1. Each speaker will disclose any conflicts of interest before their presentations. There is no relationship between the exhibitors and the content development of the program. The commercial support received from the exhibitors is very appreciated and helps to keep the cost low while enabling us to include a sack lunch.

2. Leslie Dork, MSN, CNP Renal medicine associates
Acute kidney injury
Leslie Dork, MSN, CNP
Renal medicine associates

3. Conflict of Interest
I have no conflicts of interest.

4. Acute kidney injury
A sudden decrease in GFR over hours to days that leads to failure of the kidneys to excrete the nitrogenous waste products and maintain fluid and electrolyte balance (homeostasis), (Schrier, 2005)
Life-threatening consequences: volume overload, hyperkalemia, metabolic acidosis
RIFLE (Risk, Injury, Failure, Loss, End-stage kidney disease) = staging system
AKIN (Acute Kidney Injury Network)
KDIGO (Kidney Disease: Improving Global Outcomes) Clinical Practice Guideline for Acute Kidney Injury

5. Acute Kidney injury Broad clinical syndrome
Term is meant to include the whole spectrum from small changes in markers of kidney function to the need for renal replacement therapy
AKI occurs in the community as well as in the hospital setting
AKI is a predictor of adverse outcomes, both immediately and long term
Those with chronic kidney disease are at increased risk for AKI and AKI can lead to progression of CKD

6. AKI Definition Increase in SCr by >/= 0.3 mg/dl within 48 hours; or
Increase in SCr to >/= 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
Urine volume < 0.5 ml/kg/h for 6 hours
AKI is staged for severity
The cause of AKI should be determined whenever possible
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1-138

7. Staging of AKI
Stage 1: SCr 1.5 – 1.9 time baseline OR > 0.3 mg/dl increase; urine output < 0.5 ml/kg/h for 6/12 hours Stage 2: SCr 2.0 – 2.9 times baseline; urine output < 0.5 ml/kg/h for >/= 12 hours Stage 3: SCr 3.0 time baseline OR increase in serum creatinine to >/= 4.0 mg/dl OR initiation of renal replacement therapy OR in patients < 18 years, decrease in eGFR to < 35 ml/min per 1.73 m2; urine output < 0.3 ml/kg/h for >/= 24 hours OR anuria for >/= 12 hours

8. Definitions of Terminology
Azotemia - the accumulation of nitrogenous wastes (high BUN)
Uremia – clinical manifestation (symptomatic renal failure)
Oliguria – UOP < mL/24 hours
Anuria – UOP < 100 mL/24 hours

9. Who gets AKI? Community acquired:
At least 1% of hospitalized patients have AKI on admission
50% of these patients have underlying CKD
70% of these have prerenal causes (e.g. dehydration)
17% have post renal causes (obstruction)
Mortality estimated at 15%

10. Who gets AKI? Hospital acquired
Increasingly common: especially in elderly and critically ill
Incidence: 16% in CKD patients; 5% non-CKD patients
Acute tubular necrosis (ATN) most common cause (40%)
If in-hospital dialysis required, mortality rate up to 50%; may exceed 75% in the critically ill or septic patient
About 30% who need dialysis during ICU stay will need maintenance dialysis after discharge
No drug treatment has yet been demonstrated to limit progression or speed recovery
Even small changes in SCr are associated with increased in-patient mortality

11. AKI hospital-acquired causes
Nephrotoxic medications (15%)
Radio contrast dye (CI-AKI) (10%)
AIDs-associated nephropathy
Non-ICU patients: prerenal 28% and ATN 35%
ICU patients: prerenal 18% and ATN 76%
ATN in the ICU has multiple causes and is often associated with multisystem organ failure

12. What causes AKI? Three major categories:
Decreased real blood flow (prerenal causes, 40-70%)
Direct renal parenchyma damage (intrinsic renal causes, 10-50%)
Obstructed urine flow (post renal or obstructive causes, 10%)

13. Prerenal causes: hypovolemia
Hemorrhage
Volume depletion (vomiting, diarrhea, burns, inappropriate diuresis

14. Prerenal causes: Renal hypo perfusion & edematous states
NSAIDs/COX 2 Inhibitors
ACE-I/ARBs
RAS/Occlusion
Hepatorenal syndrome
AAA
CHF
Hepatic Cirrhosis
Nephrotic syndrome

15. Prerenal causes: hypotension
Cardiogenic shock
Distributive shock (sepsis, anaphylaxis)
Antihypertensives
Massive pulmonary embolism
Severe arrhythmias
Valvular heart disease

16. Intrinsic Renal Causes of AKI
Glomerular disease: inflammation (GN), thrombosis
Tubular injury: ischemia, toxins
Interstitial nephritis
Vascular disease:
inflammation (vasculitis)
occlusion (thrombosis or embolism)

17. Post renal causes of AKI
Intrinsic:
Intra-luminal (stone, blood clot)
Intra-mural (urethral stricture, prostate hypertrophy or malignancy, bladder tumor, radiation fibrosis, neurogenic bladder)
Extrinsic:
Pelvic malignancy
Retroperitoneal fibrosis

18. Exposures Susceptibilities
Can AKI be prevented? Stratify risk according to susceptibilities and exposures
Exposures
Sepsis
Critical illness
Circulatory shock
Burns
Trauma
Cardiac surgery (especially with CPB)
Major noncardiac surgery
Nephrotoxic drugs
Radio contrast agents
Poisonous plants and animals
Susceptibilities
Dehydration
Advanced age
Female gender
Black race
CKD
Chronic diseases (heart, lung, liver)
Diabetes mellitus
Cancer
Anemia

19. AKI prevention
Identify high risk patients: elderly, hypertensives, diabetics, vascular disease, underlying CKD
Maintain BP
Avoid dehydration
Avoid nephrotoxic agents (NSAIDs, high phosphorus products like Fleets enemas)
Use caution with ACE-I/ARBs
Avoid radio contrast agents in susceptible population when possible—hydrate with IV NS preprocedure
N-acetyl cysteine used (unlikely to harm, may help)
Anuria rare: think obstruction: place foley ASAP; renal ultrasound

20. Assessing the patient with AKI
History
Review case notes
Medication review
Physical examination
Interpretation of lab tests, imaging studies, etc.

21. Is the presentation acute or chronic?
What is the baseline creatinine?
Suggestive of chronic presentation:
Long duration of symptoms
Absence of acute illness
Nocturia
Reduced kidney size (<10cm) & decreased cortical thickness on ultrasound (diabetic kidneys may be “normal” size)
Presence of anemia
Presence of renal bone disease (elevated iPTH or hyperphosphatemia)

22. presentation suggestive of acute Kidney injury
Lethargy or confusion with a creatinine of 3 to 8 mg/dl unless there is underlying stroke, infection, neurologic, or psychiatric diagnosis

23. Clinical presentation
Oliguria or anuria?
Decreased urine output (, 0.5 ml/kg X 6 hrs)
400 ml the minimum adult urine output required to eliminate daily solute production
Anuria is rare initially, suggesting renal tract obstruction. (Check renal ultrasound for dilatation of the renal pelvis and calyces – may not be present in malignancy.)

24. Clinical presentation
2. Volume status:
Intravascular volume depletion: low venous pressures; postural hypotension
Volume overload: increased venous pressure; crackles/rales in lungs
Response to diuretics? Cautious fluid challenge?

25. Clinical presentation
3. Evidence of renal parenchymal disease other than ATN?
Evidence of rashes, arthralgias, myalgias on history or physical exam?
Recent use of antibiotics?
Chronic or recent use of NSAIDs?
Recent illness/treatments/diagnostic procedures?

26. Clinical Presentation: Potential Vascular Occlusion?
Any history of renovascular or atherosclerotic disease? (34% of patients with CHF may have RAS)
Occlusion of normal renal artery—may have loin pain or hematuria
Previous occlusion (stenosed renal artery) may mean solo functioning kidney
Thrombus or emboli to artery of solitary functioning kidney can result in AKI
Usually see renal asymmetry on imaging & evidence of other vascular disease
ACE-I or diuretics may worsen the situation
Recent instrumentation of arteries/aorta may precipitate vascular occlusion
Occlusion of solitary kidney = likely anuria (likely had previous stenoisis

27. Clinical presentation: cholesterol emboli
Consider in elderly after angiography, vascular surgery, thrombolysis, anticoagulation
Classic triad: livedo reticularis, ARF/AKI, eosinophilia
Onset usually 1 to 4 weeks after intervention
Morbidity & mortality high: usually from cardiovascular causes

28. AKI Management Identify & correct pre-renal and post-renal factors
Optimize cardiac output & renal blood flow
Review medications: stop nephrotoxic agents, adjust doses & monitor drug concentrations where appropriate
Monitor fluid balance (I&O) & daily weight
Identify and treat acute complications: acidosis, hyperkalemia, pulmonary edema
Nutrition support: adequate calories, minimal nitrogenous waste, potassium restriction
Avoid protein restriction to prevent/delay RRT
g/kg/k in noncatabolic; g/kg/d in AKI on RRT; 1.7 on CRRT or hypercatabolic

29. AKI management
Identify & aggressively treat infection; minimize use of indwelling catheters and remove if anuric
Identify & treat bleeding tendencies: PPI or H2 blocker prophylaxis; avoid ASA initially; transfuse as needed
Initiate dialysis before uremic complications develop
No drug treatment has been shown to limit the progression or speed recovery from AKI – including furosemide

30. Indications for Renal replacement therapy (RRT
Hyperkalemia (not medically controllable)
Severe acidosis
Severe hyponatremia
Hypervolemia with CHF or pulmonary edema refractory to medical treatment
Severe medically refractory hypertension
Severe uremic symptoms (mental status changes, refractory nausea & vomiting)

31. AKI: Conclusions
Refer AKI cases to nephrology ASAP; early consultation may improve outcomes
AKI remains life threatening with high morbidity and mortality
AKI places huge costs & demands on the healthcare system
A fair number of patients progress to chronic dialysis management
Early recognition & institution of therapy in impro

32. Thank you
Questions? Comments.