Acute kidney injury (aki)

Acute kidney Injury(AKI)
Dr Iqbal Mahmud
MD (Phase-A) student

Renal function
• Kidney has many roles:

Renal function
- Excretory function

Renal function
- Osmolality regulation

Renal function
- Acid base balance

Renal function
• BP regulation through salt and water balance

Renal function
- Acid base balance
- BP regulation through
Salt and water balance
- Hormone secretion ( Erythropoietin, Vit D3)

Definition of Acute Kidney Injury
AKI 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.
Oliguria is usually but not invariably, a feature of AKI.
 Urine volume can be variable :
Anuria < 50 ml/day
Oliguria 100 – 400 ml/day
Non-oliguria > 400 ml/day

Definition of Acute Kidney Injury
Acute usually reversible decline in renal function*
• Rapid time course( < 48 hrs)
• Reduction of kidney function:
A) Rise in serum creatinine, defined by either:
1. absolute increase in serum creatinine of >0.3mg/dl
( >26µmol/l)
2. % increase in serum creatinine of > 50%
B) Reduction in urine output, defined as < 0.5ml/kg/hr for
more than 6 hrs
• The diagnostic criteria should only be applied after volume status has been optimized.
• Urinary tract obstruction needs to be excluded if oliguria is used as the sole criterion.
• Only one criterion (creatinine or urine output) has to be fulfilled to qualify for a stage.

RIFLE classification scheme for ARF

AKI is staged for severity according to the
following criteria

Comparison of RIFLE and AKIN criteria for
diagnosis and classification of AKI

Acute kidney disease(AKD)
• 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/1.73m2 for < 3
months or a decrease by ≥ 35% or an increase in
s.cr by>50% for <3 months.

Incidence of AKI
• Approximately 7% of all hospitalized patient ( 65% of
intensive care admission)
• 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

Acute kidney
injury
Pre renal
- ↓ Effective renal
blood flow:
1- Hemorrhage
2- Volume
depletion
3- Low cardiac
output
4- Sepsis
5- CCF
6- Cirrhosis
- Arterial
stenosis/Occlusion
- Vasomotor:
1- NSAID
2- ACEI/ ARBs
Intrinsic Post renal

Acute kidney
injury
Pre renal Intrinsic
Vascular
1- Vasculitis
2- Thrombotic
microangiopathy
3- Scleroderma
renal crisis
4- Renal vein
thrombosis
5- Cholesterol
emboli
Acute GN
Glomerluo-
nephritis
Acute TIN
tubulointestitial
nephritis
ATN
acute tubular
necrosis
Post renal

Acute kidney
injury
Pre renal Intrinsic
Vascular
1- Vasculitis
2- Thrombotic
microangiopathy
3- Scleroderma
renal crisis
4- Renal vein
thrombosis
5- Cholesterol
emboli
Acute GN
(Glomerluo-
nephritis)
Acute TIN
(tubulointestit
ial nephritis)
ATN
acute tubular
necrosis
Ischaemic Nephrotoxic
Post renal

Acute kidney
injury
Pre renal Intrinsic
Vascular
1- Vasculitis
2- Thrombotic
microangiopathy
3- Scleroderma
renal crisis
4- Renal vein
thrombosis
5- Cholesterol
emboli
Acute GN
(Glomerluo-
nephritis)
Acute TIN
(tubulointestit
ial nephritis)
ATN
acute tubular
necrosis
Endogenous
1- Haemoglobinuria
2- Myoglobinuria
3- Casts and Crystals
Exogenous
1- Nephrotoxic
drugs
2- Radiocontrast
Post renal

Acute kidney injury
Pre renal
- ↓ Effective circulatory
volume:
1- Haemorrhage
2- Volume depletion
3- Low cardiac output
4- Sepsis
5- CCF
6- Cirrhosis
- Arterial
stenosis/Occlusion
- Vasomotor:
1- NSAID
2- ACEI/ ARBs
Intrinsic
Vascular:
1- vasculitis
2- Thrombotic
microangiopathies
3- hypertensive
emergencies
Acute GN
( Glomerluo-
nephritis)
Acute TIN
(tubulo-intestitial
nephritis)
ATN
(acute tubular
necrosis)
Endogenous
1- Haemoglobinuria
2- Myoglobinuria
3- Myoglobin casts
4- Intratubular crystals
Exogenous
1- Nephrotoxic
drugs
2- Radiocontrast
Post renal
Obstruction
1- Bladder out-let
obstruction
2- Bilateral ureteral
obstruction

Etiology and Pathophysiology
• Hypovolemia leads to glomerular hypoperfusion, but
filtration rate are preserved during mild
hypoperfusion through several compensatory
mechanisms.
• During states of more severe hypoperfusion, these
compensatory responses are overwhelmed and GFR
falls, leading to prerenal AKI.

1.Hypovolemia
• Hemorrhage, burns, dehydration
• Gastrointestinal fluid loss: vomiting, surgical
drainage, diarrhea
• Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes
mellitus), hypoadrenalism
• Sequestration in extravascular space:
pancreatitis, peritonitis, trauma, burns,
• Severe hypoalbuminemia

II. Low cardiac output
• Diseases of - myocardium, valves, and
pericardium; arrhythmias; tamponade
• Other: pulmonary hypertension, massive
pulmonary embolus
III. Altered renal systemic vascular resistance
ratio
• Systemic vasodilatation: sepsis, anaphylaxis IV.
Renal hypoperfusion with impairment of renal
autoregulatory responses

IV. NSAIDS- they reduce affarent renal
vasodilation
V. ACEIs and ARBs- limit renal efferent vasoconstriction
Prerenal AKI can complicate any disease that
induces :
 hypovolemia,
low cardiac output,
systemic vasodilatation, or
 selective renal vasoconstriction.

Diagnosing pre-renal AKI
• Is the patient volume depleted?

• Is cardiac function good?

• Is the patient septic?

• Is the patient septic?
History
Examination
Investigation

Diagnosing pre renal AKI
• History
• Examination :
1. Signs of Hypovolaemia:
a) Low BP( and reduced pulse pressure)
b) Postural BP drop ( a fall in systolic BP > 10mmHg)
c) Sinus tachycardia and postural increase in heart
rate ( increase in HR > 15 beat/min).
d) Low JVP even when the patient is supine
e) Cool peripheries and vasoconstriction
f) Poor urine output

2. Sings of hypervolaemia( high extracellular fluid):
a) Increased circulating volume:
- High BP
- Elevation of the JVP
b) Increased interstitial fluid:
- Peripheral or generalized oedema
- Pulmonary oedema (tachypnoea, tachycardia,
third heart sound)
- Pleural effusion
- Ascites

Diagnosing Intrinsic Renal AKI
• Has pre-renal and post renal been excluded?
• History
- Drug, Rash, joints, nose bleed, haemoptysis, hearing loss, claudication,
IHD, diabetes, fever or night sweat, Recent infection
• Examination
- Oedema, rash, mouth ulcer, hearing loss, uveitis, ischaemic toe, bruits,
evidence of scleroderma, prosthetic valve or stigmata of Endocarditis
• Laboratory investigations
- Urine including microscopy for dysmorphic RBC, Protein, Bence Jones
protein, protein/creatinine ratio or 24hr protein excretion
- Blood – nephritic screen – ANA, dsDNA, ANCA, antiGBM,
Immunoglobulines
protein electrophoresis, Rh-factor, HBV, HCV, HIV, cryoglobulins, blood
film, CK,
C3,C4, ASO-titre , ESR and CRP
• US kidneys
. Renal biopsy

Diagnosing post renal AKI
• History
- pain, anuria, haematuria, prostatism
• Examination
- palpable bladder, central abdo mass, PR, PV
• Observation
• Laboratory investigations
- Urine
- Blood
- Imaging – US, CT

Pathophysiology of postrenal AKI
• It involves hemodynamic alterations triggered
by an abrupt increase in intratubular pressures
• An initial period of hyperemia from afferent
arteriolar dilation is followed by intrarenal
vasoconstriction from the generation of
angiotensin II, thromboxane A2, and
vasopressin, and a reduction in NO production.

Nature of Obstruction
• Outside
- Tumours, prostate, retroperitoneal fibrosis, cervical Ca
• Within wall
- Tumours, strictures
• Within lumen
- Stones, tumours

Investigations:
FBC : Hb% ↓- Haemolysis, GI bleeding
↑/ ↓ WCC: infection
↓platelets and altered coagulation : DIC, thrombotic
microangiopathy
Pancytopenia : marrow infiltration, others malignancy
PBF : fragmented RBC : send LDH,haptoglobulin,reticulocyte
count
Biochemistry :
U & E: raised s.ur,Cr ratio indicate pre-renal AKI
↑ K: needed urgent management
Na :usually normal, ↓ in case of volume overload and diuretics
↓HCO3 : metabolic acidosis

Investigations :
• LFT : ↓ albumin- imply proteinuria and GN
↑ billirubin : hepatorenal syndrome,
• Calcium and phosphates :
↑ Ca ++: myeloma, sarcoidosis, malignancy
• CRP : for infection/ inflammation,
(procalcitonin if available)
• Ck: rhabdomyolysis,
• Urate : tumour lysis/ pre-eclampsia
• Lactate : to asses underperfusion and tissue ischemia
Minimum AKI panel:
Urine dipstick, FBC, U&E, Ca, PO4, Albumin, LFT, CK,
CRP, ABG/ venous HCO3

Urinalysis in AKIUrinalysis in AKI

• 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.

3. Radiography/imaging
• 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

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

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

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.

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.

Diuretic
• Renoprotective : 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.
(1B)
• KDIGO suggest not using diuretics to treat AKI, except in
the management of volume overload. (2C)
• Indicated only for management of ﬂuid balance,
hyperkalemia, and hypercalcemia.

Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.

Fluid challenge.
2 Rule out Obstruction Physical Exam, patency of catheters, Renal
ultrasound.
Foley catheterization.

Fluid challenge.
ultrasound.
3 Renal function tests BUN, creatinine & electrolytes.
Hemoglobin, calcium & phosphorus.

Fluid challenge.
ultrasound.
4 Probable cause for renal
dysfunction
Evaluate nephrotoxic (drug) exposure –
NSAIDs, aminoglycosides, hypotension,
etc.

Fluid challenge.
ultrasound.
dysfunction
etc.
5 Urine Routine &
Microscopy
Specific gravity, protein, glucose, blood,
casts – granular &/or cellular, cells &
crystals.

Fluid challenge.
ultrasound.
dysfunction
etc.
5 Urine Routine &
Microscopy
Specific gravity, protein, glucose, blood,
casts – granular &/or cellular, cells &
crystals.
6 Urinary Indices
Fractional Excreation of
sodium (FeNa)
Obtain spot urine sodium & creatinine.

General Issues
1. Optimization of systemic and renal
hemodynamic 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

Dietary measure
• 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

Nutritional and glycaemic 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. We suggest administering
• 0.8–1.0 g/kg/d of protein in noncatabolic AKI
patients without need fordialysis (2D),
• 1.0–1.5 g/kg/d in patients with AKI on RRT (2D),
and up to a maximum of 1.7 g/kg/d In patients on
CRRT and in hypercatabolic patients. (2D)

FLUIDS
• KDIGO suggest using isotonic crystalloids in absence of
haemorrhagic 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 (e.g., a cirrhotic
patient with spontaneous peritonitis, or in burns).
• Colloids- Albumin is renoprotective and
Hyperoncotic starch shows nephrotoxicity.

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.

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 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).

Diuretic
• 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. (1B)
• KDIGO suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C)
• Indicated only for management of ﬂuid balance,
hyperkalemia, and hypercalcemia.

FENOLDOPAM
• 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

Erythropoietin
• Recent animal studies suggest a potential clinical benefit of
erythropoietin in AKI.
• The renoprotective action of erythropoietin may be related to
pleomorphic properties including antiapoptotic and
antioxidative 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 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.

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.

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 .

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.

Treatment of intrinsic renal AKI
• ATN
-aim of treatment is to keep the patient alive until
spontaneous recovery
- In-hospital mortality 19-37%*
- Recovery could take up to 6 weeks**
- Self correcting (full 60%, some 30%, dialysis 5-10%)
- Very severe – permanent cortical necrosis
* Oxford handbook of Nephrology and Hypertension 2009
** Kumar and Clark/ Clinical Medicine July 2012

Post-renal
• 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.

Indications for Dialysis
 A – Acidosis(pH<7.25)
 E – Electrolyte disturb., usually hyperkalemia
( k>6 mmol/lt 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

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

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.

Complications of AKI
• Hyperkalaemia
• Pulmonary oedema
• Acidosis
• Uremia
• Other electrolyte disturbance such as
hyperphosphataemia and hypocalcaemia

Who is a risk?
Many cases of AKI should never occur in the first place
1- Elderly
2- Pre-existing renal disease
3- Surgery, trauma, sepsis or myoglobinuria
4- Diabetes
5- Volume depletion( Nil By Mouth, bowel obstruction,
burn)
6- LV dysfunction
7- Nephrotoxic drugs
8- Cirrhosis (reduce arterial volume)

Reducing risk perioperatively
• Three principles:
1- Avoid dehydration
2- Avoid nephrotoxins
3- Review clinical status and renal function those
at risk
• Optimize volume status
1- No patient should go to theatre dehydrated
2- Review daily weight, input and output chart
3- Calculate losses especially those NBM ( use
0.9% N saline and NOT 5% Dextrose)

Reducing risk perioperatively
• Optimize blood sugar control in DM ( use
sliding scale
• Catheterize those with prostate disease
• Avoid surgery if possible immediately after a
contrast procedure
• Stop nephrotoxic drugs 24-48hrs
preoperatively
• Review the patient EARLY postoperatively

Summary
• 3 categories of AKI
• Simple clinical assessment will define which
• Be aware of life threatening complications and
emergency treatment
• Recognise those at risk

Resource materials
• Davidson’s Principles & Practice of Medicine
• Kumar & Clark Clinical Medicine
• Oxford textbook of Clinical Nephrology
• Oxford handbook of Nephrology and
hypertension
• Renal Association website( www.renal.org)
• KDIGO guideline (www.kidney.org)
• AKI network ( www.akinet.org)

Acute kidney injury (aki)

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