EDEMA

CONTENTS
EDEMA
- Pathophysiology
- How to approach
Acute poststreptococcal glomerulonephritis
Nephrotic syndrome
Renal failure

EDEMA
Defined as a palpable swelling produced
by expansion of the interstitial fluid volume
Localized or Generalized
Severe generalized edema is known as
anasarca

PATHOPHYSIOLOGY OF
EDEMA

GENERALIZED EDEMA
1) An alteration in capillary hemodynamics that
favors the movement of fluid from the vascular
space into the interstitium.
increased capillary hydrostatic pressure
decreased capillary oncotic pressure
increased capillary permeability

2) The retention of dietary or intravenously

administered sodium and water by the
kidneys.

STARLING FORCES

Capillary hydrostatic pressure

gradient
Arterial pressure (minor)
precapillary vasoconstriction

Venous pressure (major)

Causes of increased venous pressure
Intravascular volume expansion
Venous outflow obstruction

Interstitial pressure
Low compliance compartment

Capillary oncotic pressure gradient

Serum albumin concentration :
hypoproteinemia (malnutrition, cirrhosis,
nephrotic syndrome)
Interstitial oncotic pressure changes in
parallel with capillary oncotic pressure
(i.e., c i) is constant if changes c are
gradual
Acute decreases in c (e.g., rapid saline infusion)
lead to abrupt declines in and edema
formation

Capillary hydrostatic permeability

Burns
Reactive oxygen species, histamine

Cytokine/interleukin mediation

Immunotherapy (IL-2)
Sepsis (IL-2, TNF)
Diabetes mellitus
Kwarshiorkor (leukotrienes)
Ovarian hyperstimulation syndrome
Idiopathic capillary leak ( IL-2, kinins)

LOCALIZED EDEMA

LOCALIZED EDEMA
Disease of lymphatic system
- Filariasis
- Cellulitis
- Neoplasm
- Surgical excision
Disease of venous obstruction
- Thrombophlebitis
- Thrombosis
- Neoplasm
- Varicosity (Varicose veins)
- Arteriovenous fistula
- Lymph node mass

LOCALIZED EDEMA
Increased permeability of capillary wall
- infection
- burn
- trauma
Allergic reaction : angioedema

HOW TO APPROACH
EDEMA

EDEMA
Hx & PE

Localized edema
Non renal causes
1. Cardiac problems
2. Drugs, hormones
3. Hypoalbuminemia
4. Liver causes
5. Nutritional causes
6. Collagen vascular disease
7. Others : severe anemia,
Idiopathic edema, myxedema
To be continue !!!!

Generalized edema
Renal causes
1. Nephrotic syndrome
2. Acute glomerulonephritis
3. Chronic glomerulonephritis :
Hereditary nephritis, interstitial nephritis,
polycystic kidney, IgA nephropathy,
secondary glomerulonephritis
(Henoch Schoenlein purpura)
4. Acute and chronic renal failure

Non renal causes

1. Cardiac problems
Congestive heart failure
Pericardial effusion
Constrictive pericarditis
2. Drugs, hormones
Minoxidil, NSAIDs, estrogen, steroid, calcium channel blockers
3. Hypoalbuminemia
Malnitrition : Kwarshiorkor, protein losing enteropathy
4. liver causes
Biliary atresia
Cirrhosis
Hepatic failure (increased hydrostatic pressure due to portal
hypertension, decreased oncotic pressure)
5. nutritional causes
Vitamin C deficiency, beri beri
6. Collagen vascular disease : Scleroderma

RENAL CAUSES

RENAL CAUSES

Acute post streptococcal glomerulonephritis

Nephrotic syndrome
Acute renal failure
Chronic renal failure

Acute Poststreptococcal
Glomerulonephritis

Epidemiology

most common form of AGN

peak incidence 2- 15 yr
male : female 2: 1
sporadic > epidemic
attack rate in family member of affected
patient 20 - 40%
sporadic usually from pharyngitis

Epidemiology
epidemic usually from skin infection
different attack rate in difference family
due to genetic factor

Organism
Beta streptococcal gr.A
nephritogenic strain : M type
- pharyngitis 1,3,4,12,18,25,49
- skin infection 2,49,55,57,60
may be Streptococcal gr. C & G

Pathogenesis

1.
2.
3.
4.

remain incompletely understood

more 1 streptococcal Ag & mechanism
may involve
circulating immune complex
in situ immune complex : Ag-Ab in renal
molecular mimicry: Ag(renal)-Ab
direct complement activation : alternative
pathway (C3)

Clinical features
variable from asymptomatic to oliguric ARF
latent period
post pharyngitis 7-14 days
post skin infection 14-21 days
38% latent period < 7 days
9% latent period > 3 weeks)
If latent period < 7 days suggest exacerbation of
underlying

Clinical features
Edema
usually abrupt onset at periorbital area
Hematuria (100%)
> 80% microscopic ( may resolve in 1 yr )

~ 30 % gross ( resolved in 1-2 wks )

Oligulia (50%)
commonly transient , if anuria indicates
crescentic GN

Clinical features
Hypertension
> 75% pathogenesis unknow : multifactorial
partly by ECF expansion & cytokines
CHF 20%
Encephalopathy
uncommon 5-10%
more frequent in children, may be from severe HT,
CNS vasculitis
Others
N/V, anorexia, lethargy, back pain, abdominal pain

Lab findings
U/A
- proteinuria nephrotic range 10-20%
(frequent in adult)
- dysmorphic rbc, rbc cast, hyaline cast
- wbc in early phase may be predominate
(2-3 days )
- decrease Na & Ca excretion

glomerulus may produce the following

dysmorphic RBC's

Lab findings
CBC
- mild dilution of Hb concentration
- wbc & platelet usually normal
- occasionly thrombocytopenia
renal function
- rising BUN & Cr ( due to decreased GFR &
RBF )
- normal serum Na, may be mild hyponatremia

Lab findings
Serology
ASO titer in pharyngitis 80% has 4 folds
rising in skin infection may not rising 50%
Anti DNaseB rising in > 90%
complement decreased C3 but C4
normal

Typical poststreptococcal
glomerulonephritis
1. Typical presentation with no finding other
systemic disease
2. Evidence of prior streptococcal infection
- throat or skin lesion +ve
- Elevated Ab titer (acute & convalescent titer )
3. Complement abnormalities typical
- Decreased CH50 & C3 during acute phase
- levels rise toward normal by 6-8 wks
- C4 usually normal

Typical poststreptococcal
glomerulonephritis
4. Beginning recovery in 1 wk (
2 wk)
- diuresis
- BP normalized
- BUN, Cr begin to fall
5. Normalization of urine sediment
- resolution of gross hematuria by 2-3 wks
- resolution of proteinuria by 3-6 months
- resolution of microscopic hematuria by 1 yr

Treatment
admit if obvious edema, HT, rising BUN &
Cr
Bed rest as necessary
Fluid & salt restriction
Specific intervention for the following
- HT, volume overload, encephalopathy
- Hyperkalemia & acidosis

Treatment
Confirm likelihood of poststreptococcal
infection
Pen V oral * 10 days
Observe for onset of recovery within 7
days
Keep high index of suspicion for other
disease

Treatment of HT
associated with AGN
moderate
Diuretics
iv/oral
Vasodilator

Severe

Mild -

Furosemide
Furosemide iv
Hydralazine
Hydralazine

Indication for renal biopsy

1. Atypical presentation
2.
3. anuria, nephrotic range proteinuria
4. Complement
5. Creatinine raising
6.
- Oliguria, azotemia > 2 weeks
- Hypertension > 3 week
- Gross hematuria > 2 week
- C3 decrease > 3 mo
- Proteinuria > 6 mo

Other AGN in children

Less common
- MPGN (Membranoproliferative
glomerulonephritis)
- IgA nephropathy
- lupus nephritis
- Familial nephritis
- Infective endocarditis-related nephritis

Nephrotic syndrome

Nephrotic syndrome
Generalized edema
Heavy proteinuria
50 mg/kg/day or 40mg/m 2/hr
Hypoalbuminemia
albumin < 2.5 g/dl
Hyperlipidemia
cholesterol >250 mg/dl

Cause of nephrotic syndrome in

children
Primary glomerular disease
Minimal change nephrotic syndrome (MCNS)
m/c in Europe
Mesangial proliferative
glomerulonephritis(MesPGN) m/c in Thailand
Focal segmental glomerulosclerosis (FSGS)
Membranoproliferative glomerulonephritis
(MPGN) associated LE
Membranous glomerulonephropathy (MGN)

Cause of nephrotic syndrome in

children
Secondary nephrotic syndrome
- Associate with systemic disease : SLE, HSP
- Postinfectious :
syphilis, malaria, hepatitis B/C, CMV, HIV,
schistosomiasis
- malignancy : lymphoma
- Associate with drugs : NSAID, penicillamine,
gold, Heroin
- Associate with toxins or allergens : bee sting,
food allergy

Epidemiology

Incidence 2-7 new cases /100,000 children

80% age of onset < 6 yrs
peak age of onset occurs at 2-3 yrs (preschool)
male : female = 3:2
genetic predisposition : 3.4% positive family Hx
HLA B8, DR-3, DR-7

Clinical features
Edema
Distribution :
- periorbital areas
- dependent areas : lower legs
- genitalia
- pleural effusion and ascites
Often preceded by Hx of URI

Clinical features
GI : Abdominal pain (due to bowel ischemia,
peritonitis)
Diarrhea (due to bowel wall swelling)
Umbilical & inguinal hernia
HT : 20%, usually transient
May be present in hypovolemic children
(due to compensatory systemic
vasoconstriction)

Physical Examination

Height & Weight

Blood pressure
Pulse, capillary refill time
Pleural effusion, ascites, edema
Acute complication : Hypovolemia,
Infection, Thrombosis

Atypical features
1.
2.
3.
4.

Age <1yr or > 12 yrs

Persistent HT
Gross hematuria
Renal impairment (without
hypovolemia)
5. Decreased C3

Investigation
UA : proteinuria > 2+
oval fat body, hyaline cast
microscopic hematuria 20-25%
urine protein 24 hr
Serum albumin
Serum cholesteral
CBC : increased Hct
Complement : C3, C4 normal

Investigation
IgG, IgA decrease
BUN, Cr, electrolyte
electrolyte: hyponatremia, hyperkalemia (early
creatinine rising)

fat casts

Complications

Hypovolemia
Protein malnutrition & malabsorption
Infection
Acute renal failure
Thrombosis
Hypocalcemia

Infection
: Due to
- Decreased IgG, IgA
- Decreased factor B defective opsonization
: Peritonitis, cellulitis, asymptomatic UTI,
pulmonary & menigeal infection
: Organism Streptococcus, Pneumococcus,E.
coli
Hemophilus, Klebsiella spp.

ARF
Causes
- Hypovolemia ATN
- Intratubular obstruction from protein cast
- Renal vein thrombosis
- Acute interstitial nephritis (diuretics)

Thrombosis
1. Hypercoagulability from
- Loss antithrombin III, protein C & S in urine
- Hemoconcentration
- Increased coagulation factors : F I, VII, VIII, X
- Increased platelet aggregation
2. Deep vein thrombosis, renal vein thrombosis,
cerebral cortical vein thrombosis

Hypocalcemia
Decreased total calcium & ionized calcium
- Hypoalbuminemia
- Loss vitamin D binding protein in urine
- Decreased GI absorption

Definition
Remission : urine protein dipstick 0-trace for 3
consecutive days

Relapse

: urine protein > 2+ for 3 consecutive days, having

previously been in remission

Frequent relapser : > 2 in 6 months of initial remission

or > 4 within any 12 month period

Steroid-dependent : 2 consecutive relapses occuring during

after

tapering of steroid Rx or within 14 days

its cessation

Steroid-resistant : failure to achieve remission despite full

dose Rx for 8 wks

Approach to management in children with NS

1. Activity : encourage to mobilized as normal
2. Diet : no added salt
protein 1 g/kg/day (130-140% normal
requirement )
3. Fluid intake : restrict during edema
4. Immunization : no immunization during Rx with
steroid pneumococcal vaccine, varicellar
and influenza vaccine

Approach to management in children with NS

5. Edema
- salt restriction
- Diuretics
mild case : thiazide + K sparing diuretics
severe case : loop diuretics

Approach to management in children with NS

6. Intravenous 20% albumin
- in symptomatic case (respiratory distress
due to ascites & pleural effusion), genital swellin
g, cellulitis, hypovolemia
- iv 0.5-1 g/kg in 1-2 hr + furosemide 1-2 mg/
kg

Corticosteroid
First episode
Prednisolone
60 mg/m2/day(max 80 mg) x 4-6 wks then
40 mg/m2/alt day (max 80 mg) x 4-6 wks then
tapering in 3-5 months
Higher dose & longer duration decrease
relapse

Adverse effect of
corticosteroids

- susceptibility to infection
- mood and behavior disturbance
- increased appetite, wt gain, obesity
- cushinoid appearance
- acne
- hirsutism
- striae

Corticosteroid
Tuberculin test
Chest X ray
Stool concentration for parasite * 3 days

Frequent relapsing nephrotic syndrome

Rx : Prednisolone 60 mg/m2/day

(max 80 mg) until

urine protein negative x 3 days then
40 mg/m2/ alternate day
(max 80 mg) then tapering

Steroid dependent nephrotic syndrome

Rx : Prednisolone 60 mg/m2/day
(max 80 mg) until
urine protein negative x 3 days then
40 mg/m2/alt day
(max 80 mg) then tapering
and maintain at low dose for 3-12
months

Indication
for alternative immunomodulartory Rx
1. Relapse while taking prednisolone > 1 mg/kg
on alternate day
2. Relapse while taking prednisolone
> 0.5 mg/kg on alternate day, plus > 1 the
following :
- Unacceptable adverse effects of steroids
- High risk of adverse effects of steroids
approaching puberty, DM
- Unusually severe relapses
hypovolemia, thrombosis, sepsis, ARF

Indication
for alternative immunomodulartory Rx

Frequent relapse
Steroid dependent

Second line drugs : Alkylating agents

Cyclophosphamide
2 mg/kg/day x 12 wks
3 mg/kg/day x 8 wks
side effects : leukopenia, hemorrhagic cystitis,
gonadal toxicity, pulmonary
fibrosis CBC
Chlorambucil
0.2 mg/kg/day x 8-12 wks
side effects : convulsion, 2nd malignancy,
gonadal toxicity

Second line drugs : Alkylating agents

Cyclosporin
3-5 mg/kg/day
side effects : effectively maintains remission
but relapse after discontinuation
renal toxicity

Indication for kidney biopsy

Pretreatment
Onset < 6 months( 1 yr) or > 8 yr
Macroscopic hematuria
Microscopic hematuria +persistent HT
Low C3
Renal failure not attribute to hypovolemia

Posttreatment
Steroid resistance (Rx > 8 week)
Early or late non-responder, Frequent relapses

Outcomes
Mortality 2.5-7.2%
due to hypovolemia, thrombosis, sepsis
Relapse MCNS 25% single relapse
If remission > 6 months less likely relapse
MCNS < 5% ESRD
not response to steroid in 8 wks ESRD 21%
not response in 6 months ESRD 35%

ACUTE RENAL FAILURE

ACUTE RENAL FAILURE

Definition
sudden deterioration in renal function
inability to maintain fluid and electrolyte
homeostasis
accumulation of nitrogenous waste
products (urea nitrogen and creatinine)

ACUTE RENAL FAILURE

Oliguria : urine < 500 ml/1.73m2/day

< 1 ml/kg/hr in infants
or < 0.5 ml/kg/hr in children

Anuria : absence of urine production

~ 50% non oliguric

Heterogeneous Response
of Individual Nephrons
Variable Damage to
Tubular Epithelium
Anatomical Damage

Functional Damage

Primary & Secondary

Reduction in GFR

Decrease in Fractional
Reabsorption

Decreased tubular
Fluid Flow

Increased Tubular
Fluid Flow

No Contribution to
Urine Formation

Responsible for
Urine Formation

Oliguria

Polyuria

ARF
Prerenal
40-80%
Volume loss
sequestration

Postrenal
5-15%

Renal
10-30%

Intra-renal
-crystal

Vascular
-small vv
-large vv

Extra-renal
-pelvis/ureter
-bladder/
urethra
*post urethral
Valve**
*neurogenic
Bladder**

Glomerulus

Impaired CO
Hypotension

Interstitial
-inflammation
-space occupying
Tubular
- ischemic
- toxin
-pigment

BUN/Cr ratio
>20

Increased urea
formation
High protein
intake
Catabolic state
- fever

<20

Decreased urea
elimination

Decreased urea
formation

Volume depletion Starvation

Impaired CO
Obstructive
uropathy

Advanced liver
dis.
Defect of urea
cycle enzyme

Increased Cr
formation

False elevation
of Cr

Rhabdomyolysis

Cefoxitin

Decreased Cr
elimination

Ascorbic acid
Levodopa
Methyldopa

Cimetidine

Flucytocine

- corticosteroids

Trimethoprim

Barbiturates

- tetracyclines

pyrimethamine

- tissue necrosis

- sepsis

Pathophysiology
Clinical phase

Pathophysiologic correlates

Initial phase

Tubular epithelial cell injury

vasoconstriction

Maintenance phase

Tubular obstruction
Passive backflow of filtrate
Secondary vasoconstriction
Medullary congestion
Changes in glomerular capillary
ultrafiltration coefficient

azotemia

Early recovery phase Restoration of tubular epithelial cell

integrity
Phase of functional
recovery

Vasodilation
Nephron recruitment

3 phases in the course of ARF

Oliguric phase :
usually lasts a few days to 2 weeks
Diuretic phase :
Recovery phase :
vary from a few weeks to several months

History and physical examination in ARF

1. Hx of any prodomal illness
- dehydration
- acute pharyngitis / skin infection
- fever, other infection, rash, arthropathy
2. Presence or absence of urinary symptoms
- hematuria, dysuria, frequency, poor urinary stream
drugs, toxin exposure, antenatal
3. Urine output, fluid intake, fluid loss
4. Recent BW
5. Previous illness: cardiac, liver disease
6. Family Hx of renal disease

History and physical examination in ARF

Physical examination
- BW, Ht, Temp
- State of dehydration : dehydration, edema
- Respiratory status : tachypnea, fluid overload
- Abdomen : renal mass, palpable bladder, CVA
tenderness
- Neurologic exam : confusion, drowsiness, focal
neurological abnormality
- Exam for causes or sign of renal failure

Lab investigation
Blood
- Electrolyte, BUN, Cr
- Ca, PO4
- Albumin
- PTH

degree of renal impairment ,

electrolyte imbalance
degree of hypo Ca,
hyper PO4
hypoproteinemia due to
proteinuria
evidence of longstanding RF

- Immunologic : C3,C4
immunologic causes
CH50, ANA, Anti dsDNA
- CBC
hemolysis, bleeding, anemia

Lab investigation
Urine
- Protein / Cr ratio
- Microscopy
- Osmolality
- Na, Cr, urea
- myoglobin

cast suggest glomerular dz.

evidence of conc n defect
to assist distinguishing
renal from pre renal cause
rhabdomyolysis

Urine sediment in ARF

Condition Proteinuria Hematuria

Microscopy

Prerenal

Normal

Vascular
occlusion

Normal

Glomerulo
-nephritis

+++

+++

Dysmorphic rbc, granular casts

AIN

++

wbc (eosinophils) wbc cast

ATN

Muddy brown granular cast, tubular

epithelial cell casts

RBC

Hyaline cast

Dysmorphic RBC

RBC cast

Granular cast

Prerenal ARF

ATN

AIN

AGN

Obstruction
early
late
variable <1.015

Urine sp.gr
(newborn)
Uosm
U/P osm
U/P cr
UNa (mEq/L)
(newborn)

>1.020
(>1.015)
500
>2
>40
<10
(<20)

1.010
(<1.015)
<350
<1
<20
>40
(>60)

1.010

>1.020

<350
<1
<20
>40

500

>500

<350

<10

>15
<20

<15
>40

FENa (%)
(newborn)
RFI
(newborn)

1
( 2.5)
<1
(<3)

>2
(>2.5)
>1
(>3)

>2

<1

>1

>1

<1

10

>20

BUN/Cr ratio >20

FE urea
<35

10
>50

FENa (fractional excretion of sodium) = (UNa/PNa) / (UCr/PCr) x 100

RFI (renal failure index) = UNa/ (UCr/PCr)

Complications of ARF
- Metabolic : acidosis, hypo Ca, hyper PO4,
hyperkalemia,uremia, hyperuricemia ,hyper Mg
- CVS : arrythmias, hypervolemia/ hypovolemia,
CHF, uremic pericarditis, HT
- Respiratory : pulmonary edema
- Neurological : mental status changes, seizure
- Hematologic : anemia, coagulopathy
- Infectious : catheter-related infection, septicemia

Treatment
Provide supportive Rx
- Stabilize
- Monitor closely : I/O, BW, electrolyte
- Prevent sepsis : limit IV line, remove urinary
catheter
- Adjust drug according to renal function

Treatment
Prerenal failure
Administer fluid challenge
- Use isotonic solution or 5%D/N/2
- 5% albumin 10-20 cc/kg
- observe urine output 1-3 cc/kg/hr

Treatment
Postrenal failure
Removal of obstruction
Rx postobstructive uropathy
Rx voiding dysfunction and UTI
Stabilization of electrolyte abnormalities

Treatment
Intrinsic renal failure
- Restrict fluids insensible loss + urine
output
- Insensible loss
300 - 400 ml/m2 as 5-10%D/W

- Urine output
ml for ml as 0.45% NaCl

- Rx hyponatremia
maintain serum Na 130-135 mEq/L
restrict free water

Treatment
Furosemide
Increase urine flow rate
Decrease intratubular obstruction
use in 1st 24-48 hrs
Dose :
IV 1- 5 mg/kg/dose
continuous drip max 0.5 -1 mg/kg/hr
No evidence of change in renal recovery, need
for dialysis, decreased mortality

Treatment
Dopamine
- Synergistic effect with furosemide
Dose 0.5-4 g/kg/min (vasodilation effect)
- Side effect : tachycardia, arrhythmia, myocardial
ischemia, intestinal ischemia (due to precapillary
vasoconstriction)
- Evidence controversy

Treatment
- Rx metabolic acidosis
- Replace base deficit if pH < 7.2 or HCO3
< 12 mEq/L up to 16 mEq/L
base deficit = 0.6 x BW x (HCO3 desired - HCO3 observed)
2
- over 2-3 hrs, rest over next 24 hrs

- Rx hyper PO4
- Calcium carbonate

Treatment hyperkalemia
Agent

Mechanism

Dose

Onset of
effect

Complications

NaHCO3

Shifts K into cells

1 mEq/kg IV
over 10-30 min

15-30 min

Hyper Na
Change in Ca

10% Ca
gluconate

Stabilizes membrane
potential (heart)

0.5-1.0 mL/kg IV
over 5-15 min
(max 10 ml)

Immediate

Bradycardia
Arrhythmias
Hypercalcemia

Glucose and
insulin

Stimulates cellular
uptake of K

Glucose 0.5 g/kg

Insulin 0.1 U/kg IV
over 30 min

30-120 min

Hypoglycemia

-Agonists
(albuterol)

Stimulates cellular
uptake of K

5-10 mg nebulizer

30 min

Tachycardia
Hypertension

Na
polystyrene
sulfonate
(kayexalate)
Kalimate
(calcium)

Exchanges Na for K
across colonic mucosa

1 g/kg PO or PR
q 2-6 hr

Enema:60
min
Oral :2 hr

Hypernatremia
Constipation

Hyperkalemia

Treatment HT
Sodium nitroprusside 0.5 to 10 mcg/kg/min IV drip
Labetatol

0.25 to 1 mg/kg IV bolus or

0.5 to 3 mg/kg/hr drip

Diazoxide

1 to 5 mg/kg IV push
(max 150 mg/dose)

Enalapril

5 to 10 mcg/kg/day

Nicardipine

1 to 3 mcg/kg/min

Nifedipine

0.25 to 1 mg/kg/dose PO, SLQ (max

10 mg/dose)

Hydralazine

1 mg/kg IV as first dose then 0.1 to

0.3 mg/kg (max 3.5 mg/kg/day)

Treatment
Supplemental nutrition
- Goal : to provide sufficient nutrients and adequate
caloric intake
- Decreased 0.5-1% BW per day over the initial few days
- Enteral route
oral/NG feed

Parenteral
- Calories : 45-50 kcal/kg/day
CHO 70%, Fat 20%
protein 1-2 g/kg/day
low phosphate, potassium

Renal replacement therapy

Indication
1. CHF and fluid overload
2. Uremic symptoms: N/V, coma, seizure,
uremic pericarditis
3. Metabolic derangement refractory to Rx
(severe metabolic acidosis, severe hyper K,
hypo/hyper Na, hyperuricemia, hyper PO4)
4. BUN >150 mg/dl or Cr > 10 mg/dl
5. Toxin : methanol, salicylate, oxalate
options : HD, PD, CRRT

Summary of Therapy and Goals in the

Initial Phase of Acute Renal Failure
Therapy

Goal

Volume expansion/hydration

Increase in renal blood flow

Prevention of tubular epithelial
cell injury

Diuretics
Osmotic diuretics
Loop diuretics

Restoration of urine flow

Vasoactive agents
Dopamine
Atrial natriuretic peptide

Restoration of renal perfusion

Cytoprotective agents
Preservation of cell integrity
Free radical scavengers
Xanthine oxidase inhibitors
Calcium channel blocking agents
Prostaglandins

Chronic renal failure

Causes

Obstructive uropathy
Chronic glomerulonephritis
Hypoplastic / dysplastic kidneys

20.6
8.4
5

SLE nephritis
Familial nephritis
Polycystic kidney disease

1.8
1.7
0.8

Sumboonnanonda A. J Med Assoc Thai 2000;83: 894-901


( failure to thrive )

glomerular disease :


tubulo-interstitial disease :

pulmonary edema
hypertensive encephalopathy

 GFR
Phosphorus
clearance

Hyperphosphatemia,
hypocalcemia,
hyperparathyroidism
Active vitamin D deficiency
Chronic metabolic acidosis

Anemia, renal osteodystrophy

Small birth weight infants

Renal dysplasia or hypoplasia
Urologic disorders esp. obstructive uropathies
DM
SLE
Prior history of HT eg. From renal artery or renal
vein thrombosis in neonatal period
FH of polycystic kidney disease, other genetic
kidney dis
Prior history of ARF, acute nephritis, nephrotic
syndrome, hemolytic uremic,HenochSchnlein
Purpura

NKF-K/DOQI classification of the stages of CKD

Stage

GFR

description

( ml/min/1.73m2)

> 90

Kidney damage with

normal or increased GFR

60-89

Kidney damage with mild

reduction of GFR

30-59

Moderate reduction of
GFR

15-29

Severe reduction of GFR

< 15 or dialysis

Kidney failure

 GFR schwartz
Ccr = k x L / Scr
(ml /minute /1.73 m2)
K proportionality
constant

L = length ( cm)
Scr = serum creatinine
level ( mg/dl)
Ccr = creatinine
clearance

Age group

K
( mean values)

Low birth weight

< 1 yr

0.33

Term infant
< 1 yr

0.45

2-12 yr

0.55

Female
13-21 yr

0.55

male
13-21 yr

0.7

 Chronic
Kidney Dz.

Stage

GFR

Action plan

( ml/min/1.73m2)

> 90

60-89

Esstimate rate of
progression of CKD

30-59

Evaluate and treat

complications

15-29

Prepare for kidney

replacement therapy

< 15
or dialysis

Kidney replacement
therapy

Treat primary and comorbid

conditions

Investigation
Cardiovascular
system

BP, chest x-ray , ECG,

echocardiogram

Fluid and
electrolytes

Serum electrolytes

Growth and
development

Wt, height, secondary sex

characteristics

Hematological
system

CBC, reticulocyte count, bleeding

time, iron study

Investigation
Musculoskeletal
system

Calcium, phophorus,
alkaline phosphatase, long
bone x-ray, bone age, iPTH

Respiration system

CXR

Urinary system

U/S, VCUG, renal biopsy

Others ( as needed)

Uric acid, lipid profiles


Calories
Sodium
and
water

RDA
CHO : protein : fat = 50:10:40

end
stage renal disease
glomerular disease


potassium
Acidosis

Potassium exchange resin

chronic hyperkalemia
Alkaline therapy

symptomatic hypocalcemia

Aluminium
toxicity

aluminium


anemia

GI bleeding, malnutrition, uremia

Delayed sexual
development

erythropoietin

folic
Anabolicor
sex
steroid

Renal bone
disease

Growth
retardation

Adequate nutrition,
treatment of renal bone disease, dialysis, growth
hormone,
renal transplantation

phosphate binder active vitamin D

ARF & CRF

TEST
The following features are observed in the
nephrotic syndrome
A. hypoalbuminuria
B. Hyperlipidemia
C. Hypocalcemia
D. Increased intravascular volume
E. Minimal changes disease

 B
C
E

TEST
The following are associated with a good
prognosis for renal failure
A. Nephrotic syndrome caused by
glomerulosclerosis
B. NS with minimal change disease
C. Rapidly progressive GN
D. SLE related
E. Poststreptococcal GN

 B
E

TEST
The following are complications of CRF
A. osteomalacia
B. HT
C. Hypokalemia
D. Uremia
E. anemia

A
B
D
E