肾病课件——急性肾衰竭(英文)-32页PPT文档资料

Role of Tubule Dysfunction in ATN
Two Major TubularAbnormalities:
Obstrction
Backleak
Metabolic Responses of Tubule cells to Injury
ATP Depletion Cell Swelling Intyacellular Free Calcium↑ Intyacellular Acidosis Phospholipase Activation Protease Activation Oxidant Injury Inflammatory Respose
Management of ARF (一)
Correction of Reversible causes
Prevention of additional Injury Maintaining Fluid balance
Management of ARF (二)
Maintaining Fluid balance
ETIOLOGY OF ARF
Prerenal Azotemia
Intravascular Volume Depletion Decreased Cardiac Output Systemic Vasodilatation Renal Vasoconstriction Pharmacologic Agents (ACEI or NSAIDs)
急性肾小管坏死
Acute Tubule Necrosis （ATN）
ETIOLOGY OF ATN
Renal Ischemia（50%） Nrphrotoxins （35%）
Exogenous Endogenous
PATHOPHYSIOLOGY OF ATN
Intrarenal Vasoconstriction Tubular Dysfunction
Animia, RBC ↓, Hb ↓ BUN and Scr↑ Na ＋ ↓ ，K＋↑,Ca2＋↓，P3+ ↑ pH ↓，AG ↑，HCO3－ ↓
Lab Examination
Diagnostic Index Prerenal
Specific Gravity
> 1.020
Osmolality(mOsm/Kg H2O) > 500
Volume Overload Metabolic Acidosis Hyperkalemia Hyponatremia Hypocalcemia Hyperphosphatemia
The Recovery Phase
The Period of Repair and Regeneration of Renal Tissue:
< 20 <3 < 10-15
>1 >1 Brown ranular
Lab Examination
Radiologic Evaluation:
Plain Abdominal film Renal Ultrasonography IVP Renal angiography
Renal Biopsy
Management of ARF (四）
Hyperkalemia
K+<6mmol/L Restriction of Dietary Potassium Intake K+-Binding Ion Exchange Resins
K+>6mmol/L 10%Calcium Gluconate 10-20ml 5% Sodium Bicarbonate 100-200ml 20% Glucose 3ml/kg.h+Insulin 0.5U/kg.h Dialysis
Pathology
Clinical Presentation of ATN
The Clinical Course of ATN：
The Initiation Phase The Maintenance Phase The Recovery Phase
The Initiation Phase
GFR↓ Lasting Hours or Days Evidence of true Volume Depletion Decreeced Effective Circulatory Volume Treatment with NSAIDs or ACEI
Gradual Increase in Urine Output “Post-ATN” Diuresis Fall in BUN and Scr Recovery of GFR/ Tubule function
Lab Examination
Blood Routine Test and Chemistry Assays:
Management of ARF (五）
Metabolic Acidosis
HCO3－< 15mmol/L : 5% Sodium Bicarbonate 100-250ml Dialysis
Management of ARF Other Electrolyte Disorder Infection Hart failure Dialysis
The Uremic Syndrome
General Complications of ARF： Gastrointestinal Cardiovascular Respiratory Neurologic Hematologic Infectious

The Uremic Syndrome
Homeostatic Disorder of water， Electrolyte and Acid-alkali Balance：
Diagnosis Differentiation：
prerenal azotemia postrenal azotemia Glomerulonephritis/Vasculitis HUS/TTP Interstitial Nephritis Renal Artery Thrombosis Renal vein thrombosis
Role of Hemodynamic alterations in ATN
Reduction in Total Renal Blood
Flow Regional Disturbance in
Renal Blood Flow and Oxygen
Supply
Edothelin (ET) / NO (EDNO) Other Endothelial Vasoconstrctors The Tubulo-glomerular Feed Back
ARF complicates approximately 5% of hospital admissions and up to 30% of admissions to intensive care units.
CLASSIFICATION
Prerenal azotemia Intrinsic renal azotemia Postrenal azotemia
Fluid Intake ： 500ml + The Amount of Urine in The Preceding 24 Hours
Management of ARF (三）
Nutrition
Enegy Intake:147kj/d Dietary Protein: 0.8g/kg.d CRRT ( fluid > 5L/d)
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ETIOLOGY OF ARF
Postrenal Azotemia
Ureteric Obstruction
Bladder Neck Obstruction Urethral Obstruction
ETIOLOGY OF ARF
Intrinsic Renal Azotemia
Diseases Involving Large Renal Vessels Diseases of Glomeruli And Microvasculature Acute Tubule Necrosis Diseases of the Tubulointerstitium
Urinary Na+ (mmol/L)
< 10
Ucr/Scr
> 40
UUN/BUN
>8
BUN/Scr
> 20
Renal Failure Index
<1
Fractional Excretion of Na+ < 1
Urine Sediment
Hyaline
Renal
~ 1.010 ~ 300 > 20
急性肾衰竭
Acute Renal Failure （ARF）
DEFINITIONS AND INCIDENCE
Acute renal failure (ARF) is a syndrome characterized by rapid decline in glomerular filtration rate(GFR) and retention of nitrogenous waste products such as blood urea nitrogen (BUN) and creatinine.
The Maintenance Phase
GRR 5 ~ 10 ml/min Lasting 1 ~ 2 Weeks Oliguric ARF high catabolism Nonoliguric ARF Uremic Syndrome
High Catabolic State
Daily Increase in BUN >10.1~17.9 mmol/L Daily Increase in Serum Creatinine >176.8μmol/L Daily Increase in Serum Potassium >1~2 mmol/L Daily Decrease in Serum HCO 3 －>2 mmol/L