Acute kidney Injury

1. ACUTE KIDNEY INJURY
1
DR Jayakrishnan M P
PG Resident, Dept of Medicine
MGM Medical College, Indore

2. DEFINITION
• Increase in S.Cr by ≥ 0.3 mg/dl within 48 hours ; or
• Increase in S. Cr to ≥ 1.5 times baseline, which is
known and presumed to occur within the prior 7
days ; or
• Urine volume < 0.5 ml/kg/h for 6 hours
• AKI is not ATN, nor is it renal failure.
KDIGO guidelines 2012 2

3. • Anuria - Urine output < 100ml/24hrs
• Oliguria - Urine output < 400ml/24hrs
• Polyuria - Urine output > 2.5 to 3 litres/24hrs
3

4. RIFLE CRITERIA(2004)
4

5. Staging of AKI – AKIN Criteria(2007)
Stage Serum creatinine Urine output
1 1.5-1.9 times baseline or
≥ 0.3 mg/dl increase
< 0.5 ml/kg/h for 6-12
hours
2 2-2.9 times baseline < 0.5 ml/kg/h for ≥ 12
hours
3 3.0 times baseline or
Initiation of renal replacement
therapy or
In patients < 18 years, decrease
in eGFR to < 35 ml/ min per
1.73 m2
< 0.3 ml/kg/h for ≥ 24
hours or
Anuria for ≥ 12 hours
5

6. ETIOLOGY
Causes of Prerenal AKI(40-55%):
• Hemorrhage
• GI Loss – diarrhoea,vomiting,NG tube loss
• Renal loss – diuretics,DI
• Burns,Hyperthermia
• Nephrotic Syndrome,Cirrhosis
• Reduced CO: Cardiogenic shock,CHF, pericardial
diseases,vavular diseases.
• Systemic vasodilatation – Sepsis,Cirrhosis,Anaphylaxis,Drugs
• Renal Vasoconstriction – Early sepsis, HRS, Acute
hypercalcaemia,Drugs-NE,
vasopressin,NSAIDS,ACEIs,Calcineurin inhibitors, Iodinated
contrast agents
• Abdominal compartment syndrome.
BRENNER AND RECTORS - THE KIDNEY 9TH EDITION
6

7. ETIOLOGY
Causes of intrinsic AKI:
• Tubular injury: hypovolemia,sepsis,hemorrhage,cirrhosis,CHF
toxins-Myoglobin,Haemoglobin,uric acid,paraproteinemia-
antibiotics,chemotherapy,radio contrast agents,phosphate
preparations
• Tubulointerstitial injury:
- AIN- NSAIDS,antibiotics
- Infections, Infiltrations,Allograft rejection
• Glomerular injury : Glomerular diseases, Haematological
diseases
• Renal microvasculature: Malignant HTN, PIH, radiocontrast
agents,scleroderma,drugs
• Large vessels :
vasculitis,thrombosis,dissection,thromboembolism,
atheroembolism,compression,trauma
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
7

8. ETIOLOGY
Causes of Postrenal AKI(<5%):
• Extrinsic :
- Upper urinary tract: pelvic tumours,retroperitoneal tumours
or lymph nodes,fibrosis,surgical trauma
- Lower urinary tract: prostate/ bladder/urethral
pathologies,neurogenic.
• Intrinsic : stone,stricture,malignancy,sloughed papillae,blood
clots etc
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
8

9. • Most likely causes in hospitalized patients
– ATN (45%)
– Prerenal (21%)
– Acute on chronic kidney disease (13%)
– Obstruction (10%)
– Glomerulonephritis or vasculitis (4%)
– Acute interstitial nephritis (2%)
– Atheroemboli (1%)
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
9

10. 10

11. Prerenal AKI
• Most common cause of AKI in the outpatient setting
– Look for patients with hemorrhage, GI and urinary fluid
loss,severe burns
– Decreased effective arterial blood volume ( CHF, Cirrhosis
or nephrotic syndrome).
– Drugs– NSAIDS,ACEIs,ARBs
– O/E: tachycardia,signs of dehydration ,orthostatic
hypotension,reduced JVP.
CLINICAL EVALUATION
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
11

12. Intrinsic kidney Diseases
• ATN - Acute Tubular Necrosis
– Usually occurs after an ischemic event or exposure to nephrotoxic
agents.
• AIN - Acute Interstitial Nephritis
– Classic presentation is fever, rash, eosinophilia and Cr bump 7-10 days
after drug exposure.
• CIN - Contrast Induced Nephropathy
– Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration.
• Others – Glomerular Disease, Pigmented Nephropathy,
Thrombotic Microangiopathy
CLINICAL EVALUATION
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
12

13. Postrenal diseases:
• H/O of pelvic tumors, irradiation, congential abnormalities,
kidney stones, genitourinary procedures or surgeries,spinal
cord injury,DM
• Nocturia,urinary frequency,urgency,hesistency,urinary
retension
• O/E Enlarged prostate on PR examination,Distended bladder
CLINICAL EVALUATION
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
13

14. INVESTIGATIONS
Urine Analysis:
• Specific gravity: > 1.01 -1.020 – Prerenal AKI
1.010(isosthenuria) - ATN
• Haematuria – glomerulonephritis,urologic disease,interstitial
nephritis,trauma,renal infarction,pigment nephropathy.
• Urine sediment analysis:
- Normal with hyaline casts- prerenal AKI
- Pigmented granular casts- ischaemic or nephrotoxic ATN
- RBC casts – acute glomerular disease
- WBC & nonpigmented granular casts –interstitial nephritis
- Broad granular casts – CKD
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
14

15. INVESTIGATIONS
• Eosinophiluria – drug induced AIN
• Uric acid crystals – urate nephropathy
• Oxalate crystals – ethylene glycol toxicity
Proteinuria:
• < 1g/day – ischaemic and nephrotoxic ATN
• > 1g/day – glomerular diseases,multiple myeloma,drug
induced AIN.
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn15

16. • Urine biochemical parameters:
Diagnostic Index Prerenal AKI ATN
FENa <1% >2%
Urine Na <20 >40
U Cr/Pl Cr >40 <20
U urea N/Pl urea N >8 <3
Urine SG >1.018 1.010
Urine osmolality >500 300
Pl BUN/Cr >20 <10-15
Renal failure Index
Una/(UCr/Pl Cr)
<1 >1
Urine sediment Hyaline casts Muddy brown
granular casts 16

17. INVESTIGATIONS
Laboratory evaluation:
• BUN : S Cr - >20:1 - prerenal AKI
10:1 - intrinsic AKI
• Rhabdomyolysis –hyperkalemia,hyperuricemia
hyperphosphatemia,hypocalcemia,elevated CPK
• Tumor lysis syndrome/urate nephropathy –hyperkalemia,
hyperuricemia hyperphosphatemia,elevated uric acid,normal
CPK,Urine Uric acid/Cr ratio > 1
• Ethylene glycol poisoning – elevated serum anion gap and
osmolal gap
• Severe Anaemia – hemolysis,multiple myeloma,thrombotic
angiopathy
• Eosinophilia – Allergic interstitial nephritis
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn17

18. INVESTIGATIONS
• Radiologic Evaluation :
Xray KUB
Renal Ultrasonography
Noncontrast CT
MRI
• Renal biopsy: To assess the cause for intrinsic AKI after
excluding pre and post renal AKI.
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn18

19. Acute Kideny Injury
Prerenal
Uosm > 5000 mosm/kg
Una < 20meq/L
FEna < 1%
Microscopy - bland
Intrinsic Renal Diseases
Postrenal
Uosm: variable
Una: low early, high late
FEna: variable
Microscopy - bland
Ischemic / Toxic ATN
Uosm ~ 300 mosm/kg
Una > 40meq/L
FEna > 2%
Microscopy – dark pigment cast
Acute Interstitial Nephritis
Uosm: variable, ~300 mosm.kg
Una > 40 meq/L
FEna > 2%
Microscopy – leukocytes,
erythrocyts, leukocyte casts
Acute Glomerulonephritis
Uosm: variable (>400 in early GN)
Una: variable (<20meq/l in early GN)
FEna: variable, <1% in early GN
Microscopy – hematuria, proteinuria
Erythrocyte casts (dysmorphic)
19

20. COMPLICATIONS OF AKI
• Metabolic:Hyperkalemia,hyponatremia,hypocalcemia,hyperp
hosphatemia,hypermagnesemia,hyperuricemia,metabolic
acidosis.
• Cardiovascular: Pulmonary oedema, arrhythmia,
pericarditis,perricardial effusion,pulmonary
embolism,hypertension,MI.
• GI: Nausea,vomiting,malnutrition,haemorrhage.
• Neurologic: irritability,asterixis,seizures,mental status
changes.
• Haematologic: anaemia,bleeding.
• Infectious: pneumonia,septicemia,UTI
• Others: Hiccoughs,elevated PTH,Low total T3 and T4.
BRENNER AND RECTORS - THE KIDNEY 9TH
20

21. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
21

22. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Goals:
- To facilitate recovery of kidney function
- To prevent death
- To minimize the risk of CKD
• Patients be stratified& manage according to their
susceptibilities and exposure to reduce the risk of AKI.
• Test patients at increased risk for AKI with measurements of
SCr and urine output.
• Individualize frequency and duration of monitoring based on
patient risk and clinical course.
22

23. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Evaluate to determine the cause, with special attention to
reversible causes.
• Monitor with measurements of SCr and urine output to stage
the severity.
• Manage patients according to the stage and cause.
• Evaluate patients 3 months after AKI for resolution, new onset,
or worsening of pre-existing CKD.
23

24. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Prerenal AKI:
• Volume resuscitation
- Packed cell transfusion
- Crystalloids prefered than colloids
- Treat underlying cause
• Use of vasopressors in conjunction with fluids in patients with
vasomotor shock with, or at risk for AKI.
24

25. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• CHF:
- Cautious use of diuretics
- Ionotropes
- Vasodilators to reduce afterload
- Mechanical support – intra aortic balloon pumps,ventricular
assist devices.
• Liver failure and HRS:
- Intravenous Albumin
- Drugs: Terlipressin, Norepinephrine, Octreotide+Midodrine
- Peritoneovenous shunts,Portosystemic shunts

26. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Avoid using diuretics to prevent or treat AKI, except in the
management of volume overload.
• Avoid using low-dose dopamine to prevent or treat AKI.
• Avoid using fenoldopam/ atrial natriuretic peptide (ANP)/
recombinant human (rh)IGF-1 to prevent or treat AKI.
26

27. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Intrinsic AKI :
• Sepsis :
- haemodynamic targets: MAP>65mmHg,CVP-10-12mmHg,
Urine O/P-.5ml/kg/hr, central venous O2 saturation >70%
- Use crystalloid solutions, RBC transfusion, Vasopressors
- Intensive insulin therapy- Target glucose level 110- 149mg/dl
• Correct intravascular volume depletion
• Avoid nephrotoxic medications

28. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Aminoglycosides :
• Avoid unless no suitable, less nephrotoxic, therapeutic
alternatives are available.
• Single daily doses are prefered.
• Monitor drug levels if multiple daily dosing is used for more than
24 hours or single-daily dosing for more than 48 hours.
• Use topical or local applications than i.v. application, when
feasible and suitable.
28

29. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Use lipid formulations of amphotericin B .
• In the treatment of systemic mycoses or parasitic infections,
azole antifungal agents and/or the echinocandins are
prefered.
29

30. Contrast medium induced AKI:
• Screening(S Cr,r/f questionnaire,Urine protein)
• Use iso osmolar or low osmolar iodinated contrast media
• Use lowest possible dose
• Isotonic saline or sodium bicarbonate
- 1 ml/kg/hr for 12 hours before and after procedure
- OP settings – 3ml/kg/hr for 1hr before procedure f/b 1-
1.5ml/kg/hr for 6hrs after the procedure.
• Oral N Acetyl cysteine 600 BD to 1200mg BD
• Avoid Diuretics,Theophylline, Dopamine,
Fenoldopam,CCBs,Mannitol, Prophylatic haemodialysis.

31. Management of other causes of intrinsic AKI:
• Urate nephropathy – Allopurinol, Rasburicase
• Cisplatin induced nephropathy – Amifostine
• Ethylene glycol toxicity – Fomepizole
• Vasculitis and glomerular diseases – Steroids,Alkylating
agents, Plasmapheresis.
• TTP/HUS - Plasma exchange
• Scleroderma – ACEIs
• Multiple myeloma – Plasmapheresis with chemotherapy
• Acute interstitial nephritis – Discontinue the offending drug.
steroids,Mycophenolate mofetil.

32. • Use of Dopamine ,Fenoldopam,Natriuretic peptides,Mannitol
are not recommended.
• Avoid Loop diuretics for prevention and management of AKI
except in case of fluid overload.
Postrenal AKI:
• PCN, Ureteric stents
• Correction of underlying cause

33. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Indications for RRT
 Absolute :
- Volume overload unresponsive to diuretic therapy
- Refractory hyperkalemia
- Persistent metabolic acidosis
- Overt uremic symptoms – Encephalopathy, Pericarditis,
Uremic bleeding diathesis.
 Relative:
- Progressive azotemia without uraemic manifestations
- Persistent oliguria
33

34. Modalities of RRT:
• Intermittent Haemodialysis
• Continuous renal replacement therapy
- Continuous venovenous haemofiltration(CVVH)
- Continuous venovenous haemodialysis(CVVHD)
- Continuous venovenous haemodiafiltration(CVVHDF)
• Hybrid therapies :
- Sustained low efficiency dialysis(SLED)
- Extended daily dialysis(EDD)
- Sustained low efficiency daily diafiltration(SLEDD-f)
• Peritoneal dialysis

35. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Initiate RRT emergently when life-threatening changes in
fluid, electrolyte, and acid-base balance exist.
• Consider the broader clinical context, the presence of
conditions that can be modified with RRT, and trends of
laboratory tests—rather than single BUN and creatinine
thresholds alone.
• Discontinue RRTwhen it is no longer required, either because
intrinsic kidney function has recovered to the point that it is
adequate to meet patient needs, or because RRT is no longer
consistent with the goals of care.
• Avoid using diuretics to enhance kidney function recovery, or
to reduce the duration or frequency of RRT.
35

36. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
Anticoagulation:
• In a patient with AKI requiring RRT, base the decision to use
anticoagulation for RRT on assessment of the patient’s
potential risks and benefits from anticoagulation.
• Anticoagulation during RRT in AKI is recommended if a
patient does not have an increased bleeding risk or impaired
coagulation and is not already receiving systemic
anticoagulation.
36

37. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• For patients without an increased bleeding risk or impaired
coagulation and not already receiving effective systemic
anticoagulation:
- In intermittent RRT, use either UF or LMW heparin.
- In CRRT, use regional citrate anticoagulation rather than
heparin in patients who do not have CIs for citrate.
- In patients with contraindications for citrate, use either UF
or LMW heparin.
37

38. • For patients with increased bleeding risk who are not receiving
anticoagulation:
- Regional citrate anticoagulation can be used, rather than no
anticoagulation, during CRRT .
- Avoid regional heparinization during CRRT .
• In patients with heparin-induced thrombocytopenia (HIT), direct
thrombin inhibitors (argatroban) or Factor Xa inhibitors
(danaparoid or fondaparinux) are recommended rather than
other or no anticoagulation during RRT.
38

39. • Initiate RRT via an uncuffed nontunneled dialysis catheter,
rather than a tunneled catheter.
• Vein for insertion of a dialysis catheter:
- Right jugular vein > femoral vein > left jugular vein
- Last choice: subclavian vein(dominant side).
- use USG guidance for dialysis catheter insertion.
• Take a CXR promptly after placement and before first use of
an IJV or subclavian dialysis catheter.
39

40. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Avoid topical antibiotics over the skin insertion site of a
nontunneled dialysis catheter.
• Avoid using antibiotic locks for prevention of catheter-related
infections of nontunneled dialysis catheters.
• Use dialyzers with a biocompatible membrane for IHD and
CRRT .
• Use continuous and intermittent RRT as complementary
therapy.
• Use CRRT for hemodynamically unstable patients.
• Use CRRT for AKI patients with acute brain injury or
increased ICP or generalized brain edema.
40

41. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Use bicarbonate as a buffer in dialysate and replacement fluid
for RRT in patients with AKI and circulatory shock/ liver failure
and/ lactic acidemia.
• Dialysis fluids and replacement fluids in patients with AKI, at a
minimum, should comply with American Association of
Medical Instrumentation (AAMI) standards regarding
contamination with bacteria and endotoxins.
41

42. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Provide RRT to achieve the goals of electrolyte, acid-base,
solute, and fluid balance that will meet the patient’s needs.
• A Kt/V of 3.9 per week is recommended when using
intermittent or extended RRT in AKI.
• An effluent volume of 20–25 ml/kg/h is recommended for
CRRT in AKI.
42

43. Supportive management of AKI
• Intravascular volume overload :
- Salt and water restriction,diuretics,Ultrafiltration
• Hyponatremia :
- Restriction of oral and iv free water
• Hyperkalemia:
- Dietary restriction
- Discontinue K+ supplements/K+ sparing diuretics
- K+ binding resins, Loop diuretics
- Glucose(50 ml 50%)+ Regular Insulin 10-15U IV
- Sodium bicarbonate
- Calcium gluconate
- RRT

44. Supportive management of AKI
• Metabolic Acidosis :
- Restriction of dietary protein
- Sodium bicarbonate, RRT
• Hyperphosphatemia :
- Diet restriction,
- PO4- binding agents(Ca carbonate,ca acetate,Sevelamer)
• Hypocalcemia :
- Calcium Carbonate
Hypermagnesemia :
- Discontinuation of Mg containing Antacids

45. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Nutrition :
• Total energy intake of 20–30 kcal/kg/d any stage of AKI.
• Avoid restriction of protein intake.
- 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients
without need for dialysis.
- 1.0–1.5 g/kg/d in patients with AKI on RRT
- up to a maximum of 1.7 g/kg/d in patients on CRRT and
in hypercatabolic patients.
• Enteral route is prefered for nutrition.
45

46. Supportive management of AKI
• Drug dosage :
- Adjustment of all dosages for GFR and renal replacement
modality.

47. AKI Stage
Discontinue all nephrotoxic agents when possible
Ensure volume status and perfusion pressure
Consider functional hemodynamic monitoring
Monitor serum creatinine and urine output
Avoid hyperglycemia
Consider alternative to radiocontrast procedures
Non invasive diagnostic work up
Consider invasive diagnostic work up
Check for changes in drug dosing
Consider renal replacement therapy
Consider icu admission
Avoid subclavian catheters if possible
High Risk Stage 1 Stage 2 Stage 3
47

48. • Identify AKI early on
– Monitor serum Cr for at risk patients
– Make sure I/Os are recorded correctly
• Diagnose as Prerenal, Intrinsic or Postrenal
– Detailed history
– Order routine labs including UA, Uosm, Ucr, Una
(Urine Urea if on diuretics)
– Imaging studies as necessary
• Begin appropriate treatment
– Stop offending agent
– Fluids if appropriate
– Relieve obstruction
– Renal dosing of medicines
Take Home Points
48

49. THANK YOU
49