ACUTE KIDNEY INJURY 1.pptx presentation.

renal

1. Acute Kidney Injury PAMELA JOY DIZON DECENA ESPINOZA 2ND YEAR IM RESIDENT

2. OBJECTIVES At the end of this 1-hour lecture, the listeners will be able to: Define Acute Kidney Injury and Identify its causes Determine the Treatment and Prevention of AKI based on KDIGO guidelines Discuss Contrast Induced AKI including its risk factors, prevention and treatment

3. CASE J.C. 35 MALE FILIPINO CATHOLIC PARANAQUE CITY RIGHT KNEE PAIN AND SWELLING

4. HISTORY OF PRESENT ILLNESS 1 month prior to admission (+) gradual onset dull pain (PS 4/10) on the right knee; NO associated erythema, warmth, swelling, limited ROM, nor fever Medications: Tramadol + Paracetamol 37.5/325mg/tab 1 tab q6h PRN for pain Uridine monophosphate + Vitamin B12 + Folic Acid (Keltican) 1 tab OD Right knee APL ray done which revealed no fracture or dislocation, with probable knee joint effusion; MRI R knee was requested but was not done at this time.

5. HISTORY OF PRESENT ILLNESS Interim (+) increasing pain (PS 7/10) on the R knee (+) swelling, warmth, and erythema (+) undocumented fever despite compliance to medications

6. HISTORY OF PRESENT ILLNESS 1 week PTA (+) persistent R knee pain and swelling hence consult at IM OPD. Prescribed with Celecoxib 200mg/cap 1 cap q12h for pain. Crea BUN Na K BUN were requested. Few hours PTA Persistence of symptoms, Advised admission

7. PAST MEDICAL HISTORY No known comorbids (HTN, DM, PTB, BA) No known allergies No previous hospitalizations No blood transfusion history Covid vaccine: Pfizer x 2 doses

8. FAMILY HISTORY (-) HTN, DM, BA, Malignancy, Kidney disease

9. PERSONAL SOCIAL HISTORY Previous 3PY smoker Occasional alcoholic Denies illicit drug use

10. PHYSICAL EXAMINATION 120/80 > 110 > 18 > 38.0 > 98% RA Ht 162cm Wt 60 BMI 22.9 (N) Awake, alert, speaks in sentences, not in cardiorespiratory distress Anicteric sclerae, pink palpebral conjunctivae, no neck vein enlargement, no cervical lymphadenopathies, moist lips and oral mucosa Symmetrical chest expansion, clear breath sounds, Adynamic precordium, tachycardic regular rhythm, no murmurs Flabby, soft, nontender abdomen, no masses R knee erythema, swelling, tenderness with no limited ROM

11. BASELINE LABORATORIES WBC 16.54 RBC 4.94 HGB 140 HCT 0.43 N 0.88 L 0.04 M 0.08 E B MCV 86 MCH 28 MCHC 330 RDW 13 PLT 362 BUN 5.50 CREA 62.88 NA 126.59 K 4.41 CL 87.64 PROCAL 1.02 ESR 13 URINALYSIS: Amber Slightly cloudy pH 6 SG 1.030 RBC 10-12 WBC 0-3 Epithelial cells: Few Bacteria:Moderate Glucose +1 Protein +3 Blood, ketones, nitrite, bili, leuk - negative

12. COURSE IN THE WARDS Patient was managed as a case of septic arthritis Right knee arthrocentesis was done Patient was then started on Vancomycin Diagnostics were requested for monitoring where in creatinine was noted to be elevated Hydration with NSS was done (2cc/kg) Patient also underwent MRI of the right knee

13. CREATININE TRENDS 12/19 12/23 12/28 1/3 1/12 1/17 1/21 1/27 1/29 Crea 62.8 58.8 135.7 134.7 405 331.3 241.9 208.9 184.3 BUN 5.5 4.5 6.70 4.60 18.60 13.3 6.90 6.8 5.6 eGFR 123 125 60 51 16 21 30 36 42 BCR 21.6 18.9 12.19 8.43 11.34 9.91 7.07 8.04 7.51 01/12: POST MRI W/ IV CONTRAST

14. BASELINE LABORATORIES Repeat urinalysis

15. ACUTE KIDNEY INJURY

16. WORKING IMPRESSION: Acute Kidney Injury Stage 2 intrinsic probably secondary to 1) infection secondary to Septic arthritis 2) drug-induced (vancomycin) 3)t/c CIN (MRI-gadoliunium)

17. QUESTION 1 Based on our case, having the patient presenting with AKI, according to KDIGO, AKI is defined as which of the following Increase in SCr by >/=0.3mg/dl within 48hrs Increase in SCr to >/=1.5x baseline within the prior 7 days Urine volume <0.5ml/kg/h for 6hrs All of the above

18. QUESTION 1 AKI is defined as which of the following Increase in SCr by >/=0.3mg/dl within 48hrs Increase in SCr to >/=1.5x baseline within the prior 7 days Urine volume <0.5ml/kg/h for 6hrs All of the above

19. ACUTE KIDNEY INJURY Increase in SCr by >/=0.3mg/dl within 48hrs Increase in SCr to >/=1.5x baseline within the prior 7 days Urine volume <0.5ml/kg/h for 6hrs Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

20. AKI STAGING Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32 Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

21. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

22. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

23. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32 Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

24. QUESTION 2 WHICH OF THE FOLLOWING STATEMENT IS FALSE AKI IS NOT A DISEASE EVALUATE PATIENTS 1 MONTH AFTER AKI FOR RESOLUTION, OR WORSENING OF PREEXISTING CKD MONITOR PATIENT WITH AKI USING SCr AND UO TO STAGE THE SEVERITY THE CAUSE OF AKI SHOULD BE DETERMINED WHENEVER POSSIBLE

25. QUESTION 2 WHICH OF THE FOLLOWING STATEMENT IS FALSE AKI IS NOT A DISEASE EVALUATE PATIENTS 1 MONTH AFTER AKI FOR RESOLUTION, OR WORSENING OF PREEXISTING CKD MONITOR PATIENT WITH AKI USING SCr AND UO TO STAGE THE SEVERITY THE CAUSE OF AKI SHOULD BE DETERMINED WHENEVER POSSIBLE

26. ACUTE KIDNEY INJURY AKI IS NOT A DISEASE BUT RATHER A CLINICAL SYNDROME WITH MULTIPLE ETIOLOGIES THE CAUSE OF AKI SHOULD BE DETERMINED WHENEVER POSSIBLE STRATIFY RISK OF AKI ACCORDING TO THEIR SUSCEPTIBILITIES AND EXPOSURES TEST PATIENTS AT INCREASED RISK FOR AKI WITH MEASUREMENTS OF SCr AND UO AND MONITOR THEM TO STAGE THE SEVERITY MANAGE PATIENT WITH AKI ACCORDING TO THE STAGE AND CAUSE Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

27. ACUTE KIDNEY INJURY EVALUATE PATIENTS 3 MONTH AFTER AKI FOR RESOLUTION, NEW ONSET, OR WORSENING OF PREEXISTING CKD Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

28. CAUSES OF AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

29. CAUSES OF AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32 Vancomycin Gadolinium

30. STAGE-BASED MANAGEMENT OF AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

31. EVALUATION OF AKI ACCORDING TO STAGE AND CAUSE Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

32. EVALUATION OF AKI ACCORDING TO STAGE AND CAUSE Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

33. EVALUATION OF AKI ACCORDING TO STAGE AND CAUSE Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

34. TREATMENT OF AKI Patients with AKI and increased risk of AKI require careful attention to paid to their hemodynamic status FLUIDS In the Absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids as initial management for patients with AKI SAFE study (Saline vs Albumin fluid Evaluation) RCT comparing 4% human albumin in 0.9% saline with isotonic saline in ICU patients indicate that albumin is safe and no more effective than isotonic saline Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

35. TREATMENT OF AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32 Patient J.C. started on hydration PNSS 1L x 150cc/hr (2cc/kg/hr)

36. TREATMENT HYDROETHYLSTARCH VS SALINE Hypertonic HES may induce “osmotic nephrosis” VISEP study (Volume substitution and Insulin therapy in severe sepsis) HES vs Isotonic modified Ringer’s lactate solution HES group showed greater mortality rate at 90 days Hypertonic HES - higher rates of AKI and longer days on which RRT was required Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

37. TREATMENT VASOPRESSORS Vasopressin vs Norepinephrine Increases BP and enhances diuresis but has not been proven to enhance survival nor reduce need for RRT In patients in the RIFLE-R category, vasopressin was associated with lower rate of progression of F or L categories and lower rates of RRT Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

38. TREATMENT Glycemic control and nutritional support In critically ill patient, we suggest insulin therapy targeting plasma glucose 110-149 mg/dl Protein-calorie malnutrition is an important independent predictor of in-hospital mortality in patients with AKI Achieving a total energy intake of 20-30kcal/kd/day in patients with any stage of AKI is suggested Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

39. TREATMENT NUTRITIONAL ASPECTS IN THE PREVENTION AND TREATMENT OF CRITICALLY ILL PATIENTS WITH AKI Avoid Restriction of protein intake with the aim of preventing or delaying initiation of RRT Administer 0.8-1.0 g/kg/d of protein in noncatabolic AKI patients w/o RRT Administer 1.0-1.5 g/kg/d in patients w/ AKI on RRT Up to Maximum 1.7 g/kg/d in patients on continuous renal replacement therapy and in hypercatabolic patients Enteral Route is preferred Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

40. TREATMENT USE OF DIURETICS Diuretics is not recommended in preventing AKI Do not use Diuretics to treat AKI except in the management of volume overload Growth Factor Intervention Using Recombinant Human IGF-I to prevent or treat AKI is not recommended Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

41. Prevention of Aminoglycoside and Amphoterin- related AKI 3.8.1: We suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephrotoxic, therapeutic alternatives are available. (2A) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

42. In patients with normal and stable kidney function, once-daily dosing of aminoglycosides should be used to limit aminoglycoside nephrotoxicity. True or False

43. Prevention of Aminoglycoside and Amphoterin- related AKI 3.8.2: We suggest that, in patients with normal kidney function in steady state, aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens. (2B) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

44. 3.8.3: We recommend monitoring aminoglycoside drug levels when treatment with multiple daily dosing is used for more than 24 hours. (1A) 3.8.4: We suggest monitoring aminoglycoside drug levels when treatment with single-daily dosing is used for more than 48 hours. (2C) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

45. 3.8.5: We suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible and suitable. (2B) Aminoglycoside-loaded beads for the prevention and treatment of bone and joint infections Aminoglycoside aerosol delivery systems are now in use to provide high intrapulmonary antibiotic levels with minimal systemic and kidney concentrations of the antibiotic Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

46. AMPHOTERICIN B NEPHROTOXICITY This polyene antifungal agent is insoluble in water and needs to be solubilized with deoxycholate and given i.v. in the absence of electrolyte solutions to maintain solubility. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

47. AMPHOTERICIN B NEPHROTOXICITY AKI related to amphotericin B is clinically significant and is associated with higher mortality rates, increased LOS, and increased total costs of health care when managing patients with systemic fungal infection Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

48. 3.8.6: We suggest using lipid formulations of amphotericin B rather than conventional formulations of amphotericin B. (2A) Three amphotericin lipid formulations includes the following except ? Amphotericin B colloidal dispersion Amphotericin B lipid complex Amphotericin B micellar complex Liposomal amphotericin B Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

49. Amphotericin B colloidal dispersion is formulated by amphotericin B complexed with cholesteryl sulfate. Amphotericin B lipid complex is composed of amphotericin B complexed with dimyristoyl phosphatidylcholine and dimyristoyl phosphatidylglycerol. Liposomal amphotericin consists of amphotericin B complexed with hydrogenated soy phosphatidylcholine, distearoylphosphatidylcholine, and cholesterol. Other formulations that might further reduce the risk of AKI from amphotericin B include nanoparticle packaging in micelles with polyaspartic acid Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

50. 3.8.7: In the treatment of systemic mycoses or parasitic infections, we recommend using azole antifungal agents and/or the echinocandins rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed. (1A) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

51. Other methods of prevention of AKI in the critically ill 3.9.1: We suggest that off-pump coronary artery bypass graft surgery not be selected solely for the purpose of reducing perioperative AKI or need for RRT. (2C) 3.9.2: We suggest not using NAC to prevent AKI in critically ill patients with hypotension. (2D) 3.9.3: We recommend not using oral or i.v. NAC for prevention of postsurgical AKI. (1A) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

52. Contrast Induced AKI

53. A rise in SCr of more than or equal to 0.5 mg/dl ( >44 mmol/l) or a 25% increase from baseline value, assessed at 48 hours after a radiological procedure Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

54. Contrast Induced AKI In a minority of cases, the peak increase of SCr may occur up until 5 days after contrast exposure. However, a recent prospective study showed that the percentage change of SCr 12h after contrast vs. the basal value was the best predictor of CI-AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

55. Contrast Induced AKI Cystatin C as early marker of AKI Cystatin C increase concentration of >10% at 24 hours after contrast-media exposure In patients with CKD, cystatin C may be a useful marker for the early diagnosis of CI-AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

56. Epidemiology It is accepted that, in patients with normal renal function— even in the presence of diabetes—the risk for CI-AKI is low (1–2%) 25% in patients with pre-existing renal impairment CKD and diabetes, CHF, advanced age, and concurrent administration of nephrotoxic drugs 11%- Contrast induced AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

57. Epidemiology In critically ill patients, even with an apparently ‘‘normal’’ renal function, i.v. administration of iodinated contrast media is associated with a significant incidence of CI-AKI. Radiological procedures performed in an emergency would be associated with an increased risk of CI-AKI Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

58. Prognosis Patients with CI-AKI greater risk for death or prolonged hospitalization, as well as for other adverse outcomes, including early or late cardiovascular events (PCI). When patients with CI-AKI require dialysis, the mortality is higher compared to those not requiring dialysis. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

59. 4.2.1: 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. (Not Graded) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

60. Screening for pre-existing renal impairment Pre-existing renal functional impairment is the most important risk factor above all other risk factors for developing CI-AKI screening for both acute and chronic kidney disease is highly recommended. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

61. Screening for pre-existing renal impairment Risk of CI-AKI becomes clinically important when the baseline SCr concentration is >1.3 mg/dl (>115 mmol/l) in men and >1.0 mg/dl (>88.4 mmol/l ) in women, equivalent to an eGFR less than 60ml/min per 1.73 m2 Precautions to reduce the risk should be implemented in patients with a baseline eGFR <60ml/min per 1.73 m2 . The threshold could probably be lowered to 45 ml/min per 1.73 m2. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

62. Screening for pre-existing renal impairment In emergent imaging/intervention, where the benefit of very early imaging outweighs the risk of waiting, should not be delayed Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

63. Risk factor questionnaire Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

64. Urine Protein screening Dipstick testing for urine protein rapid screen to identify patients who can undergo studies requiring contrast media without SCr measurement Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

65. Other risk factors for contrast induced AKI Diabetes Hypertension CHF Advanced age Volume depletion Hemodynamic instability Nephrotoxic medications large volume or high osmolality of the contrast agent Metabolic syndrome Prediabetes Hyperuricemia Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

66. Other risk factors for contrast induced AKI Circulatory collapse or CHF patients delayed until their hemodynamic status is corrected Repeated exposure should be delayed: 48 hours in patients without risk factors for CI-AKI 72 hours in those with diabetes mellitus or pre-existing chronic renal dysfunction. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

67. Other risk factors for contrast induced AKI If acute renal dysfunction develops after contrast-media administration, repeated exposure should preferably be delayed until the SCr level has returned to baseline levels. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

68. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32 Risk Models of CI-AKI

69. 4.2.2: Consider alternative imaging methods in patients at increased risk for CI-AKI. (Not Graded) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

70. Nephrotoxicity of Gd Chelates Gd chelates are widely used as MRI contrast agents, and are considered to have a good overall safety profile. However, more recent studies raised the possibility of nephrotoxicity, although it is not clear whether it approaches the incidence of AKI associated with iodine-containing contrast media. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

71. Non pharmacological prevention strategies of CI- AKI

72. 4.3.1: Use the lowest possible dose of contrast medium in patients at risk for CI-AKI. (Not Graded) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

73. The risk of CI-AKI appears to be greater after arterial compared to venous administration of contrast media. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

74. 4.3.2: We recommend using either i so-osmolar or low- osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media in patients at increased risk of CI-AKI. (1B) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32 Selection of Contrast Agent

75. High-osmolar vs iso osmolar or low osmolar contrast media In patients with normal renal function, Risk for CI AKI is LOW in both High and Low osmolar agents In patients with pre existing kidney function impairment Low osmolar contrast are less nephrotoxic Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

76. Low osmolar vs iso-osmolar contrast media Iodixanol is thus not associated with a significantly reduced risk of CI- AKI compared to the low-osmolar contrast media pooled together. However, in patients with decreased kidney function, iodixanol is associated with a reduced risk of CI- AKI compared to iohexol. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

77. Pharmacological prevention strategies of CI- AKI

78. Fluid Administration Extracellular volume expansion at the time of radiocontrast- media administration may serve to counteract both the intrarenal hemodynamic alterations and the direct tubulo-toxic effects that play a role in the pathophysiology of CI- AKI. Reduce cellular damage by dilution of the contrast medium, particularly in the medullary tubular segments Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

79. 4.4.1: We recommend i.v. volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions, rather than no i.v. volume expansion, in patients at increased risk for CI-AKI. (1A) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

80. Fluid Administration Fluids should be started at least 1h before and continued for 3–6 hours after contrast-media administration . A ‘‘good’’ urine output (>150ml/h) in the 6 hours after the radiological procedure has been associated with reduced rates of AKI in one study Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

81. Fluid Administration Since not all of i.v. administered isotonic crystalloid remains in the vascular space, in order to achieve a urine flow rate of at least 150 ml/h, >1.0–1.5 ml/kg/h of i.v. fluid has to be administered for 3–12 hours before and 6–12 hours after contrast-media exposure. The sustained administration of isotonic saline before and after radiocontrast injection seems, thus, to be more protective than equivalent volumes of hypotonic saline. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

82. 4.4.2: We recommend not using oral fluids alone in patients at increased risk of CI-AKI. (1C) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

83. 4.4.3: We suggest using oral NAC, together with i.v. isotonic crystalloids, in patients at increased risk of CI-AKI. (2D) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

84. 4.4.4: We suggest not using theophylline to prevent CI-AKI. (2C) 4.4.5: We recommend not using fenoldopam to prevent CI-AKI. (1B) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

85. Effects of Hemodialysis or Hemofiltration

86. 4.5.1 We suggest not using prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI. (2C) Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

87. Hemodialysis or Hemofiltration In summary, the evidence profile for IHD vs. HF showed low-quality evidence and an uncertain benefit vs. harm balance of HF/IHD in preventing CI-AKI in patients with severe CKD. Given the costs and logistical difficulties, the use of HF modalities for CI-AKI prevention can only be advocated if future studies will convincingly show clear benefit. Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

88. JOURNAL

89. JOURNAL APPRAISAL

90. CLINICAL QUESTION Among diabetic patients diagnosed with STEMI and underwent PCI, are SGLT2 inhibitors protective against contrast-induced AKI?

91. Journal case P DM patients with STEMI and underwent PCI I SGLT2 inhibitor O Prevention of renal failure M Case control study

92. RESULT The cause of AKI (HRS vs ATN) was not significantly associated with mortality in patients with cirrhosis The Transplant Status, MELD score, and indicators of critical illness were more closely associated with survival

93. Thank you!