12 renal failure_ptii
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patholophysiology of Renal Failure Pathophysiology（病理生理学） Pathology uploaded by prabesh 杰诗
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12 renal failure_ptii
- 1. Dept. of PathologyDept. of Pathology Medical CollegeMedical College Hunan Normal UniversityHunan Normal University (( 湖南 范大学医学院病理学教研室师湖南 范大学医学院病理学教研室师 )) 1 Chapter 12Chapter 12 Renal FailureRenal Failure （ 衰竭）肾脏（ 衰竭）肾脏
- 2. Outline 11 22 33 44 2 Introduction Acute Renal Failure Chronic Renal Failure Uremia
- 3. 33 Chronic Renal FailureChronic Renal Failure a.a. DefinitionDefinition b.b. Etiology and ClassificationEtiology and Classification c.c. PathogenesisPathogenesis d.d. Clinical CourseClinical Course e.e. Alterations of Function andAlterations of Function and MetabolismMetabolism
- 4. 4 Section 3 Chronic Renal Failure Definition A pathologic process caused by progressive and irreversible damage of nephrons, which results in fewer and fewer intact nephrons that leads to the retention of waste products and toxic metabolites, water-electrolyte and acid-base imbalance and endocrine dysfunction.
- 5. 5 Section 3 Chronic Renal Failure Causes Progressive damage IntactNephrons Endocrine Dysfunction OrganDysfunction
- 6. 66 Chronic Renal FailureChronic Renal Failure a.a. DefinitionDefinition b.b. Etiology and ClassificationEtiology and Classification c.c. PathogenesisPathogenesis d.d. Clinical CourseClinical Course e.e. Alterations of Function andAlterations of Function and MetabolismMetabolism
- 7. 7 Section 3 Chronic Renal Failure Etiology Renal Diseases Chronic glomerulonephritis Systemic Diseases Diabetes mellitus, Hypertension
- 8. 8 Section 3 Chronic Renal Failure CauseCause %% Chronic glomerulonephritisChronic glomerulonephritis 64.464.4 Chronic pyelonephritisChronic pyelonephritis 14.814.8 CollagenosisCollagenosis 7.87.8 Renal tuberculosisRenal tuberculosis 4.94.9 HypertensionHypertension 3.13.1 Polycystic kidneyPolycystic kidney 2.72.7 Diabetes mellitusDiabetes mellitus 0.50.5 Causes of Chronic Renal Failure
- 9. 99 Chronic Renal FailureChronic Renal Failure a.a. DefinitionDefinition b.b. Etiology and ClassificationEtiology and Classification c.c. PathogenesisPathogenesis d.d. Clinical CourseClinical Course e.e. Alterations of Function andAlterations of Function and MetabolismMetabolism
- 10. 10 Section 3 Chronic Renal Failure Pathogenesis of CRF ♠Intact nephron hypothesis ♠Glomerular hyperfiltration hypothesis ♠Trade-off hypothesis
- 11. 11 Section 3 Chronic Renal Failure Intact Nephron Hypothesis
- 12. 12 Section 3 Chronic Renal Failure Chronic renal diseases Chronic renal diseases Progressive damage of nephrons Progressive damage of nephrons Intact nephrons work excessively Intact nephrons work excessively Intact Nephron HypothesisIntact Nephron Hypothesis Glomerular- tubular balance disrupted Glomerular- tubular balance disrupted BUN and serum creatinine ↑↑ BUN and serum creatinine ↑↑ Filtration rate and solute load per nephron ↑↑↑ Filtration rate and solute load per nephron ↑↑↑
- 13. 13 Section 3 Chronic Renal Failure Renal fibrosis Glomerulosclerosis Renal fibrosis Glomerulosclerosis Progressive decrease of nephrons Progressive decrease of nephrons Chronic renal diseases Chronic renal diseases Glomerular filtration pressure in intact nephrons ↑↑ Glomerular filtration pressure in intact nephrons ↑↑ Glomerular Hyperfiltration HypothesisGlomerular Hyperfiltration Hypothesis
- 14. GFR ↓ Vit D3 ↓ Osteolysis Renal osteodystrophy Serum HPO4 2- ↑ PTH↑ Ca2+ ↓ Excretion of HPO4 2- ↓ Serum Ca2+ N Correction Disturbance Nephrons ↓ Renal diseases Reabsorption of HPO4 2- ↓ Serum HPO4 2- N Trade-off hypothesis Trade-off hypothesis Section 3 Chronic Renal Failure Acidosis Trade-off
- 16. 1616 Chronic Renal FailureChronic Renal Failure a.a. DefinitionDefinition b.b. Etiology and ClassificationEtiology and Classification c.c. PathogenesisPathogenesis d.d. Clinical CourseClinical Course e.e. Alterations of Function andAlterations of Function and MetabolismMetabolism
- 18. 18 18 Renal reserve ↓ Renal insufficiency Renal failure Uremia Clinical Manifestations Clearance of Endogenous Creatinine (%) 25 50 75 100 Relationship Between Renal Function and Clinical Manifestations
- 19. 1919 Chronic Renal FailureChronic Renal Failure a.a. DefinitionDefinition b.b. Etiology and ClassificationEtiology and Classification c.c. PathogenesisPathogenesis d.d. Clinical CourseClinical Course e.e. Alterations of Function andAlterations of Function and MetabolismMetabolism
- 20. 20 Section 3 Chronic Renal Failure Alterations of function and metabolism Urine volume: Polyuria (or Nocturia) at early stage (to oliguria) Urine osmolarity: Hypotonic (hyposthenuria) to Isotonic (isosthenuria) Urine component: Proteinuria, hematuria, pyuria and different type of casts 1. Disorders of Urine
- 23. 23 Section 3 Chronic Renal Failure ♠Proteinuria – Increase of the permeability of glomerular filtration membrane – Damage of tubular epithelial cells ♠Pyuria, Hematuria – Filtration of WBC and RBC Normal urine Pyuria Hematuria
- 25. 25 Section 3 Chronic Renal Failure ♠ Early stage ─ Normal potassium with normal urine volume ♠ Advanced stage ─ Hypokalemia: inadequate food intake, vomiting, diarrhea, long-term use of diuretics, etc. ─ Hyperkalemia: oliguria, severe acidosis, infection, transfusion of stored blood, excess potassium intake, etc. Potassium disorder
- 26. 26 Section 3 Chronic Renal Failure Hypocalcemia ♠ Increase of serum H2PO3 - → ↓Ca2+ ♠ Decreased absorption of calcium ↓ 1,25-(OH)2-Vit D3 formation in the kidney Intestinal mucosa damage by toxic metabolites ♠ Inadequate intake caused by anorexia and low protein diet
- 27. 27 Section 3 Chronic Renal Failure Hyperphosphatemia Excretion of Pi ↓Excretion of Pi ↓ Serum H2PO3 - ↑Serum H2PO3 - ↑ GFR↓GFR↓ HyperphosphatemiaHyperphosphatemia
- 28. 28 Section 3 Chronic Renal Failure 3. Acidosis Early stage Secretion of H+ and reabsorption of HCO3 - Absorption of Cl - from gut Acidosis (normal AG) Advanced stage Excretion of non- volatile acid (sulphate, phosphate, etc) Acidosis (high AG)
- 29. §3. Classification ： 2) High AG metabolic acidosis ： primary HCO3-↓ AG↑ due to any kind of fixed acids except Cl- (Normochloremic MAc) e.g., shock, renal failure 1) Normal AG metabolic acidosis ： primary HCO3 - ↓ compensatory ↑ of Cl- (Hyperchloremic MAc) HCO3 - losing ↑ : diarrhea, intestinal fistulas; HCO3 - reabsorption ↓ : RTAⅡ Normal Normal AG MAc High AG MAc Metabolic acidosis
- 30. 31 Section 3 Chronic Renal Failure 4. Azotemia GFR ↓ Accumulation of NPN Urea nitrogen Creatinine nitrogen Uric acid nitrogen NPN: Non-protein nitrogen
- 31. 32 Section 3 Chronic Renal Failure Relationship between non-protein nitrogen and GFR
- 32. 33 Section 3 Chronic Renal Failure 5. Renal hypertension Renal diseasesRenal diseases HypertensionHypertension
- 33. 35 Section 3 Chronic Renal Failure 6. Renal anemia and bleeding tendency ♠ Renal anemia (seen in 97% of CRF patients) ─ Reduced production of EPO ─ Shortened survival time of RBC ─ Inhibition of bone marrow hemopoiesis by uremic toxins ♠ Bleeding tendency (seen in 17-20% of CRF patients)
- 34. 36 Section 3 Chronic Renal Failure 6. Renal osteodystrophy CRFCRF Renal osteodystrophyRenal osteodystrophy
- 35. 37 Formation of calcium nodules in knuckles during renal osteodystrophy.
- 36. 38 Osteoporosis (pathological fracture) occurring in renal osteodystrophy.
- 37. 39 ARF CRF Course of disease Acute, short Chronic, long Urine volume Oliguria→polyuria Polyuria→oliguria Serum potassium Hyperkalemia→Hypokalemia Hypokalemia→Hyperkalemia Clinical manifestations Mainly urinary dysfunction Mainly endocrine dysfunction Prognosis Good Bad Comparison between ARF and CRF
- 38. Outline 11 22 33 44 40 Introduction Acute Renal Failure Chronic Renal Failure Uremia
- 39. ♠ End-stage of renal failure. ♠ A pathological process that occurs in addition to the urinary dysfunction and endocrine dysfunction. ♠ A series of symptoms of auto-intoxication induced by accumulation of metabolic wastes and endogenous toxins may be observed. 41 Section 4 Uremia Concept
- 40. 42 Section 4 Uremia Etiology ♠ Uremic toxins PTH Guanidine compound Urea Amines etc
- 41. 43 Section 4 Uremia Alterations ♠ Alterations ─ Intracellular Ca2+ ↑, metastatic calcification ─ Disturbance of metabolism: proteolysis ↑ → non-protein nitrogen ↑ ─ Stimulates the secretion of gastrin → promotes the development of gastric ulcer ─ Inhibits erythropoiesis (anemia) ─ Inhibits immunological function (Inflammation) ─ Promotes formation of renal osteodystrophy
- 42. 44 Section 4 Uremia Prevention and treatment ♠ Primary disease and risk factors control ♠ Diet therapy: Low sodium, low protein, low phosphate High calory ♠ Dialysis ♠ Renal transplantation
Editor's Notes
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- No endocrine dysfunction for ARF.
- No endocrine dysfunction for ARF.
- Polycystic kidney disease, obstruction, and infection are among the less common causes of CRF.
- Data from China. Polycystic kidney disease, obstruction, and infection are among the less common causes of CRF.
- Actually, the pathogenesis of CRF is poorly understood. Three hypotheses are proposed to explain the impaired function of the kidneys in CRF.
- Nephron destroyed, the remaining counterparts adapt by increasing GFR, tubular resorption and excretion. When the intact nephron is decreasing to a certain degree, it goes to non-compensatory stage, CRF.
- This occurs in compensatory stage.
- This occurs in decompensatory stage.
- As the nephrons are progressively destroyed, increased blood concentration of some solutes stimulate over-secretion of some related regulatory factors (such as hormones) in order to increase the excretion function. At the same time, however, high blood levels of the regulatory factors will result in some other metabolic disorders. ①secondary hyperparathyroidism ②disorder in Vit D metabolism ③acidosis ④aluminum intoxication
- As the nephrons are progressively destroyed, increased blood concentration of some solutes stimulate over-secretion of some related regulatory factors (such as hormones) in order to increase the excretion function. At the same time, however, high blood levels of the regulatory factors will result in some other metabolic disorders. ①secondary hyperparathyroidism ②disorder in Vit D metabolism ③acidosis ④aluminum intoxication
- Compensatory stage: stage of decreased renal reserve.
- Clearance of creatinine (not BUN, not serum creatinine) is the best parameter of renal function.
- Isotonic urine: 1.010 specific gravity; 285 mOsm/L.
- Casts include hyaline casts, cellular casts, granular casts.
- Anorexia:厌食症 Calcium x phosphorus is a fixed value.
- Na+, Cl-, HCO3- are determined ions. Undetermined anions include: negatively charged proteins, phosphate, sulfate, lactate, ketone bodies, etc.
- NPN > 40mg/dl
- Non-protein nitrogen ＞ 28.6 mmol/L (or＞4 g/L).
- Seen in 97% of CRF patients.
- Bleeding tendency: Decreased release of platelet factor III Decreased adhesiveness and aggregation of platelet Decreased platelet counts
- Rickets, osteoporosis, metastatic calcification,
- 肾性骨营养不良时指关节的钙结节形成
- 肾性骨营养不良时的骨质疏松（病理性骨折）
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- gastric ulcer (nausea and vomiting)
- hemodialysis, peritoneal dialysis