FARMAKOTERAPI OBAT

PADA PENYAKIT
BATU SALURAN KEMIH
 Obat
Metode lain:
aa _
+
Tx BG/SK
Litotripsi
Pembedahan
OT Di Ind. dikenal
sbg obat u/ BSK
Tempuyung Heyne, 1987
 Why is it important?
Prevalence
2% to 3%
Likelihood that a white man will develop stone
disease by age 70
1 in 8.
Recurrence rate without treatment for calcium
oxalate renal stones
10% at 1 year, 35% at 5 years, and 50% at 10
years
(Uribarri et al, 1989).
(Laerum & Murtagh, 2001)
 Epidemiology
Rare in Native Americans, blacks of African
or American decent, and native born Isrealis
Bladder stones more common in
malnourished, kidney disease more
common in affluent
 Epidemiology
Genetic
Evidence not clear
Does appear in certain genetic disorders
Familial renal tubular acidosis
Cystenuria
Hereditary xanthinuria
dehydroxyadeninuria
 Epidemiology
Age and sex
Peak occurrence in 20s to 40s
Males > females
Women are more likely to have infectious or
hereditary cause
 Ind. termasuk daerah sabuk batu (stone
belt) BSK (Subadi,1999)
Retensi urin; 28,58 % karena BKM & Ure-
tra (Barus, 1999)

Wiranto, 1999 meneliti BSK di RSUP Dr.

Sarjito dari Jan 93-Des 97 menemukan
317kasus
 Batu saluran kemih dapat diderita siapa saja
dari bayi sampai usia lanjut.
Gilsanz, dkk 1985 10 bayi prematur dg
Nefrolithiasis. Penderita BSK di RSUP
Dr.Sardjito termuda laki-laki usia 2,5 th. &
tertua 86 th. Pasien 79,6 %; 20,4 %
dan terbanyak ditemukan umur dekade
kelima yaitu 30 % (Wiranto, 1999).
Patogenesis terjadinya BSK
* Teori presipitasi kristalisasi
* Teori pembentukan inti matrik
* Teori ketiadaan inhibitor
* Teori penghambatan sistem limfa
Teori yg konsisten pd bbrp pmbntk batu:
pengeluaran bhn/unsur pokok pmbtk
batu & pH. ( Teori presipitasi kristalisasi)
 Stones apparently form in an organized manner
influenced by:
-Composition of the environment
-urinary solutes
-urinary particles, i.e. bacteria, sloughed
urothelium
-uromucoids large arrays or protein formed in
the urinary tract
-glycoaminoglycans group of substances which
coat the urinary tract
-Nature of the bed of origin
-urothelium (transitional cell epithelium)
-Field characteristics
-magnetic
-gravitational possibly influence
of gravity on certain particles
-Nature of Nidal forces it is assumed
that every stone starts as a central core
 Physical Chemistry
Supersaturation
Central event in stone formation
Dependant on concentration, temperature, pH,
other chemicals
Urine
Contains inhibitors which allow supersaturation
metastable concentration
 Stone formation once the
process stone formation has
begun, we are no longer dealing
with a biological driven system,
it is all a chemical process from
that point on.
 Symptoms/signs

Moderate to severe colicky flank pain, may radiate

towards the testis, vulva or loin
Radiation indicates that the stone has migrated
toward lower third of ureter
Some may even present with ureteral obstruction,
unexplained persistent UTIs, or painless hematuria
 Full workup

Pt. have h/o diarrhea, UTIs, or gout?

FHx of stones?
Urine pH, culture if UA shows signs of infection
Serum calcium, phosphorous, parathyroid hormone,
sodium, oxalate, citrate, uric acid, creatinine
24 hour urine collection for: calcium, sodium,
oxalate, citrate, urate, creatinine
Further imaging
Treatment
Percutaneous
Ultrasound
Laser
Electrohydrolic
ESWL
the most frequent treatment modality for
stones in the upper ureter and the kidneys
Endourolology
Laser
ultrasound
Extraction
Open lithotomy
 Treatment

Normal calcium intake (lowers stone events by 50%)

Low sodium diet
High fluid intake (UO should be >2L/day)
Hypercalcuria worsened by: high sodium diet, loop
diuretics, high intake of animal protein
For recurrent stones: thiazide diuretic and/or
amiloride
 What is amiloride?

Mild potassium-sparing diuretic

Unique class, acts on distal convoluted tubule
and collecting duct
Action is independent of aldosterone
Cannot use in patients with renal insufficiency
Can cause hyperkalemia

go
 Hyperoxaluria

Results from fat malabsorption (IBD, chronic

pancreatitis, jejunoileal bypass) excessive
dietary consumption (leafy greens), or
recessive metabolic syndrome
Treatment: cholestyramine, low-fat, low
oxalate diet, calcium supplements given with
meals
go
 Hypocitrauria
Citric acid helps to prevent calcium stones by
complexing wth free urinary calcium
May be alone or found in combination with other
disorders (RTA, chronic diarrheal illness
Treatment: alkali, usually complexed with
potassium instead of sodium
Alkali increase urinary excretion of citrate

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 Hyperuricosuria
Can cause calcium oxalate stones
High urinary uric acid causes supersaturation
of calcium oxalate
Mainly from excessive dietary purine
consumption
Treatment: low dietary purine, allopurinol
 Uric acid stones
Urate stones are radiolucent
Hyperuricosuria AND low urinary pH (usually less
than 5.5)
Assoc. conditions: myeloprolferative disorders (with
or without chemo), Lesch-Nyhan
Treatment: alkalinization of urine with bicarb or
citrate, hydration, allopurinol
 Struvite stones
From urease-producing organisms, most often
Proteus mirabilis
Infection can occur from chronic obstruction,
instrumentation, or chronic antibiotic therapy
Treatment: antibiotics, removal of staghorn
calculus, which is frequently infected
 Cystine Stones
Genetic defect in amino acid transport in the GI
brush border and renal tubules
Suspect when stones are formed at a young age
Stones are radioopaque
Treatment: hydration (UO>3L/day), alkalinization,
and D-penicillamine or alpha-mercaptoproprionyl
glycine
Penanganan batu saluran kemih
Konservatif : Hidrasi, Diet.
Obat (Simptomatik: Analgesik, spasmolitik),
(kausatif).
Tindakan (Invasif, noninvasif)
Obat tradisional dari berbagai jenis tana-
man: daun (keji beling, gempur batu,
tempuyung, urat,wungu, kaki kuda); akar
(pohon enau, bt. Pepaya); rimpang
(temulawak). Farmakologinya ???
other
Tanaman Tempuyung (Sonchus arvensis L.
other
 Allopurinol - Zyloric
Cholestyramin - Questran
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other