Professional Documents
Culture Documents
FOR KIDNEY
Budi Raharjo
Function of Kidney
Excretion of waste product
e.g.Hydogen ion, Water
Regulation of homeostasis
e.g. Fluid, Electrolyte and Acid-base
balance
Serum Creatinine
(Male 0,6-1,2 mg/dL; Female 0,2-0,4
mg/dL)
Creatinine Clearance
Measurement of creatinine
clearance give an estimate of GFR
(Glomerular Filtration Rate)
Creatinine clearance varies with
age, sex, and size
Measurement:
Urine collection
Cockroft and Gault Equation
Creatinine Clearance
Normal reference = 120 ml/min
Renal disorder if: 60 < CrCl < 120
ml/min symptomless
Renal insuficiency:
Mild
Moderate
Severe
ESRD
(End State
20 50 ml/min
10 20 ml/min
< 10 ml/min
< 5 ml/min
of Renal Disease)
Urine Collection
Accurate collection of over 24 hour
periode (note problems with patient
compliance)
Plasma sample midway through 24 hour
periode
U x V
Clcr = ------------S
U = Urine Creatinine concentration (mg/dL)
V = Urine flow rate (ml/min)
S = Serum Creatinine concentration
(mg/dL)
Females
TB > 152,4 cm IBW = 45,5 + [(TB - 152,4) x 0,89]
TB < 152,4 cm IBW = 45,5 - [(152,4 - TB) x 0,89]
Limitation of
Cockroft & Gault Equation
Cannot be used if
Age < 15 years old or age > 90 years old
Renal function is changing rapidly
Pregnancy (GFR + 20 %)
Serum creatinine > 3 x normal range
Amputated limb
Miscellaneous
Increased potassium
Decreased bicarbonate
Increased phosphate
Decreased calcium
Altered sodium levels
Disturbed fluid balance
Pharmacokinetics
Absorption
Oral absortion reduce by vomitting, nausea,
diarrhoea, GI oedema & changes in blood pH
Little clinical significance
Distribution
Volume distribution (Vd) due to
oedema/ascites; Vd due to dehydration
(Little clinical significant: Aminoglycoside,
Lithium)
Protein binding (Pb) due to protein loss or Pb
due to uraemia; increase free drugs;
temporary effect; caution in interprete drug
level (Clinical Significant: Phenytoin, Warfarin)
Pharmacokinetics
Metabolism
Hepatic metab. unaffected in renal impairment
Clinical significant of impaired renal
metabolism:
Accumulation of active metabolite
Vitamin D replacement
Insulin requirement
Excretion
Elimination of drug or its metabolites may be
decreased
Most important parameter to consider when
making dosage decissions
General Guidelines
Only use drugs if a definite indication
Choose drugs with minimal nephrotoxic
effect and avoid potentially nephrotoxic
drugs
Increased sensitivity to certain drug
effects
Monitor and act on plasma levels
Check appropriate dosage adjustment
Avoid prolonged courses of potentially
toxic drugs
Monitor for clinical efficacy and evidence
of toxicity
Dosage Adjustment
Loading dose is usually unchanged (except
for digoxin and gentamycin)
The most common maintenance dosage
changes are to decrease the dosage or
increase the dosage interval or both
Refference sources:
BNF
Data Sheet / Drugs leaflet
Bennett: Drugs and renal desease
Dosage Adjustment
DRrf = DRn x [(1 - Feu) + (Feu x RF)]
Patient creatinine clearance (ml/mnt)
RF =
Ideal creatinine clearance (120ml/mnt)
DRrf = Dosing Rate in renal failure
DRn = Dosing Rate in normal state
RF = the extent of Renal Failure
Feu = Fraction of drugs normally excreting unchage
in the urine
RENAL DISEASE
Acute Renal Failure
Chronic Renal
Failure
Acute Renal
Failure
Pre-Renal ARF
Hipovolemia
sweating,vomiting,
diarhoe,blood loss
Cardiac Output
AMI, CHF
Renal hypoperfusiondrug induce
ARF:Diuretic,ACEI
NSAID (PgE2D2I2)
Intra-Renal ARF
Post-Renal ARF
Examination of ARF
1. Full history, including medication history
2. Physically Examination:
Postural hypotension & skin turgor Pre-Renal
Drug rashes / vasculitic lession Intra-Renal
Sizes of bladder & kidneys Post Renal
4. Examination of Blood
5. Radiological Study
Vasokonstriktor Afferent:
Inhibitor Prostaglandin
- NSAID
- COX-2 inhibitor
Vasokonstriktor langsung
- Cyclosporine
- Amphotericine-B
- Kontras Media (ionik)
- Vasopresor
Tekanan
Hidrostatik
Glomerolus
Ultrafiltrat
Tubulus Proximal
Arteri Efferent
Aliran Darah
Vasodilator Efferent:
Renin-Angiotensin Aldosteron
- ACE Inhibitor
- Angiotensin II Antagonis
Vasokonstriktor langsung
- CCB dihydropiridin
- Diltiazem
- Verapamil
Treatment of ARF
1.Early Management:
Correction of fluid & Electrolide imbalance
If not respons Loop diuretic & Manitol; or Dopamine
2.Establish ARF:
a.Uraemia protein intake + Fat & CH Catabolism
b.Hyperkalaemia (K excresion + Cell damage) Cardiotoxic Ca gluconate i.v.; Soluble insulin + glucose; Ca resin
ion exchange
c.Acidosis H+ excresion Na bicarbonate
d.Hypocalcaemia (Ca malabsorption) Ca Supplement
e.Hyperphosphataemia (retention) Ca carbonat
Chronic Renal
Failure
Causes of CRF:
Chronic Glomerulonephritis (nephrotic
syndro-me): Pitting Oedema; Proteinuria 3-5
gram/day; Hypoalbuminaemia 25-30 gr/L
Hypertension
Chronic Pyelonephritis
Urinary Obstruction: BPH, Renal calculi,
Veico-ureteric reflux, indwelling urinary
cathethers
Interstitial Nephritis
Congenital Abnormalities
Metabolic Disease: DM, Amyloidosis can
lead to chronic glomerulonephritis
Examination of CRF
1. Full history, including medication history
2. Physically Examination: Nocturia, Fatigue,
Breathless, Anemia, Skin coloration with
Hypertension, Oedema
3. Examination of The Urine: Proteinuria
4. Examination of Blood: Creatinine Serum
and/or Clearence, Electrolyte disturbance
(Hyperkalaemia,Serum bicarbonateAcidosis,Hypercalcaemia,Hyperphospataemia
)
5. Radiological Study: Intravenous Urography
(IVU) with Contrast Media
Hypertension
Sodium and
fluid
Retention
Renal Parenchymal
damage
Reduce ability
to excrete Na
ions
Activation
of RAA
System
Cycle of events leading to hypertension
in
Renal
Ischaemic
CRF
R.A.A. System
Perdarahan
Masif
TD
Iskhaemia
Ginjal
Angiotensinogen
RENIN
Juxtaglomerolus App.
Stimulasi
Angiotensin I
Prostaglandin
TD
Angiotensin III
Vol.Cairan
Retensi Air
Aldosteron
Retensi Na
Renal Failure
1,25 dihydroxycholecalciferol
Ca
absorption
from GI
tract.
OSTEOMALACIA
Phosphate excretion
Serum phosphate
Serum calcium
Hyperparathyroidism
OSTEOSCLEROSIS
Treatment of CRF
Terima
Kasih