急性肾损伤
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7
ATN (acute tubular necrosis)
• Etiology • Pathogenesis • Pathology • Clinical Presentations • Laboratory Examinations • Diagnosis & Differentiation • Management
• Postrenal: 5-10 %
• The 2 most common causes of acute renal failure in hospitalized patients are prerenal azotemia and acute tubular necrosis（ＡＴＮ）.
• There is a continuum from prerenal physiology to ischemic pathology.
• Oliguria is a common finding but not necessary. ARF is sometimes asymptomatic and is diagnosed by increase in the urea and creatinine.
3
Acute kidney injury (AKI)
8
Etiology
9
Renal Ischemia
Supply of O2 Nutrients to Kidney
ATP
Abnormal Metabolic Levels
Nephrotoxins
Lipid Peroxidation Oxygen-Derived Free Radicals
Thromboxane Norepinephrine
Tubuloglomerular
Feedback
Afferent Arteriolar Constriction
Kf
Glomerular Capillary Pressure
RBF
Tubular Obstruction
Backleak
Reduced Glomerular Filtration Rate
12
ＨＥ
病理
Clinical Course of ATN
• Initiation Phase • Maintenance Phase • Recovery Phase
15Baidu Nhomakorabea
Initiation Phase
• Causes: Hypotension,Sepsis,Renal Toxins
• with usually normal urine output, varies in duration depending on causative factors (eg, the amount of toxin ingested, the duration and severity of hypotension).
Acute kidney Injury
Department of Nephrology, Tongji Hospital Hongyu Gao
Definition of AKI
Acute kidney Injury(AKI) is a syndrome characterized by rapid decline in GFR hours to days, retention of nitrogenous waste products and disturbances in the extracellular volume, electrolyte and acid base homeostasis.
Pathology of ATN
• Tubule vacuolization, Tubule dilation and brush border losses
• Degenerated and sloughed, frank necrosis tubular cells
• Denuded basement membrane and the presence of intraluminal casts
Functional or structural abnormalities or markers of kidney damage including abnormalities in blood , urine or tissue tests or imaging studies present for＜3 months
Classification and Major Causes of AKI
5
Classification and Major Causes of AKI
6
Classification and Major Causes of AKI
• Prerenal: 50-80 %
• Renal: 10-40 %
• Clinical Syndrome • Quick decline of GFR • Accumulation of nitrogenous products :
Rising Serum Creatinine(≥44.2µmol/L /day)
2
• It is seen as a complication in about 5% of hospital admissions, and up to 30% of intensive care admissions.
Tubular Sodium Pump inhibition
Cell structure changes
Membrane Integrity Cytoskeleton Damaged
Mitochondria Swell
Pathologic Changes
Tubular Dysfunction: Leakage, Obstruction, Loss of Filtration, Necrosis
The Pathophysiology of ATN
Ischemic / Toxic Renal Injury
Hemodynamic Abnormalities
Tubular Damage
Endothelial Swelling Reduced EDRF
Vasoconstrictor Release Endothelin Angiotensin
ATN (acute tubular necrosis)
• Etiology • Pathogenesis • Pathology • Clinical Presentations • Laboratory Examinations • Diagnosis & Differentiation • Management
• Postrenal: 5-10 %
• The 2 most common causes of acute renal failure in hospitalized patients are prerenal azotemia and acute tubular necrosis（ＡＴＮ）.
• There is a continuum from prerenal physiology to ischemic pathology.
• Oliguria is a common finding but not necessary. ARF is sometimes asymptomatic and is diagnosed by increase in the urea and creatinine.
3
Acute kidney injury (AKI)
8
Etiology
9
Renal Ischemia
Supply of O2 Nutrients to Kidney
ATP
Abnormal Metabolic Levels
Nephrotoxins
Lipid Peroxidation Oxygen-Derived Free Radicals
Thromboxane Norepinephrine
Tubuloglomerular
Feedback
Afferent Arteriolar Constriction
Kf
Glomerular Capillary Pressure
RBF
Tubular Obstruction
Backleak
Reduced Glomerular Filtration Rate
12
ＨＥ
病理
Clinical Course of ATN
• Initiation Phase • Maintenance Phase • Recovery Phase
15Baidu Nhomakorabea
Initiation Phase
• Causes: Hypotension,Sepsis,Renal Toxins
• with usually normal urine output, varies in duration depending on causative factors (eg, the amount of toxin ingested, the duration and severity of hypotension).
Acute kidney Injury
Department of Nephrology, Tongji Hospital Hongyu Gao
Definition of AKI
Acute kidney Injury(AKI) is a syndrome characterized by rapid decline in GFR hours to days, retention of nitrogenous waste products and disturbances in the extracellular volume, electrolyte and acid base homeostasis.
Pathology of ATN
• Tubule vacuolization, Tubule dilation and brush border losses
• Degenerated and sloughed, frank necrosis tubular cells
• Denuded basement membrane and the presence of intraluminal casts
Functional or structural abnormalities or markers of kidney damage including abnormalities in blood , urine or tissue tests or imaging studies present for＜3 months
Classification and Major Causes of AKI
5
Classification and Major Causes of AKI
6
Classification and Major Causes of AKI
• Prerenal: 50-80 %
• Renal: 10-40 %
• Clinical Syndrome • Quick decline of GFR • Accumulation of nitrogenous products :
Rising Serum Creatinine(≥44.2µmol/L /day)
2
• It is seen as a complication in about 5% of hospital admissions, and up to 30% of intensive care admissions.
Tubular Sodium Pump inhibition
Cell structure changes
Membrane Integrity Cytoskeleton Damaged
Mitochondria Swell
Pathologic Changes
Tubular Dysfunction: Leakage, Obstruction, Loss of Filtration, Necrosis
The Pathophysiology of ATN
Ischemic / Toxic Renal Injury
Hemodynamic Abnormalities
Tubular Damage
Endothelial Swelling Reduced EDRF
Vasoconstrictor Release Endothelin Angiotensin