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Kesimpulan Gagal ginjal kronis atau penyakit renal tahap akhir (ESRD) merupakan gangguan fungsi renal yang progresif dan irreversible dimana kemampuan tubuh gagal untuk mempertahankan metabolisme dan keseimbangan cairan dan elektrolit, menyebabkan uremia (retensi urea dan sampah nitrogen lain dalam darah). Asuhan Keperawatan Pada Chronic Renal Failure ( Crf) - Free download as. (.ppt /.pptx), PDF File (.pdf), Text File (.txt) or view presentation slides online. Gagal ginjal kronik adalah sindrom klinis yang umum pada stadium lanjut dari.

Background: Patients with chronic kidney disease undergoing hemodialysis suffer changes in lifestyle, which cause physical and psychosocial problems, particularly anxiety. Progressive Muscular Relaxation is considered as an intervention to reduce anxiety. Objective: This study aims to examine the effect of progressive muscular relaxation in in reducing anxiety in patients with chronic kidney disease undergoing hemodialysis. Methods: This study used a quasi-experimental design involved 78 respondents, with 38 randomly assigned in the intervention and control group. The progressive muscular relaxation was performed on 14 muscle groups for 4-week period. Hamilton Anxiety Rating Scale was used to measure anxiety.

Univariate, bivariate and multivariate analyses were performed for data analyses. Results: The results showed a statistically significant difference in anxiety values between the intervention and control group with p-value 0.000 (.

Eddy Susatyo, SpPD FinaSIM RSU dr. Sutrasno Rembang Gangguan sistem urologi fokus gagal ginjal 2. STRUCTURE OF THE KIDNEYS 3. Chronic Kidney Disease?

Definition of CKD • Kidney damage for >3 months – Defined by structural or functional abnormalities of the kidney, with or without decreased glomerular filtration rate (GFR) • Reduced GFR for >3 months • New staging for chronic kidney disease (CKD) is primarily based on kidney function. National Kidney Foundation (NKF). Am J Kidney Dis. 2002;39(2 suppl 1):S1-S266. Prevalence of CKD 6.

How About the Function of Renal? Fungsi ginjal Regulasi volume cairan tubuh Regulasi keseimbangan elektrolit Regulasi keseimbangan asam basa Regulasi tekanan darah (RAAS) Ekskresi sampah metabolik Regulasi erithropoesis Metabolisme vit D Sintesis prostaglandin 8. ADH Angiotensin II Ang II Adrenal Aldosteron Kidney Na+ excretion H2O excretion Angiotensin I Angiotensinogen Renin Brain Lung Hepar RAAS 9.

The Most Common Causes of CKD Glomerulonefritis Penyakit ginjal herediter Hipertensi Uropathy obstruktif Infeksi Nefropati diabetik 10. The Most Common Causes of CKD Primary Diagnosis for Patients Who Start on Dialysis Diabetes 50.1% Hypertension 27% Glomerulonephritis 13% Other 10% GlomerulonephritisOther 11. Hipertrofi sel renal Ggn konstentrasi urin Penurunan GFR CKD Ggn fs ekskresi Ggn fs non ekskresi Pe↓ ekskr ion H Pe↓ ekskr PO4 Pe↓ ekskr kalium Pe↓ eksr sisa metab Pe↑ Reabs Na Ggn Imun ↓ prod eritropoetin Pe↓ abs Ca Ggn Reproduksi 12. JENIS PEMERIKSAAN PENUNJANG • Urinalisis • Evaluasi Fungsi Ginjal • Evaluasi Serologis • Pemeriksaan Radiologis • Biopsi Ginjal 13. Equations for Estimating GFR Abbreviated MDRD Study Equation GFR (mL/min/1.73 m2 ) = 186.3 X SCr -1.154 X Age-0.203 X 0.742 (if female) X 1.210 (if African American) MDRD = Modification of Diet in Renal Disease; Ccr = creatinine clearance. Ann Intern Med. Cockcroft-Gault Equation Ccr = (mL/min) (140 – Age) X Weight in kg 72 X SCr = 0.85 if female 14.

CKD Progresses in Stages Defined by Kidney Function: GFR 20 Million People With CKD (1 in 9 adults) in the United States, Many More at Risk 70 (145-160 by 2010)* 300,000 0.5mg% Specificity 35. Klasifikasi/staging AKI modifikasi RIFLE Stadium kriteria kreatinin kriteria urin output 1. Risk serum kreatinin meningkat > 0,3 mg/dl atau meningkat lebih dari 150-200% dari awal 6jam 2. Injury serum kreatinin meningkat sampai > 200% sampai 300% dari data awal 300%, (serum kreatinin > 4mg/dl dengan peningkatan akut 0,5mg/dl, indikasi untuk renal replacement therapy 4 weeks ESRD Persistent renal failure for >3 months Murray PT, Palevsky PM.

Nephrology Self Assesment Program, Vol 6, No 5, Sept 2007 36. Sepsis Ischemic insult Nephrotoxic insult Complement activationEndotoxin releaseIschemia-reperfusion Cellular activation (PMN, endothelial cells) Arachidonic acid metabolities Proteases Chemokines Platelet activating factor ↑ Serum creatinine Oxygen free radicals Nitric oxide Heat shock proteins Endothelins Acute kidney injury↑ Urinary KIM-1, NAG ↓ Urine output ↓ GFR Anti-inflamatory mediators Pro-inflamatory mediators - + Pathogenic mechanism of sepsis related acute kidney injury 37. (1) Vasoconstriction Renin-angiotensin endothelin PGI2 NO (2) Obstruction by casts (3) Tubular backleak Ischemia Nephrotoxins Tubular damage (proximal tubules and ascending thick limb) (5)? Direct glomerular effect GFR Oliguria Tubular fluid flow Intratubular pressure Possible pathogenetic mechanisms in ATN. (4) Interstitial inflammation 38. Effects of ischemia on renal tubules in the pathogenesis of ischemic AKI Schrier et al, J Clin Invest 2004, 114:5-14 39. Renal protection, there is damage before any symptom MAP> 65 mmHg CVP 8-12 mmHg (no ventilator) 12-15 mmHg (ventilator) Urine > 0,5ml/BW/hour SaO2 >70% Koloid,albumin?