Acute kidney injury

1. Acute kidney injury/acute renal failure Prepared by Abera D(EMCCN)

2. Out line • Introduction • Epidemiology • Etiology and Pathophysiology • Diagnostic Evaluation • Clinical features • Complications • Treatment

3. 1) Introduction • Acute kidney injury (AKI), previously known as acute renal failure, is characterized by the sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys.

4. There are two different classification for diagnostic and staging of AKI ;this are RIFLE criteria AKIN classification Both classification uses creatinine level and urine output.

5. RIFLE Criteria consists • Three graded levels of injury (Risk, Injury, and Failure) • And two outcome measures (Loss and End-stage renal disease).

6. Risk — 1.5-fold increase in the serum creatinine or GFR decrease by 25 percent or urine output <0.5 mL/kg per hour for six hours • Injury — Two fold increase in the serum creatinine or GFR decrease by 50 percent or urine output <0.5 mL/kg per hour for 12 hours

7. Failure — Three fold increase in the serum creatinine or GFR decrease by 75 percent or urine output of <0.5 mL/kg per hour for 24 hours, or anuria for 12 hours. • Loss — Complete loss of kidney function (eg, need for renal replacement therapy) for more than one months. • ESRD — Complete loss of kidney function for more than three months.

8. The AKIN proposed both diagnostic criteria for AKI and a staging system that was based on the RIFLE criteria • An abrupt (within 48 hours) absolute increase in the serum creatinine concentration of ≥0.3 mg/dL (26.4 micromol/L) from baseline, a percentage increase in the serum creatinine concentration of ≥50 percent, or oliguria of less than 0.5 mL/kg per hour for more than six hours .

9. The diagnostic criteria should be applied only after volume status had been optimized • Urinary tract obstruction needed to be excluded if oliguria was used as the sole diagnostic criterion. • comprised of three stages of increasing severity, which correspond to risk (stage 1), injury (stage 2), and failure (stage 3) of the RIFLE criteria.

10. 2) Epidemiology • AKI complicates 5–7% of acute care hospital admissions. • 30% of admissions to the intensive care unit • A prospective study in Ethiopian patients done by WorkuZewdu in 1992, sowed that septicabortionwas the leading cause of AKI followed by P.falciparummalaria and nephrotoxicagents

11. 3) Etiology and Pathophysiology • Divided into three broad categories A) prerenal azotemia B) intrinsic renal parenchymal disease, and C) postrenal obstruction

12. A) prerenal azotemia • Hypovolemia (hemorrage,burns,vomiting…) • Low cardiac output • medications that interfere with renal autoregulatory responses(NSAID and ACEI) • Prerenal azotemia involves no parenchymal damage to the kidney and is rapidly reversible once intraglomerular hemodynamics are restored.

13. Compensatory mechanisms to maintain GFR • Renal vasoconstriction and salt and water reabsorption. • Myogenic reflex which leads to the dilation of the afferent arteriole. • Tubuloglomerular feedback renal autoregulation usually fails once the systolic blood pressure falls below 80 mmHg.

14. B) Intrinsic renal parenchymal disease, • Ischemia • Sepsis • Nephrotoxins (endogenous vs exogenous) Rhabdmyolisisvs tumor lysis Antibiotics Contrast agent

15. C) postrenal obstruction • UretericCalculi, blood clot, sloughed papillae, cancer, external compression (e.g.,retroperitoneal fibrosis) • Bladder neck Neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot

16. What are the signs and symptoms of acute kidney injury Signs and symptoms of acute kidney injury differ depending on the cause and may include: • Too little urine leaving the body • Swelling in legs, ankles, and around the eyes • Fatigue or tiredness • Shortness of breath • Confusion • Nausea • Seizures or coma in severe cases • Chest pain or pressure

17. 4) Diagnostic Evaluation ¤ Careful historyand physical examination is essential • Exposure to nephrotoxins and drugs • Anuria/no urinemay indicate post-renal causes • Skin rashes may indicate allergic nephritis • Evidences of volume depletion: diarrhea, bleeding • Pelvic and per-rectal examination: look for evidence of abortion. • Ischemia or trauma to the legs or arms may indicate rhabdomyolysis. • Recent surgical or radiologic procedures • Past and present use of medications • Family history of renal diseases

18. Laboratory evaluation A)The urinalysis and urine sediment ● in case of prerenal azotemia the most common urinary findings are trace/no proteniuria and few hyaline casts are possible • in case of intrinsic causes of AKI the urinary findings are different with underlying problem.

19. ● Due to ischemia/nephrotoxins mild to moderate proteinuria pigmented granular casts, renal tubular epthileal cells. ● acute interstitial nephritis mild to moderate proteinuria WBC, Eosinophils,Casts,Red cells ● Acute glomerulonephritis moderate to severe proteinuria, redcells and red cell casts; and red cells can be dysmorphic

20. B) Blood Laboratory Findings • CBC (anemia, leukocytosis) • Serum electrolyte (hyperkalemia, hyperphosphatemia, and hypocalcemia) • Creatinine phosphokinase levels and serum uric acid • Renal function(BUN/Cr) BUN : Cr ratio around 20 suggest prerenal problem

21. C) Renal Failure Indices • The fractional excretion of sodium (FeNa) is the fraction of the filtered sodium load that is reabsorbed by the tubules. • With prerenal azotemia, the FeNa may be below 1%, • ischemic AKI, the FeNa is frequently above 1% • Postrenal AKI, the FeNa is usually above 1%

22. D)Imaging • Ultrasound • CT scan • MRI best used

23. 5)Complication • Uremia/high level of urea • Hypervolemia / Hypovolemia • Hyponatremia • Hyperkalemia • Acidosis • Hyperphosphatemia and Hypocalcemia • Malnutrition

24. 6)Treatment • The basic principles of the general mx are; 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

25. 1)Optimizing the hemodyanamic status This can be corrected according to the cause for severe hemorrage we have to give whole blood for less sever hemorrage we can administer Isotonic crystalloid and/or colloid

26. 3) . Initiation of renal replacement therapy when indicated Methods for renal replacment therapy are; intermittent hemodialysis peritoneal dialyis continousvenovenoushemodifiltration

27. Indications for renal replacment therapy are when medical management fails to control • volume overload • hyperkalemia • acidosis • in some toxic ingestions • uremia

28. Management of the complication 1). Hyperkalemia     a. Restriction of dietary potassium intake   b. Loop diuretics to promote urinary potassium loss   c. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry of potassium intracellularly     d. Inhaled beta-agonist therapy to promote entry of potassium intracellularly     e. Calcium gluconateor calcium chloride (1 g) to stabilize the myocardium

29. 2. Volume overload    a. Salt and water restriction      b. Diuretics c. Ultrafiltration • 3. Hyponatremia     a. Restriction of enteral free water intake, minimization of hypotonic intravenous solutions including those containing

30. 4). Metabolic acidosis     a. Sodium bicarbonate (if pH <7.2 to keep serum bicarbonate >15 mmol/L)     b. Administration of other bases e.g., THAM    c. Renal replacement therapy

31. THANK YOU

32. REFERNCES • Tintinalli Emergency 7th edition • Harrison's Principles of Internal Medicine 18th • Up to date 19.3