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Objectives Anatomy Function Chronic Renal Failure (CRF) Causes Symptoms Dialysis
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Anatomy and Physiology The Kidneys Hilum Medulla Pyramids Papilla Renal Pelvis
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Anatomy 2 Kidneys 2 Ureters Bladder Urethra
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Kidney Function Detoxify blood Increase calcium absorption calcitriol Stimulate RBC production erythropoietin Regulate blood pressure and electrolyte balance renin
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Formation of Urine Glomerular Filtration GFR Reabsorption and Secretion Simple diffusion and osmosis Facilitated diffusion Active transport
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Azotemia: elevated blood urea nitrogen not from an intrinsic renal disease Oliguria:urine output less than 500cc/24hr. Nonoliguria:urine output greater than 500cc/24hr. Anuria:urine output less than 50cc/24hr.
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Acute Versus Chronic Acute sudden onset rapid reduction in urine output Usually reversible Tubular cell death and regeneration Chronic Progressive Not reversible Nephron loss 75% of function can be lost before its noticeable
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ARF versus CRF Neuropathy Renal osteodystrophy Small size Kidney Past history of CKD Broad cast
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Chronic renal failure Chronic renal failure: slowly progressive and non- reversible loss of kidney function Uraemia: metabolic outcome of chronic renal failure End-stage renal disease: requirement for renal replacement therapy
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ETIOLOGY Diabetes mellitus (28%) Hypertension (25%) Glomerulonephritis (21%) Polycystic Kidney Diease (4%) Other (23%): Obstruction, infection, etc.
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Progression of chronic renal failure Factors causing progression sustaining primary disease systemic hypertension Intraglomerular hypertension Proteinuria Nephrocalcinosis Dyslipidaemia Imbalance between renal energy demands and supply
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Slowing the Progression of Chronic Renal Failure Control BP to <130 /80 Diet Anaemia Calcium and Phosphate Dyslipidaemia Obesity Smoking Cessation
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Old Chinese saying ……. Good doctor relieve disease Better doctor cure disease Superior doctor prevent disease
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Symptoms of chronic renal failure Many are symptom free until 2/3 of renal mass lost. Often no physical examination findings or history. Several common modes of presentation: progressive lethargy, anorexia, (and later vomiting) hypertension, and /or heart failure unexplained anaemia serendipitous findings on biochemistry
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The Medical Burden Of Chronic Renal Failure Prevention of ESRD may prevent other co-morbid conditions from developing In particular, there is a high prevalence of Cardiovascular diseases in patients with Chronic kidney disease
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CHRONIC RENAL FAILURE: CLINICAL MANIFESTATIONS Sodium and water retention Hyperkalemia Metabolic Acidosis Mineral and Bone metabolism Cardiovascular and Pulmonary Disorders Hematologic Abnormalities Neuromuscular Abnormalities Gastrointestinal Abnormalities Endocrine Abnormalities Dermatologic Abnormalities
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Sodium and Volume Balance Sodium and water retention: CHF, Hypertension, ascites, edema Enhanced sensitivity to extra-renal sodium and water loss vomiting, diarrhea, fever, sweating Symptoms: dry mouth, dizziness, tachycardia, etc. Recommendations Avoid excess salt and water intake Diuretics or dialysis
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Potassium Balance Hyperkalemia (GFR below 5 mL/min) GFRs >5 mL/min: compensatory aldosterone-mediated K transport in the DCT K-sparing diuretics, ACEis, beta-blockers impair Aldosterone-mediated actions Exacerbation of hyperkalenia: Exogenous factors: K-rich diet, etc. Endogenous factors: infection, trauma, etc.
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Hyperkalemia & EKG K > 5.5 -6 Tall, peaked T ’ s Wide QRS Prolong PR Diminished P Prolonged QT QRS-T merge – sine wave
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Hyperkalemia Symptoms Weakness Lethargy Muscle cramps Paresthesias Hypoactive DTRs Dysrhythmias
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Metabolic Acidosis Decreased acid excretion and ability to maintain physiologic buffering capacity: GFR < 20 mL/min: transient moderate acidosis Treat with oral sodium bicarbonate Increased susceptibility to acidosis
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Mineral and Bone Bone disease (Figure 16-6) from: Decreased Ca absorption from the gut Over-production of PTH Altered Vitamin D metabolism Chronic metabolic acidosis
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Cardiovascular and Pulmonary Abnormalities Volume and salt overload CHF and pulmonary edema Hypertension Hyperreninemia: Hypertension Pericarditis: Remic toxin accumulation Accelerated atherosclerosis: linked to factors above and metabolic abnormalities (Ca alterations, hyperlipidemia)
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Hematological Abnormalities Anemia: lack of erythropoietin production Bone marrow suppression: uremic poisons: leukocyte suppression - infection bone marrow fibrosis: elevated PTH an aluminum toxicity from dialysis Increased bruising, blood loss (surgery) and hemorrhage Lab Abnormalities: Prolonged bleeding time, abnormal platelet aggregation
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Neuromuscular Abnormalites CNS Abnormalities: Mild-Moderate: Sleep disorders, impaired concentration and memory, irritability Severe: Asterixis, myoclonus, stupor, seizures and coma Peripheral neuropathies: “ restless legs ” syndrome Hemodialysis-related neuropathies
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Gastrointestinal Abnormalities Peptic Ulcer disease: Secondary hyperparathyrodism? Uremic gastroenteritis: mucosal alterations Uremic Fetor: bad breath (ammonia) Non-Specific abnormalities: anorexia, nausea, vomiting, diverticulosis, hiccoughs
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Endocrine Abnormalities Insulin: Prolonged half-life due to reduced clearance (metabolism) Amenorrhea and pregnancy failure: low estrogen levels Impotence, oligospermia and geminal cell dysplasia: Low testosterone levels
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Dermatologic Abnormalities Pallor: anemia Skin color changes: accumulation of pigments Ecchymoses and hematomas: clotting abnormalities Pruritus and Excoriations: Ca deposits from secondary hyperparathyroidism
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Conclusion – chronic renal failure Progressive chronic disease leading to end-state renal failure Different primary disease can cause chronic renal failure Diabetic nephropathy is a frequent cause for chronic renal failure Symptoms can be very different and depend on primary disease and stage of chronic renal failure Stages of renal failure can be associated with a progressive decrease of GFR The consequences are complex according to the different function of the kidney and involve many organ systems
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Pre-Dialysis Treatment 1.Maintain normal electrolytes a.Potassium, calcium, phosphate are major electrolytes affected in CRF b.ACE inhibitors may be acceptable in many patients with creatinine >3.0mg/dL c.ACE inhibitors may slow the progression of diabetic and non-diabetic renal disease [13]13 d.Reduce or discontinue other renal toxins (including NSAIDS) e.Diuretics (eg. furosemide) may help maintain potassium in normal range f.Renal diet including high calcium and low phosphate
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1.Reduce protein intake to <0.6gm/kg body weight a.Appears to slow progression of diabetic and non-diabetic kideny disease b.In type 1 diabetes mellitus, protein restriction reduced levels of albuminuria c.Low protein diet did not slow progression in children with CRF 1.Underlying Disease a.Diabetic nephropathy should be treated with ACE inhibitors until creatinine >2.5- 3mg/dL b.Hypertension should be aggressively treated (ACE inhibitors are preferred)
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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
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Hemodialysis 1.Indications a.Uremia - azotemia with symptoms and/or signs b.Severe Hyperkalemia c.Volume Overload - usually with congestive heart failure (pulmonary edema) d.Toxin Removal - ethylene glycol poisoning, theophylline overdose, etc. e.An arterio-venous fistula in the arm is created surgically f.Catheters are inserted into the fistula for blood flow to dialysis machine
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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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1.Procedure for Chronic Hemodialysis a.Blood is run through a semi-permeable filter membrane bathed in dialysate b.Composition of the dialysate is altered to adjust electrolyte parameters c.Electrolytes and some toxins pass through filter d.By controlling flow rates (pressures), patient's intravascular volume can be reduced e.Most chronic hemodialysis patients receive 3 hours dialysis 3 days per week
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1.Efficacy a.Some acids, BUN and creatinine are reduced b.Phosphate is dialyzed, but quickly released from bone c.Very effective at reducing intravascular volume/potassium d.Once dialysis is initiated, kidney function is often reduced e.Not all uremic toxins are removed and patients generally do not feel "normal" f.Response of anemia to erythropoietin is often suboptimal with hemodialysis
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1.Chronic Hemodialysis Medications a.Anti-hypertensives - labetolol, CCB, ACE inhibitors b.Eythropoietin (Epogen ® ) for anemia in ~80% dialysis pts c.Vitamin D Analogs - calcitriol given intravenously d.Calcium carbonate or acetate to phosphate and PTH e.RenaGel, a non-adsorbed phosphate binder, is being developed for hyperphosphatemia f.DDAVP may be effective for patients with symptomatic platelet problems
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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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Temporary Catheter
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AV Fistula & Graft
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Chronic Renal Failure Long-Term Management Renal Dialysis Hemodialysis Common complications
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What This Means For You No BP on same arm as fistula Protect arm from injury Control obvious hemorrhage Bleeding will be arterial Maintain direct pressure No IV on same arm as fistula A thrill will be felt – this is normal
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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 reverse symptoms
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Peritoneal Dialysis Abdominal lining filters blood 3 types Continuous ambulatory Continuous cyclical Intermittent
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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
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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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