1 / 45

renal training

renal training. Judith Coombes Pharmacist Princess Alexandra Hospital And School of pharmacy University of Queensland Material provided by Jo Sturtevant Renal and Transplant pharmacist Princess Alexandra Hospital and Graham Davies, Kings College London.

ziazan
Télécharger la présentation

renal training

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. renal training Judith Coombes Pharmacist Princess Alexandra Hospital And School of pharmacy University of Queensland Material provided by Jo Sturtevant Renal and Transplant pharmacist Princess Alexandra Hospital and Graham Davies, Kings College London

  2. “a significant % of patients with renal impairment are admitted to hospital on inappropriately high doses of drugs, with a high fractional renal excretion and low therapeutic index” (Pillans et al 2003)

  3. DRUG USE IN RENAL DISEASE • OBJECTIVES • At the end of this series of lectures, students should be able to: • Identify patients who are at risk of renal failure • Describe how a patient’s renal function should be monitored • Classify renal function • Describe the influence of renal failure on drug pharmacokinetics • List the drugs commonly associated with renal failure • Describe the treatment of the complication of chronic renal failure

  4. At risk patients • Elderly – Glomerular Filtration Rate (GFR) may be significantly reduced due to ↓ muscle mass and protein intake even though creatinine is within normal range. • Transplant patients – all antirejection drugs • Diabetics • Congestive Heart Failure

  5. Multiple co-morbidities & complex frequently changing medication regimens = unwanted effects drug interactions confusion

  6. MONITORING PATIENTS’ DRUG THERAPY • ROLE OF THE PHARMACIST • Efficacy of treatment, e.g.Oedema and weight following diuretic therapy • BP following antihypertensive therapy • Adjust drug dosing regimens in line with renal status, e.g. antibiotics • 3. Monitor renal function of patients receiving nephrotoxic agents

  7. CLASSIFICATION OF RENAL FILURE Appendix 3 : BNF

  8. MONITORING PATIENTS’ RENAL FUNCTION • Patient’s clinical condition • Biochemical Data • Other biochemical abnormalities

  9. 2(a) Serum Creatinine (40 to 120 Micromoles/Litre) Increased by: • Large muscle mass, dietary intake • Drugs Interfere with analysis (Jaffe reaction) e.g. methyldopa, levodopa, dexamethasone, cephalosporins Inhibit tubular secretion e.g. cimetidine, trimethoprim, aspirin • Ketoacidosis Decreased by: • Reduced muscle mass (elderly) • Severe renal disease (increased secretion) • Cachexia / starvation • Immobility • Pregnancy

  10. 1(a). Clinical Assessment

  11. Dosing in kidney impairment What should I use??

  12. Predicting GFR using serum and urine creatinine concentrations. Cockcroft and Gault Equation GFR = F (140 – age [yrs]) Ideal Body Wt (kg) Serum creatinine (mol/L) Where: F = 1.23 for males and 1.04 for females IBW = 50 kg + 2.23 kg for every 1” > 5 feet in height (male) IBW = 45.5 kg + 2.3 kg for every 1” > 5 feet in height (female)

  13. Examples – estimating renal function using serum creatinine. Patient details Mr JB 75 yr old gentleman admitted to the renal unit with a longstanding history of NIDDM and hypertension. Ideal body weight = 80 kg, serum creatinine = 400 mol/L, urine creatinine = 3.7 mmol/L, 24 hr urine volume = 2400 mls Method 1: British National Formulary Appendix 3 Classification GFR (mls/min/1.73m2) Serum Creatinine (mol/L) Mild 20 to 50 150 to 300 Moderate 10 to 20 300 to 700 Severe < 10 > 700

  14. Patient details Mr JB 75 yr old gentleman admitted to the renal unit with a longstanding history of NIDDM and hypertension. Ideal body weight = 80 kg, serum creatinine = 400 mol/L, urine creatinine = 3.7 mmol/L, 24 hr urine volume = 2400 mls Method 2: Cockcroft and Gault Equation GFR = 1.23 (140 – (age) 75) x 80 400 = 1.23 x 65 x 80 400 = 13 x 1.23 = 16 ml/min = Moderate renal impairment

  15. Limitations of Cockcroft-Gault equation • Accurate only when renal function is stable • Inaccurate when serum creatinine values > 450 mol/L • Becomes inaccurate when GFR < 20 mls/min • Not valid in pregnancy Limitations of creatinine as a marker: • Retrospective indicator of renal function • May only increase when < 50% of nephrons not functioning

  16. Method 3: 24 hr urine collection Urine is collected over 24 hours (or 12 hours) Blood sample taken at the midpoint of the collection period and creatinine measured GFR (mls/min) = UV P Where: U = urine creatinine concentration (mol/L) V = volume of urine collected (mls) P = serum creatinine concentration (mol/L)

  17. Dosage Adjustment Mr JB 75 yr old gentleman admitted to the renal unit with a longstanding history of NIDDM and hypertension. Ideal body weight = 80 kg, serum creatinine = 400 mol/L, urine creatinine = 3.6 mmol/L, 24 hr urine volume = 2400 mls What dose of:- • Ciprofloxacin would you recommend for a UTI? • Metformin would you recommend for NIDDM? Patient has moderate renal impairment

  18. Dosage Adjustment in Renal Impairment

  19. Serum Urea (BUN – blood urea nitrogen) (2.5 – 7.5 mmoles/Litre) Limitations as a marker: • It varies with the dietary protein intake • Reabsorbed by the tubules • Reabsorption varies with urine flow. Its clearance is independent of GFR at low urine flow rates Factors increasing serum urea • High protein diet • Hypercatabolic conditions e.g. severe infection, burns, hyperthyroidism • Gastrointestinal bleeding • Muscle injury • Drugs e.g. Glucocorticoids (with catabolism) Tetracycline • Hypovolaemia Factors decreasing serum urea • Malnutrition • Liver disease • Sickle cell anaemia

  20. . Other biochemical abnormalities seen in renal impairment a) Raised Serum Potassium (3.5 to 5 mmol/L) When GFR < 5 ml/min – hyperkalaemia develops When serum potassium > 7 mmol/L – life threatening b) Raised Serum Phosphate (0.8 to 1.2 mmol/L) Chronic Renal Failure leads to hyperphosphataemia c) Decreased Serum Calcium (2.2 to 2.6 mmol/L) Linked to vitamin D production Patients with CRF are typically hypocalcaemic

  21. Managing Complications • Hypertension • Fluid retention • Electrolyte control - Potassium • - Calcium & Phosphate • Anaemia

  22. 1.Principle Drug Classes used in initial treatment of Hypertension • Diuretics (thiazides) • Beta blockers • ACE-I • AT II receptor antagonists • Calcium channel blockers • Alpha adrenergic blockers

  23. 2 FLUID RETENTION • Fluid restriction - 800 to 1000 ml/day • Low salt diets • Loop diuretics Oral Frusemide Effective when GFR as low as 5 ml/min • Thiazides – ineffective (as a diuretic) if GFR < 25 ml/min • Metolazone – synergism with loop diuretics – short term therapy • Avoid potassium sparing diuretics - hyperkalaemia

  24. 3 ELECTROLYTE DISTURBANCES 1. HYPERKALAEMIA (Normal serum concentration 3.5 to 5.0 mmol/L) • Mainly excreted by active tubular secretion • Small contribution from aldosterone • When GFR < 5 ml/Min potassium raises rapidly • Life-threatening condition when > 7 mmol/L – cardiac arrhythmias (peaked T-waves)

  25. Electrolyte Disturbances 4. CALCIUM AND PHOSPHATE BALANCE • Normal serum values : Calcium 2.2 to 2.6 mmol/L Phosphate 0.8 to 1.2 mmol/L • Deficiency in vitamin D synthesis – hypocalcaemia • Decreased phosphate clearance – hyperphosphotaemia- deposits on coronary arteries

  26. Electrolyte Disturbances 2. CALCIUM AND PHOSPHATE BALANCE TREATMENT • Active Vitamin D alfacalcidol or calcitriol • Oral phosphate binders – complex phosphate in GIT Calcium Carbonate or Aluminium Hydroxide • Dietary control

  27. EPO THERAPY WHEN Hb<11-12g/dl Hct <33-37%

  28. Chronic Renal Failure – a typical prescription • Oral hypoglycaemic or insulin – often • Antihypertensive – often needed (ACEI should be considered early) • Loop diuretic – control fluid balance (especially as disease progresses) • Phosphate binder – beware binding of drugs prescribed • Active Vitamin D – calcitriol or alfacalcidol • Iron supplementation – according to degree of anaemia • EPO – according to degree of anaemia • Ion-exchange resins – to bind potassium (usually end-stage renal impairment only) - avoid potassium sparing drugs - consider influence of resin on bioavailability of other drugs

  29. Is the patient on dialysis? • What type of dialysis are they on? • Haemodialysis • Continuous Ambulatory Peritoneal Dialysis (CAPD) • CVVHD

  30. Haemodialysis Access "Access” is the term used to describe the way we “tap” into your blood stream. • Fistula - the most common access used. Created by joining your artery and vein together under the skin. • Graft - the use of synthetic material to join an artery to a vein. • Vascath or Permacath - a catheter surgically placed in a neck or leg vein

  31. How does it work? 1. Sterile dialysis fluid is drained into the peritoneal cavity. 2. Glucose (sugar) in the dialysis fluid attracts excess water from the blood into the peritoneal cavity.

  32. How does it work? 4. Waste products such as creatinine and urea also filter into the dialysis fluid. 5. Drain out the old fluid and re-fill.

  33. Pharmacists Role “ EDUCATE, ACHIEVE MAXIMUM EFFICACY PREVENT HARM”

  34. NSAID/Metformin counselling • Patients should cease NSAIDS/metformin if they are in a situation where they may become dehydrated: • vomiting • diarrhoea • sepsis • pre-surgery • excessive exercise • If on metformin they should seek medical advice

  35. Metformin induced lactic acidosis • Metformin largely eliminated via kidneys • Metformin increases production and decreases clearance of lactate • Impaired ability of liver to remove lactate as pH falls • Hepatic conversion of lactate to glucose impeded.

  36. Metformin induced lactic acidosis • Typically occurs in patients with renal impairment. • Other pre-disposing factors: • high dose • chronic hepatic disease • severe cardiovascular disease • severe pulmonary insufficiency • alcohol abuse • increasing age • nephrotoxic medication (contrast) • surgery (cease 2/7 before)

  37. Group 4 • Mrs HR • 78 years, wt 57kg • Admitted to outlying hospital acute exacerbation COPD • Baseline Cr 80mol/L • Charted gentamicin 160mg daily for 5/7 • CrCl = 45ml/min • What action would you take? Level after 1st dose

  38. 21/6 Gent level still 1.4!!!! • 23/6 complaining of dizziness, unsteady feeling, vestibular symptoms, vomiting • 1/7 Cr 0.21 recovering

  39. Summary • Identify at risk patients • Know which drugs are renally cleared • Reduce doses accordingly • Empower the patient

More Related