Renal Failure and Treatment

1. Renal Failure andTreatment Vicky Jefferson, RN, CNN Capital Dialysis of Texas

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. Renin secretion and the regulation of volume and composition of extracellular fluid. Excretion Blood pressure control Vitamin D activation Acid-base balance regulation. Erythropoietin production Urine formation Functions of the Kidneys

4. Renin • Renin is important in the regulation of blood pressure. • It is released from the granular cells of the efferent arteriole in response to decreased arteriole blood pressure, renal ischemia, extracellular fluid depletion, increased norepinephrine, and increased urinary Na+ concentration.

5. Blood Pressure Regulation 4 mechanisms are involved • Volume control • Aldosterone effect • Renin-angiotensin-aldosterone • Renal prostaglandin

6. Prostaglandin Prostoglandins (PGs)- synthesized by most body tissues. In the kidney, PGs are synthesized in the medulla and have a vasodilating action and promote Na+ excretion. PGs counteract the vasoconstrictor effect of angiotensin and norepinephrine. Renal PGs systemically lower blood pressure by decreasing systemic vascular resistance.

7. Vitamin D • Acquired by the body through diet or through synthesis by ultraviolet radiation on the cholesterol in the skin. • The liver and the kidney make the vitamin active in the body.

8. Erythropoietin • Erythropoietin is produced and released by the kidneys in response to decreased oxygen tension in the renal blood supply that is created by the loss of red blood cells. • Erythropoietin stimulates the production of RBCs in the bone marrow. • Erythropoietin deficiency leads to anemia in renal failure.

9. RBC Synthesis & Maturation Kidney secrete Erythropoietin, it stimulates the bone marrow to produce RBC’s •  in oxygen delivery simulates release • in response the RBC count rises in 3 - 5 days • speeds the maturation of RBC’s

10. Acid Base Balance Kidneys regulate acid-base balance by stabilizing body fluid volume & flow rate to enhance the reabsorption or excretion of bicarbonate & hydrogen ions

11. Electrolyte Regulation • Sodium • Potassium • Calcium Need to Know: • Phosphate Normal Values • Magnesium Functions • Chloride Factors affect

12. Excretion of Metabolic Waste • Over 200 waste products excreted • Only 2 are used for clinical assessment • BUN • Creatinine

13. Excretion of Metabolic Waste • Over 200 waste products excreted • Only 2 are used for clinical assessment • BUN • Creatinine

14. BUN • Normal 8 - 20 mg/dl • Nitrogenous waste product of protein metabolism • Unreliable in measurement of renal function • Relevance is assessed in conjunction with Creatinine

15. Factors Affecting BUN • Urine flow • low renal perfusion • Volume depletion • Metabolic rate • Protein metabolism • Drugs

16. Creatinine • A waste product of muscle metabolism • Normal value0.6 - 1.5 mg/dl • 2 times normal = 50% damage • 8 times normal = 75% damage • 10 times normal = 90% damage • Exception - severe muscular disease can greatly  Creatinine levels

17. Diagnostic Tools for Assessing Renal Failure • Blood Tests • BUN elevated (norm 10-20) • Creatinine elevated (norm 0.7-1.3) • K elevated • PO4 elevated • Ca decreased • Urinalysis • Specific gravity • Protein • Creatinine clearance

18. Diagnostic Tools • Biopsy • Ultrasound • X-Rays

19. Acute Renal Failure (ARF) • Sudden onset - hours to days • Often reversible • Severe - 50% mortality rate overall; generally related to infection.

20. Characteristics of ARF • Homeostatic functions affected most • Electrolyte imbalances • Volume regulation • Blood pressure control • Endocrine functions affected lease • Require time to evolve • Renal size is preserved • Evidence of acute illness or insult exists

21. Chronic Renal Failure • Slow progressive renal disorder related to nephron loss, occurring over months to years • Culminates in End Stage Renal Disease

22. Characteristics of Chronic Renal Failure • 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

23. Causes of Chronic Renal Failure • Diabetes • Hypertension • Glomerulonephritis • Cystic disorders • Developmental - Congenital • Infectious Disease

24. Causes of Chronic Renal Failure • Neoplasms • Obstructive disorders • Autoimmune diseases • Lupus • Hepatorenal failure • Scleroderma • Amyloidosis • Drug toxicity

25. Stages of Chronic Renal FailureOld System • Reduced Renal Reserve • Renal Insufficiency • End Stage Renal Disease (ESRD)

26. Stages of Chronic Renal FailureNKF Classification System Stage 1: GFR > 90 ml/min despite kidney damage

27. Stages of Chronic Renal FailureNKF Classification System 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.

28. During Stage 1 - 2 • No symptoms • Serum creatinine doubles • Up to 50% nephron loss

29. Stages of Chronic Renal FailureNKF Classification System Stage 3:Moderate reduction (GFR 30 – 59 ml/min) 1. Calcium absorption decreases 2. Malnutrition onset 3. Anemia secondary to Erythropoietin deficiency 4. Left ventricular hypertrophy

30. Stages of Chronic Renal FailureNKF Classification System Stage 4: Sever reduction (GFR 15 – 29 ml/min) 1. Serum triglycerides increase 2. Hyperphosphatemia 3. Metabolic acidosis 4. Hyperkalemia

31. During Stage 3 - 4 • Signs and symptoms worsen if kidneys are stressed • Decreased ability to maintain homeostasis

32. During stages 3 - 4 • 75% nephron loss • Decreased: glomerular filtration rate, solute clearance, ability to concentrate urine and hormone secretion • Symptoms: elevated BUN & Creatinine, mild azotemia, anemia

33. Stages of Chronic Renal FailureNKF Classification System Stage 5: Kidney failure (GFR < 15 ml/min) 1. Azotemia

34. During Stage 5 • Residual function < 15% of normal • Excretory, regulatory and hormonal functions severely impaired. • metabolic acidosis • Marked increase in: BUN, Creatinine, Phosphorous • Marked decrease in: Hemoglobin, Hematocrit, Calcium • Fluid overload

35. During Stage 5 • Uremic syndrome develops affecting all body systems • can be diminished with early diagnosis & treatment • Last stage of progressive CRF • Fatal if no treatment

36. What happens when the kidneys don’t function correctly?

37. Manifestations of CRF -Nervous System • Mood swings • Impaired judgment • Inability to concentrate and perform simple math functions • Tremors, twitching, convulsions • Peripheral Neuropathy • restless legs • foot drop

38. Manifestations of CRFSkin • Pale, grayish-bronze color • Dry scaly • Severe itching • Bruise easily • Uremic frost

39. Manifestations of CRFEyes • Visual blurring • Occasional blindness

40. Manifestations of CRF Fluid - Electrolyte - pH • Volume expansion and fluid overload • Metabolic Acidosis • Electrolyte Imbalances • Hyperkalemia

41. Manifestations of CRFGI Tract • Uremic fetor • Anorexia, nausea, vomiting • GI bleeding

42. Manifestations of CRF Hematologic • Anemia • Platelet dysfunction

43. Manifestations of CRF Musculoskeletal • Muscle cramps • Soft tissue calcifications • Weakness • Related to calcium phosphorous imbalances

44. Calcium-Phosphorous Balance

45. Manifestations of CRFHeart - Lungs • Hypertension • Congestive heart failure • Pericarditis • Pulmonary edema • Pleural effusions

46. Manifestations of CRF Endocrine - Metabolic • Erythropoietin production decreased • Hypothyroidism • Insulin resistance • Growth hormone decreased • Gonadal dysfunction • Parathyroid hormone and Vitamin D3 • Hyperlipidemia

47. Treatment Options • Hemodialysis • Peritoneal Dialysis • Transplant • Nothing

48. Hemodialysis • Removal of soluble substances and water from the blood by diffusion through a semi-permeable membrane.

49. History • Early animal experiments began 1913 • 1st human dialysis 1940 by Dutch physician Willem Kolff (2 of 17 patients survived) • Considered experimental through 1950’s, No intermittent blood access; for acute renal failure only.

50. History cont’d • 1960 Dr. Scribner developed Scribner Shunt • 1960’s Machines expensive, scarce, no funding. • “Death Panels” panels within community decided who got to dialyze.