MANAGEMENT OF ACUTE RENAL FAILURE

1. MANAGEMENT OF ACUTE RENAL FAILURE PROF.DR M.ABDELAZIZ CLINICAL PHARMACOLOGY COLLEGE OF MEDICINE

2. . • Human beings are essentially big bags of water, the volume of which must be kept under tight control, to prevent us from either drying out or drowning…..

3. Highlights… • FOLLOWING THE TRENDS…. • CAPTURE THE KEYS TO OPEN THE DOOR • HOW TO PREVENT ARF • REPLACING KIDNEY […very difficult]

4. ‘ACUTE KIDNEY INJURY’ • Abrupt reduction [<48 hrs] in kidney function, defined as an absolute increase in S creatinine of ≥0.3 mg/dL • A percentage increase in S creatinine of ≥ 50% [1.5 fold from baseline] or • a reduction in urine output-- documented oliguria of < 0.5 ml/kg/hr, for more than six hours.

5. STAGING SYSTEM FOR A.K.I.

6. RIFLE criteria

7. CLASSIFICATION

8. PRERENAL ARF • Most common • Renal hypo perfusion • Important form in perioperative period

9. .

10. HYPOVOLEMIA- extrinsic

11. HYPOVOLEMIA- intrinsic • Tubuloglomerular feedback • Afferent arteriolar vasodilatation • Preferential efferent arteriolar vasoconstriction Aim is to utilize the existing filtration reserve maximally

12. In short…. • EXTRINSIC INCREASE MAP, IMPROVE INTRAVASCULAR VOLUME • INTRINSIC IMPROVE RENAL PLASMA FLOW, GFR & GLOMERULAR PRESSURE

13. When the insult cross the limits…. • Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall • Decreased O2 delivery needs to decrease its work decrease filtration oliguria • Increased Na reabsorption = more work by medulla blood flow towards medulla ,i.e. away from cortex GFR decrease oliguria • “acute renal success” • Increase perfusion pressure • If we wait …..ATN

14. INTRINSIC ARF

15. Ischemic ATN

16. The so called diuretic phase… • Recovery phase • Filtration recovers early • Recovery of epithelial function lags behind

17. Nephrotoxic ATN RISK FACTORS • Advanced age • Preexisting kidney disease • Hypovolemia • CCF • Multiple myeloma

18. Toxins….

19. Contrast nephropathy

20. POSTRENAL ARF • Obstruction is always the most likely cause when there is anuria • B/L ureteric • U/L ureteric if single functioning kidney • Bladder neck obstruction • Urethral

21. Perioperative oliguria - pathophysiology • Anesthetic agents: no renal vasodilation per se ; effects by reducing CO & BP • EDB & high spinal anesthesia reduce sympathetic tone • PPV decrease renal blood flow • ACE-I cause significant reduction in perfusion pressure during anesthesia • Narcotics can increase ADH response

22. Clinical features

23. Pre renal • vomiting , diarrhoea • Intestinal obstruction…. • Carry over cases..NPOOOOOOO Look for • Thirst • Reduced JVP • Decreased skin turgor • Dry mucus membrane

24. Intrinsic renal • oliguria,edema,hypertension AGN • Intake of nephrotoxic drugs • h/o atrial fibrillation : renal artery thrombus • h/o vascular surgeries : atheroembolic ARF • Muscle trauma : rhabdomyolysis

25. Post renal • Anuria • Flank pain • h/o prostatic disease

26. INVESTIGATIONS

27. URINE MICROSCOPY

28. Assessment of GFR

29. Blood urea • 15-40mg/dL • Increased in dehydration , post G-I bleed • May be a better guide in timing dialysis to avoid uremic complications

30. Serum creatinine • Normal: <1.5 mg/dL • Overestimate GFR • Lags behind renal injury & recovery • Rise by 1-2 mg/dL in ARF,>2mg/dL in rhabdomyolysis • Critically ill patient: a “normal” value may not be normal

31. Creatinine clearance • Volume of plasma cleared off creatinine per unit time • Earlier warnings, 2hr samples • [140-age] x body wt / S.Creatinine x 72 • 91-130 ml / min • CrCl = U. Creatinine [mg/dL] x volume [mL/min] • P Creatinine[mg/dL] • S cystatin C

32. Assessment of tubular function • Renal Failure Indices

33. Assessment of tubular function • Differentiate pre renal from intrinsic renal failure • FeNa is the most useful • Ratio of Na clearance to Creatinine clearance • Prerenal intact tubules Na reabsorption avidly takes place  Cr Cl high FENa <1 • ATNNa absorption impaired FENa > 1 • CKD & diuretics also FENa >1 • Metabolic alkalosis  FECl better

34. Radiology • Abdominal USG • Small  Htve Nephrosclerosis , CRF • Normal / large DM , Amyloidosis • Large kidneys with large dilated pelvis and ureters • Pyelography : localization • MRA/ Doppler US : arterial /venous obstruction

35. Others • renal biopsy • Increased potassium ,phosphorus , CK-MM, Uric Acid, decreased Calcium rhabdomyolysis

36. Complications • .

37. Complications • .

38. Complications • .

39. Also… • hyperphosphatemia • Infection • Uremic syndrome • Hypovolemia due to vigorous diuresis in recovery

40. Prevention of ARF- in perioperative period

41. Avoid nephrotoxins • ACE-I & ARB • NSAIDs • AMINOGLYCOSIDES • AMPHOTERICIN-B • CISPLATIN • ASPIRIN • CYCLOSPORIN • LMW-DEXTRAN • ACYCLOVIR,INDINAVIR • METHOTREXATE

42. Management of AKI 1. Prevention: • Because there are no specific therapies for ischemic or nephrotoxicAKI, Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients, such as the elderly and those with preexisting renal insufficiency.

43. • Indeed, aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma, burns, or cholera prevention is of paramount importance.

44. The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR; for example, reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment

45. Preliminary measures • Exclusion of reversible causes: Obstruction should be relived , infection should be treated • Correction of prerenal factors: intravascular volume and cardiac performance should be optimized

46. Maintenance of urine output: Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form. • High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses

47. Specific Therapies: • To date, there are no specific therapies for established intrinsic renal ARF due to ischemia or nephrotoxicity. • Management of these disorders should focus on elimination of the causative hemodynamic abnormality or toxin, avoidance of additional insults, and prevention and treatment of complications. • Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology.

48. Prerenal ARF: • The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid. • Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells, whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (e.g., burns, pancreatitis).

49. Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic. Hypotonic solutions (e.g., 0.45% saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses, although isotonic saline may be more appropriate in severe cases

50. Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids. Serum potassium and acid-base status should be monitored carefully.