Approach to Acute renal failure

dr Putra Hendra SpPD

UNIBA

Acute renal failure (ARF) or acute

kidney injury (AKI)
Deterioration of renal function over a period of hours to days,
resulting in
the failure of the kidney to excrete nitrogenous waste products and
to maintain fluid and electrolyte homeostasis

ARF Rapid deterioration of renal function

(increase of creatinine of >0.5 mg/dl in <72hrs.)

azotemia (accumulation of nitrogenous wastes)
elevated BUN and Creatinine levels
GFR < 10 ml/min
decreased urine output (usually but not always)

Oliguria: <400 ml urine output in 24 hours

Anuria: <100 ml urine output in 24 hours

Assessment of Renal Function

(cont.)
Creatinine Clearance
Best way to estimate GFR
GFR = (creatinine clearance) x (body surface area in
m2/1.73)
Ways to measure:
24-hour urine creatinine:
Creatinine clearance = (Ucr x Uvol)/ plasma Cr
Cockcroft-Gault Equation:
(140 - age)xlean body weight [kg]
CrCl (mL/min)= x 0.85 if
Cr [mg/dL]x72
female
Limitations: Based on white men with non-diabetes kidney disease

Modification of Diet in Renal Disease (MDRD) Equation:

GFR (mL/min./1.73m2) = 186 X (SCr)-1.154 X (Age)-0.203 X
(0.742 if female) X (1.210 if African-American )

Assessment of Renal
Function
Glomerular Filtration Rate (GFR)
= the volume of water filtered from the plasma per
unit of time.
Gives a rough measure of the number of
functioning nephrons
Normal GFR:
Men: 130 mL/min./1.73m2
Women: 120 mL/min./1.73m2

Cannot be measured directly, so we use creatinine

and creatinine clearance to estimate.

Stages of Renal Failure

Stages of Renal
Failure
Stage 1

GFR (cc/min)
>90

Stage 2 (Mild)

60-90

Stage 3 (Moderate)

30-59

Stage 4 (Severe)

15-29

Stage 5 (End-stage)

<15

Epidemiology
It occurs in
5%of all hospitalized patients and
35% of those in intensive care units
Mortality is high:
up to 7590% in patients with sepsis
3545% in those without

Median hospital length of stay (LOS) stratified by single acute organ system
dysfunction (AOSD), including acute renal failure (ARF).

Etiology of ARF

Underlying Cause
CHRONIC
KIDNEY DISEASE

PRE-RENAL

RENAL

POST-RENAL

GLOMERULAR

INTERSTITIAL

VASCULAR

Pre-renal ARF
Volume depletion

Renal losses (diuretics, polyuria)

GI losses (vomiting, diarrhea)
Cutaneous losses (burns, Stevens-Johnson syndrome)
Hemorrhage
Pancreatitis

Decreased cardiac output

Heart failure
Pulmonary embolus
Acute myocardial infarction
Severe valvular heart disease
Abdominal compartment syndrome (tense ascites)

Renal
Glomerular
Antiglomerular basement membrane (GBM) disease
(Goodpasture syndrome)
Antineutrophil cytoplasmic antibody-associated
glomerulonephritis (ANCA-associated GN) (Wegener
granulomatosis, Churg-Strauss syndrome, microscopic
polyangiitis)
Immune complex GN (lupus, postinfectious, cryoglobulinemia,
primary membranoproliferative glomerulonephritis)

Tubular
Ischemi
Totoxic
Heme pigment (rhabdomyolysis, intravascular hemolysis)
Crystals (tumor lysis syndrome, seizures, ethylene glycol
poisoning, megadose vitamin C, acyclovir, indinavir,
methotrexate)
Drugs (aminoglycosides, lithium, amphotericin B,
pentamidine, cisplatin, ifosfamide, radiocontrast agents)

Renal
Interstitial
Drugs (penicillins, cephalosporins, NSAIDs,
proton-pump inhibitors, allopurinol, rifampin,
indinavir, mesalamine, sulfonamides)
Infection (pyelonephritis, viral nephritides)
Systemic disease (Sjogren syndrome, sarcoid,
lupus, lymphoma, leukemia, tubulonephritis, uveitis

Acute Tubular Necrosis

Most common cause of intrinsic cause of ARF
Often multifactorial
Ischemic ATN:
Hypotension, sepsis, prolonged pre-renal state

Nephrotoxic ATN:
Contrast, Antibiotics, Heme proteins

Contrast nephropathy
(Contrast Induce Nephropathy/CIN)
12-24 hours post exposure, peaks in 3-5 days
Non-oliguric, FE Na <1% !!
RX/Prevention: 1/2 NS 1 cc/kg/hr 12 hours
pre/post
Mucomyst 600 BID pre/post (4 doses)
Risk Factors: CKD, Hypovolemia ,DM,CHF

Ischemic Acute Renal Failure

Intravascular volume depletion and hypotension
Gastrointestinal, renal, dermal losses, hemorrhage, shock

Decreased effective
intravascular volume: CHF,

Large vessel renal vascular disease:

Renal artery thrombosis or embolism,
operative arterial cross clamping, renal
artery stenosis

cirrhosis, nephrosis, peritonitis

Medications: ACE
inhibitors, NSAIDS,
radiocontrast agents,
Ampho B, Cyclosporin

Generalized
or localized reduction in
renal blood flow

Small vessel renal vascular disease:

Atheroembolism, vasculitis, malignant
hypertension, hypercalcemia,
transplant rejection

Hepatorenal syndrome
Sepsis

Ischemic
Acute Renal Failure

Causes
Hypertension

Congestive Heart Failure

Chronic Glomerulonephritis

Diabetes (most common cause)

Causes
Systemic Lupus Erythrematosus

Amyloidosis

Polycystic Kidney Disease

Atherosclerosis

Aminoglycoside nephrotoxicity
(Gentamycin, Azithromycin)

Causes
IV contrast medium

Long term use of NSAIDS

Post-renal AKI
Ureteric obstruction

Stone disease,
Tumor,
Fibrosis,
Ligation during pelvic surgery

Bladder neck obstruction

Benign prostatic hypertrophy [BPH]

Cancer of the prostate
Neurogenic bladder
Drugs(Tricyclic antidepressants, ganglion blockers,
Bladder tumor,
Stone disease, hemorrhage/clot)

Urethral obstruction (strictures, tumor)

Causes
Nephrolithiasis

Prostate Cancer

Clinical Presentation of
Acute Renal Failure

A c u t e R e n a l F a ilu re
P re re n a l
d e c r e a s e d r e n a l p e r f u s io n
8 0 % o f ca ses

R enal
in t r in s ic r e n a l d is e a s e
1 0 % o f ca ses

P o s tre n a l
o b s t ru c t io n
10%

Clinical feature-2
Symptoms and/or signs of renal failure:

weakness and
easy fatiguability (from anemia),
anorexia,
vomiting, mental status changes or
Seizures
edema

Systemic symptoms and findings:

fever
arthralgias,
pulmonary lesions

Acute Renal Failure

Diagnosis
Blood urea nitrogen and serum creatinine
BUN/Cr helpful in classifying cause of ARF
ratio> 20:1 suggests prerenal cause

CBC, peripheral smear, and serology

Urinalysis
Urine electrolytes
U/S kidneys
Serology: ANA,ANCA, Anti DNA, HBV, HCV, Anti GBM,
cryoglobulin, CK, urinary Myoglobulin

Renal failure
Differentiation between acute and chronic renal failure

Acute

Chronic

History

Short
week)

(days-

Long
(month-years)

Haemoglobin
concentration

Normal

Low

Renal size

Normal

Reduced

Renal osteodystrophy

Absent

Present

Peripheral neuropathy

Absent

Present

Serum Creatinine
concentration

Acute reversible
increase

Chronic
irreversible

RF: Differences
ARF

CRF

ESRD

GFR

Rapid decline
Reversible

Slow,
progressive,
irreversible

Permanent no
function

Urine output

Anuria, oliguria
on non-oliguria

Polyuria

Polyuria or
normal

Urine
analysis

Sp.gr.:>1.020
May be active
sediment

Sp.gr.: 1.010
Bland sediment

1.010
Bland Sediment

Serum K+

Usually high
May be normal

Usually low
May be normal
or high

Usually low
May be normal
or high

Uremic bone
disease

Not present

Usually present

Always present

Management of acute renal

failure
Management of volume homeostasis
Management of electrolyte
homeostasis
Management of acid- base homeostasis
Management of uremia
Nutritional management in acute renal
failure
Dialysis in acute renal failure

Management of volume
homeostasis

Record I/O
Physical examination
Fluid = urine output + 300-500
Sodium intake<2 g/day
Diuretics
Low dose dopamin ( 0.3 ug/kg/min)
CVP or pulmonary capillary wedge
pressure

Management of acid- base

homeostasis
Dietary protein restriction 0.81.0g/kg of body weight 30 kcal
/kg/day ( except hypercatabolism )
Look for cause of acidosis
Sodium bicarbonate
Dialysis

Management of electrolyte
homeostais

Hypernatremia and hyponatremia

Hyperkalemia
Hypocalcemia
Hypomagnesemia
Hyperphosphatemia

Management of uremia
Fatigue, lethargy, mental dullness,
norexia and nausea
More serious myoclonus, confusion,
delirium or coma, seizure and
pericarditis
Diet protein control
Check GI bleeding
Hemodialysis

Nutritional management in
acute renal failure
Minimal recommand protein
intake0.6-0.8g/kg/day
Carbohydrate and lipid should
maximal with a target of providing
30-65kcal /kg/day
Limit fluid volume potassium ,
magnesium, and phosphorus should
avoid.

Indication for renal replacement

therapy

Symptoms of uremia ( encephalopathy,)

Uremic pericarditis
Refractory volume over load
Refractory hyperkalemia
Refractory metabolic acidosis

Dialysis

Method of removing toxic substances from the

blood.
Blood is diverted from the access through a filter.
The blood flows counter-current to a special
solution called the dialysate. The electrolyte
imbalances and toxins in the blood are corrected
and the is returned to the body.
Peritoneal

Hemodialysis

Hemodialysis
Works by circulating the blood,
from an access in the body,
through a semi-permeable filter
in the dialysis machine that
helps remove toxins. The
cleansed blood is then returned
to the body.
Typically, most patients
undergo hemodialysis for three
sessions every week. Each
session lasts 3-4 hours
Patients on hemodialysis are
always heparinized to prevent
clotting of the AV access.
Indicated in chronic tx and
obese patients

Terima kasih

Tubular-Cell Injury and Repair in Ischemic Acute Renal Failure.

Thadhani, R. et al. N Engl J Med 1996;334:1448-1460

Urine Indices in ARF

Pre Renal

Intrinsic ATN

Post Renal

> 500

< 350

< 350

< 20

> 40

> 40

> 20:1

< 10:1

< 10:1

< 1%
<35%

>3%
>55%

>3%
>55%

Hyaline casts

Brown,
Granular
casts,

Bland

Uosm
Na (meq/L)
Bun/Cr (mg/dL)
FENa
FEUrea

Sediment

What is FENa
The fraction of filtered
sodium excreted in the
urine.
FeNa = (urine Na x plasma Cr)
(plasma Na x urine Cr)

Urine output?
The obstruction:
Complete

InComplete

Anuria

Manifestasi klinis
Fase Oliguria (1 hr 3 mgg)
Oliguri < 40 ml/hr
Anuria pd oklusi bilateral arteri renalis, obstruktif uropati,
cortical nekrosis
Non oliguri pd cedera ringan

Peningkatan BUN & Kreatinin

Hiperkalemia & hiperpospatemia pada kerusakan sel
berat spt: trauma, pembedahan, status katabolik
Edema dari retensi cairan, edema pulmonal, efusi
perikardium dan pleura
Gejala2 gagal jantung pd kelainan jantung
Mual, muntah & fatigue karena uremia &
ketidakseimbangan elektrolit
Asidosis metabolik
Dialisis

Fase Oliguri ARF

Volume urin
BJ urin
Osmolality urin
Sodium urin
BUN/Cr plasma
FE Na
FE Na:

Prerenal

ATN

< 400 ml
1,016 1,020
>500 mOsm
< 10 mEq/L
>15 : 1
<1%

< 400 ml
1,010 1,012
< 400 mOsm
>30 mEq/L
< 15 : 1
>1%

Urin Na/Plasma Na
Urin kreatinin/plasma kreatinin

x 100

Manifestasi klinis
Fase Diuresis (1 3 mgg)
Kehilangan sodium & potasium karena
kerusakan tubulus risti hipokalemia
Urin output 3 4 lit/hr
Monitor keseimbangan cairan & elektrolit
Penggantian cairan
Monitor kreatinin plasma

Fase Recovery (1 bln 1 thn)

GFR meningkat, BUN & kreatinin menetap dan
menurun

Manajemen ARF
Awal: koreksi keseimbangan cairan dan
elektrolit dan urea
Resusitasi cairan pada kekurangan cairan
Furosemide (lasix) pada kelebihan cairan.
Diberikan IV tiap 6 jam 20 100 mg atau kontiniu
Kalsium glukonat untuk kardioprotektif
Insulin IV (10 unit) & glukosa (25 gr), inhalasi
beta agonis atau sodium bikarbonat IV untuk
transport kalium ke intrasel
Diuretik atau sodium polystyrene sulfonate untuk
membantu ekskresi potasium
Sodium bikarbonat IV (bila bikarbonat serum < 15
mEq/L atau pH 7,2)
Diet 30 45 kcal/kgBB/hr, kombinasi karbohidrat
dan lemak. Protein < 0,6 gr/kgBB/hr (non dialisis),
1 1,5 gr (dialisis)

FeNa = (urine Na x plasma Cr)

(plasma Na x urine Cr)
FeNa <1%
1. PRERENAL
Urine Na < 20. Functioning tubules reabsorb lots of filtered Na
2. ATN (unusual)
Postischemic dz: most of UOP comes from few normal nephrons,
which handle Na appropriately
ATN + chronic prerenal dz (cirrhosis, CHF)
3. Glomerular or vascular injury
Despite glomerular or vascular injury, pt may still have wellpreserved tubular function and be able to concentrate Na

More FeNa
FeNa 1%-2%
1. Prerenal-sometimes
2. ATN-sometimes
3. AIN-higher FeNa due to tubular damage
FeNa >2%
1. ATN Damaged tubules can't reabsorb Na
Calculating FeNa after pt has gotten Lasix.
1. Fractional Excretion of Lithium (endogenous) (<7% in prerenal )
2. Fractional Excretion of Uric Acid (<7% in prerenal )