In the name of GOD

1. In the name of GOD

2. ischuriarenalis, was by William Heberden in 1802. • At the beginning of the twentieth century, Acute Bright’s disease, was well described in William Osler’s Textbook for Medicine (1909), as a consequence of toxic agents, pregnancy, burns, trauma, or operations on thekidneys. • During the First WorldWarthe syndrome was named ‘‘war nephritis’’, and was reported in several publications.

3. The syndrome was forgotten until the Second World War, when Bywaters and Beall published their classical paper on crush syndrome. • It is Homer W. Smith who is credited for the introduction of the term ‘‘acute renal failure’’, in a chapter on ‘‘Acute renal failure related to traumatic injuries’’ in his textbook The kidney-structure and function in health and disease (1951).

4. A recent survey revealed the use of at least 35 definitions in the literature. • Kellum JA, Levin N, Bouman C, et al. Developing a consensus classification system for acute renal failure. CurrOpinCrit Care 2002; 8: 509–514.

5. AKI is defined by an abrupt decrease in kidney function that includes, but is not limited to, ARF.

6. Because the manifestations and clinical consequences of AKI can be quite similar (even indistinguishable) regardless of whether the etiology is predominantly within the kidney or predominantly from outside stresses on the kidney, the syndrome of AKIencompasses both direct injury to the kidney as well as acute impairment of function.

7. AKI Definition

8. AKI is defined as any of the following : • Increase in SCr by >=0.3 mg/dl within 48 hours • Increase in SCr to>= X1.5 times baseline, which is known or presumed to have occurred within the prior 7 days • Urine volume of <0.5 ml/kg/h for 6 hours.

9. Staging of AKI

10. The cause of AKI should be determined whenever possible.

17. Risk assessment

18. We recommend that patients be stratified for risk of AKI according to their susceptibilities and exposures.

20. Manage patients according to their susceptibilities and exposures to reduce the risk of AKI .

21. Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI. • Individualize frequency and duration of monitoring based on patient risk and clinical course.

22. Evaluation and general management of patients with and at risk for AKI

23. Evaluate patients with AKI promptly to determine the cause, with special attention to reversible causes.

24. Monitor patients with AKI with measurements of SCr and urine output to stage the severity.

25. Manage patients with AKI according to the stage and cause.

27. Evaluate patients 3 months after AKI for resolution, new onset, or worsening of pre-existing CKD. • If patients have CKD, manage these patients as detailed in the KDOQI CKD Guideline. • If patients do not have CKD, consider them to be at increased risk for CKD and care for them as detailed in the KDOQI CKD Guideline 3 for patients at increased risk for CKD.

31. Diagnostic approach to alterations in kidney function and structure

36. Contrast-induced AKI

37. Contrast-induced AKI: definition,epidemiology, and prognosis

38. Define and stage AKI after administration of intravascular contrast media as per Recommendations. • In individuals who develop changes in kidney function after administration of intravascular contrast media, evaluate for CI-AKI as well as for other possible causes of AKI.

39. Many studies have now shown that patients who develop CI-AKI have a greater risk for death or prolonged hospitalization, as well as for other adverse outcomes, including early or late cardiovascular events. • when patients with CI-AKI require dialysis, the mortality is higher compared to those not requiring dialysis.

40. Assessment of the population at risk for CI-AKI

41. Assess the risk for CI-AKI and, in particular, screen for pre-existing impairment of kidney function in all patients who are considered for a procedure that requires intravascular (i.v. or i.a.) administration of iodinated contrast medium.

44. Consider alternative imaging methods in patients at increased risk for CI-AKI.

45. Nonpharmacological preventionstrategies of CI-AKI

46. Use the lowest possible dose of contrast medium in patients at risk for CI-AKI.

47. Additional radiological measures to reduce CI-AKI • Some CT strategies in patients at risk of CI-AKI • Perform CT, when possible, without contrast media. • Dosing per kilogram body weight to reduce the amount of contrast media is needed in thin patients. • Adapt injection duration to scan duration when performing CT-angiography, so that the injection is not still running when the scan is finished. • Use a saline chaser to decrease the amount of contrast media, by using the contrast medium that otherwise would remain in the dead space of the arm veins; this may save 10–20 ml of contrast media.

48. …Some CT strategies in patients at risk of CI-AKI • Further reduction of contrast media may be instituted in patients with known decreased cardiac output (not unusual in patients with renal impairment) undergoing CT-angiographic studies.

49. Some angiographic strategies in patients at risk of CI-AKI • Avoid test injections; the same amount may be enough for a diagnostic digital-subtraction angiography run. • Scrutinize each series before performing the next; avoid unnecessary projections. • Decrease kilovoltage in a thin patient; a lower iodine concentration may be used.

50. Avoid ventriculography: echocardiography (and ‘‘echo contrast’’) is always a reasonable alternative. • Use plasma isotonic contrast-media concentrations for renal artery injections. • CO2 may be used as contrast medium in venous examinations and below the diaphragm for arterial examinations or alternatively use iodinated contrast media with the same contrast effect, i.e., about 40mg iodine per milliliter.