Update and Management of

Acute Kidney Injury

Dr. Tam Chun Hay
Specialist in nephrology
Honorary Clinical Associate professor, CUHK
Honorary Clinical assistant professor, HKU
 Why AKI?
1.Is it related to me?

2. Is it related to me??

3. Is it related to me???
 Contents
• Definition

• Etiology and pathophysiology

• Workup

• Management
 Case 1 – Uncle Tung
• M/70, good past health
• Lower limb pain 4/52 ago
• seen in GP: given voltaren, pantoloc, panadol
• Pain improved, but persistent malaise
• Blood test: Cr 300, urea 20
 Question:
• Is this a case of acute • What would you do?
kidney injury? A. Urgent refer to AED
A. Yes B. Refer to medical clinic
B. No C. No need to follow-up
C. Don’t know as this is normal in
elderly
 Definition of AKI
• a clinical syndrome with:
– An abrupt decline in glomerular filtration rate (GFR)
– sufficient to decrease the elimination of nitrogenous
waste products (urea and creatinine) and other
uremic toxins
• abrupt (<48 hours) ↓kidney function
serum Cr

– SCr > 0.3mg/dL, or divided by 88 to convert to SI unit used in HK

– SCr > 50%, or

– ↓urine output (<0.5ml/kg/hr for >6 hours)
 Useful terms
less urine

• oliguria (<500ml/day)
• Anuria (<100ml/day)
• azotemia: Rise in urea without renal intrinsic
cause
Staging of AKI
decrease in urine and increased SCr and increased duration

Himmelfarb J Kidney Int 2007;71(10):971-6

 acute vs chronic
acute chronic ultrasound grey white differentiation poor

1. normal kidney size 9-10cm

1. small, echogenic kidneys
need at least 3yrs
PTH less accurate

2. normal bone and PTH as can have hyper

with 3 months RF 2. renal bone & hyperPTH
3. Recent RFT normal 3. Recent RFT
4. no past history 4. past history of DM/HT, etc
5. less associated with 5. more associated with
normocytic anemia & normocytic anemia &
hypoCa no so accurate as would change over 2-3 months
hypoCa
 Case 1 – Uncle Tung
• M/70, good past health
• Lower limb pain 4/52 ago
• seen in GP: given voltaren, pantoloc, panadol
• Pain improved, but persistent malaise
• Blood test: Cr 300, urea 20
 Question:
• Is this a case of acute • What would you do?
kidney injury? A. Urgent refer to AED
A. Yes B. Refer to medical clinic
B. No C. No need to follow-up
C. Don’t know as this is normal in
elderly
D. Don’t know
 case 1 – Uncle Tung (cont)
• blood test showed glucose 22, HbA1c 15; Hb
9.6 normocytic
• USG showed bilateral renal parenchymal
disease, left kidney 7.9cm, right kidney 8.1cm

• Answer: chronic, refer to medical clinic

Examples of USG reports

around normal size but need to relate to the body build

or nobulated kidney
 Contents
• Definition

• Etiology and pathophysiology

• Workup

• Management
 Case 2
• M/60
• Recent chemotherapy for CA lung
• High fever, BP 75/35, ANC 0.1 neutrophil count
so neutropenic fever

• Admitted ICU, noted anuria and after 3 days,

Cr rise from 76 to 500AKI definite

• DDx?
Standard Classification of Acute Renal
Failure
Hilton: BMJ 2006; 333: 786-790
 Pre-renal causes of AKI
hypotension, less fluid, dehydration

• Impaired renal perfusion, commonly ∵

depletion of extracellular fluid volume, e.g.
– GI loss: vomiting, diarrhea
– Renal loss: diuretics, DM polyuria as too much glucose in urine drawing more water

– Dermal loss: burn, excessive sweating

– Sequestration of fluid to 3rd space, e.g. heart
failure, liver cirrhosis eg lower limb edema causing decreased vascular fluid volume
 Post-renal causes of AKI

stones tumor

Blood eg BPH

clot compression
Standard Classification of Acute Renal
Failure
Hilton: BMJ 2006; 333: 786-790

related to drugs, usu NSAIDS

interstitial: between glomerulus

Acute tubular
necrosis
 ATN acute tubular necrosis

• differentiate between pre-renal & ATN

• check urine Na and osmol pre-renal: concentrated
ATN; lower osmol

• pre-renal: preserved ability to retain Na &

concentrate urine
• ATN: failed to retain Na and concentrate urine
 nephrotic vs nephritic syndrome
• nephrotic • nephritic AKI

– proteinuria >3g/d – rapid onset

– hypoalbuminemia – edema, HT, oliguria
– edema – heavy proteinuria,
– hyperlipidemia hematuria
 Case 2
• M/60 renal cause
affecting interstitial or tubular

• Recent chemotherapy for CA lung

pre-renal cause

• High fever, BP 75/35, ANC 0.1

• Admitted ICU, noted anuria and after 3 days,
Cr rise from 76 to 500
• DDx?
 Case 3
• M/60
• History of DM on metformin, HT on lisinopril,
OA knee on regular OTC pain killers
• CT thorax with contrast for suspected CA lung
1 week ago
• Cr 76 to 200
Question: What is the offending agent?
A. metformin, lisinopril, painkiller
B. Metformin, lisinopril, contrast
C. Metformin, painkiller, contrast
D. Lisinopril, painkiller, contrast
 Drugs - NSAID
• Mechanism
– Renal vasoconstriction (usually reversible)
– Interstitial nephritis commonly caused by NSAID

– ATN or papillary necrosis

• COX-2 inhibitor? smaller GI side effect only

– Similar renal effects to NSAID

 Drugs – ACEI/ARB
high K would be the concern

• Impaired renal perfusion ∵impaired

vasoconstriction of the efferent arterioles
• Patients with pre-existing renal vascular
disease or dehydration may have higher risk of
AKI
• NOT absolutely contraindicated in chronic
kidney disease
 Drugs – radioiodine contrast
• Pathology
– Oxidant injury to proximal tubular cells
– Contrast osmolarity persistent afferent
vasoconstriction
• Clinical course
– Starts within 24 hours,
– peak at 3-4 days,
– resolve at ~ 2 weeks
– usually reversible
– Typically non-oliguric
 Drugs - metformin
• Increase risk of lactic acidosis in renal
impairment
• Reduce dose in renal impairment, not
recommend for use if CrCl <30ml/min CrCl <60 need reduce dose
CrCl <30 need to stop

• Withhold in occasions when patient

predispose to risk of AKI
 Drugs - acyclovir
• Intratubular crystal formation
– Birefringent needle-shaped crystals in urine
microscopy
• Direct tubular toxicity
• Reduce dose in patients with renal
impairment ∵ neurotoxicity
confusion for few days until diminish of drug effect
400 bd vs normal people 800 5xperday
Answer: What is the offending agent?
A. metformin, lisinopril, painkiller
B. Metformin, lisinopril, contrast
C. Metformin, painkiller, contrast
D. Lisinopril, painkiller, contrast
 Contents
• Definition

• Etiology and pathophysiology

• Workup

• Management
 Workup for AKI
History
• Past history (e.g. DM) and
renal function (? Underlying
renal disease)
• Recent illness, e.g. vomiting
or diarrhea (pre-renal)
• Recent imaging or drugs
Physical exam
• Hypotension/postural
hypotension
• Dehydration
• Distended bladder
• Evidence of vasculitis or
rheumatological disease
 Workup for AKI
normal should be dark outside and grey inside

Imaging
• USG: hydronephrosis now

– obstructive uropathy,
– renal parenchymal disease
• Doppler USG: renal artery
stenosis/occlusion
 Workup for AKI
Lab tests - blood Lab tests - urine
• Ur/Cr ratio 1:20 usu abnormal would >1:20
• Urinalysis & microscopy
– Pre-renal causes urea – RBC, WBC, nitrite, protein,
– False +ve in occasions like eosinophils
steroid use – Na/osmol
• Immune markers, e.g. ANA, – Culture
ANCA
• Myeloma screening
abnormal protein would be
produced by the body Invasive
blocking the tubules

• Hepatitis serology • Renal biopsy

• CK (rhabdomyolysis)
Novel biomarkers for AKI

CJASN
January 07,
2015 vol. 10
no. 1 147-155
 Contents
• Definition

• Etiology and pathophysiology

• Workup

• Management
 Prevention of AKI -
• Optimize volume & hemodynamic status
• Avoid offending agents and drugs
• Renal dose dopamine
Prevention of contrast-induced nephropathy

high dose 化痰藥

 Management of AKI
• SUPPORTIVE!!
– fluid balance
– Electrolytes
– Treatment of AKI complications
– nutrition
– dialysis
 Dialysis
• KDIGO – guideline:
– Initiate RRT emergently when life-threatening
changes in fluid, electrolyte, and acid-base
balance exist
• Indications:
– metabolic acidosis
– electrolyte disturbance, esp hyperK
– volume overload refractory to diuretics
– Uremic complications, e.g. pericarditis
 Pitfall 1 - Dialysis
• Movement of fluid and molecules across a
semi-permeable membrane from one
compartment to another
• Dialysis does not correct renal dysfunction
• Dialysis replaces function of kidney when
kidney failure
• Correct fluid & electrolytes
• Remove waste
Pitfall 2
 gadolinium induced irreversible nephrogenic sytemic
fibrosis if CrCl <30

Take home message

• Differentiate between AKI & CKD
– Kidney size, past RFT, renal bone
• Understand different causes of AKI
– Pre-renal, post-renal, renal (Glom, tub, vas, int)
• Comprehensive workup for AKI
– History, PE, blood, urine, USG
• Management:
– Prevention, Supportive dialysis
• 譚雋熹醫生
• Email: drtamchunhay@gmail.com
• Whatsapp:59391001
Thank you