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CRONIC KIDNEY DISEASE(CKD)

CRONIC KIDNEY DISEASE(CKD). oleh : RENTA S.M.A. SIANTURI Anis, puji, tere, nana,mia, wita. Defenition of CKD.

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CRONIC KIDNEY DISEASE(CKD)

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  1. CRONIC KIDNEY DISEASE(CKD) oleh: RENTA S.M.A. SIANTURI Anis, puji, tere, nana,mia, wita

  2. Defenition of CKD • Ketidakmampuan ginjal mempertahankan keseimbangan internal tubuh karena penurunan fungsi ginjal bertahap diikuti penumpukan sisa metabolisme protein dan ketidakseimbangan cairan elektrolit. • GagalGinjalKronik (CKD) ataupenyakitginjaltahapakhiradalahgangguanfungsiginjal yang menahunbersifatprogresifdanirreversibel. • Gagalginjalkronismerupakankegagalanfungsiginjal (unit nefron) yang berlangsungpelahan-lahankarenapenyebabberlangsung lama danmenetap yang mengakibatkanpenumpukansisametabolit (toksikuremik) sehinggaginjaltidakdapatmemenuhikebutuhanbiasalagidanmenimbulkangejalasakit (Hudak & Gallo, 1996).

  3. KIDNEY ANATOMY • Renal capsule • Hilus • Ureter • Renal vein • Renal artery • Kidney cortex • Medulla • Renal columns • Renal pelvis • Major calyces • Minor calyces

  4. 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.

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

  6. 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.

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

  8. Patient meets definition of Chronic Kidney Disease? YES NO Risk Factor Reduction Determine Stage of CKD Determine underlying cause Identify risk factors for progression Identify comorbidites

  9. Picture of function kidney

  10. 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.

  11. Summary of Blood Flow Through Kidney and Nephron

  12. 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 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

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

  14. Management of Patients with Chronic Kidney Disease

  15. PROGRESSIVE RENAL DAMAGE: The Final Common Pathway RENAL INJURY Reduction in nephron mass Glomerular capillary hypertension Increased glomerular permeability to macromolecules Increased BP Increased filtration of plasma proteins Proteinuria Excessive tubular protein reabsorption Tubulointerstitial inflammation RENAL SCARRING

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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: • Strict glucose control in diabetes; • Strict blood pressure control; • ACEI and ARBs • Interventions that may be effective, but studies are inconclusive, include: • Dietary protein restriction; • Lipid-lowering therapy; • 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.

  21. PROGRESSIVE RENAL DAMAGE: The Final Common Pathway RENAL INJURY ACEI ARB Reduction in nephron mass Glomerular capillary hypertension Increased glomerular permeability to macromolecules ACEI ARB Increased BP Increased filtration of plasma proteins Proteinuria Excessive tubular protein reabsorption Tubulointerstitial inflammation ACEI ARB RENAL SCARRING

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

  23. 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 EVALUATION OF ANEMIA

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

  25. Preexisting Iron Deficiency Poor nutrition Blood loss Iron deficiency with erythropoiesis-stimulating agents Increased iron needs IRON DEFICIENCY IN CKD

  26. Manifestasi klinik • GangguanpernafasanUdema, kelainan mata, pada visus, retina, dan saraf mataHipertensi, CHF, perikarditis, edema paruAnoreksia, nausea, vomitusUlserasilambungStomatitisProteinuriaHematuria • Letargi, apatis, penurunankonsentrasiAnemia defisiensi eritropoetin, retensi uremiaPerdarahanTurgorkulitjelek, gatakgatalpadakulit, kulit kering bersisik, uremic frostDistrofi renalHiperkalemiaAsidosis metabolic

  27. 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

  28. ACID/BASE BALANCE Renal NH4+ Excretion 40 mEq/day Endogenous Renal Net Acid H+ 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

  29. 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

  30. 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

  31. 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

  32. Goal Serum HCO3- > 20 mEq/L pH > 7.35 Agents Sodium bicarbonate tablets (650 mg = ~ 8 mEq HCO3-) Sodium citrate (Shohl’s solution) Dose of HCO3- 1.0 – 1.5 mEq/kg/day Dependent upon initial serum HCO3- and degree of renal insufficiency Dubose TD. Harrison’s Principles of Internal Medicine. 1998:277 TREATMENT OF METABOLIC ACIDOSIS IN CKD

  33. 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

  34. ↑ 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 EXERCISE

  35. Pemeriksaan diagnostik • Urine :VolumeWarnaSedimenBeratjenisKreatininProtein 2. Darah : Bun / kreatinin Hb, Ht, faktor pembekuan darahHitungdarahlengkapSeldarahmerahNatrium serumKaliumMagnesium fosfatProteinOsmolaritas serum AGD 3. Penunjang Foto polos abdomen USG renogram Pielografi retrograde

  36. Pengkajian keperawatan

  37. Dialysis • ½ 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

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

  39. 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

  40. AV Fistula & Graft

  41. 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

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

  43. 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

  44. 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

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