cronic+kidney+disease(ckd)+by+rensi

7/30/2019 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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5

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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11

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



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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



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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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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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