1. AETIOPATHOGENESIS & MANAGEMENT OF ACUTE RENAL FAILURE

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. DEFINITION Acute renal failure (ARF) or acute kidney injury (AKI), as it is now referred to in the literature, is defined as an abrupt or rapid decline in renal filtration function. This condition is usually marked by a rise in serum creatinine concentration or azotemia (a rise in blood urea nitrogen [BUN] concentration). However, immediately after a kidney injury, BUN or creatinine levels may be normal, and the only sign of a kidney injury may be decreased urine production

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. STAGES.CREATININE CRITERIA URINE OUTPUT CRITERIA 1INCREASE IN S.CREATININE ≥0.3mg/dL OR INCREASE TO ≥ 150- 200% FROM BASELINE 6HRS 2INCREASE IN S.CREATININE TO >200- 300%[2-3 FOLD] FROM BASELINE 12 HRS 3INCREASE IN S. CREATININE TO >300%[>3 FOLD] FROM BASELINE OR S.CREATININE OF ≥4mg/dL WITH AN ACUTE INCREASE OF ATLEAST 0.5 mg/dL <0.3ml/kg/hr FOR 24 HRS OR ANURIA FOR 12 HRS

6. RIFLE Classification System

7. Risk factors Baseline renal insufficiency DMCHF Large volume of contrast NSAIDs or ACEI Volume depletion

8. CLASSIFICATION PRERENAL ARFINTRINSIC ARFPOSTRENAL ARF

9. PRERENAL ARF as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons GFR is reduced as a result of hemodynamic disturbances that decrease glomerular perfusion.

10. . CAUSES-PRERENAL ARF HYPOVOLEMIA >HEMORRHAGE >G-I LOSSES >DECREASED INTAKE >URINARY LOSSES >SKIN LOSSES >OTHERS:BURNS,PANCREATITIS,SEVERE HYPOALBUMINEMIA

11. INTRINSIC ARF The so called diuretic phase… Recovery phase Filtration recovers early Recovery of epithelial function lags behind

12. CAUSES ISCHEMIA >MAJOR CARDIOVASCULAR >TRAUMA >HEMORRHAGE >HYPOVOLEMIA TOXINS Exogenous: Antibiotics-Aminoglycosides,Chemotherapeutic agents-Cisplatin, Endogenous: myoglobin,hemoglobin,calcium,bilirubinSEPSIS INTERSTITIUM Allergic: Antibiotics : b-lactam,quinolone, rifampin NSAIDs B/L pyelonephritis INTRATUBULAR OBSTRUCTION acyclovir, methotrexate, indinavir, myeloma proteins

13. POSTRENAL ARF Obstruction is always the most likely cause when there is anuria Bladder neck obstruction

14. 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”

15. Clinical features

16. Pre renal vomiting, diarrhoea Intestinal obstruction…. Look for Thirst Reduced JVP Decreased skin turgor Dry mucus membrane

17. Intrinsic renal oliguria,edema,hypertension Intake of nephrotoxic drugs atrial fibrillation

18. Post renal Anuria Flank pain

19. INVESTIGATIONS

20. Laboratorium Urine microscopic Assessment GFR Radiology (Abdominal USG, Pyelography, MRA)

21. Assessment of GFR

22. Blood urea 15-40mg/dL Increased in dehydration, post G-I bleed

23. Serum creatinine Normal: <1.5 mg/dL Rise by 1-2 mg/dL in ARF

24. 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

25. INTERVENTION Hemodynamic &urinary output monitoring Aggressive fluid loading Adequate oxygenation Pharmacologic strategies Renal replacement therapy

26. Hemodynamic &urinary output monitoring Blood pressure CVP PAWP Urine output  ensure catheter is not compressed  ensure good urine flow from start  monitor output hourly  ensure output >1ml/kg/hr

27. Aggressive fluid loading Trauma Compartment syndrome Limb revascularization ….high chance for rhabdomyolysis

28. Pharmacologic strategies

29. Mannitol Improve urinary flow Pulmonary edema, intra renal vasoconstriction, Aortic surgeries, Renal transplantation, CABG 6.25-12.5g is given 15 mins prior to the defined insult / repeated 4-6 hrs 24 hr cumulative dose not >1.5 mg/kg

30. Furosemide Renal vasodilation Shouldn’t be given if pt is not adequately fluid loaded 2-10 mg/kg for converting oliguric to non oliguric renal failure Continuous infusion 1-10mg/hr after a LD of 10- 20mg

31. others Metabolic acidosis: NaHCO3 to keep its level >15mmol/L or pH >7.2 Hyperphosphatemia :Ca carbonate, Al(OH)3 Hypocalcemia :Ca gluconate, CaCl2 Nutrition : Because potassium and phosphorus are not excreted optimally in patients with AKI, blood levels of these electrolytes tend to be high. Frequent measurements are mandatory to initiate early treatment and avoid complications. In the polyuric phase of AKI, potassium and phosphorus may be depleted and patients require dietary supplementation and intravenous replacement. Calculation of the nitrogen balance can be challenging, especially in the presence of volume contraction, hypercatabolic states, gastrointestinal bleeding, and diarrheal disease. Critically ill patients should receive at least 1 g/kg/day protein intake but should avoid hyperalimentation, which can lead to elevated BUN level and water loss resulting in hypernatremia.

32. Renal replacement therapy

33. Criteria for initiation of RRT Anuria Oliguria Pulmonary edema Hyperkalemia >6.5mmol/L Ureum > 200 mg % Overhydrasi

34. hemodialysis Intermittent HD: 3-4hrs per day,3-4 times per week Slow Low Efficiency Dialysis ^-12 hrs per day

35. peritoneal dialysis Less effective than HD Useful if HD not available Impossible to attain vascular access Hemodynamically unstable No anticoagulation is needed

36. Peritoneal dialysis Access via a peritoneal catheter Allowed to dwell for a short period of time [2-4hrs]

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