ACUTE KIDNEY INJURY

Acute Renal Failure

An abrupt and sustained decrease (days to weeks/within

48 hours) in renal function resulting in retention of
nitrogenous (urea and creatinine) and non-nitrogenous
waste products.
Depending on severity and duration of the renal
dysfunction, this accumulation is accompanied by
metabolic dysturbance, such as metabolic acidosis and
hyperkalaemia, changes in body fluid balance, and effects
on many other organ systems.
 Acute Renal Failure/Acute kidney
injury

An acute and sustained increase in serum creatinine

concentration of 0.5 mg% if the baseline is < 2.5 mg%,
or an increase in serum creatinine concentration of >
20% if the baseline is > 2.5 mg%/. An Increase % more
than or equal 50%/1.5 fold from base line
Reduction in urine out put(documented oliguria of less
then 0.5 ml/kg perhour for more than six hours)
TABEL 2 : RIFLE criteria ADQI
Bellomo et al, Curr Opin Crit Care 2002;6:505-8
 Acute Renal Failure

Oligouric

Non-oligouric
 EPIDEMIOLOGY

1% of hospitalized patients
20% of patients treated in ICU
4-15% of patients after cardiovascular surgery
Cause of mortality
1. (75%) : Sepsis/multy organ dysfuntion syndrome
2. Cardiopulomonal( 50%)
 Acute Renal Failure
Dialysis Treatments

Creatinine
M/l
Urine
l/day

Zllner,
Innere Medizin,
modified

Time / days

1. Damage 2. Oliguria / Anuria 3. Polyuria 4. Recovery

Damage to Complete Loss of Uncontrolled slow Recovery of
Renal Tissue Renal Function Urine Quantities Renal Function
(minutes to days) (up to 6 weeks) (1 - 2 weeks) (several months)
 Prerenal 35 %

CLASSIFICATION
OF Renal 50 %

ACUTE RENAL FAILURE

Postrenal 10 %
 ACUTE RENAL FAILURE

PRERENAL

Absolute decrease in effective blood volume

Haemorrhage
Volume depletion

Relative decrease in blood volume (ineffective arterial volume)

Congestive heart failure
Decompensated liver cirrhosis
Arterial occlusion or stenosis of renal artery

Haemodynamic form
NSAIDs
ACE-inhibitors or angiotensin-II
receptor antagonists in renal-artery
stenosis or congestive heart failure
Hypovolemia Baroreceptor activation Reduced affective
circulation volume

Respons neurohormonal

Axis renin-angiotensin Vasopressin Sympathetic nervous system

aldosterone

Vasoconstriction
contraction of mesangial cells
Reabsorpsi natrium and water

Reduced renal blood flow and glomerular filtration rate

Acute renal failure pre-renal
 ACUTE RENAL FAILURE

INTRINSIC RENAL

Vascular Glomerulonephritis Acute interstitial nephritis

Acute tubular
Vasculitis, Drugs
necrosis
Malignant HT Allergy

Ischaemic (50%) Nephrotoxic (35%)

Exogenous Endogenous
Antibiotics (gentamicin) Intratubular pigments (haemoglobinuria,
Radiocontrast agents myoglobinuria)
Cisplatin Intratubular proteins (myeloma)
Intratubular crystals (uric acid, oxalate)
 ACUTE RENAL FAILURE

POSTRENAL

Obstruction of collecting system or

extrarenal drainage

Bladder-outlet obstruction
Bilateral ureteral obstruction or
unilateral in one functioning kidney
 Causes for Kidney Failure Location of the
Cause?
Upstream
of the Kidney
- prerenal -
Heavy Blood Loss
Stenosis of the
Renal Artery
Within the Kidney ...
- intrarenal -
Drugs
Diabetes Downstream
Inflammatory of the Kidney
Diseases - postrenal -
... Prostatic
Hypertrophy
Renal Calculus
...

R E N AL AN AE M I A
 Assessment of a Patient with
Acute Renal Failure (1)
Procedure Information Sought

Clinical history and Clues to the cause of acute renal failure

examination Indicators of severity of metabolis disturbance
Estimate of volume status (hydration)

Urinalysis and urine Markers of glomerular or tubulointerstitial

microscopy inflammation, urinary tract infection or crystal
uropathy

Plasma biochemistry To assess extent of GFR reduction and metabolic

consequences

Urine biochemistry To differentiate prerenal from established renal

failure

To determine presence of anemia, leucocytosis, and

Full blood count
platelet consumption
Findings that suggest prerenal causes
Volume depletion
Congestive heart failure
Severe liver disease or other edematous state
Findings that suggest postrenal causes
Palpable bladder or hydronephrotic kidneys
Enlarge prostat
Abnormal pelvic examination
Large residual bladder urine volume
History of renal calculi (perform USG to screen obstruction)
Findings that suggest intrinsic renal disease
Hypotension, exposure to nephrotoxic drugs
Recent radiographic procedure with contrast
Finding in the urine sediment

If no abnormalities: suspect prerenal or postrenal azotemia

If eosinophils: suspect acute interstitial nephritis

If red blood cell casts: suspect glomerulonephritis or vasculitis

If renal tubular ephitelial cells and muddy brown casts: suspect

acute tubular necrosis
 Assessment of a Patient with
Acute Renal Failure (2)

Procedure Information Sought

Renal ultrasound To determine kidney size, presence of obstruction,

abnormal renal parenchymal texture
Plus, where appropriate :

Abdominal CT-Scan To define structural abnormalities of the kidneys or

urinary tract

Radionuclide scan To assess abnormal renal perfusion

Cystoscopy +/- retragrade To evaluate / relieve urinary tract obstruction

pyelograms

Renal biopsy To define pathology of renal parenchymal disease

 WHEN ?
Reverse An-/Oliguria to
Normouria
-volume replacement
-osmotic diuresis
(mannitol 12.5-25 g in 30m)
-forceed diuresis
(furosemide 40-300mg/4-6h)
-correct acidosis &
hyperkalemia)
-reverse hypercatabolism)
Maintain homeostasis Avoid hypovolemi
-electrolite imbalance Caused by polyuria
-Nutrition
-Normohydration Increase metabolism
-Acid-base balance
Avoid persistent
-RENAL Causative of decrease
-REPLACEMENT RF
-& SUPPORT
 Management priorities in patients
with acute renal failure
Search for and correct prerenal and postrenal factors.
Review medications and stop administration of nephrotoxins.
Optimise cardiac output and renal blood flow.
Monitor fluid intake and output; measure bodyweight daily.
Search for and treat acute complications (hyperkalaemia,
hyponatraemia, acidosis, hyperphospataemia, pulmonary oedema).
Provide early nutritional support.
Search for and aggressively treat infections.
Expert nursing care (management catheter care and skin in general;
physicological support).
Initiate dialysis before uraemic complication emerge.
Give drugs in doses appropriate for their clearance.
 Indications for dialysis in acute renal failure

Indications Characteristics
Uremia Asterixis, seizures, nausea & vomiting, pericarditis

Hyperkalemia K+ >6.5 mmol/L; K+ 5.5-6.5 mmol/L if ECG

changes

Fluid overload Fluid overload resistant to diuretics, especially

pulmonary edema

Metabolic pH < 7.2 despite sodium bicarbonate therapy;

acidosis sodium bicarbonate not tolerated because of fluid
overload
 Proposed criteria for the initiation of renal replacement therapy in adult critically ill
patients

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.
11.
Severe dysnatremia ([Na] > 160 or < 15 mmol/liter)
Hyperthermia/Hypothermia
WHEN ?
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.
 CAVHD
CVVHD
CAVHF
CVVHF
CAVH CAVHDF
KRAMER CVVHDF
Willem KOLF 1943-1944
1977
Dialysis in 15 pts
(1 survived)l IHD
HYBRID
EDD
HD DIALYSIS
CAPD
Renal SLED
Replacement Belding SCRIBNER 1960,
1960 Fred BOEN
begin chronic dialysis
1961
PD
George Haas 1914-1915 APD
Dialysis in Animal
SELLIGMENT & FINE
1945
 Dialysis modalities for acute renal failure

Intermittent therapies Continuous therapies

(up to 12 hours) (24 hours)
Hemodialysis Peritoneal dialysis
intermittent Ultrafiltration (SCUF)
daily Hemofiltration (CAVH, CVVH)
Hemodiafiltration Hemodialysis (CAVHD, CVVHD)
Slow Continous Ultra-Filtration Hemodiafiltration (CAVHDF, CVVHDF)
Extended Daily Dialysis
Sustained Low Efficient Dialysis

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.

WHICH ?
# Proses difusi
( Perpindahan molekul melalui membran semi permeable
Dengan cara difusi)

# Dipengaruhi oleh :
- berat molekul
- perbedaan konsentrasi
- Resistensi/ jenis membran

# Proses Filtrasi
(Perpindahan cairan dengan cara convective)
# Dipengaruhi oleh :
- Perbedaan tekanan (transmembrane)
- Koefisien ultrafiltrasi
Proses difusi dan ultrafiltrasi
 Dengan dialisis darah dibersihkan dengan proses difusi dan filtrasi
Melalui membran semi-permeable dalam Ginjal Buatan
Darah
Darah kotor dialisat bersih
masuk
Proses
difusi
Proses yang terjadi
dialisat
masuk
Proses
Filtrasi
ultrafiltrat
keluar
Ultra- Darah
Filtrat

Darah bersih
keluar Membran semi-permeable
Didalam ginjal buatan
GINJAL BUATAN
a. Modifikasi proses dialysis, dengan
- Qb = 150 cc/menit
- Qd = 300 cc/menit
- tD = 6 12 jam / hari

b. Dimulai Juli, 1998 di University of Arkansas, Amerika

c. Indikasi untuk ARF dengen hemodinamik tidak stabil

d. Merupakan alternatif terapi dari CAVHD atau CVVHD

e. Biasanya menggunakan Mesin Fresenius 4008, dengan

ginjal BUKAN Cellulosa Acetate
THAN
K
YOU