Approach to a

patient with
Acute Kidney
Injury
Dr. Sayan Chakraborty
JR-3, Dept. of Tropical Medicine,
School of Tropical Medicine, Kolkata
Email: dr.sayan@gmail.com
 Epidemiology
• 5-7% of acute care hospital admissions
• 30% of ICU admissions with mortality rates –
50%
• AKI worsens CKD
• Severe AKI requiring dialysis increases risk of
developing dialysis-requiring-ESRD.
• Community-acquired AKI: Volume depletion,
ADRs & obstruction of the urinary tract.
• Hospital-acquired AKI: Sepsis, major surgical
procedures, heart or liver failure, IV iodinated
contrast and nephrotoxic drugs
 AKI in
Tropics
• Diarrhoeal diseases
• Envenomations from snakes, spiders,
caterpillars, and bees
• Malaria
• Leptospirosis
• Crush injuries from earthquakes and
resultant rhabdomyolysis
Definition of
AKI
 KDIGO criteria
(ungraded)
• Increase in SCr by ≥0.3 mg/dl (≥26.5
umol/l) within 48 hours;
or
• Increase in SCr to ≥1.5 times baseline,
which is known or presumed to have
occurred within the prior 7 days;
or
• Urine volume <0.5 ml/kg/h for 6
hours.
KDIGO- Staging of
AKI
RIFLE
Criteria
R isk
I njury
F ailure
L oss of function
E nd-Stage Renal
disease
 RIFLE
Criteria
R isk
 Increase in Cr of 1.5-2.0 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
 RIFLE
Criteria
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
 RIFLE
Criteria
R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6
hrs I njury: Inc Cr 100-200% 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
 RIFLE
Criteria
R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr 100-200% 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

 RIFLE
Criteria
R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr 100-200% 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.
Etiopathogenesi
s of
AKI
 Classification of
AKI Acute Kidney Injury
55% 40% 5%

Pre-renal Intrinsic Post-renal

Glomerular Interstitial Tubula Vascula

r r
<5% 10% 85% <5%
Pre-renal AKI
 Non- oliguric
AKIIn hospital set-up, secondary
• Non- Oliguric:
Nephrotoxic agents like:
Aminoglycosides (10-30%), even in therapeutic
ranges, manifestation after 5-7 days of therapy
Amphotericin B: Dose & duration dependent;
polyuria, hypomagnesemia, hypocalcemia,
&nongap metabolic acidosis

• Non-oliguric has better prognosis than oliguric

one.
 ICU vs Non-ICU
AKI
• Non-ICU AKI, kidney usually being the only
failed organ, mortality rates of up to 10%.

• ICU AKI often associated with sepsis and

with non-renal multi-organ system
failure, mortality rates of over 50%
 Diagnostic Evaluation
 History and Physical examination:
• Pre-renal:
 History: vomiting, diarrhoea,
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
 Diagnostic Evaluation
INTRINSIC RENAL:
 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
 Diagnostic Evaluation
• 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.
 Blood Tests
• CBC
• BUN/creatinine
• Electrolytes
• Uric acid
• PT/aPTT
 Urine
Analysis
• Volume
• Osmolality
• Proteinuria
•Urinary Indices: FeNa
& Urinary Sodium
• Sediments
 Imaging
• 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.
 Important
biomarkers
• Cystatin C

•Neutrophil gelatinase-associated lipocalin (NGAL)

•Interleukin-18

•Kidney injury molecule-1

•N-acetyl-D-glucosaminidase
 Cystatin-C

• Superior to serum creatinine, as a

surrogate marker of early and subtle
changes of kidney function.
• Identifies kidney injury while
creatinine levels remain normal
• Allows detection of AKI, 24-48 hours
earlier than serum creatinine
 Kidney Injury Molecule-
1 (KIM-1)
• 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.
 Neutrophil gelatinase-
associated lipocalin(NGAL)
• Highly upregulated after
inflammation and kidney injury
• Can be detected in the plasma & urine
within 2 hours of cardiopulmonary
bypass–associated AKI.
• Considered equivalent to troponin in acute
coronary syndrome.
Complications
of AKI
Major causes of
AKI in Specific
Clinical settings
Treatment of
AKI
 General
Issues
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
 Pre-Renal
AKI
• Prevention and treatment of prerenal
azotemia requires optimization of renal
perfusion.

• Severe acute blood loss should be

treated with PRBC transfusion.
 FLUID
S of isotonic crystalloids
• KDIGO advocates use
rather than colloids (albumin or starches) .

• Colloids may be chosen to avoid excessive fluid

administration 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.
 Vasopressors
• Appropriate use of vasoactive agents
improve kidney perfusion in volume-
resuscitated patients with vasomotor shock.

• Dopamine associated with a greater

number of adverse events than Nor-
epinephrine.
 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)
 Cirrhosis and Hepatorenal
Syndrome
•Albumin may prevent AKI in those treated
with antibiotics for SBP

•Bridge therapies [in combination with IV

Inf albumin (25–50 mg/d)] include:
 terlipressin (a vasopressin analog),
 combination therapy with octreotide (a
somatostatin analog) and midodrine (an
α 1-adrenergic agonist), and
norepinephrine
 Cardio-Renal Syndrome
• Optimization of cardiac function .

• May require use of

inotropic agents
preload- and afterload-reducing agents,
antiarrhythmic drugs,
mechanical aids such as an intra-aortic
balloon pump.
Treatment of
Intrinsic
AKI
 Diureti
c lessening ischemic injury
• Renoprotective : Potentially

•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.
 FENOLDOPA
M mesylate: pure dopamine
• Fenoldopam
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.
 Erythropoietin
•Potential clinical benefit of erythropoietin in AKI in
animal studies.

•Renoprotective action of erythropoietin related to

pleomorphic properties including anti-apoptotic &
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.
 Growth factor intervention
•IGF-1 is a peptide with renal vasodilatory,
mitogenic and anabolic properties.

•KDIGO Work Group recommends against its

use in patients with AKI.
 Rhabdomyolysis
•Aggressive volume repletion (may require 10 L of
fluid/day)

• Alkaline fluids beneficial

•Diuretics may be used if fluid repletion is adequate &

no urine output

• Dialysis

•Focus on calcium and phosphate status because of

precipitation in damaged tissue
 Glomerulonephriti
s 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.
 Aminoglycoside Induced
•
AKI
KDIGO suggest not using aminoglycosides for the t/t of
infections unless no suitable, less nephrotoxic, therapeutic
alternatives are available

•Avoid in high risk patients of age > 65 years, DM, septic

shock

• Single dose daily rather than multiple-dose daily t/t

regimens

•Topical or local applications of aminoglycosides (e.g.,

respiratory aerosols, instilled antibiotic beads), rather than I.V.
application, when feasible
 AMPHOTERICIN B
•KDIGO suggest using lipid formulations of
NEPHROTOXICITY
amphotericin B rather than conventional formulations

•Use 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 lipid complex or
colloidal dispersion forms
 Post-
renal
• Prompt relief of urinary tract obstruction.

• Relief of obstruction is usually followed by

an appropriate diuresis and may require
continued administration of IVF &
electrolytes for a period of time.
 Indications for
 A – Acidosis
Dialysis
 E – Electrolyte disturb, usually
hyperkalemia
 I – Intoxications (lithium, ethylene glycol,
etc)
 O – Overload (volume overload)
 U – Uremia (symptoms, signs )
 Modes Of
Dialysis
• Hemodynamically stable- IHD

• Hemodynamically unstable
1. CRRT
2. PD
3. SLED
 Prognosi
s
• 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.
Recent
Publications
Recent
Publications
• Diagnose early – Biomarkers have great
potential
• Look for etiology
• Prevent rather than treat
• No role of low dose dopamine, diuretics in
prevention and treatment
• Initiate RRT when indicated
 References
• Brenner and Rector's The Kidney 9th ed. - M. Taal (Saunders,
2012)
• Harrison's Principles of Internal Medicine, 19th edition (2015)
• Paul Marino The ICU Book(3rd Ed)
• The Washington manual of Critical care 2nd edition
• Kidney Disease: Improving Global Outcomes (KDIGO) Acute
Kidney Injury Work Group. KDIGO Clinical Practice Guideline
for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1–138
• Rahman et al Acute kidney injury: A guide to diagnosis and
management; American Family Physician, Volume 86, Number
7 October 1, 2012
• Ronco C Acute Kidney Injury: from clinical to molecular
diagnosis; Ronco Critical Care (2016) 20:201