR :
• Vascular component: loss of renal
autoregulation (Pgs / N2O and ANG II)
• Tubular component: obstruction, backleak and
inflammation

13. Course of Ischemic ATN
• Initiation – direct injury to TEC & endothelial cells
• Extension – activation of inflammatory mediators amplify
cellular injury & result in extension
• Maintenance - (1-2 weeks)
• Recovery/diuretic phase (10-25 days) – TEC repair &
regeneration & improvement in GFR

14. MAJOR COMPLICATIONS OF AKI
• Volume overload
• Hyperkalemia
• Metabolic acidosis
• Hypocalcemia
• Hyperphosphatemia
• Hyperuricemia and hypermagnesemia
• Signs of uremia

15. Distinguishing AKI from CKD
• Review h/o kidney disease and old records
• Ultrasonography
• Anemia (GFR < 30ml/min , absence of anemia
suggests AKI( exception HUS/TTP)

16. Prevention of AKI
• Identify patients at increased risks
advanced age,low eGFR,proteinuria,low
albumin, DM, previous AKI
• Avoidance of renal insults
Volume depletion, nephrotoxic drugs (NSAIDS,
ACEI/ARB, contrast, TLS, amphotericin,
aminoglycosides etc.)
• Prophylactic treatments
Good hydration, ?NAC, IV Sodabicarbonate

17. TREATMENT OF AKI
• Determine cause of AKI with special attention
to reversible causes
• Stage severity of AKI according to creatinine
and urine output
• Manage as per AKI stage and specific cause
• Management of complications of AKI

18. Treatment of AKI
• No specific Pharmacologic treatment
• Correct reversible causes
stop toxins, treat sepsis, volume resuscitation and
maintain kidney perfusion in non fluid responsive
by vasopressor/ inotropes (noradrenaline).
• Avoid in AKI
High dose diuretics, renal dose dopamine,
nephrotoxics, contrasts, volume overload
• General supportive management
Drug dosages, Correct hyperglycemia, Nutritional
support

19. RRT in AKI-1
• Conservative vs RRT?
• When to start RRT?
• Early vs late? (no survival benefit of early
start, concern of harm exists)
• What modality (IHD vs CRRT) of RRT to use
• What dose of RRT to give?

20. RRT in AKI-2
• What type of temporary dialysis access to
use?
• What type of dialysis membranes to use?
• What choice of anticoagulation?
• When to stop RRT in AKI? ( CRRT to IHD,
recovery of kidney function)

21. Modality of dialysis in ITU
• IHD (rapid removal of solute & water)
• SLED
• Hemofiltration
• Hemodiafiltration
• UF (Aquapharesis)
• Approx. 10% pts with AKI cannot be treated with IHD
because of hemodynamic instability
• SLED and CRRT meta-analysis: no difference in
outcome (Zhang et al AJKD Aug 2015)

22. Initiation of RRT in AKI
• Extremely variable and empirical on clinical
situation, if no improvement to optimal
medical/supportive interventions.
• RRT indicated in severe (stage 3) kidney injury.
• Absolute/urgent (objective) and
relative/elective (subjective) indications
• ICU:(early/low threshold to start in MOF)
• Renal ward:(single organ AKI)

23. Timing and indications of CRRT in ICU
• Optimal timing and indications for CRRT initiation(no
consensus, wide variation)
1.Start electively before the development of overt
complications of AKI.
2.Observational studies - early initiation prevent other
organ dysfunction ?
• 3 large RCT have not demonstrated benefit with earlier
initiation of dialysis.
Akiki study group NEJM MAY 2016,Jamale et al AJKD
DEC 2013,Canadian critical care trial KI OCT 2015

24. IHD vs CRRT – which patients
• Ideal method of treatment in unstable patients in
icu : IHD vs. CRRT- no survival benefit/recovery of
renal function as in Hemodiafe study or other RCT.
• In Hemodynamic stable pts CRRT not superior to
IHD.
• When IHD is unable to control volume or metabolic
derangement in catabolic/septic pts switch to
CRRT.
• Current literature support no differences in
mortality among the 3 RRT modalities.

25. Dialysis method and dose
• Controversy between CVVD (diffusion) vs. CVVHF
(convection) benefits. Convection removes
inflammatory cytokines as well.
• Most appropriate dialysis intensity/dose and
patient outcome -
Recent study suggests intensive renal support in
critically ill pts with AKI does not decrease
mortality or accelerate recovery or alter rate of
non renal organ failure c/w usual care (kt/v 3.9
and 20-25ml/kg/hour)
(Renal study and VA/NIH ARF trial network)

26. Anticoagulation
(risk and benefits)
• For IHD : Unfractionated heparin or use LMWH.
• For CRRT : Use of regional citrate anticoagul. if no C/I
to citrate, otherwise use unfractionated or LMWH.
• HIT: Argatroban, Fondaparinux or danaparoid
• For bleeding risk: proceed without
anticoagulation or use RCA.

27. Outcome of AKI
• Recovery, Predialysis-CKD, ESRD (10-30%) and
Death

28. How does AKI progress to CKD
• Host predisposition: genetics/co-morbidities
• Nephron loss followed by glomerular
hypertrophy
• Fibrosis and maladaptive repair
• Vascular drop out as a consequence of
endothelial injury

29. Conclusion
• AKI is a multisystem disease that affects lung,
brain, liver, metabolic function and immune
function.
• These multisystem effects likely contribute to
increased mortality observed in patients with
AKI

30. Thank you for kind attention!!