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the definition and clinical

practice guidelines

sudden impairment of kidney function
resulting in the retention of nitrogenous
and other waste products normally
cleared by the kidneys.
Harrisonss Principle of I nternal Medicine
8
th
edition



AKI is one of a number of conditions that
affect kidney structure and function.
AKI is defined by an abrupt decrease in
kidney function that includes, but is not
limited to, ARF.

Increase in SCr by X0.3 mg/dl (X26.5
lmol/l)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
RIFLE
AKIN


NONOLIGURIC: Urine output > 400ml/day
OLIGURIC: Urine output < 400ml/day
ANURIC: Urine output < 100ml/day

Pre-renal = 50%, mc
Intrinsic Renal = 40%
Post renal = 5%
Retention of
nitrogenous
waste products
Expansion of
ECF volume
Disorders on
electrolytes and
Acid-Base
balance

azo, meaning nitrogen, and -emia
rise in SCr or BUN concentration due to
inadequate renal plasma flow and
intraglomerular hydrostatic pressure to
support normal glomerular filtration.

Reduce effective extracellular volume
1. Hypovolemia
2. Systemic Vasodilation
3. Cardiac Failure
Impaired Renal Autoregulation
1. Postglomerular (efferent arteriolar)
vasodilation
2. Postglomerular (afferent arteriolar)
Vasoconstriction

Problem within the kidney
Major site of renal parenchymal
damage:
Glomeruli
Tubulointerstitial
Vessels

Diseases of large renal
vessels:
Renal artery
stenosis/thrombosis/
embolism/obstruction/
atherosclerotic plaque
Operative arterial cross
clamping
Bilateral renal vein
thrombosis/occlusion

Diseases of renal
microvasculature:
Vasculitis
Thrombotic
microangiopathies
Hemolytic Uremic
syndrome
Malignant HPN
Thrombotic
thrombocytopenic
purpura
Toxemia of pregnancy
HELLP

Glomerular disease:
AGN
RPGN


Tubular debris and casts in the urine

Arterial
Vasodilation
Inc NO
synthase
Reduced
GFR
Kidney: site of one of the most hypoxic
regions in the body, the renal medulla.
outer medulla--vulnerable to ischemic
damage because of the architecture of
the blood vessels that supply oxygen
and nutrients to the tubules.
Ischemia associated AKI
Ex:
cardiac surgery with cardiopulmonary
bypass (particularly for combined valve
and bypass procedures)
vascular procedures with aortic cross
clamping
intraperitoneal procedures
underlying CKD
older age
diabetes mellitus
congestive heart
failure
Emergency procedures
nephrotoxic agents
including iodinated
contrast
longer duration of
cardiopulmonary
bypass
atheroembolic
disease after
percutaneous
catheterization of the
aorta,
foreign body reaction


Extensive fluid losses into the extravascular
compartments
AKI --an ominous complication of burns,
affecting 25% of individuals with more than
10% total body surface area involvement.
Kidney is highly susceptible --extremely
high blood perfusion and concentration
of circulating substances along the
nephron where water is reabsorbed and
in the medullary interstitium

high-concentration exposure of toxins to
tubular, interstitial, and endothelial cells.

Diabetic nephropathy
Clinical course: rise in SCr beginning 2448
hours following exposure, peaking within 35
days, and resolving within 1 week.
Iodinated contrast
agents:cardiovascular
and CT imaging
high-dose gadolinium used for MRI and
oral sodium phosphate
solutions used as bowel purgatives

Aminoglycosides
Nonoliguric AKI
Hypomagnesem


Amphotericin B
Polyuria
hypomagnesemia,
hypocalcemia
non gap metabolic
acidosis

Vancomycin
Acyclovir
Foscarnet , pentamidine , and cidofovir
penicillins , cephalosporins , quinolones ,
sulfonamides , and rifampin-- AKI
secondary to acute interstitial nephritis

Cisplatin and carboplatin
Ifosfamide
mitomycin C and gemcitabine

Ethylene glycol
metabolite 2-hydroxyethoxyacetic acid
(HEAA)
Melamine
Aristolochic acid
myoglobin
Hemoglobin
uric acid
myeloma light chains
drugs
inflammatory infiltrate
peripheral and urinary eosinophilia
Total or partial blockage of urine flow
( functional or structural)--renal pelvis to
the tip of the urethra

increased retrograde hydrostatic
pressure and interference with
glomerular filtration.

CAUSES:
1. bladder neck obstruction-mc
2. prostate disease (benign prostatic
hypertrophy or prostate cancer)
3. neurogenic bladder
4. therapy with anticholinergic drugs.
5. obstructed foley catheters

hemodynamic alterations triggered
by an abrupt increase in intratubular
pressures
Initial: hyperemia from afferent arteriolar
dilation is followed by intrarenal
vasoconstriction from the generation of
angiotensin II, thromboxane A2, and
vasopressin, and a reduction in NO
production.
Ureteric Obstruction
Intraluminal: Stones blood clot, sloughed
renal papillae, uric acid or sulfonamide
crystals, fungus balls
Intramural: postoperative edema after
ureteric surgery, BK virus-induced ureteric
fibrosis in renal allograft
Extraureteric: Iatrogenic (ligation during
pelvic surgery)
Periureteric: Hemorrhage, tumor, or fibrosis

Intraluminal: Stones, blood clots,
sloughed papillae
Intramural: bladder CA, bladder
infection w/mural edema, neurogenic,
drugs (eg tricyclic antidepressants,
ganglion blockers)
Extramural: Prostatic hypertrophy,
prostatic carcinoma
Phimosis, congenital valves, stricture,
tumor

Oliguria
S/S fluid overload/volume depletion
S/S of underlying causes of ARF
S/S electrolytes imbalance, acid base
disorders
Changes in sensorium


History:
Fluid losses and fluid intake
Urine volume
Infection: Viral, bacteria, fungal
Drug/s intake
Radiologic procedures, Surgery
Symptoms of underlying disease
Diseases or clinical situation that lead
todevelopment of endogenous toxins
Renal calculi
Cardiac disease

State of hydration BP, HR, JVP, mucous
membrane, skin turgor
Signs of chronic liver disease
Skin Lesions
Edema
Abdominal findings (+) KP, distended

Volume depletion:
Hx thirst, oliguria/anuria
Excessive fluid losses
Fluid balance I & O, daily weights

PE dry mucosa, poor skin turgor
Absent axillary sweat
Reduced JVP
Postural tachycardia/hypotension
Supine tachycardia/hypotension


Increase in BUN
Increased in BUN and Creatinine
Oliguria urine < 400 ml/day

Normal or Few RBC
or WBC
Prerenal Azotemia
Arterial thrombosis or
embolism
PreglomerularVasculi
tis
HUS or TTP
Scleroderma crisis
Postrenal Azotemia

White Blood Cell
Casts
Acute intestinal
nephritis or
exudative
glomerulonephritis
Sever Pyelonephritis
Marked leukemic or
lymphomatous
infiltration
Granular casts
Acute tubule
necrosis (muddy
brown)
Glomerulonephritis or
vasculitis
Interstitial nephritis

Eosinophils (>5%)
Allergic interstitial
nephritis(antibiotics
NSAIDs)
Athereombolic
Disease

Red Blood Cell Casts
Glomerulonephritis or
vasculitis
Malignant
Hypertension
Rarely interstitial
nephritis
Crystalluria
Acute
uratenephrophaty
Calcium Oxalate
Acyclovir
Indinavir
Sulfonamides
Radiocontrast
Agents

BUN and SERUM
Creatinine
Rapid elevation
(within 24- 48 hrs)

Laboratory
evaluation:
UTZ
X-ray - KUB
-IVP, retrogade
pyelography
Ct scan stonogram/
unenhanced helical
Ct, CT angio
MRI/MRA
Doppler UTZ

Volume overload
Electrolyte disorders
Metabolic acidosis
Hyperphosphatemia/ hypocalcemia
Anemia, bleeding time
Uremic syndrome
Infection- common and accounts for 75%of
deaths
Cardiac abnormalities: arrhythmia, AMI,
pulmonary embolism
GI bleeding 10 -30% due to stress ulceration
on gastric or small intestinal mucosa

GOAL: Renal perfusion


packed RBC

severe acute
blood loss
isotonic crystalloid
and/or colloid
less severe acute
hemorrhage
burns and pancreatitis
Isotonic crystalloid
(e.g., 0.9% saline) or
colloid
severe hypovolemia
hypotonic crystalloids
(e.g., 0.45% saline)
less severe
hypovolemia.

acute glomerulonephritis
or vasculitis

immunosuppressive agents
and/or plasmapheresis
AIN due to medications
discontinue
Rhabdomyolysis

10 L of fluid per day
tubular injury and
cast formation
75 mmol sodium
bicarbonate
added to 0.45%
saline
site of obstruction defines the treatment
approach
transurethral or suprapubic bladder
catheterization--urethral strictures or
functional bladder impairment
Ureteric obstruction--percutaneous
nephrostomy tube placement or
ureteral stent placement
Volume Management
furosemide may be given as a bolus (200
mg) followed by an intravenous drip (10
40 mg/h), with or without a thiazide
diuretic.
metabolic acidosis: dextrose water
with 150 mEq sodium bicarbonate
Hyperphosphatemia
---phosphate binders (calcium
carbonate, calcium acetate,
sevelamer, or aluminum hydroxide).
Immediate Onset:
Calcium gluconate
10% 10ml soln over 2-3
mins
Intermediate Onset:
Shift K+ into the cells
Insulin + Glucose
Sodium bicarbonate
Dose is 50-150 meq/L
B2 Adrenergic Agonist
Albuterol 10 mg
nebulization






Delayed Onset:
Normal renal function
Cation Exchange Resin
Sodium Polystyrene
sulfonate
(Kayexalate)
Oral: 20-40g with
100mL 20% sorbitol
Absent Renal Function
Cation Exchange Resin
Na polysterene
Sulfonate
(Kayexalate)
Oral:
20-40 gm w/ 100 ml
20% sorbitol
Onset is 2 hrs; rptd
every 4-6hrs

Absent Renal Function
Cation exchange
Resin
Dialysis:
Onset immediate
Hemodialysis is
preferred
Removes 25-30
meq/hr on total
body K+


Uremic encephalopathy
Intractable fluid overload
Nonresponsive hyperkalemia
Refractory metabolic acidosis
BUN > 100mg/dl

3.1.1: In the absence of hemorrhagic
shock, we suggest using isotonic
crystalloids rather than colloids (albumin
or starches) as initial management for
expansion of intravascular volume in
patients at risk for AKI or with AKI. (2B)
3.1.2: We recommend the use of
vasopressors in conjunction with fluids in
patients with vasomotor shock with, or at
risk for, AKI. (1C)

3.1.3: We suggest using protocol-based
management of hemodynamic and
oxygenation parameters to prevent
development or worsening of AKI in high-
risk patients in the perioperative setting
(2C) or in patients with septic shock (2C).
3.3.1: In critically ill patients, we suggest
insulin therapy targeting plasma glucose
110149mg/dl (6.18.3mmol/l). (2C)
3.3.2: We suggest achieving a total energy
intake of 2030 kcal/kg/d in patients with
any stage of AKI. (2C)
3.3.3: We suggest to avoid restriction of
protein intake with the aim of preventing or
delaying initiation of RRT. (2D)
3.3.4: We suggest administering 0.81.0
g/kg/d of protein in noncatabolic AKI
patients without need for dialysis (2D),1.0
1.5 g/kg/d in patients with AKI on RRT (2D),
and up to a maximum of 1.7 g/kg/d in
patients on continuous renal
replacement therapy (CRRT) and in
hypercatabolic patients. (2D)
3.3.5: We suggest providing nutrition
preferentially via the enteral route in
patients with AKI. (2C)
3.4.1: We recommend not using diuretics to
prevent AKI. (1B)
3.4.2: We suggest not using diuretics to treat
AKI, except in the management of volume
overload. (2C)
3.5.1: We recommend not using low-dose
dopamine to prevent or treat AKI. (1A)
3.5.2: We suggest not using fenoldopam to
prevent or treat AKI. (2C)
3.5.3: We suggest not using atrial natriuretic
peptide (ANP) to prevent (2C) or treat (2B) AKI.
3.6.1: We recommend not using recombinant
human (rh)IGF-1 to prevent or treat AKI. (1B)
3.7.1: We suggest that a single dose of
theophylline may be given in neonates with
severe perinatal asphyxia, who are at high risk
of AKI. (2B)
3.8.1: We suggest not using aminoglycosides
for the treatment of infections unless no
suitable, less nephrotoxic,therapeutic
alternatives are available. (2A)
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)
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)
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)
3.8.6: We suggest using lipid formulations of
amphotericin B rather than conventional
formulations of amphotericin B. (2A)
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)

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