ANALISIS DRP

TRESA
• Nama : Tn. A / UST
• RM / Reg : 00-90-78-95 / 1212300009
• Umur : 43 th
• Tgl masuk : 30/12/2012
• Tgl keluar : 7/1/2013
• Dokter : J, Sp. S
• Keluhan : hemiparese sinistra, pelo
• Riw. Penyakit: HT uncontrolled
• Diagnosa : CVD Ischemic
 Hasil pemeriksaan Laboratorium
Pemeriksaan Hasil pemeriksaan Nilai normal
Neutrofil 76 50-70 %
Limfosit 16 20-40 %
Ureum serum 57,9 10-50 mg/dL
BUN 27 10-20 mg/dL
eGFR 14,122 Kidney failure (<15)
ml/min/1,73 m2
Rasio BUN : kreatinin 6 (10-20):1
Asam urat 10,1 3,4-7 mg/dL
Total kolesterol 290,2 150-200 mg/dL
HDL 40 ≥45 mg/dL
LDL 210 <130 mg/dL
Trigliseride 206,8 <200 mg/dL
Pemeriksaan Hasil
penunjang

NCCT -Lacunar infark di paraventrikel dextra

- ventriculomegaly

Thorax normal
USG Ginjal PNC (Pyelonephritis Chronic) bilateral,
ukuran ginjal ka=8,3 cm, tebal
cortex=1,3 cm
Ukuran ginjal kiri=9,4 cm, tebal cortex=
1,8 cm
 Daftar Pemberian Obat (DPO)
Nama obat Signa 30/ 31/ 1 2 3 4 5 6 7
12 12 / / / / / / /
1 1 1 1 1 1 1
Plavix 75 mg 1x1 √ √ √ √ √ √ √ √ √
Neurosanbe 5000 1x1 √ √ √ √ √ √ √ √ √
Tylonic 300 mg 1x1 √ √ √ √ √ √ √ √
Atofar 20 mg 1x1 √ √ √ √ √ √ √ √
Canderin 16 mg 1x1 √ √ √ √ √ √ √
Ketosteril 3x2 √ √ √ √
PARENTERAL
Farmabes 2 ampul dlm NaCl 0,9% 100 10-12 √ √ Habis stop, ganti canderin
cc (microdrip) tts/mnt 1x16 mg
Neulin 500 mg 2x1 √ √ √ √ √ √ √ √ √

Tanggal 3/1/13 konsul dr. Ian

Kesan : CKD stage V
Saran : ketosteril 3x2, diet protein 40 g
 PEMBAHASAN
• Indikasi pemakaian Atofarkolesterol
‘Clinical Guideline for stroke management 2010’
1. statin memiliki good safety profile dan tidak
menyebabkan toksisitas hepar.
2. Terapi statin menurunkan kejadian stroke
ischemic, serious vascular event (non fatal
stroke, non fatal MI, vascular death).
‘Guidelines for the Management of Absolute Cardiovascular Disease Risk (2012)’
 Indikasi pemakaian Plavix antiplatelet

‘Clinical Guideline for stroke management 2010’

Indikasi pemakaian Canderin anti-
hipertensi

Dipiro, 2008
KDOQI Clinical Practice Guidelines on
Hypertension and Antihypertensive
Agents in Chronic Kidney Disease 2004
 Additional Antiproteinuric Effect of Ultrahigh Dose
Candesartan: A Double-Blind, Randomized, Prospective Study
Roland E. Schmieder, Arnfried U. Klingbeil, Erwin H. Fleischmann,
Roland Veelken, and Christian Delles
Department of Medicine IV, University of Erlangen-Nu¨ rnberg,
Erlangen, Germany
J Am Soc Nephrol 16: 3038–3045, 2005. doi:
10.1681/ASN.2005020138

The ultrahigh dose of the ARB candesartan (64

mg/d) produced greater antiproteinuric effect
than doses of 16 or 32 mg/d.
 Supramaximal dose of candesartan in
proteinuric renal disease.
Burgess E, Muirhead N, Rene de Cotret P, Chiu A, Pichette V, Tobe
S
J Am Soc Nephrol. 2009 Apr;20(4):893-900. doi:
10.1681/ASN.2008040416.

• there was no significant change in protein

excretion when the standard dose of 16
mgs/day was compared with 64 mgs/day, but
the administration of 128 mgs/day brought
about a 33% decrease in protein excretion,
95% CI (−45% to −17%), P < 0.001, in patients
with >1 g of protein/day.
 Long-Term, High-Dosage Candesartan Suppresses
Inflammation and Injury in Chronic Kidney Disease:
Nonhemodynamic Renal Protection
Chen Yu,*† Rujun Gong,* Abdlla Rifai,‡ Evelyn M. Tolbert,* and Lance D.
Dworkin*
*Division of Renal Disease, Department of Medicine, and ‡Department of
Pathology, Rhode Island Hospital, Brown
J Am Soc Nephrol 18: 750–759, 2007. doi: 10.1681/ASN.2006070770
• Conclusion
The AT1R blocker candesartan attenuates proteinuria, ameliorates renal fibrosis,
and suppresses renal inflammation in a dosage-dependent manner in the SHR
model of chronic renal.
Standard dosages of candesartan failed to block completely the Ang II receptor, but
complete inhibition was obtained at very high dosages. The renoprotective actions
of high-dosage therapy seem to be independent of the drug’s hemodynamic effects.
Instead, high-dosage candesartan suppressed activation of NF-B, tubular
expression of MCP-1 and RANTES, and renal inflammation and injury. Our findings
suggest that long-term, high-dosage candesartan is safe and may be superior to
regular-dosage therapy in preventing progression of chronic renal disease.
Chen S, Ge Y, Si J et al. Candesartan suppresses chronic
renal inflammation by a novel antioxidant action
independent of AT1R blockade. Kidney Int 2008; 74:
1128–1138.
• Reactive oxygen species are thought to be critical
inducers of renal inflammation and destruction.
• candesartan, a highly selective angiotensin II type I
receptor (AT1R) blocker suppressed TNF-induced
chemokine expression and NFjB activation independent
of AT1R blockade in cultured renal tubular epithelial
cells.
• decreased reactive oxygen generation elicited by either
TNF or the pro-oxidant hydrogen peroxide and
reinstated redox homeostasis, suggesting a direct
antioxidant effect.
 ‘Guidelines for the Management of Absolute
Cardiovascular Disease Risk (2012)’

Terapi ARB telah terbukti menurunkan perkembangan

makroalbuminuria
 Indikasi pemakaian neurosanbe 5000
Reduction in stroke recurrence (reduced
the level of homocysteine)
• Hyperhomocysteinemia is common in patient
stage 5 CKD which associated with increased
risk of cardiovascular event
Indikasi pemakaian Tylonic asam urat

• .
 2012 American College of Rheumatology
Guidelines for Management of Gout. Part 1:
Systematic Nonpharmacologic and Pharmacologic
Therapeutic Approaches to Hyperuricemia

• Xanthine oxidase inhibitor (XOI) therapy with

either allopurinol or febuxostat is
recommended as the first-line pharmacologic
urate-lowering therapy (ULT) approach in gout
 Guideline on Urigical Infection

European Association of Urology 2011

 INVESTIGATION
• Urinalysis: the urine is often cloudy with an offensive smell. It may be positive on dipstick
urinalysis for blood, protein, leukocyte esterase and nitrite. A midstream specimen of urine
(MSU) should be sent off for microscopy and culture, although there is often poor
correlation between symptoms and bacteriuria. A catheter specimen will be acceptable if a
catheter is in situ and special arrangements may be needed for collecting a sample from a
child (eg peroneal bag, suprapubic aspiration). Microscopy of urine shows pyuria.
• Inflammatory markers: CRP, ESR, and plasma viscosity are raised.
• Recent studies identified procalcitonin as a biological marker in diagnosing acute
pyelonephritis in children of 2 years of age or under. [6]
• FBC: this shows elevated white cell count with neutrophilia.
• Blood cultures: these are positive in approximately 12-20% of patients with pyelonephritis.
• Imaging:
– Imaging is useful if the clinical picture or biochemical markers are ambivalent, as
structural problems are not uncommon. It is mandatory in patients with recurrent
pyelonephritis and may help to identify obstruction or stones. [7]
– Contrast-enhanced helical/spiral CT (CECT) scan is the best investigation in adults where
diagnosis is in doubt or deterioration occurs. Non-contrast helical/spiral CT scans will
pick up moderate to severe disease but may be normal in milder cases.
Chronic Pyelonephritis/ reflux nephropathy/
vesico-ureteric reflux
• characterized by scarring and shrunken volume (atrophy)
of the kidneys , renal inflammation and fibrosis induced
by recurrent or persistent renal infection, vesicoureteral
reflux, or other causes of urinary tract obstruction.
• Unlike acute pyelonephritis in which there is bacterial
infection of the kidney, chronic pyelonephritis is a kidney
condition that develops over time due to damage of
kidney tissue. In adults, infection usually plays a role, but
the underlying disorder usually involves an underlying
structural or functional abnormality in the urinary tract
that predisposes an individual to kidney infections. It
results in decreased ability of the kidneys to function
(renal failure).

http://www.mdguidelines.com/pyelonephritis-chronic
 Treatment
• If a urinary tract infection is the cause, antibiotics are
the first line of therapy.
• Obstruction surgery
• variety of procedures designed to correct the
vesicoureteral reflux condition itself (reimplantation of
ureters).
• Medications may be prescribed to control
hypertension. If kidney failure has occurred,
medications, diet changes, and dialysis may be
necessary.
http://www.mdguidelines.com/pyelonephritis-chronic
 ANALISIS DRP
1. Obat yang yang tidak diperlukan pada terapi
(unnecessary drug therapy)
Tidak ada
 2. Perlu tambahan terapi (needs additional
drug therapy)
• Guideline on Urological Infection perlu
antibiotik namun dlm kasus ini tidak perlu
karena hanya terjadi peningkatan neutrofil
(neutrofilia) sedangkan WBC normal.
Neutrofilia belum tentu menandakan infeksi,
neutrofilia bisa juga disebabkan adanya
peradangan dan nekrosis. Dari TTV pasien
seperti suhu dan nadi tidak menunjukkan
terjadi infeksi.
 3. Ketidakefektifan pemilihan obat
(ineffective drug)
• Belum ada
4. Dosis berlebih (dosage too high)
Dose adjusment berdasarkan DIH:
• Atovastatin  no necessary
• Candesartan  no necessary
• Clopidogrel  no necessary
• Allopurinol  Clcr 20 ml/min: 100 mg/day
 Clcr 10 ml/min: 100 mg tiap 2
hari sekali
 EULAR evidence based recommendations
for gout. Part II: Management. Report of a task
force of the EULAR Standing Committee for International
Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum
Dis 2006, 65:1312-1324.

Chao J, Terkeltaub R: A critical reappraisal of allopurinol

dosing, safety, and efficacy for hyperuricemia in gout. Curr
Rheumatol Rep 2009, 11:135-140.

• FDA and more recent EULAR dosing guidelines

for allopurinol have suggested the use of
reduced doses in renal failure in order to
lessen the risk of drug toxicity.
• the FDA-recommended maximum allopurinol
dose is 200 mg daily with a creatinine
clearance of 10 to 20 ml/min, and 100 mg daily
with a creatinine clearance of <10 ml/min
 2012 American College of Rheumatology
Guidelines for Management of Gout. Part 1:
Systematic Nonpharmacologic and
Pharmacologic
Therapeutic Approaches to Hyperuricemia

• The starting dosage of allopurinol should be no

greater than 100 mg/day and less than that in
moderate to severe chronic kidney disease
(CKD), followed by gradual upward titration of
the maintenance dose, which can exceed 300
mg daily even in patients with CKD.
 5. Dosis yang kurang (dosage too low)

• Tidak ada
 6. Efek samping obat yang merugikan
(adverse drug reaction)
• Tidak ada interaksi obat

7. Ketidakpatuhan pasien(noncompliance)
• Tgl 3/1/2013
Pasien menolak untuk minum obat ketosteril, namun
tgl 4/1 sampai seterusnya pasien taat minum
ketosteril.