Renal Megan McClintock, RN, MS 10/27/11

1. RenalMegan McClintock, RN, MS10/27/11 “TO PEE IS TO LIVE”

2. "Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But should the kidneys fail … neither bone, muscle, gland, nor brain could carry on.” • Smith HW: Fish to philosopher, Boston, 1953, Little, Brown.

3. Chronic kidney disease (CKD) KIDNEY DISEASE Acute kidney injury (AKI) Sudden onset Acute decrease in urine output and/or increase in creatinine Potentially reversible Mortality 60% Usually die from infection Gradual onset GFR < 60 mL/min for > 3 months Progressive and irreversible Mortality 19-24% (need dialysis to survive) Usually die from CV disease

4. ACUTE KIDNEY INJURY • Prerenal causes – external to the kidney, sudden reduction in blood flow to the kidneys • Usually resolve quickly with correction of cause • Intrarenal causes – infections, toxins, drugs, or direct trauma, ATN • Postrenal causes –urinary tract obstructions • Usually resolve quickly with correction of cause

5. ACUTE KIDNEY INJURYCLINICAL COURSE • Oliguric Phase (10-14 days) • Urine output less than 400 mL/day • UA w/ casts, RBCs, WBCs, SG fixed at 1.010, urine osmo of 300 mOsm/kg (may have proteinuria) • Volume depletion but oftentimes fluid retention • Metabolic acidosis • Sodium imbalance • Potassium increase • Hematologic disorders • Waste product accumulation • Neuro disorders

6. ACUTE KIDNEY INJURY CLINICAL COURSE • Diuretic Phase (1-3 weeks) • Begins with a gradual increase in daily urine output to 1-3 L • Nephrons still not fully functional • Kidneys can excrete waste, but still can’t concentrate the urine • Hypovolemia • Hypotension • Hyponatremia, hypokalemia

7. ACUTE KIDNEY INJURY CLINICAL COURSE • Recovery Phase (12 months) • Begins when the GFR increases • BUN and creatinine plateau, then decrease

8. ACUTE KIDNEY INJURYTREATMENT • Eliminate the cause, manage signs & symptoms, prevent complications • #1 goal is to ensure adequate cardiac output and intravascular volume • Careful monitoring of I/Os • Prevent hyperkalemia • Use RRT (renal replacement therapy) only if needed • Nutritional management

9. ACUTE KIDNEY INJURYTREATMENT • Avoid exposure to contrast media • Watch for nephrotoxic drugs • ACE inhibitors • Meticulous aseptic technique • Meticulous skin care • Meticulous mouth care

10. ACUTE KIDNEY INJURYNURSING DIAGNOSES • Decreased cardiac output • Excess fluid volume • Risk for infection • Imbalanced nutrition: less than body requirements • Fatigue • Anxiety • Dysrhythmias • Sensory/perceptual alterations

11. CHRONIC KIDNEY DISEASE

12. CHRONIC KIDNEY DISEASE • Frequently asymptomatic • Early on have no change in urine output, may even have polyuria • Uremia develops when GFR is <10 mL/min • Persistent proteinuria • Tend to die of CV disease before needing dialysis

13. Fig 45-3 clinical manisfestations of chronic uremia

14. CHRONIC KIDNEY DISEASETREATMENT • Treat high potassium • Control HTN • Treat anemia (EPO) • Treat hyperlipidemia • Restrict proteins • Restrict fluids • Restrict sodium, potassium, phosphates • Lots of teaching and reteaching

15. TREATING HYPERKALEMIA • Insulin • Sodium Bicarbonate • Calcium Gluconate IV • Dialysis • Sodium Polystyrene Sulfonate (kayexalate) • Dietary Restriction

16. Dialysis Peritoneal Dialysis (PD) Hemodialysis (HD)

22. PERITONEAL DIALYSIS • Three phases of PD • Manual vs Continuous • Complications

25. Fig 45-12 Temporary catheters Fig 45-13 placement of jugular vein temporary dialysis catheter

26. Fig 45-14 components of hemodialysis system

28. HEMODIALYSIS • Pre & Post Dialysis Interventions • Complications • Hypotension • Muscle cramps • Blood loss • Hepatitis

29. PYELONEPHRITIS • Cause – Bacteria (most common) • S/S – abrupt onset of chills, fever, vomiting, malaise, CVA pain, dysuria, urinary urgency and frequency • Labs – UA w/ pyuria, bacteriuria, hematuria, WBC casts; CBC w/ left shift (increase in bands) • Cx – Urosepsis leading to septic shock and death, chronic pyelonephritis

30. Pyelonephritis: glomerular hemorrhage

31. Pyelonephritis - papillary necrosis

32. PYELONEPHRITIS INTERVENTIONS • Early tx for cystitis • Take antibiotics as prescribed • Follow-up urine culture • Drink at least 8 glasses of fluid daily • Rest

33. GLOMERULONEPHRITIS • Cause – Antibody-induced injury (exposure to drugs, immunizations, microbial/viral infxn) • S/S – generalized edema, HTN, oliguria, hematuria, proteinuria, abd/flank pain • Labs – UA w/ proteinuria, hematuria, WBC casts; increased BUN and creatinine, ASO titer • Cx – Renal insufficiency, destruction of renal tissue

34. GLOMERULONEPHRITIS INTERVENTIONS • REST • Diuretics, restricted sodium and fluids • Restrict dietary protein if in BUN. • Treat severe HTN with anti-hypertensives • No abx unless infection still present • Prevention - Take the FULL course of antibiotics (treat strep)

35. NEPHROTIC SYNDROME • Cause – systemic disease, allergens, drugs, infxn, glomerulonephritis • S/S – edema, massive proteinuria, HTN, hypoalbuminemia, hyperlipidemia • Labs – low albumin, low protein, high cholesterol • Cx – Infection, thromboembolism, skin breakdown, malnourishment, body image problems

38. NEPHROTIC SYNDROME INTERVENTIONS • ACE inhibitors, corticosteroids, diuretics, lipid-lowering agents • Low sodium, low-moderate protein diet (focus on preventing malnutrition) • Strict I/Os, daily weights • Protect skin • Prevention of infection

39. Minute paper • On the provided 3x5 card answer the following: • What was the most important thing you learned today. • What important point remains unclear to you?