Acute kidney injury prevention new microsoft power po.int presentation
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Transcript of Acute kidney injury prevention new microsoft power po.int presentation
objectives Definition of acute kidney injury
Diagnosis , prevalence , aetiology , RIFLE crietria , AKI crieteria ,………. Already discussed
Clinical Approach to AKI:
Pre-, Intra-, and Post-Renal
History Volume status
Ultrasound Urinalysis US shows
Hydronephrosis
Post-Renal
Urinalysis Normal
Urinalysis Abnormal
Tubulointerstial Disorders
Glomerular and Vascular Disorders
Pre-renal
Urinalysis in Acute Kidney Injury
Prerenal Postrenal Oncotic AKI
Glomerulopathy Vasculitis
Thrombotic MA
Pyelonephritis Interstitial nephritis
AIN Athero- embolic
AKI
ATN Myoglobin Hemoglobin
Uric acid Toxins Drugs
Plasma cell dyscrasia
Hematuria RBC casts proteinuria
WBC WBC casts
Eosinophils RTE cells Pigmented
casts
Crystalluria Non- albumin
proteinuria
Abnormal sediment Normal/bland
Schrier, Diseases of the Kidney
Pathophysiology of Ischemic and Toxic Acute
Renal Failure
MICROVASCULAR TUBULAR
Vasoconstriction
endothelin, adenosine,
angiotensin II, thromboxane A2,
leukotrienes, sympathetic nerve
activity
Vasodilation
nitric oxide, PGE2, acetylcholine
bradykinin
Cytoskeletal
breakdown
Loss of polarity
Apoptosis and
Necrosis
Desquamation of
viable and necrotic
cells
Tubular obstruction
Backleak
Glomerular Medullary
O2/TOXINS
Inflammatory
and
vasoactive
mediators
Endothelial and vascular smooth
muscle cell structural damage
Leukocyte-Endothelial adhesion
vascular obstruction, leukocyte
activation, and inflammation
Schrier, Diseases of the Kidney
However ……..
What about MRI….. US IT SAFE
AKI: Rhabdomyolysis Precipitated by trauma/crush injury, extreme exertion,
statins, cocaine, envenomation, hypoK, hypoPO4
Multifold injury, with volume depletion, direct tubular toxicity, and obstructing pigment casts
UA: granular casts, (+) bld on dipstick but (-) microscopy
due to myoglobin pigment
CK levels not always consistent in predicting AKI, but general consensus is that low likelihood exists with CK levels less than 5k-10k
Rhabdomyolysis
Endotoxin cascade
Activation of ET NO
scavenging
Muscular vasodilatation and uptake of
ECF in damaged muscles
Increased load of PO4 and urate
Myoglobinemia Hyperuricemia
Hypovolemia, CV suppression due
to hi K, lo Ca, Met Acidosis
Myoglobinuria Uricosuria
Renal vasoconstriction, ischemia
Pigment nephrotoxicity
Tubular cast formation and stasis
Depletion of ATP stores,
synergistic tubular damage
ATN
Zager RA, Kidney Int 1996; 49: 314-326
AKI: Rhabdomyolysis Treatment is via forced saline diuresis: goal of UOP >
200-300 mL/hr
Early hydration: in crush victims, IV begun in field, advised even before full extrication (Turkey earthquake, 1999)
Urinary alkanization
Treatment for symptomatic hypocalcemia only: watch for hyperK
Atheroembolic (AE) AKI
Renal and systemic AE occur in patients with diffuse atheroscerotic disease
Risk factors include manipulation of the aorta or other large arteries during angiography or CV surgery
Also can occur spontaneously with ulcerated plaques
Destabilization of plaque may be enhanced in the setting
of anticoagulation or thrombolytic therapy
Atheroembolic AKI
Clinical Manifestations
AKI days to weeks after manipulation, anticoagulation
Systemic signs, signals of inflammation
Rash
Livedo reticularis
Decreased complement due to activation by exposed atheromata
Eosinophilia/eosinophiliuria
Occlusion of distal arteriolar beds
AKI
Visual field deficits
Gangrenous digits, palpable pulses
Pancreatitis
GI bleeding
Acute Kidney Injury
Clinical features of Acute Interstitial Nephritis Onset usually 3-5 days with most drugs, but may be sooner with
rifampin, or much later with NSAIDS
Rising SCr which resolves upon d/c of offending drug
Fever, hematuria, pyuria: Urine eosinophils
Mild to moderate proteinuria; much higher to NS in NSAIDS
Eosinophilia and morbilliform rash also s/sx in AIN
Occasionally see hyperkalemia and distal RTA
Prednisone 40 mg PO x 2 wks sometimes utilized to shorten AKI interval
Schrier, Diseases of the Kidney
Schrier, Diseases of the Kidney
Acute Kidney Injury: AIN causes
DRUGS ACEI
Allopurinol
Cephalosporins
Cimetidine
Fluoroquinolones
Loop diuetics
NSAIDS
Phenytoin
Rifampin
Sulfonamides
Tegretol
Thiazides
INFECTION Bacterial
Agents causing pyelonephritis
Legionella
Brucella
Yersinia
Viral
Hantavirus
HIV
CMV,EBV,HSV
Acute Kidney injury Crystal-induced AKI:
Common factors include high excretion in urine, and low solubility in acidic urine; exacerbated by hypovolemia; examination of urine critical to Dx
Common agents Uric acid
Acyclovir
Sulfa
Methotrexate
Ethylene glycol
Pre-exposure hydration, Urinary alkalinization
Hemolytic Uremic Syndrome
One of the most common causes of community-acquired
AKI in young children
Triad of microangiopathic hemolytic anemia,
thrombocytopenia, and renal insufficiency
HUS has clinical features in common with thrombotic
thrombocytopenic purpura (TTP) which is also characterized
by these features but can include central nervous system
(CNS) involvement and fever and can have a more gradual
onset
A low platelet count can usually, but not always, be detected
early in the illness, but it can then become normal or even
high. If a platelet count obtained within 7 days after onset of
the acute gastrointestinal illness is not <150,000/mm3, other
diagnoses should be considered
Terminology and Classification
Microangiophathic hemolytic anemia with fragmented erythrocytes (schistocytes)
Acute Kidney Injury
Indications for Renal Biopsy in AKI:
Acute nephritic syndrome
Hematuria, cellular casts, proteinuria in setting of new-onset or exacerbation of HTN, rising SCr
May also have serologic (+) i.e. ANA, ANCA, aGBM that tissue dx also provides treatment options and prognosis
Unexplained AKI
Uncertain or multiple competing ddx, of which treatment differs greatly with definitive dx; AIN vs ATN considerations are seen not uncommonly in hospitalized pts
Young pts with AKI often are considered based on long-term renal survival outcomes maximized with definitive dx
Renal TPL: Acute Rejection
aeiou
Classic Indications for RRT
A—acidosis
E—electrolyte disturbances
I—intoxication
O—overload
U—uremia