Acute Kidney Injury (Kuliah Khusus, Sabtu 13 Sep 08)

8/4/2019 Acute Kidney Injury (Kuliah Khusus, Sabtu 13 Sep 08)

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Ketut Suwitra

Division of Nephrology Department of Medicine

Faculty of Medicine Udayana University – Sanglah Hospital

DENPASAR



Definition

Acute Kidney Injury (AKI)

a. abrupt of kidney function (< 7 days)

b. changes in blood chemistry (rise in serum creatinine)

c. decrease of urine out put

d. or both (b and c)



Risk of renalDysfunction

Serum creatinine increased1.5 fold (1.5 – 2. mg/dL) or

GFR decreased by morethan 25%

Less than 0.5 ml/kg/h ofurine for 6 hours

Serum cretainine increased2 fold (2 – 4 mg/dL) or

GFR decreased than 50%

Less than 0.5 ml/kg/hof urine for 12 hoursInjury to the

Kidney

Failure ofKidneyFunction

Serum cretainine increased3 fold or An Acute rise inceratenine of greater than

44 mol/L so that newcreatinine is greater than

350 mol/L(>4 mg/dL)GFR decreased more than

75%

Less than 0.3 ml/kg/h ofurine for 24 hours oranuria for 12 hours

Loss of Kidneyfunction Complete loss of kidney for longer than 4 weeks

End-stage renal

Disease

The need for dialysis for longer than 3 months

GFR criteria Urine output criteriaAND/OR

Goldsmith D, 2007. ABC of Kidney Disease

RIFLE Criteria



Aetiology

Acute Kidney Injury

Pre-renal Renal (intrinsic) Post-renal



Pre-renal (40- 80% of cases)

Pre renal

Hypotension Hypovolaemia(reduced intravascular volume)

Low cardiac output

Total loss Volume redistribution

Reduced effectivecirculating volume

(Ascites, oedema, “3rd spacing”,

congestive cardiac failure)

Altered vascularcapacitance

(Sepsis: shunting, vasodilatation.Hepatorenal syndrome HRS)

GI loss(Vomiting, diarrhea, surgical

fistulae)

Haemorrhage(Visible and occult)

Renal loss(Diuretics, polyuria)

Skin loss(Exessive sweating, burns)

Blakeley S, 2008. Renal Failure and replacement Therapy



Renal (Intrinsic) (20- 40% of cases)

Intrinsic

Glomerular(Glomerulonephritis)

Tubular Interstitial

(Autoimmune, toxic, infectious)Vascular

Toxic

Ischaemic(Extreme pre renal,sepsis, pancreatitis)

Large vessel

(Renovascular disease,atheroembolic)

Small vessel

(Vasculitis, HRS,renovascular, malignanthypertension)

Intrinsic toxins(Rhabdomyolysis, massive

aemolysis tumour lysis, myeloma)

Extrinsic toxins (Radio contrast, drugs, antibiotics)

Blakeley S, 2008. Renal Failure and replacement Therapy



Post-renal (10- 20% of cases)

Intrinsic Extrinsic

Intra-luminal: e.g. stone, blood

cloth, papillary necrosis

Pelvic malignancy

Intra-mural: e.g. urethral stricture,

prostatic hypertophy or

malignancy, bladder tumour,

radiation fibrosis

Retroperitoneal fibrosis




Causes of AKI

Pre-renal (volume responsive) Intrinsic Post-renal

Hypovolaemia

• Vomiting and diarrhoea

• Hemorrhage

Decrease in effectivecirculating volume

• Cardiac failure

• Septic shock

• Cirrhosis

Drugs• ACE inhibitors

Glomerular

• Glomerulonephritis

Glomerular endothelium

• Vasculitis

• HUS

• Malignant hypertension

Tubular

• Acute tubular necrosis

• Rhabdomyolysis• Myeloma

Interstitial

• Intersitial nephritis

Obstruction

• Renal calculi

• Retroperitoneal fibrosis

• Prostatic hypertrophy

• Carcinoma

• Cervical carcinoma

• Urethral stricture

• Bladder neoplasm

• Pelvic neoplasm

• Retroperitoneal neoplasm

Davenport A, 2008. Clinical Practice Guidelines; Module 5: Acute Kidney Injury.



Prerenal



Renal



Postrenal



Investigation of the causes

A. History

1. Presence of risk factors

- hemorrhage, water loss

- DM, advanced age, hypertension, heart disease

2. Previous episodes of renal disease (stone, cystic disease)

3. History of medication (anti TB, NSAID, aminoglycoside)

4. Systemic disease (SLE, hyperuricemia)

5. Family history



B. Physical Finding 1. Blood pressure

2. Volaemic state

3. Loan pain 4. Ballotment

5. Retensio urinae

6. Prostate hyperthropy



C. Laboratory finding

1. Oligouria

2. Anemia

3. Elevated serum urea and creatinine

4. Elevated serum cystatin C (?)

5. Hyperkalemia



D. Imaging

1. Plain foto abdomen

2. Ultrasound



Diagnostic step

1. Is this acute or chronic

renal failure ?

• history & examination

• Anemia

• hypertension

• Edema

• previous Sc

• small kidney in USG

2. Present a sign of

obstruction ?

• complete anuria

• ballotment/palpable blader

• USG



3. Volaemic state ? Blood pressure, pulse

JVP/CVP

Urea/SC >20

heart failure

Urine Na < 20 mmol/L

4. Renal parenchymal

disease ?

history and examination

urine dipstic & microscopic

- proteinuria

- hematuria

- cast

Diagnostic step



MANAGEMENT OF AKI

A. Conservative management

1. Exclude reversible/treatable causes of AKI 2. Obtain and maintain euvolemic state

3. Attempt to establish a urine output if patients oligouric

4. Provide adequate nutrition

5. Minimize use of invasive lines and procedures 6. Monitor drug usage, carefully, and modify dosage or

interval appropriately

7. Monitor and treat for clinical and biochemical

complications

B. Active management

• Renal Replacement Therapy



Use of Diuretic and Renal vasodilators in AKI

1. success for converting an oligouric to an nonoligouric stateoccurs when the duration of oliguric was brief

2. respond more readly to a continuous infusion rather than abolus of loop diuretic

3. a small controlled study suggest dopamine may be synergistic

with lop diuretic in conversion an oligouric to nonoligouricstate , but this issue still controversy

4. the complication rate of low-dose dopamine and continuousinfusion of loop diuretic appears to be low

Important : obstructive uropathy must be excluded and prerenal factors corrected

Schrier, 2007



Other Pharmacologic Agents :

Inotropic support (norapenephrine)

Some studies suggest that in patients with septic shock,

norepinephrine induces a diuresis more effectively than

other vasoactive agents as dopamine

Atrial Natriuretic Peptide

No consistent evidence for a beneficial role of ANP in the

treatment of AKI

Insulin like growth factor 1

No beneficial effect



Nutritional support in AKIThe goal of nutritional support :

1. Restoration of metabolic homeostasis with

maintenance of fluid, electrolyte, and acid-base

balance

2. Preservation of lean body mass

3. Maximization of protein synthesis

4. Prevention of vitamin, mineral, and trace element

depletion



Recommendation of nutrition in AKI : • 35 kcal/kg body weight/day

in sepsis, energy requirement can be increased by 25%

• 0.8 gm protein/kg body weight

• ratio between glucose and fat 70/30

Careful attention to electrolyte (Potassium & Sodium )



RENAL REPLACEMENT THERAPY

The issues regarding renal replacement therapy in AKI

are currently the source of much debate and

investigations

• when to start ?

• what modality to use

• how much is enough ?



When to start ?

earlier renal replacement therapy

“prophylactic” to keep BUN 90-100 mg/dl,creatinine 9-10 mg/dl

Schier, 2007



Indications and criteria for initiating

renal replacement therapy in the intensive care unit

Bellomo R, Ronco C : Kidney int 1998;53 (66):S106-109

1. Oliguria (urine output < 200 ml/12 hr)

2. Anuria/extreme oliguria (urine output < 50 ml/12 hr)

3. Hyperkalemia ([K+] > 6.5 mmol/liter)

4. Severe acidemia (pH < 7.1)

5. Azotemia (urea) > 30 mmol/liter)

6. Clinically significant organ (especially lung) edema

7. Uremic enchepalopathy

8. Uremic pericarditis

9. Uremic neuropathy/myopathy

10. Severe dysnatremia ([Na] > 160 or < 115 mmol/liter)

11. Hyperthermia/Hypothermia

12. Drug overdose with dialysable toxin

The presence of :• one of the above criteria is sufficient to initiate renal replacement therapy in a critically ill

patients• two of these criteria makes renal replacement urgent and mandatory.• combined derangements suggest initiation of renal replacement therapy even before the

above mentioned limits have been reached.



Dialysis modalities for acute kidney injury

Intermittent therapies

(up to 12 hours)

Continuous therapies

(24 hours)

Hemodialysis

intermittent

daily

Hemodiafiltration

Slow Continuous Ultra-Filtration

Extended Daily Dialysis

Sustained Low Efficiency Dialysis

Peritoneal dialysis

Ultrafiltration (SCUF)

Hemofiltration (CAVH, CVVH)

Hemodialysis (CAVHD, CVVHD)

Hemodiafiltration (CAVHDF,

CVVHDF)

Adapted from Mehta RL. Supportive therapies; intermittent hemodialysis, continuous

renal replacement therapies and peritoneal dialysis. In : Schrier RW, editor. Atlas of

diseases of the kidney, Current Medicine, Philadelphia: Blackwell Science; 1998: with

permission.



ADVANTAGES DISADVANTAGES

Intermittent

hemodialysis

Efficient and rapid removal of

volume and small molecules

Cost effective

Readily available

Central venous access required

Anticoagulation may be required

May not be tolerated by

hemodynamically unstable

patients

Continuoushemofiltration

Excellent control of volumeenabling liberal use of

hyperalimentation, blood

products, etc.

Good removal of larger

molecules

Can be used in relatively

hypotensive patients

Central venous access requiredAnticoagulation may be required

Labor intensive and expensive

Peritoneal dialysis No need for anticoagulation

Cost-effective

Slow removal of uremic toxins

Risk of peritonitis

May be tolerated poorly in patients

with splanchnic hypo perfusion

The advantages and disadvantages of intermittent versus

continuous renal replacement therapies

Nephrology Secret, 2006



NATURAL HISTORY OF AKI

INSULT1 – FULL RECOVERY

2 – AKI TO CKD

3 – ACUTE-ON-CHRONICKIDNEY DISEASE

4 – AKI TO ESRD

100

0

TIME

Clin J Am Soc Nephrol 3: 881-886, 2008



SUMMARY

ACUTE KIDNEY INJURY

• A common critical condition with high mortality

• The classification depends on site of position and

etiology

• Loss of autoregulation, vasoconstriction,

glomerulotubular damage, and inflammation is a main

pathogenesis

• Some modality of treatments with a different result



Treatment Evidence of benefit Comment

Loop diuretics No difference in renal revovery or mortality compared with placebo

May promote diuresis inoliguric AKI, but may be

ototoxic in high doses

Dopamine No difference in mortality or need for

dialysis compared with placebo

Potential adverse effects

include tachycardia,

extravasation necrosis

and peripheral gangrene

Natriuretic peptides No difference in dialysis-free survival

compared with placebo

Renal replacementtherapy

No significant difference in dialysis-dependency or mortality between

continuous and intermittent renal

replacement therapy

Continuous renalreplacement therapy is

less likely to ptovoke

haemodynamic

instability

Summary of Treatment


Acute Kidney Injury (Kuliah Khusus, Sabtu 13 Sep 08)

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