GANGGUAN FAAL

GINJAL

Renal Physiology, Electrolytes and

Renal Failure

FUNGSI GINJAL
Mempertahankan HOMEOSTASIS
1. Mempertahankan keseimbangan H2O
2. Mengatur jumlah dan konsentrasi sebagian besar
ion CES
3. Memelihara volume plasma
4. Keseimbangan asam-basa
5. Memelihara osmolaritas
6. Eliminasi sisa metabolisme tubuh
7. Sekresi senyawa asing
8. Membentuk hormon eritropoetin
9. Sekresi renin
10.Mengubah vit D menjadi bentuk aktif

What you need to know:

Renal anatomy
Control of vascular
tone
Tubular function
Handling Na+/water
Handling K, CI
Handling acid
Pathophysiology of
renal failure

Electrolyte disorders
Acid-Base disorders
Water disorders
Conduit/pouch effects
Obstruction effects
Stones/RTA
Diuretic effects
Surgical issues in renal
failure patient

NEFRON satuan fungsional

ginjal
1 juta nefron / ginjal
Nefron adl satuan terkecil yang mampu
membtk urin
Susunannya didlm ginjal: kortek dan medula
Tiap nefron : komponen vaskular + tubulus
komponen vaskular: Arteriol aff kapiler
glomerolus arteriol eff kapiler
peritubulus venula
Komponen tubulus: kapsula Bowman tub
proksimal lengkung Henle tub distal
tub pengumpul

3 Proses pembentukan urin

1. Filtrasi glomerolus
2. Reabsorbsi tubulus
3. Sekresi tubulus
180 liter (47 galon) filtrat glomerolus /hari
178.5 lt diserap kembali
1.5 lt dikeluarkan sebagai urin
Setiap yang difiltrasi atau disekresi tetapi
tidak direabsorbsi akan dieksresikan
dalam urin
(bedakan istilah eksresi dan sekresi)

Paediatric
Urology

Physiology

Liquids flow from high pressure low pressure

Heart the driving force for urine flow
Disruption of urine flow occurs if collecting
system pressure rises above 30 cmH2O
The collecting system runs from the renal
pelvis to the bladder and is a dynamic structure
designed to store and then to conduct urine to
the outside while maintaining a low and safe
pressure.

Renal Hemodynamic Definitions

Renal Blood Flow (RBF)
- blood to kidneys per minute (1200 ml/min)

Renal Plasma Flow (RPF)

- plasma flow to kidneys per minute (670 ml/min)

Glomerular Filtration Rate (GFR)

- volume of plasma filtered per minute by the
glomeruli (125 ml/min males, 100 ml/min
females)

Filtration Fraction (FF)

- GFR:RPF (about .18-.22)

GFR
balance of hydrostatic and oncotic
pressures
hydrostatic pressure controlled by relative
tonicity of pre- and post-glomerular
arterioles
hyper-renin state will maintain GFR by postglomerular arteriolar constriction
GFR may be approximated by creatinin
clearance, since Cr filtered, not reabsorbed
and minimally secreted

Control of Renal Artery

Tone
Vasoconstrictors
- Endothelin
- angiotensin II
- atrial natriuretic peptide

Vasodilators
- PGE-2
- acetylcholine

serotonin/bradykinin (NO mediated)

glucocorticoids

Tubular Function
maintain appropriate water, acid and
electrolyte balance using passive and
active mechanisms
reabsorb selectively up to 99% of the
glomerular filtrate
respond to endocrine signals to make
necessary changes

Tubular Organization

Proximal Tubule
reabsorbs 100% of glucose and amino
acids, 90% of bicarbonate and 80-90%
of inorganic
phosphate and water
solutes active, water passive
Na reabsorption through Na-H and Nasolute active transporters

HCO3 generated in cell and absorbed

with Na ammonium secretion

Loop of Henle
early water and urea permeability,
filtrate becomes hypertonic
later Na-CI permeability
final, Na-CI actively transported,
filtrate hypotonic
creates high interstitial osmolality
which permits urinary concentration

Thick Ascending Limb

the "diluting" segment
active transport of NH4 and Na
aldosterone and ADH augment Na
reabsorption
PGE2 reduces Na reabsorption

Collecting Duct
provides final touches to Na, HCO3 and
K
Na absorbed, K secreted (stimulated by
aldosterone)
H secreted based on blood pH
NH3 secreted into lumen and can trap H
to make NH4
If ADH present, permeable to water and
water is drawn by hypertonic medulla

Thiazide Diuretics
HCTZ, chlorthalidone, metolazone
inhibit Na and CI reabsorption in
distal convoluted tubule
reduce GFR and RBF
decrease urinary calcium
in DI, they have an anti-diuretic
effect

Loop Diuretics
furosemide, ethacrinic acid,
bumetanide
inhibit Na/K/CI cotransporter
increased diuresis and excretion of
Na, K, CI, Ca and Mg
reduce medullary solute content and
impair urinary concentrating and
diluting capacity

Disorders of Water/Sodium
Primary goals:
maintain blood pressure
excrete wastes
Mechanisms
thirst
ADH

- aldosterone

Tubular Handling of Water

Hyponatremia Evaluation

Acid-Base Disorders
normal arterial blood pH ranges from 7.37 to
7.43, maintained by lungs (PCO2) and
kidneys (HCO3)
sudden changes tempered by buffers in blood
first determine primary disorder, then check
compensation
if compensation not appropriate, suspect
mixed disorder
check anion gap in metabolic acidosis (Na
(Cl+HCO3)) looking for "extra" anions

Acute Renal Failure

sudden reduction in GFR with
retention of Cr/BUN and often oliguria
significant mortality, often iatrogenic
divided by pathophysiology into
prerenal, renal and post-renal
assess by history, fluid status, blood
and urine electrolytes, residual urine,
imaging and/or renal biopsy

Pre-Renal ARF
reduction in renal perfusion below 60
mm Hg will disrupt glomerulotubular
balance
most common cause of ARF
BUN/Cr ratio greater than 10:1
may have hyaline casts but seldom
others
treatment to correct cause of
hypoperfusion

Post-Renal ARF
infravesical obstruction or bilateral
ureteral obstruction
may require retrogrades to confirm
electrolyte imbalances usually
correct in 1-3 days but loss of
concentrating ability may last 2
weeks

Intrarenal ARF
typically follows ischemic or
nephrotoxic insult
multiple hits can be synergistic (eg IV
contrast in a dehydrated diabetic on
gentamycin)
related to vasomotor changes,
tubular obstruction and decrease in
ultrafiltration
UNa >40, UP osm <1.2, often have
casts

Chronic Renal Failure

chronic loss of renal excretory and regulatory
functions
most common causes in US are:
hypertension, diabetes, glomerulonephritis,
APCKD and chronic pyelonephritis
Seldom symptomatic until CrCI < 20 ml/min
May not need dialysis until CrCI < 5 ml/min
Typical symptoms/signs:
fatigue, nausea, hypertension, bleeding,
cardiomyopathy, pericarditis, pruritis,
osteodystrophy, parathesia, seizures

CRF Features
hyperkalemia
metabolic acidosis
anemia
hypocalcemia -> secondary hyper
PTH
hyperphosphatemia
osteomalacia (lack of vitamin D)

CRF Supportive Therapy

Treat hypertension
Restrict dietary protein and salt (if HTN or
edema)
Correct acidosis (Na bicarb)
Prevent bone disease (Ca supplements,
PO4 binders)
Treat anemia (erythropoietin)
Modify drug dosages if renally excreted

Surgical Issues in CRF

Bleeding
platelet defect: DDAVP, cryoprecipitate,
conjugated estrogens
Calculated fluid management
Control of hypertension
Prevent hyperkalemia (bleeding,
hemolysis)
Appropriate timing of dialysis
Drug dose modifications

Dialysis
usually instituted for uremic symptoms
fluid overload, hyperkalemia, acidosis,
hypoalbinemia, drug intoxication (EtOH)
hemodialysis most common in USA
peritoneal dialysis most common in Canada
and Europe
fewer hemodynamic effects and greater
freedom
but less efficient dialysis and limited by
peritonitis

Postobstructive Diuresis
requires bilateral obstruction or obstruction
of solitary unit
mechanisms
Na leak, urea osmotic diuretic, loss of
concentrating ability from urea washout in
medulla
mild form can be corrected by oral intake
severe requires partial IV replacement and
electrolyte monitoring