CKD/ESRD & Management

1. CKD/ESRD&Management Note-when viewing lab values in PPT-note that values are given as both as “common values” as also the specific values given in textbook (remember, sources vary slightly-think ranges.)2010

2. Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But -- should kidneys fail.... neither bone, muscle, nor brain could carry on. Homer Smith, Ph.D.

3. REVIEW Recall functions of the kidneys? Recall normal creatinine & BUN; other lab tests? Review Diagnostic Tools

4. CKD- Elderly Risk (Review) • Older Adult-normal aging (plus co-morbidities) > risk kidney dysfunction/renal failure • Must: • Identify/prevent damage • Monitor/risk multiple RX/OTC meds (altered renal blood flow/dec. renal clearance etc) • Monitor/risk associated with dehydration (ie diuretics) • Monitor/risk with dec ability to respond to changes to fluid/electrolyte status (manifestation may be atypical

5. Functions of the Kidneys Regulates volume and composition of extracellular fluid Excretion of nitrogenous waste products BP control via renin-angiotensin-aldosterone system- Recall RAAS Vitamin D activation Acid-base balance (HCO3 & H) regulation through process of _____, ____ and ______. Prostaglandin synthesis Erythropoietin production filtration, secretion, reabsorpton

6. Functions of the Kidneys (cont) Erythropoietin Release If a patient has chronic renal failure, what condition will occur? WHY??? EPO- glycoproteinhormone that controls erythropoiesis, or red blood cell production 6 6/9/2014

7. Diagnostic Tools for Assessing Renal Failure Blood Tests BUN elevated (norm 10-20 mg/dl) (text 10-30mg/dl) Creatinine elevated (norm 0.6 - 1.2 mg/dl) (text 0.5-1.5mg/dl) K elevated (text norm 3.5-5.0 mEq/L) PO4 elevated (text norm 2.8-4.5mg/dl) Ca decreased (text norm 9-11mg/dl) Urinalysis Specific gravity (text norm 1.003-1.030 Protein (text norm 0-trace) Creatinine clearance (text norm 85-135ml/min)

8. BUN Normal 8 - 20 mg/dl (text 10-30mg/dl) Nitrogenous waste product of protein metabolism Unreliable in measurement of renal function Relevance assessed in conjunction with serum creatinine

9. Creatinine A waste product of muscle metabolism Normal value 0.6 - 1.2 mg/dl (text 0.5-1.5mg/dl) 2 times normal = 50% damage 8 times normal = 75% damage 10 times normal = 90% damage Exception - severe muscular disease can greatly  serum creatinine levels

10. Diagnostic Tools Ultrasound X-Rays Biopsy *most definitive

11. Chronic Renal Failure/ Chronic Kidney Disease (CKD) Slow progressive renal disorder related to nephron loss, occurring over months to years Culminates in End Stage Renal Disease (ESRD)

12. Characteristics of CKD > ESRD Cause & onset often unknown Loss of function precedes lab abnormalities Lab abnormalities precede symptoms Symptoms (usually) evolve in orderly sequence Renal size is usually decreased

13. Causes of CKD *Diabetes *Hypertension Glomerulonephritis Cystic disorders Developmental - Congenital Infectious Disease • Neoplasms • Obstructive disorders • Autoimmune diseases (lupus) • Hepatorenal failure • Scleroderma • Amyloidosis • Drug toxicity-(overuse some common drugs, as aspirin, NSAID as ibuprofen, cocaine and acetaminophen) NSAIDs-…cause prerenal ARF by blocking prostaglandin production > also alters local glomerular arteriolar perfusion… (reduces renal blood flow)

14. Glomerular Filtration Rate (GFR)-determine stage CKD (most accurate evaluation) 24 hour urine for creatinine clearance Formula- urine creatinine X urine volume serum creatinine Can estimatecreatinine clearance by: 140 – {age x weight (kg)} 72 x serum creatinine What is normal GFR? 90 - 120 mL/min

15. Stages of CKD (“old” terminology) Reduced Renal Reserve Renal Insufficiency End Stage Renal Disease (ESRD)

16. Stages of CKDNKF Classification System Stage 1: GFR > 90 ml/min despite kidney damage Stage 2: Mild reduction (GFR 60 – 89 ml/min) 1. GFR of 60 may represent 50% loss in function. 2. Parathyroid hormones starts to increase. (why?) *kidneys unable to reabsorb calcium, blood calcium levels fall, stimulating continual secretion of parathyroid hormone to maintain normal calcium levels in blood.

17. During Stage 1 - 2 No symptoms Serum creatinine doubles* (Up to 50%nephron loss FYI-older adult- may impaired renal function even in presence of normal serum creatinine

18. Stages of CKDNKF Classification System Stage 3:Moderate reduction (GFR 30 – 59 ml/min) 1. Calcium absorption decreases (from the GI tract) 2. Malnutrition onset 3. Anemia 4. Left ventricular hypertrophy

19. Stages of CKDNKF Classification System Stage 4: Severe reduction (GFR 15 – 29 ml/min) 1. Serum triglycerides 2. Hyperphosphatemia 3. Metabolic acidosis 4. Hyperkalemia Oops-trouble! K Effect & EKG

20. During Stage 3 - 4 Signs and symptoms worsen if kidneys stressed ability to maintain homeostasis 75% nephron loss glomerular filtration rate, solute clearance, ability to concentrate urine and secrete hormone Symptoms: BUN & Creatinine, mild azotemia, anemia

21. Stages of CKD-NKF Classification System Stage 5: Kidney failure (GFR < 15 ml/min) Azotemia Residual function < 15% of normal Excretory, regulatory, hormonal functions severely impaired Metabolic acidosis (Kussmaul breathing) Marked : BUN, Creatinine, Phosphorous Marked : Hemoglobin, Hematocrit, Calcium Fluid overload ESRD!!!

22. During Stage 5 Uremicsyndrome develops- affecting all body systems can be diminished with early diagnosis & treatment Last stage of progressive CKD Fatal if no treatment

23. Manifestations of Chronic Uremia Syndrome- combination of common symptoms *greater build-up waste products = greater symptoms Fig. 47-5

24. What happens when kidneys don’t function correctly?

25. Manifestations of CKD -Nervous System Mood swings Impaired judgment Inability to concentrate and perform simple math functions Tremors, twitching, convulsions Peripheral Neuropathy restless legs foot drop Manifestations due to inc nitrogenous waste products, electrolyte imbalances, metabolic acidosis and axonal atrophy and demyelination of nerve fibers & dec erythropoietin*

26. Manifestations of CRFSkin Pale, grayish-bronze color Dry scaly Severe itching Bruise easily, petechiae, ecchymosis *Uremic frost • *Manifestations due to…calcium-phosphate deposition in skin, sensory neuropathy, platelet abnormalities; urea crystallizes (uremic frost) >if BUN extremely high

27. Medical Mystery? What do lab studies, etc indicate ? What causes uremic frost? *57-year-old with HTN and CKD (Stage 5), refused dialysis found in respiratory distress after week of upper respiratory symptoms due to viral infection Before admission to hospital >developed asystolic cardiac arrest, was resuscitated by EMT, admitted to ICU, required vasopressor support. PE- diffuse deposits tiny white crystalline material on skin > lab studies- BUN 208 mg/dl; creatinine 15 mg/dl; bicarbonate level 5 mmol per liter; anion gap-26; arterial pH of 6.74, and arterial partial pressure of carbon dioxide of 50 mm Hg. Blood cultures- revealed-Staphylococcus aureus pneumonia, likely due to prior influenza infection. *Aggressive care measures withdrawn after consultation with patient's family >patient died. Walsh S and Parada N. N Engl J Med 2005;352:e13 *Uremic frost- uncommon skin manifestation due to profound azotemia; occurs when urea and other nitrogenous waste products accumulate in sweat and crystallize after evaporation.

28. Manifestations of CKDEyes Visual blurring Occasional blindness “Red eye” Due to calcium-phosphate deposits in eyes

29. Manifestations of CKD Fluid - Electrolyte - pH Volume expansion and fluid overload Metabolic Acidosis Electrolyte Imbalances Potassium Magnesium Sodium Due to impaired kidneys unable to excrete acid load (mostly from NH3); defective reabsorption/regeneration of HCO3. Due to dec excretion by kidneys, breakdown of cellular protein, bleeding, metabolic acidosis, food, drugs, etc Kidneys unable to excrete (too much magnesium causes hyporeflexia and can lead to cardiac arrest) Kidneys retain > water retention> fluid overload

30. Manifestations of CKDGI Tract/Bleeding Risk Uremic fetor Anorexia, nausea, vomiting GI bleeding Anemia Platelet dysfunction Due to GI irritation, platelet defect; diarrhea from hyperkalemia Anemia-due to insufficient production of erythropoietin, protein naturally produced in functioning kidneys…circulates through bloodstream to bone marrow, stimulating production of RBCs. Platelet dysfunction-subnormal platelet aggregation -due to fibrinogen fragments, usually absent in normal human blood but present in uremic plasma may lead to platelet dysfunction in uremia.

31. Manifestations of CKD-Musculoskeletal Muscle cramps Soft tissue calcifications Weakness Related to calcium phosphorous imbalances RENAL OSTEODYSTROPHY Fracture risk!

32. Manifestations of CKD- Heart & Lungs Hypertension Heart failure > pulmonary edema Pericarditis due to uremia Pulmonary edema Pleural effusions- “Uremic Lung” Atherosclerotic vascular disease* Cardiac dysrhythmias (from HF, electrolyte imblaances) *Major Problem!

33. Manifestations of CKD- Endocrine - Metabolic Erythropoietin Hypothyroidism Insulin resistance Growth hormone Gonadal dysfunction Parathyroid hormone and Vitamin D3 Hyperlipidemia

34. Treatment Options Conservative Therapy * (Severe restrictions, dietary, fluids maintain renal function as long as possible- if GFR > 10ml/min) Hemodialysis Peritoneal Dialysis Transplant Nothing > Death

35. Conservative Treatment Goals Detect/treat potentially reversible causes of renal failure Preserve existing renal function Treat manifestations Prevent complications Provide for comfort

36. Conservative Treatment • Control • Hyperkalemia • Hypertension • Hyperphosphatemia • Hyperparthryoidism • Anemia • Hyperglycemia • Dyslipidemia • Hypothyroidism • Nutrition : Describe a renal diet? Depends on lab values-usually low NA, K, restricted protein, phosphorous, & fluids (See text)

37. Hemodialysis Removal of soluble substances and water from the blood by diffusion through a semi-permeable membrane. Early animal experiments began 1913 1st human dialysis 1940’s by Dutch physician Willem Kolff (2 of 17 patients survived) Considered experimental through 1950’s, No intermittent blood access; for acute renal failure only. 1960 Dr. Scribner developed Scribner Shunt-1960’s machines expensive, scarce, no funding. “Death Panels” panels within community decided who got to dialyze.

38. Hemodialysis Process Blood removed from patient into extracorporeal circuit. Diffusion and ultrafiltration take place in dialyzer. Cleaned blood returned to patient.

39. Extracorporeal Circuit

40. How Hemodialysis Works

41. . How Dialysis Works-Interactive! An Introduction to Dialysis-How Stuff Works! (Step by Step) YouTube- Hemodialysis! Great!

42. Vascular Access(click) Arterio-venous shunt (External Shunt) *used now for Continuous Renal Replacement Therapy (CRRT)-temporary access Arterio-venous (AV) Fistula (AKA-native or primary fistula) PTFE Graft Temporary catheters “Permanent” catheters

43. External Shunt (Schribner Shunt) External- one end into artery, one into vein. Advantages place at bedside use immediately Disadvantages infection skin erosion accidental separation limits use of extremity *Used now only for CRRT-temporary

44. Arterio-venous (AV) FistulaPrimary (native) Fistula Patients own artery and vein surgically anastomosed. Advantages patient’s own vein/artery longevity low infection and thrombosis rates Disadvantages long time to mature, 1- 6 months “steal” syndrome requires needle sticks davita.com

45. PTFE (Polytetraflourethylene) Graft Synthetic “vessel” anastomosed into an artery and vein. Advantages for people with inadequate vessels can be used in 1-4 weeks prominent vessels Disadvantages clots easily “steal” syndrome more frequent requires needle sticks infection may necessitate removal of graft

46. Temporary Catheters Dual lumen catheter placed into a central vein-subclavian, jugular or femoral. Advantages immediate use no needle sticks Disadvantages high incidence of infection subclavian vein stenosis poor flow-inadequate dialysis clotting Restricts movement

47. Cuffed Tunneled Catheters (Dacron cuff) Dual lumen catheter with Dacron cuff surgically tunneled into subclavian, jugular or femoral vein. Advantages immediate use; *permanent/long term use can be used for patients that can have No other permanent access no needle sticks Disadvantages high incidence of infection poor flows result in inadequate dialysis clotting

48. Above Native fistula (in place for over 20 years) *Remember- assess circulation-listen for bruit, feel for thrill! “Temporary” vascular access catheters- if tunnelled, with Dacron cuff, can be used long-term as Permacath, below. Buttonhole technique-individual cannulates own fistula for home dialysis YouTube video

49. Care of Vascular Access NO BP’s, needle sticks to arm with vascular access. This includes finger sticks. Place ID bands on other arm whenever possible. Palpate thrill and listen for bruit. Teach patient nothing constrictive, feel for thrill.

50. Potential Complications of Hemodialysis During dialysis Fluid and electrolyte related hypotension Cardiovascular arrhythmias Associated with the extracorporeal circuit exsanguination Neurologic Disequilibrium Syndrome & seizures Musculoskeletal cramping Other fever & sepsis blood born diseases