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Acute kidney injury

acute kidney injury
latest kdigo guidelines

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Acute kidney injury

  1. 1. Acute Kidney Injury Siddhesh Kalantri Medicine Unit-1 GNDH Amritsar
  2. 2. Epidemiology • 5–7% of acute care hospital admissions • 30% of admissions to the intensive care unit ( mortality rates may exceed 50%.) •India- community acquired, yet 90% being potentially reversible •Developed nations AKI is almost hospital-acquired occurring in an ICU setting
  3. 3. TOP FIVE CAUSES OF AKI IN INDIA 1. Diarrhoeal diseases. 2. Sepsis: Pregnancy related septicaemia. 3. Acute Malaria- P.falciparum. 4. Drug induced. 5. Hospital Acquired.
  4. 4. Definition: Kidney Disease Improving Global Outcomes (KDIGO)
  5. 5.  Increase in SCr by ≥0.3mg/dl ( 26.5lmol/l) within 48 hours;  Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days;  Urine volume < 0.5ml/kg/h for 6 hours.
  6. 6. Risk Injury Failure Loss of function End-Stage Renal disease Rifle Criteria for stratifying AKI
  7. 7. Risk  Increase in Cr of 1.5-2.0 X baseline or  urine output < 0.5 mL/kg/hr for more than 6 hours. Injury Failure Loss of function End-Stage Renal disease
  8. 8. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for more than 6 hrs Injury  increase in Cr 2-3 X baseline (loss of 50% of GFR) or  urine output < 0.5 mL/kg/hr for more than 12 hours. Failure Loss of function End-Stage Renal disease
  9. 9. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs Failure  increase in Cr rises > 3X baseline Cr (loss of 75% of GFR) or  an increase in serum creatinine greater than 4 mg/dL, or  urine output < 0.3 mL/kg/hr for more than 24 hours or anuria for more than 12 hours. Loss of function End-Stage Renal disease
  10. 10. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours Loss of function  persistent renal failure (i.e. need for dialysis) for more than 4 weeks. End-Stage Renal disease
  11. 11. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours Loss of function: Need for dialysis for more than 4 weeks End-Stage Renal disease  persistent renal failure (i.e. need for dialysis) for more than 3 months.
  12. 12. Classification Patho-Physiological basis :  I. Pre-renal  II. Intrinsic  III. Post-renal
  13. 13. Classification of AKI (ARF) Acute Kidney Injury Pre-renal Intrinsic Post-renal Glomerular Interstitial VascularTubular 55% 40% 5% 85%10%<5% <5%
  14. 14. Oliguric Vis-à-vis Non- oliguric AKI: Non- Oliguric: In hospital set-up, secondary Nephrotoxic agents. Non-oliguric has better prognosis than oliguric one.
  15. 15. ICU vs. Non-ICU AKI:  Non-ICU AKI, in which the kidney is usually the only failed organ, with mortality rates of up to 10%.  ICU AKI is often associated with sepsis and with non-renal multi-organ system failure), with mortality rates of over 50%
  16. 16. Diagnosis  History and Physical examination: Pre-renal:  History: vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.  Examination : Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in prerenal azotemia
  17. 17. Post- Renal: Colicky flank pain radiating to the groin suggests acute ureteric obstruction.  Nocturia and urinary frequency or hesitancy can be seen in prostatic disease. Abdominal fullness and suprapubic pain can accompany massive bladder enlargement. Definitive diagnosis of obstruction requires radiologic investigations.
  18. 18.  Review all medications • Cause of AKI . • Dose Adjustment.  Systemic vasculitis with Glomerulonephritis: • Palpable purpura • Pulmonary hemorrhage, • Sinusitis.  Atheroembolic • Livedo reticularis and other signs of emboli to the legs.  Rhabdomyolysis. • Signs of limb ischemia
  19. 19. Blood Tests  CBC,  BUN/creatinine,  Electrolytes,  Uric acid,  PT/PTT,
  20. 20. Urine Analysis  Volume  Proteinuria  Urinary Indices: FENA and Urinary Sodium  Sediments
  21. 21. Radiologic studies  Renal ultrasound (useful for obstructive forms)  Doppler (to assess renal blood flow)  CT Scan  Pyelography  Nuclear Medicine Scans : DMSA: anatomy. DTPA and MAG3: renal function, urinary excretion and upper tract outflow.
  22. 22. Creatinine is a functional marker of organ damage Functional Markers: Old and Busted
  23. 23. Biomarkers are Foot Prints of Actual Organ Damage Biomarkers, New Hotness
  24. 24. •Cystatin C •Neutrophil gelatinase-associated lipocalin(NGAL) •Interleukin-18 •Kidney injury molecule-1 •N-acetyl-D-glucosaminidase. Important Biomarkers:
  25. 25. Cystatin-C  Superior to serum creatinine, as a surrogate marker of early and subtle changes of kidney function.  It identifies kidney injury while creatinine levels remain in the normal range.  Allows detection of AKI, 24-48 hours earlier than serum creatinine
  26. 26. Kidney Injury Molecule-1 (KIM-1)  KIM-1 is a type 1 trans-membrane glycoprotein  Served as a marker of severity of AKI  Can be used to predict adverse outcomes in hospitalized patients better than conventionally used severity markers.
  27. 27. Neutrophil gelatinase-associated lipocalin(NGAL)  NGAL is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 hours of cardiopulmonary bypass–associated AKI.  Considered equivalent to troponin in acute coronary syndrome.
  28. 28. Complications  Uremia  Hypervolemia and Hypovolemia  Hyponatremia  Hyperkalemia  Hyperphosphatemia and Hypocalcemia  Bleeding  Infections  Cardiac Complications.  Malnutrition
  29. 29. Treatment
  30. 30. General Isssues 1. Optimization of systemic and renal hemodynamics through volume resuscitation and judicious use of vasopressors 2. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs, aminoglycosides) if possible 3. Initiation of renal replacement therapy when indicated
  31. 31. Pre-Renal AKI  Prevention and treatment of prerenal azotemia requires optimization of renal perfusion.  Severe acute blood loss should be treated with packed red blood cells.
  32. 32. FLUIDS  KDIGO suggest using isotonic crystalloids rather than colloids (albumin or starches) .  Colloids may be chosen in some patients to avoid excessive fluid administration in patients requiring large volume resuscitation, or in specific patient subsets (e.g., a cirrhotic patient with spontaneous peritonitis, or in burns).  Colloids- Albumin is renoprotective and Hyperoncotic starch shows nephro- toxicity.
  33. 33. Vasopressors  The Work Group emphasized that vasoactive agents should not be withheld from patients with vasomotor shock over concern for kidney perfusion.  Indeed, appropriate use of vasoactive agents can improve kidney perfusion in volume- resuscitated patients with vasomotor shock.  The use of dopamine was associated with a greater number of adverse events than Nor- epinephrine.
  34. 34. Low Dose Dopamine • Its use has been abandoned by most subsequent to negative results of various studies . • KDIGO recommends not using low-dose dopamine to prevent or treat AKI. (1A)
  35. 35. Cirrhosis and Hepatorenal Syndrome  Albumin may prevent AKI in those treated with antibiotics for spontaneous bacterial peritonitis.  Bridge therapies that have shown promise include terlipressin (a vasopressin analog), combination therapy with octreotide (a somatostatin analog) and midodrine (an α 1-adrenergic agonist), and norepinephrine, all in combination with intravenous albumin (25–50 mg per day, maximum 100 g/d).
  36. 36. Cardio-Renal Syndrome  Optimization of cardiac function .  May require use of inotropic agents, preload- and afterload-reducing agents,antiarrhythmic drugs, and mechanical aids such as an intraaortic balloon pump.
  37. 37. Intrinsic Acute Kidney Injury
  38. 38. Diuretic • Renoprotective : Potentially lessening ischemic injury. • Can also be harmful, by worsening established AKI. • No evidence of incidence reduction. • KDIGO recommend not using diuretics to prevent AKI. (1B) • KDIGO suggest not using diuretics to treat AKI, except in the management of volume overload. (2C) • Indicated only for management of fluid balance, hyperkalemia, and hypercalcemia.
  39. 39. FENOLDOPAM  Fenoldopam mesylate is a pure dopamine type-1 receptor agonist  Without systemic adrenergic stimulation.  No conclusive studies available.  For critically ill patients with impaired renal function, a continuous infusion of fenoldopam 0.1mg/kg/min improves renal function when compared to low dose dopamine.
  40. 40. Erythropoietin • Recent animal studies suggest a potential clinical benefit of erythropoietin in AKI. • The renoprotective action of erythropoietin may be related to pleomorphic properties including antiapoptotic and antioxidative effects, stimulation of cell proliferation, and stem- cell mobilization. • Although one recent RCT in the prevention of human AKI was negative, the usefulness of erythropoietin in human AKI should be further tested in RCTs.
  41. 41. Growth factor intervention • IGF-1 is a peptide with renal vasodilatory, mitogenic and anabolic properties. • KDIGO Work Group recommends against its use in patients with AKI.
  42. 42. Rhabdomyolysis • Aggressive volume repletion (may require 10 L of fluid per day). • Alkaline fluids are beneficial. • Diuretics may be used if fluid repletion is adequate and there is no urinary output. • Dialysis. • Focus on calcium and phosphate status because of precipitation in damaged tissue.
  43. 43. Glomerulonephritis or Vasculitis • May respond to immunosuppressive agents and/or plasmapheresis . • Allergic interstitial nephritis due to medications requires discontinuation of the offending agent. • Glucocorticoids have been used, but not tested in randomized trials. • AKI due to scleroderma (scleroderma renal crisis) should be treated with ACE inhibitors.
  44. 44. Aminoglycoside Induced AKI • KDIGO suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephro - toxic, therapeutic alternatives are available. • Avoid in high risk patients age more than 65 years, DM, cases of septic shock. • KDIGO suggests using single dose daily rather than multiple- dose daily treatment regimens. • It also suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible .
  45. 45. AMPHOTERICIN B NEPHROTOXICITY • KDIGO suggest using lipid formulations of amphotericin B rather than conventional formulations of amphotericin B. • KDIGO recommend using azole antifungal agents and/or the echinocandins rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed. • Some studies indicate that the liposomal form of amphotericin B is less nephrotoxic than amphotericin B lipid complex or amphotericin B colloidal dispersion.
  46. 46. Postrenal  Prompt relief of urinary tract obstruction.  Relief of obstruction is usually followed by an appropriate diuresis and may require continued administration of intravenous fluids and electrolytes for a period of time.
  47. 47. Indications for Dialysis  A – Acidosis  E – Electrolyte disturb., usually hyperkalemia  I – Intoxications (lithium, ethylene glycol, etc)  O – Overload (volume overload)  U – Uremia (symptoms, signs )
  48. 48. Modes Of Dialysis  Hemodynamically stable- IHD  Hemodynamically unstable 1. CRRT 2. PD 3. SLED (Slow Low-efficiency dialysis).
  49. 49. Prognosis  Pre-renal and Post- renal better prognosis.  Kidneys may recover even after dialysis requiring AKI.  10% of cases requiring dialysis develop ckd.  Die early even after kidney function recovers completely.
  50. 50. Carry Home Message  Diagnose early – Biomarkers have great potential.  Look for Aetiology.  Prevent rather than treat.  No role of low dose dopamine, diuretics in prevention and treatment.  Initiate RRT when indicated.
  51. 51. Thank You

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