1. Acute Kidney Injury SUSAN BUDNICK, MD

2. What is an Acute Kidney Injury?  AKI is a heterogeneous group of conditions that are all characterized by an acute impairment of renal function, causing an increase in waste products normally filtered by the kidneys  All of these conditions are associated with rise in serum creatinine, BUN and (sometimes) decreased urine output (UOP).  Divided into 3 broad categories: Prerenal, intrinsic renal and postrenal

3. Why do AKIs matter?  AKI is associated with increased risk of mortality, both while in-hospital and long term.  Patients with AKI are more likely to die prematurely after hospitalization, even if renal function returns to baseline.  AKI is associated with longer hospital stays and increased cost of stay  Patients with severe AKI, requiring CRRT or HD are at a high risk of developing progressive CKD and 10% eventually developed ESRD requiring HD.

4. How is AKI defined?  A rise in serum creatinine of at least 0.3mg.dL within 4 hours or 50% increase from baseline within 1 week  OR  A decrease in UOP to <0.5ml/kg lasting longer than 6 hours

5. The RIFLE criteria for kidney injury

6.  The RIFLE classification is based on Creatinine and UOP.  It includes 3 classes of AKI severity (Risk, Injury and Failure) and 2 classes of post-AKI outcomes (loss of function and ESRD).  If UOP and creatinine differ in AKI severity, use the criteria that gives the most severe diagnosis/prognosis.

7. Etiologies of AKI  Generally divided into 3 categories:  Prerenal: The most common form  Intrinsic renal: Either due to direct damage by nephrotoxins or secondary to ATN, ischemia or sepsis (etc.)  Postrenal/Obstructive: Obstruction causing increased retrograde hydrostatic pressure that interferes with GFR.

8. Prerenal Azotemia  Decreased renal blood flow which causes insufficient hydrostatic pressure for normal GFR  Can be due to hypotension, decreased cardiac output and medications that interfere with autoregulation of glomerular blood flow.  Can be rapidly reversed with improvement in RBF

9. Prerenal Azotemia Remember this? Common medications (NSAIDs, ACEi/ARBs) can affect RBF by decreasing autoregulatory functions

10. Intrinsic Renal Parenchymal Disease  Causes are numerous…  ATN (ischemic or toxic)  Sepsis  Ischemia- can progress from prerenal azotemia  Nephrotoxic agents  DIC  TTP/HUS  HTN  Endogenous toxins (Hb, myoglobin, uric acid, light chain proteins)

11. Postrenal Obstruction  Can occur anywhere from the renal pelvis to the tip of the urethra  AKI occurs when either both of the kidneys are obstructed or the unobstructed kidney is dysfunctional.  Causes are numerous: BPH, neurogenic bladder, anticholinergics, intraluminal calculi and clots, and compression/damage to normal structures.

12. Diagnostic evaluation  Don’t forget your History and Physical! It can give important clues to the etiology of AKI.  Hypotension?  History of vomiting and diarrhea?  New medications?  Dry mucous membranes?  Do they appear septic?

13. Patterns of Creatinine Rise  Contrast induced Nephropathy : Rise in SCr within 24-48 hrs. Peak within 3-5 days and back to baseline in 5-7 days.  Prerenal azotemia : A rise in creatinine that downtrend when volume status is corrected.  Atheroembolic disease : Typically a subacute rise in SCr (Can be rapid rise and severe in some cases).  Nephrotoxic agents like aminoglycosides, carboplatins: Rise in SCr delayed 3-14 days after exposure

14. Diagnostic workup?

15. Kidney Biopsy  A biopsy can give diagnostic information when prerenal, postrenal, ischemia and nephrotoxic etiologies are unlikely.  Useful in diagnosing glomerulonephritis, vasculitis, interstitial nephritis, myeloma kidney, HUS and TTP, and allograft dysfunction.  This procedure carries a risk of serious bleeding, especially when patients are coagulopathic.

16. Complications of AKI  Hypervolemia  Uremia  Uremia poses little direct toxicity at levels below 100 mg/dL.  At higher concentrations can cause mental status changes and bleeding  Electrolyte abnormalities including hyperkalemia, hyponatremia, hyperuricemia, hyperphosphatemia, hypocalcemia, and hypomagnesemia  Metabolic acidosis  Cardiac complications can include arrhythmias, pericarditis, and pericardial effusion

17. Indications for Emergent Dialysis  AEIOU mnemonic:  Acidemia: Persistent academia that is either non-responsive to bicarb or when giving bicarb would result in volume overload  Electrolyte abnormalities such as hyperkalemia in setting of EKG changes  Intoxications: Salicyclic acid, lithium, isopropanol, magnesium and ethylene glycol  Overload  Uremia causing complications such as pericarditis, encephalopathy, bleeding

18. Treatment of AKI  Treatment depends on the etiology and focuses on treating underlying insult  For instance, in setting of post-renal obstruction, relieving the obstruction or in prerenal etiologies such as hypovolemia, correcting the hypovolemia.  Patients may need medications renally dose in the setting of AKI.  Avoid NSAIDs and consider holding ACEi/ARBs in the setting of acute AKI