Renal insufficiency

• 肾功能不全


  renal insufficiency
• 肾功能不全


  • Oliguria or anuria
  • Retention of nitrogenous wastes (azotemia)
  • Water/electrolyte acid-base disturbance
  • Rapidly and severely decline of GFR
  • Kidneys fail to excrete and regulate in hours to days
• 急性肾功能不全的表现


  • Water intoxication
  • Azotemia
  • Hyperkalemia
  • Metabolic acidosis
• 急性肾功能不全的类型


  • Oliguria type
  • Non oliguria type
• 急性肾功能不全的病程


  • Oliguric stage
  • Polyuria stage
  • Convalescence
• 急性肾功能不全的分级


  Ⅰ: Serum creatinine increased ≥0.3mg/dl or ≥150%-200%, urine output <0.5ml/kg.h for ≥6h

  Ⅱ: Serum creatinine increased ≥200%-300%, urine output <0.5ml/kg.h for ≥12h

  Ⅲ: Serum creatinine increased >300%, urine output <0.3ml/kg.h for ≥24h or anuria ≥12h
• 急性肾功能不全的分类


  • Prerenal
  • Intrarenal
  • Postrenal
• Prerenal


  • Functional: Hypovolemia, Cardiac pump dysfunction, Increased vascular bed volume, Early stages of various types of shock

  Decreased effective circulating blood volume leads to rapid decrease in renal blood flow and GFR, with unchanged renal tubular reabsorption
• Intrarenal


  • Organic: Glomerulus, Renal interstitium, Renal blood vessels, Renal tubule

  Most common and important cause is acute tubular necrosis due to renal ischemia/reperfusion injury, endogenous/exogenous toxins
• Postrenal


  • Caused by obstruction of the urinary tract below the kidney, such as bilateral urinary tract stones, prostatic hypertrophy, pelvic tumor compression
• Pathogenesis of acute renal failure


  1. Decreased glomerular filtration rate

  2. Renal vascular and hemodynamic changes

  3. Renal tubular injury

  4. Decrease in glomerular filtration coefficient
• Renal vascular and hemodynamic changes


  • Decreased renal perfusion pressure due to decreased circulating blood volume, sympathetic activation, renin-angiotensin system, endothelial cell damage

  2. Renal vasoconstriction

  3. Swelling of renal capillary endothelial cells

  4. Intrarenal vascular coagulation
• Renal tubular injury


  • Tubular obstruction by cell fragments, myoglobin, hemoglobin

  2. Backflow of urine due to basement membrane rupture

  3. Dysfunction of tubular-juxtaglomerular feedback
• Glomerular filtration coefficient


  Represents the permeability of the glomerulus, related to the state of filtration membrane area and permeability
• Characteristics of urine changes in functional vs organic ARF


  • Specific gravity, Urine osmolality, Urinary sodium, Urine/blood creatinine ratio, Urinary protein content, Urine sediment
• Oliguric stage


  • The most dangerous stage, with water intoxication, hyperkalemia, and metabolic acidosis
• Diuretic effect of mannitol is effective in functional ARF but poor in organic ARF
• ＜20


  Urine/blood creatinine ratio
• oliguric stage


  1. The most dangerous stage in the course of the disease

  2. Water intoxication

  3. Renal drainage↓

  4. Decomposition release↑→Endogenic water↑

  5. Cell edema, diluted hyponatremia
• oliguric stage


  1. Hyperkalemia: Fewer urine and less potassium excretion

  2. Tissue damage, decomposition and release↑

  3. Acid replacement

  4. Hyponatremia, Na+-K+ exchange↓

  5. Ingestion↑: Stock blood transfusion, high potassium content

  6. The most dangerous complication
• oliguric stage


  1. metabolic acidosis: Urinary insufficiency, accumulation of acidic substances

  2. hydrogen and ammonia secretion↓, Reabsorption HCO3↓

  3. catabolism↑, Fixed acid production↑

  4. Progressive, difficult to correct
• oliguric stage


  1. azotemia: Urinary insufficiency, excretion↓

  2. Decomposition enhancement generation↑

  3. Toxin related symptoms
• Polyuria stage


  1. Urine volume exceeding 2000ml/24h

  2. Release of renal tubular obstruction

  3. The concentration function of neonatal renal tubular epithelial cells has not yet been restored

  4. Osmotic diuresis

  5. Gradual recovery of renal blood flow and glomerular filtration function
• Convalescence


  1. Lasting for approximately June to 1 year

  2. No clear boundary between polyuria and polyuria

  3. The longer the oliguria period, the longer it takes for renal function to recover

  4. Reversible pathological process
• Prevention and treatment


  1. Actively treat the primary disease

  2. Correct internal environmental disorders

  3. Anti-infection and nutritional support

  4. Treatment based on pathogenesis
• Prevention and treatment


  hyperkalemia
• Outline


  • I. II. III. IV. CRF Catalogue Concept Classification and Causes Pathogenesis Functional metabolic changes Treatment principles V.
• Chronic renal failure (CRF)


  Various chronic kidney diseases cause chronic progressive and irreversible destruction of the nephron, resulting in retention of metabolic wastes, imbalance of water, electrolyte and acid-base balance, renal endocrine dysfunction, and a series of pathological processes with clinical symptoms.
• Causes of chronic renal failure


  • Primary: Chronic glomerulonephritis, Renal arteriosclerosis, Renal tuberculosis
  • Secondary: Hypertension, diabetes
• Stages of chronic kidney disease (CKD)

  • Kidney damage with normal or increased GFR (≥90 ml/(min·1.73m2))
  • Kidney damage with mild decrease in GFR (60-89 ml/(min·1.73m2))
  • Moderate decrease in GFR (30-59 ml/(min·1.73m2))
  • Severe decrease in GFR (15-29 ml/(min·1.73m2))
  • Kidney failure and ESRD (<15 ml/(min·1.73m2) or dialysis)
• Mechanisms of chronic renal failure


  1. The role of primary disease

  2. Secondary progressive glomerulosclerosis: Changes in hemodynamics of surviving nephrons, Increased proliferation of mesangial cells and production of extracellular matrix

  3. Renal tubulointerstitial injury: Inflammation, Chronic hypoxia, Hypermetabolism of renal tubules
• Changes in urine in CRF


  1. Changes in urine volume: Enuresis nocturna, Excessive urine output greater than 2000ml/24h, Urinary output is less than 400ml/24 hours (Too few residual nephrons), Osmotic diuresis, Urine concentration dysfunction

  2. Change of urine osmotic pressure: Early stage - hypotonic urine, Late stage - isotonic urine

  3. Changes in urine composition: Proteinuria, hematuria, tubular urine
• CRF azotemia


  plasma urea nitrogen, creatinine, plasma uric acid nitrogen
• Disturbance of water electrolyte and acid-base balance in CRF


  1. Disorders in water and sodium metabolism: hyponatremia, Increased blood sodium

  2. Potassium metabolism disorders: Early stage: blood potassium normal, Late: oliguria, severe acidosis, infection, hyperkalemia, hypokalemia

  3. Magnesium metabolic disorders

  4. Abnormal calcium and phosphorus metabolism

  5. metabolic acidosis, tetany
• Complications of CRF


  • Renal osteodystrophy, Renal anemia, Renal bleeding, renal hypertension
• Factors affecting calcium and phosphorus metabolism in CRF


  • Disordered calcium and phosphorus metabolism, Vitamin D, Acidosis, Aluminum accumulation, Sodium water retention, Increased secretion of renin, Reduced blood pressure lowering substances in the kidneys
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