1. RIFLE Study: Application to Practice
Cammy House-Fancher, ACNP
University of Florida

2. RENAL BLOOD FLOW Kidney’s receive 20-25% of CO
Autoregulation: maintains constant in GFR
MAP mmHg prevents changes in GFR
Afferent arteriole’s ability to dilate or constrict
Filtration ceases MAP <40 to 60 mmHg

3. Constriction of Efferent
Mesangial
Cell Relaxation
Capillary Loop
↓effects of
Angiotensin-II,
Vasopressin
Aldosterone
Endothelial
Cell
Dilation of Afferent
Arteriole
Constriction of Efferent
Arteriole
Juxtaglomerular Apparatus

4. RENAL ASSESSMENT Weight and fluid changes
Serum osmolality: mOm/liter
BUN:Creatinine ratio: 10:1
If BUN is elevated disproportionate to Creatinine.
Dehydration (prerenal)
Catabolism
Blood in gut

5. ARF ARF is a common complication of critical illness
Associated with high mortality and
And has an Independent Increase risk of death %

6. Risk, Injury and Failure
ARF
ARF 1-25% of critical care patients
Carries 28-90% mortality
Today--AKI, Acute Kidney Injury
Acute Dialysis Quality Initiative (ADQI) published RIFLE Study (2006) to define Acute Kidney Injury (AKI)
Risk, Injury and Failure

7. RIFLE Study: 5,383 Risk Stratification of patients in the ICU
Study: 21% of pts had acute kidney injury on admission to the ICU
During entire ICU stay: 67.2% an episode of acute kidney injury -- 50% of these pts reached renal failure within 2 days of ICU admission

8. Proposed classification scheme for acute renal failure (ARF)
Proposed classification scheme for acute renal failure (ARF). The classification system includes separate criteria for Creatinine and urine output (UO). A patient can fulfill the criteria through changes in serum Creatinine (SCreat) or changes in UO, or both. The criteria that lead to the worst possible classification should be used. Note that the F component of RIFLE (Risk of renal dysfunction, Injury to the kidney, Failure of kidney function, Loss of kidney function and End-stage kidney disease) is present even if the increase in SCreat is under threefold as long as the new SCreat is greater than 4.0 mg/dl (350 μmol/l) in the setting of an acute increase of at least 0.5 mg/dl (44 μmol/l). The designation RIFLE-FC should be used in this case to denote 'acute-on-chronic' disease. Similarly, when the RIFLE-F classification is achieved by UO criteria, a designation of RIFLE-FO should be used to denote oliguria. The shape of the figure denotes the fact that more patients (high sensitivity) will be included in the mild category, including some without actually having renal failure (less specificity). In contrast, at the bottom of the figure the criteria are strict and therefore specific, but some patients will be missed. *GFR = Glomerular Filtration Rate; ARF Acute Renal Failure

9. Loss Persistent ARF=Complete loss
of Kidney Function>4 weeks
ESKD End Stage Renal Failure
(>3 months)

10. Critical Care Environment AKI is marker of Mortality

11. ACUTE RENAL FAILURE: ARF
Definition: any sudden severe impairment or cessation of kidney function: characterized by accumulation of nitrogenous wastes and fluid and electrolyte imbalances:
Prerenal: disrupted blood flow to the kidney
<Intravascular volume, <CO, vasodilation, renovascular disease: most common is floor pt

12. Cortical: intrarenal damage to renal tissue
glomerulonephritis, vasculitis, interstitial nephritis (renal capillary swelling)

13. ARF Medullary: Acute Tubular Necrosis
Nephrotoxic drugs, prolonged ischemic injury, any causes of prerenal failure that is prolonged: prolonged ischemia destroys tubular basement membrane: most common in ICU pt
Postrenal: disrupted urine flow
Mechanical obstruction, functional obstruction: neurogenic bladder, diabetic neuropathy

15. STAGES OF ARF
Onset: period of time from the precipitating event to beginning of oliguria or anuria
Duration: hours to days
BUN/Creatinine: normal or slightly decreased
Mortality: 5%

16. STAGES OF ARF Oliguric-Anuric: when urine output is <400cc/24h
Duration: 1-2 weeks
BUN/creatinine: >>
Mortality: %
Other: metabolic acidosis, water gain w/ dilutional hyponatremia, hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, azotemia

17. STAGES OF ARF
Diuretic: urine output is >400cc/24h until lab values stabilize
Duration: 1-2 weeks
Urine output: may > 3L/24h ( normal)
BUN/creatinine:
Mortality: 25%
Other: metabolic acidosis, Na may be normal or low, high K continues

18. STAGES OF ARF
Recovery: period of time between when the lab values stabilize until they are normal
Duration: months
BUN/creatinine: back to 100% normal
Mortality: %
Other: uremia, acid-base imbalances, and electrolyte imbalances gradually resolve

19. TREATMENT Support renal perfusion and improve GFR Volume
Inotropes, vasopressors (dopamine)?????? NO!
Administer diuretic challenge
Maintain fluid, lyte, and acid-base balanced
Na, K, phosphorus, magnesium
Diminish accumulation of nitrogenous wastes
Protein restriction, dialysis

20. TREATMENT Prevent further damage to kidney
Eliminate nephrotoxic agents
Monitor peak and trough levels of drugs
Nutrition
Prevent infection
Monitor and treat anemia (Epogen)

21. MANAGEMENT: COMPLICATIONS
Renal failure increases mortality overall
Renal: chronic RF in 25-30% of ARF
CV: dysrhythmias, HTN, pericarditis, pulmonary edema, HF
Neurologic: coma, seizures
Metabolic: lyte imbalance
GI: PUD, hemorrhage, anorexia, N/V, abd distention, pancreatitis, ileus

22. MANAGEMENT: COMPLICATIONS
Hematologic: anemia, uremic coagulopathies, >WBC, plts dysfunction
Infection: pneumonias, Immunosuppressed
Pulmonary: pulmonary edema, hyperventilation, acid- base imbalance
Nutrition

23. RENAL REPLACEMENT THERAPIES
Dialysis
Semipermeable membrane Blood/dialysate
Principles:
Types:
Peritoneal
Hemodialysis
Continuous Renal Replacement Therapy

24. Reasons for CVVHD Electrolyte disorder Hypoxemia Met acidosis
Symptomatic uremia
Bleeding: plts
(DDAVP)
Pericarditis
Intolerance to HD
Clear Myoglobin
Rhabdomyolysis
Obese Pt undergoing surgery
⇑ ICP w liver failure

25. Evidence
Unknown at present time which form of dialysis is best for renal recovery
There is an increase in CRRT esp. in the pt with sepsis and liver/GI disease
NO change in mortality
Is more costly

26. Look for AKI
Can we prevent AKI?

27. Preventing AKI
Limit dehydration, hypotension, exposure to nephrotoxins
Maintaining renal perfusion pressure: not just pressure remember abdominal compartment syndrome

28. Strategies to Prevent AKI
IV isotonic hydration
Maintenance of adequate MAP (>65)
Minimizing nephrotoxin exposure

29. Strategies to Prevent Contrast Nephropathy
N-acetylcysteine
Hydration with sodium bicarb
Strategies that are under investigation
ANP, fenoldopam with septic pts, theophylline, and hemofiltration

30. Acute Renal Failure
Chronic renal failure occurs in about 25% of patients with acute renal failure
Careful renal protection must continue

31. Real Deal Think Renal Protection
Thank You

32. CRF
CRF is a slowly progressive disease that causes gradual loss of kidney function. It can range from mild dysfunction to severe renal failure
Over number of years
Asymptomatic
Progression may be so slow: symptoms occur when RF is 1/10th of normal

33. Incidence 2 out of 1000 people in US
DM and HTN are the two most common causes and account for most cases
Other Causes
Heart Failure, Hypotension, Glomerulonephritis, kidney stones, obstructive uropathy, Polycystic disease

34. CRF
Categorized as diminished renal reserve, renal insufficiency, or renal failure.
Decreased renal function interferes with the kidney’s ability to maintain fluid and electrolyte homeostasis. Changes precede predictability

35. CRF First: ability to concentrate urine declines early
Followed by decreases in ability to excrete phosphate, acid and Potassium
RF advanced: (GFR < 10mL/min/1.73m2)
Ability to dilute UA is lost--volume ⇓

36. CRF
As RF progresses
Abn of Ca, phosphate, PTH, vit D metabolism, renal osteodystrophy occur
Decreased renal excretion of Calcitrol leads to hypocalcemia
2º hyperparathyroidism is common
SO---monitoring PTH is recommended

37. Symptoms Fatigue: anemia Frequent hiccups General ill feeling
Generalized itching (pruritus)
Headache
Nausea and vomiting
Unintentional weight loss

38. Late Symptoms Hyper vomiting , uremic frost
Confusion, change is behavior and LOC
Decreased sensation in the hands, feet
Easy bruising or bleeding
Increased or decreased urine output
Muscle twitching or cramps
Seizures

39. Diagnosis UA Creatinine Creatinine clearance
Potassium--Electrolyte Disturbances
Metabolic Acidosis
CT scan, Abd MRI, ultrasound
Renal Biopsy

40. Classification Stage 1: normal GFR (>90mL/min/1.73m2)
Plus persistent albuminuria
Stage 2: GFR 60 to 89
Stage 3: GFR 30 to 59
Stage 4: GFR 15 to 39
Stage 5: GFR < 15

41. ESRD A. 90% nephrons damaged
B. Renal function has deteriorated that chronic and persistent abnormalities exit
C. Patient requires artificial support to sustain life
D. Uremic syndrome

42. Treatment
Goal: control symptoms, reduce complications, and slow the progression of the disease (tx underlying problem)
Fluid restriction, diet control, BP monitoring and control, DM control, Vit D supplements, electrolyte control
Doses of all drugs adjusted
Dialysis ??

43. Treatment
Underlying disorders and contributory factors must be controlled. Hyperglycemia
BP--110 to 130/<80
ACE-I, ARBs decrease rate of decline in GFR in pts with most causes of CRF

44. Activity: need not be restricted, although fatigue and lassitude usually limit exercise
Nutrition: Severe protein restriction is controversial--mod restriction key
0.8g/kg/day if GFR 25 to 55
0.6g/kg/day if GFR 13 to 24

45. More Nutrition Vit D supplements Vit A+E is unnecessary
Calcitrol: as indicated by PTH levels
Stage of renal failure = and phosphate
Target Ca = 8.4 to 9.5
Starting dose 0.25ug po daily
Vit A+E is unnecessary
Statin if cholesterol is elevated

46. Inversely proportional to GFR
RENAL PEARLS
S+S of hypophosphatemia=reciprocal hypercalcemia, weakness, apathy and confusion, TPN, ETOH
Seizures are seen with hyperphos
Creatinine best indicator of renal function:
Inversely proportional to GFR
<<sodium causes aldosterone release