cronic+kidney+disease(ckd)+by+rensi
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CRONIC KIDNEY DISEASE(CKD)
oleh:
RENTA S.M.A.
SIANTURI
Anis, puji, tere,
nana,mia, wita
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Defenition of CKD
Ketidakmampuan ginjal mempertahankan keseimbanganinternal tubuh karena penurunan fungsi ginjal bertahapdiikuti penumpukan sisa metabolisme protein danketidakseimbangan cairan elektrolit.
Gagal Ginjal Kronik (CKD) atau penyakit ginjal tahap akhir
adalah gangguan fungsi ginjal yang menahun bersifatprogresif dan irreversibel.
Gagal ginjal kronis merupakan kegagalan fungsi ginjal (unitnefron) yang berlangsung pelahan-lahan karena penyebab
berlangsung lama dan menetap yang mengakibatkanpenumpukan sisa metabolit (toksik uremik) sehinggaginjal tidak dapat memenuhi kebutuhan biasa lagi danmenimbulkan gejala sakit (Hudak & Gallo, 1996).
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KIDNEY ANATOMY
Renal capsule
Hilus
Ureter
Renal vein
Renal artery
Kidney cortex
Medulla
Renal columns Renal pelvis
Major calyces
Minor calyces
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FUNCTION OF URYNARY SYSTEM
Excretion refers to the elimination of
metabolic wastes that were cell metabolites;
this is the function of the urinary system.
Kidneys play a role in homeostasis of the
blood by excreting metabolic wastes, and by
maintaining the normal water-salt and acid-
base balances of blood.
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Excretion of Metabolic Wastes
Kidneys excrete nitrogenous wastes, including
urea, uric acid, and creatinine.
Urea is a by-product of amino acid metabolism.
The metabolic breakdown of creatine phosphate
in muscles releases creatinine. Uric acidis produced from breakdown of
nucleotides.
Collection of uric acid in joints causes gout.
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Maintenance of Water-Salt Balance
Kidneys maintain the water-salt balance of thebody which, in turn, regulates blood pressure.
Salts, such as NaCl, in the blood cause osmosis
into the blood; the more salts, the greater theblood volume and also blood pressure.
Kidneys also maintain correct levels of
potassium, bicarbonate, and calcium ions inblood.
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Secretion of Hormones
Kidneys secrete or activate several hormones:
1) They secrete the hormone erythropoietin tostimulate red blood cell production,
2) They activate vitamin D to the hormonecalcitriolneeded for calcium reabsorptionduring digestion, and
3) They release renin, a substance that leads to
the secretion of aldosterone.
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YES NO
Risk Factor ReductionDetermine Stage of CKD
Determine underlying causeIdentify risk factors for
progression
Identify comorbidites
Patient meets definition of Chronic
Kidney Disease?
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Picture of function kidney
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NEFRON Unit fungsional ginjal
adalah nefron, 1 ginjalterdiri dari 1 juta nefron
Each nephron has itsown blood supply.
An afferent arterioleapproaches theglomerular capsule anddivides to become theglomerulus, a knot ofcapillaries.
The efferent arteriole
leaves the capsule andbranches into theperitubular capillarynetwork.
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Summary of Blood Flow Through
Kidney and Nephron
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MULTIPLE RISK FACTORS FOR CKD
Diabetes
Hypertension
Autoimmune disease
Systemic infections Exposure to drugs
associated with acute
decline in kidney function
Recovery from acute kidneyfailure
NKF. Am J Kidney Dis. 2002;39:S46
Pinto-Sietsma. Ann Intern Med. 2000;133:585
Older age
Family history of kidney
disease
Reduced kidney mass
Racial/ethnic background
Smoking
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CRF Symptoms Malaise
Weakness
Fatigue
Neuropathy
CHF
Anorexia
Nausea
Vomiting
Seizure
Constipation
Peptic ulceration
Diverticulosis Anemia
Pruritus
Jaundice
Abnormal hemostasis
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Management of Patients with Chronic Kidney Disease
Blood glucose control
BP Control
ARBs
ACE Inhibitors
Interventions that delay p rogression
Reduced Functioning and Well-being
Malnutrition
Osteodystrophy
Anemia
Prevention of Uremic Complications
(GFR < 60 cc/min/1.73 m2)
Cardiovascular Disease
Modifcation of Comorbidity
Pre-emptive Transplantation
Kidney Transplant Evaluation
Timely Dialysis Initiation
Timely Dialysis Access Placement
Choice of Dialysis Modality
Education
An "ESRD Clinic"
Preparation for Renal Replacement Therapy
(GRF < 30 cc/min/1.73m2)
Early Detection of CKD
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RENAL INJURY
Reduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability
to macromolecules
Increased filtration of plasma proteins Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
RENAL SCARRING
PROGRESSIVE RENAL DAMAGE:
The F inal Common Pathway
Increased BP
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EVALUATING PATIENTS AT RISK FOR CKD
Evaluating risk factors and identifying GFR
declines are essential to the prompt and
appropriate management of CKD
GFR or age/weight-sensitive eGFR
Blood pressure
Glucose
Urinalysis
Microalbuminuria/proteinuria
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COMORBIDITIES AND COMPLICATIONS OF
CKD
Anemia
Hypertension
Cardiovascular disease
Diabetes
Osteodystrophy
Malnutrition
Metabolic acidosis
Dyslipidemia
Deficits in functioning
and well-being
Zabetakis. Am J Kidney Dis. 2000;36(suppl 3):S31
NKF. Am J Kidney Dis. 2002;39:S17
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DELAYED DIAGNOSIS OF CKD LEADS TO
UNDERUSE OF INTERVENTIONS
Lack of interventions to treat HTN, CVD, DM,
anemia, and malnutrition
Under use and delayed consultations with
nephrologists, cardiovascular specialists, or
dietitians
Lack of patient education
Lack of a permanent vascular access at
initiation of hemodialysis
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MANAGEMENT OF PATIENTS WITH CKD
Blood pressure control
Diabetes control
Cardiovascular disease management
Anemia management
Iron management
Vitamin D and vital bone protection
Eating well and exercise
Access planning
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GUIDELINE 13. LOSS OF KIDNEY FUNCTION IN CKD
Interventions to slow the progression should be considered in all patients with CKD
Interventions proven to be effective include:
1. Strict glucose control in diabetes;2. Strict blood pressure control;
3. ACEI and ARBs
Interventions that may be effective, but studies are inconclusive, include:
1. Dietary protein restriction;
2. Lipid-lowering therapy;
3. Partial correction of anemia.
Attempts should be made to prevent acute renal failure:
Volume depletion;
IV contrast;
Some antibiotics (for example, aminoglycosides and amphotericin B);
NSAIDs, including COX 2 inhibitors;
Other drugs: ACEI, ARBs, calcineurin inhibitors
Obstruction.eGFR should be obtained at least yearly in CKD, and more often in patients with:
GFR
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RENAL INJURYReduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability
to macromolecules
Increased filtration of plasma proteins Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
RENAL SCARRING
PROGRESSIVE RENAL DAMAGE:
The F inal Common Pathway
Increased BP ACEIARB
ACEI
ARB
ACEI
ARB
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http://www.kidney.org/professionals/kdoqi/guidelines_ckd/Gif_File/kck_t148.gif -
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BP CONTROL: INTERVENTIONS
ACE inhibitors
Angiotensin-receptor blockers (ARBs)
Calcium channel blockers (CCBs) Diuretics
Low-sodium diet
Combination therapy
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EVALUATION OF ANEMIA
Hemoglobin and/or hematocrit
Red-blood-cell indices
Reticulocyte count
Iron parameters
Test for occult-blood in stool
NKF. Am J Kidney Dis. 2001;37:S192
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TREATMENT OF ANEMIA
Iron supplementation (IV/PO)
Erythropoiesis stimulating agents
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IRON DEFICIENCY IN CKD
Preexisting Iron
Deficiency
Poor nutrition
Blood loss
Iron deficiency with
erythropoiesis-
stimulating agents
Increased iron needs
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Manifestasi klinik Gangguan pernafasan
Udema, kelainan mata, pada visus, retina, dan saraf mata
Hipertensi, CHF, perikarditis, edema paruAnoreksia, nausea, vomitusUlserasi lambungStomatitisProteinuria
Hematuria Letargi, apatis, penurunan konsentrasi
Anemia defisiensi eritropoetin, retensi uremiaPerdarahanTurgor kulit jelek, gatak gatal pada kulit, kulit kering bersisik,
uremic frostDistrofi renalHiperkalemiaAsidosis metabolic
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ASSESSMENT OF IRON STATUS
Frequently used tests
Serum ferritin
Transferrin saturation
Target
100 ng/mL
>20%
Additional measurements
Reticulocyte Hb content
% Hypochromic RBCs
Erythrocyte ferritin
NKF. Am J Kidney Dis. 2001;37(suppl 1);S182
Macdougall. Curr Opin Hematol. 1999;6:121
Goodnough. Blood. 2000;96:823
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ACID/BASE BALANCE
Renal NH4+
Excretion
40 mEq/day
Endogenous Renal Net AcidH+ Production Renal Excretion
70 mEq/day Excretion 70 mEq/day
30 mEq/day
Normal Acid/Base Balance
[HCO3] = 24 mEq/L
Alpem. Am J Kidney Dis. 1997;29:291
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CONSEQUENCES OF METABOLIC ACIDOSIS
Abnormal renal handling of ions
tubular-phosphate reabsorption
filtered load of calcium and phosphate tubular-calcium reabsorption
Increased resorption of bone
Increased muscle catabolism
Franch. J Am Soc Nephrol. 1998;9:S78
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CONSEQUENCES OF METABOLIC ACIDOSIS
Abnormal renal handling of ions
tubular-phosphate reabsorption
filtered load of calcium and phosphate tubular-calcium reabsorption
Increased resorption of bone
Increased muscle catabolism
Franch. J Am Soc Nephrol. 1998;9:S78
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CONSEQUENCES OF METABOLIC ACIDOSIS
Abnormal renal handling of ions
tubular-phosphate reabsorption
filtered load of calcium and phosphate tubular-calcium reabsorption
Increased resorption of bone
Increased muscle catabolism
Franch. J Am Soc Nephrol. 1998;9:S78
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TREATMENT OF METABOLIC ACIDOSIS IN
CKD
Goal
Serum HCO3- > 20 mEq/L
pH > 7.35
AgentsSodium bicarbonate tablets
(650 mg = ~ 8 mEq HCO3-)
Sodium citrate (Shohls solution)
Dose of HCO3-1.0 1.5 mEq/kg/day
Dependent upon initial serum HCO3- and degree ofrenal insufficiency
Dubose TD. Harrisons Principles of Internal Medicine. 1998:277
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Recommendations in Metabolic
Acidosis Treatment
Alkali therapy to maintain plasma bicarbonate
concentration above 22 meq/L (K/DOQI
guideline recommendation)
Sodium bicarbonate Agent of choice; may
cause bloating.
Sodium Citrate Avoid when also taking
aluminum-containing anti-acids since itmarkedly enhances aluminum absoption
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EXERCISE
Physical functioning Blood pressure control
Muscle, bone strength
Level of cholesterol and
triglycerides
Better sleep
Control of body weight
NKF. Staying fit with Kidney Disease
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Pemeriksaan diagnostik1. Urine :
Volume
WarnaSedimenBerat jenisKreatininProtein
2. Darah :
Bun / kreatininHb, Ht, faktor pembekuan darahHitung darah lengkapSel darah merahNatrium serumKalium
Magnesium fosfatProteinOsmolaritas serum
AGD
3. Penunjang
Foto polos abdomen
USG renogram
Pielografi retrograde
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Pengkajian keperawatan
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Dialysis of patients with CRF eventually require
dialysis
Diffuse harmful waste out of body
Control BP Keep safe level of chemicals in body
2 types
Hemodialysis Peritoneal dialysis
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Hemodialysis 3-4 times a week
Takes 2-4 hours
Machine filters
blood and
returns it to
body
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Types of Access Temporary site
AV fistula
Surgeon constructs by combining an artery and a vein
3 to 6 months to mature
AV graft
Man-made tube inserted by a surgeon to connect artery
and vein
2 to 6 weeks to mature
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AV Fistula & Graft
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Access Problems AV graft thrombosis
AV fistula or graft bleeding
AV graft infection
Steal Phenomenon
Early post-op
Ischemic distally
Apply small amount of pressure to reversesymptoms
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Peritoneal Dialysis Abdominal lining filters blood
3 types
Continuous ambulatory
Continuous cyclical
Intermittent
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EMS Considerations Make sure the dressing remains intact
Do not push or pull on the catheter
Do not disconnect any of the catheters
Always transport the patient andbags/catheters as one piece
Never inject anything into catheter
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Dialysis Related Problems Lightheadedgive fluids
Hypotension
Dysrhythmias
Disequilibration Syndrome
At end of early sessions
Confusion, tremor, seizure
Due to decrease concentration of blood versusbrain leading to cerebral edema
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