CRONIC KIDNEY DISEASE(CKD)

oleh: RENTA S.M.A. SIANTURI Anis, puji, tere, nana,mia, wita

Defenition of CKD
Ketidakmampuan ginjal mempertahankan keseimbangan internal tubuh karena penurunan fungsi ginjal bertahap diikuti penumpukan sisa metabolisme protein dan ketidakseimbangan cairan elektrolit. Gagal Ginjal Kronik (CKD) atau penyakit ginjal tahap akhir adalah gangguan fungsi ginjal yang menahun bersifat progresif dan irreversibel. Gagal ginjal kronis merupakan kegagalan fungsi ginjal (unit nefron) yang berlangsung pelahan-lahan karena penyebab berlangsung lama dan menetap yang mengakibatkan penumpukan sisa metabolit (toksik uremik) sehingga ginjal tidak dapat memenuhi kebutuhan biasa lagi dan menimbulkan gejala sakit (Hudak & Gallo, 1996).

KIDNEY ANATOMY
Renal capsule Hilus
Ureter Renal vein Renal artery

Kidney cortex Medulla Renal columns Renal pelvis

Major calyces Minor calyces

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 acidbase balances of blood.

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 acid is produced from breakdown of nucleotides. Collection of uric acid in joints causes gout.

Maintenance of Water-Salt Balance

Kidneys maintain the water-salt balance of the body which, in turn, regulates blood pressure. Salts, such as NaCl, in the blood cause osmosis into the blood; the more salts, the greater the blood volume and also blood pressure. Kidneys also maintain correct levels of potassium, bicarbonate, and calcium ions in blood.

Secretion of Hormones
Kidneys secrete or activate several hormones: 1) They secrete the hormone erythropoietin to stimulate red blood cell production, 2) They activate vitamin D to the hormone calcitriol needed for calcium reabsorption during digestion, and 3) They release renin, a substance that leads to the secretion of aldosterone.

Patient meets definition of Chronic Kidney Disease?

YES NO

Determine Stage of CKD Determine underlying cause Identify risk factors for progression Identify comorbidites

Risk Factor Reduction

Picture of function kidney

NEFRON
Unit fungsional ginjal adalah nefron, 1 ginjal terdiri dari 1 juta nefron Each nephron has its own blood supply. An afferent arteriole approaches the glomerular capsule and divides to become the glomerulus, a knot of capillaries. The efferent arteriole leaves the capsule and branches into the peritubular capillary network.

Summary of Blood Flow Through Kidney and Nephron

11

MULTIPLE RISK FACTORS FOR CKD

Diabetes Hypertension Autoimmune disease Systemic infections Exposure to drugs associated with acute decline in kidney function Recovery from acute kidney failure Older age Family history of kidney disease Reduced kidney mass Racial/ethnic background Smoking

NKF. Am J Kidney Dis. 2002;39:S46 Pinto-Sietsma. Ann Intern Med. 2000;133:585

CRF Symptoms
Malaise Weakness Fatigue Neuropathy CHF Anorexia Nausea Vomiting Seizure Constipation Peptic ulceration Diverticulosis Anemia Pruritus Jaundice Abnormal hemostasis

Management of Patients with Chronic Kidney Disease

Early Detection of CKD

Interventions that delay progression

Prevention of Uremic Complications (GFR < 60 cc/min/1.73 m2)

Modifcation of Comorbidity

Preparation for Renal Replacement Therapy (GRF < 30 cc/min/1.73m2)

ACE Inhibitors

Anemia

Cardiovascular Disease

Education An "ESRD Clinic"

ARBs

Osteodystrophy

Kidney Transplant Evaluation

Choice of Dialysis Modality

BP Control

Malnutrition

Pre-emptive Transplantation

Timely Dialysis Access Placement

Blood glucose control

Reduced Functioning and Well-being

Timely Dialysis Initiation

PROGRESSIVE RENAL DAMAGE:

The Final Common Pathway
RENAL INJURY

Reduction in nephron mass

Glomerular capillary hypertension

Increased BP

Increased glomerular permeability to macromolecules Increased filtration of plasma proteins

Proteinuria

Excessive tubular protein reabsorption

Tubulointerstitial inflammation RENAL SCARRING

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

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

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

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

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 <60 mL/min/1.73 m2; Fast GFR decline in the past Risk factors for faster progression; Ongoing treatment to slow progression; Exposure to risk factors for acute GFR decline.

PROGRESSIVE RENAL DAMAGE: The Final Common Pathway

RENAL INJURY

ACEI ARB

Reduction in nephron mass Glomerular capillary hypertension

Increased BP

Increased glomerular permeability

to macromolecules
Increased filtration of plasma proteins Excessive tubular protein reabsorption Tubulointerstitial inflammation RENAL SCARRING

ACEI ARB
Proteinuria

ACEI ARB

BP CONTROL: INTERVENTIONS
ACE inhibitors Angiotensin-receptor blockers (ARBs) Calcium channel blockers (CCBs) Diuretics Low-sodium diet Combination therapy

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

TREATMENT OF ANEMIA
Iron supplementation (IV/PO) Erythropoiesis stimulating agents

IRON DEFICIENCY IN CKD

Preexisting Iron Deficiency Poor nutrition Blood loss Iron deficiency with erythropoiesisstimulating agents Increased iron needs

Manifestasi klinik
Gangguan pernafasan Udema, kelainan mata, pada visus, retina, dan saraf mata Hipertensi, CHF, perikarditis, edema paru Anoreksia, nausea, vomitus Ulserasi lambung Stomatitis Proteinuria Hematuria Letargi, apatis, penurunan konsentrasi Anemia defisiensi eritropoetin, retensi uremia Perdarahan Turgor kulit jelek, gatak gatal pada kulit, kulit kering bersisik, uremic frost Distrofi renal Hiperkalemia Asidosis metabolic

ASSESSMENT OF IRON STATUS

Frequently used tests Serum ferritin Transferrin saturation 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

Target 100 ng/mL >20%

ACID/BASE BALANCE
Renal NH4+ Excretion 40 mEq/day Endogenous H+ Production 70 mEq/day Renal Excretion 30 mEq/day Renal Net Acid Excretion 70 mEq/day

Normal Acid/Base Balance [HCO3] = 24 mEq/L Alpem. Am J Kidney Dis. 1997;29:291

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

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

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

TREATMENT OF METABOLIC ACIDOSIS IN CKD

Goal Serum HCO3- > 20 mEq/L pH > 7.35 Agents Sodium bicarbonate tablets (650 mg = ~ 8 mEq HCO3-) Sodium citrate (Shohls solution) Dose of HCO31.0 1.5 mEq/kg/day Dependent upon initial serum HCO3- and degree of renal insufficiency
Dubose TD. Harrisons Principles of Internal Medicine. 1998:277

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 it markedly enhances aluminum absoption

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

Pemeriksaan diagnostik
1. Urine : Volume Warna Sedimen Berat jenis Kreatinin Protein 2. Darah : Bun / kreatinin Hb, Ht, faktor pembekuan darah Hitung darah lengkap Sel darah merah Natrium serum Kalium Magnesium fosfat Protein Osmolaritas serum AGD 3. Penunjang Foto polos abdomen USG renogram Pielografi retrograde

Pengkajian keperawatan

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

Hemodialysis
3-4 times a week Takes 2-4 hours Machine filters blood and returns it to body

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

AV Fistula & Graft

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 reverse symptoms

Peritoneal Dialysis
Abdominal lining filters blood 3 types
Continuous ambulatory Continuous cyclical Intermittent

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 and bags/catheters as one piece Never inject anything into catheter

Dialysis Related Problems

Lightheaded give fluids Hypotension Dysrhythmias Disequilibration Syndrome
At end of early sessions Confusion, tremor, seizure Due to decrease concentration of blood versus brain leading to cerebral edema