医学ppt课件：英文肾小球疾病.ppt

Chapter 2 Outline of Renal Glomerular Diseases Definition Glomerular Diseases are characterized by a group of similar clinical manifestations,such as hematuria,proteinuria,hypertension,but their etiology,pathogenesis,pathology and prognosis are different,involving bilateral glomerulus changes ClassificationPrimarySecondaryHeredityClassification of primary glomerular diseases:1.Clinical types:acute glomerulonephritisrapidly progressive glomerulonephritischronic glomerulonephritislatent glomerulonephritis nephrotic syndrome2.Pathological types:minimal glomerular abnormalitiesfocal segmental lesionsdiffuse glomerulonephritismembranous nephropathyproliferative glomerulonephritis:mesangial proliferative glomerulonephritisendocapillary proliferative glomerulonephritismesangiocapillary glomerulonephritiscrescentic&necrotizing glomerulonephritissclerosing glomerulonephritis unclassified glomerulonephritisminimal glomerularfocal segmental lesionsmembranousMesangiocapillaryMesangiocapillaryMesangialMesangial proliferative proliferativeEndocapillaryEndocapillary proliferative proliferative crescenticcrescentic necrotizingSclerosing Most of the glomerulonephritis are immune mediated inflammatory disease,however the reaction is a primary cause for the glomerulonephritis.Inflammatory mediators(such as complement,interleukin),taking part in immune reaction,results in glomerular injury and clinical symptoms.In the chronic development of glomerular disease,it can also be due to non-immune and non-inflammatory mechanisms Pathogenesis:1.Immunoreaction:humoral immunity：circulatory immune complex(CIC)immune complex format in situs autoantibody cellular immunity：important for some types;circulatory immune complex(CIC)immune complex format in situs2.Phlogistic reaction:Inflammatory cell monocyte macrophages,neutrocytes,acidophils&platelet Mediators of inflammation complement,leukotriene,etc.3.Non-immunologic mechanism:important factors of diseases persistence&deterioration large amount of proteinuria,hyperlipemia,loss of body fluid,etc Clinical manifestation:1.proteinuria:positive150mg/d;large amount of proteinuria3.5/d;protein of molecular weight24104 can pass normal renal filter membrance(lysozyme,2microglobulin,light chain protein)protein in normal urine3/HP of centrifuged hematuria microscopic hematuria;blood1ml/l urine gross hematuria;painless&whole hematuria,RBC casts,protein excretion500mg/d may glomerulus originated hematuria distinguish the origin of hematuria:fresh urine sediment test under phase contrast microscope distortion RBC hematuria indicate glomerular originatedreason:GBM rupture,when RBCs passing,they will be pressed to distortion.Irregular shapes of RBCs may also occur due to PH and osmolarity changes found in the distal tubule.distribution curve of urine RBC volumeIsomorphic red blood cells in urine 50 100 150 200a50 100 150 200b50 100 150 20050 100 150 200c50 100 150 200d3.edema:nephropathy:hypoproteinemia&retention of sodium and water;begin from lower limbs;clinically heavy proteinuria hypoalbuminemia and diminished colloid osmotic pressure promotes a net movement of fluid into interstitium hypovolia and initiates the edema-forming sequence.nephritis GFR retention of sodium and water;begin from eyelids;Be local and evident in the very soft tissues of the eyelids/face and tends to be most pronounced in the morning.the increased capillary permeability GRF.4.hypertention:90%of CKD patients gets HBp persistent deterioration of renal function mechanism:retention of sodium and waterrenin excretedecompressing materials in kidney(prostate,kinin)5.Renal function damage Chapter 3 Primary Glomerular Diseases Definition AGN:The acute nephritic syndrome is the clinical correlate of acute glomerular inflammation.In its most dramatic form,the acute nephritic syndrome is characterized by sudden onset of azotemia、edema、hyertension、hematuria and proteinuria.Section 1.Acute Glomerulonephritis AGN 【Pathogeny&pathogenesis】Pathogeny hemolytic streptococcus infection (upper respiratory tract infection)pathogenesis CIC accumulate in glomeruli/immune complex in situ activate complements endothelial cells&mesangial cells regeneration and soakage of neutrocytes&monocytes renal pathological changes.【Pathology】Endocapillary proliferative glomerulonephritis endothelial&mesangial cellsCrescents are uncommon.Immunofluorescence microscopy reveals diffuse granular deposition of IgG and C3 in subendothelial and mesangial areas.The characteristic finding on election microscopy is the presence of large electron-dense immune deposits in the subepithelial areas.Endocapillary proliferative Normal glomerulus【Clinical manifestation&Lab.Exam】1.Often kids(2-6 years)are involved,Male is more than female;Incubation period for about 13 weeks(mean 10 days).Prognosis may be satisfied.2.Urine abnormality:glomerular originated hematuria(almost all);dysmorphic RBC,moderate proteinuria;WBC and epithelium,granular casts and RBC cast in early stage;【Clinical manifestation&Lab.Exam】3.Edema;typical eyelid4.HBp:water&sodium retention 5.olyguria(400ml/d),moderate azotemia.mild acute renal failure6.heart failure:water&sodium retention and hypertension 7.C3 decrease but restore in 8 weeks,serumal ASO may increase8.Generalized symptoms:anorexia,nausea,vomiting,malaise.Swelling of the renal capsule can cause flank or back pain.【diagnosis&deferential diagnosis】1.Other acute nephritis syndrome:pathogen(bacteria/virus/parasite)C3 is normal;mesangiocapillary nephritis continuous hypocomplementemia can not restore in 8 weeks,nephrotic syndrome,no spontaneous cure.mesangial proliferative nephritis normal C3;no spontaneous cure;hematuria earlier【diagnosis&deferential diagnosis】2.RPGN:rapidly deteriorate renal failure3.Systematic disease:SLE or purpura4.Indication of renal biopsy:olyguria for more than 1 week or gradually olyguria companied by azotemia course continue beyond 2 months AGN companied by nephrotic syndrome【treatment】1.Rest until the symptom alleviated;salt,water and protein should be limited.2.Antibiotics penicillin 1014days3.Diuretics and antihypertensive agents are employed to control extracellular fluid volume and blood pressure;4.Dialyze short time;5.Chinese herb【prognosis】1.symptoms,signs&lab exam recover in 48 weeks2.1%die for acute renal failure3.6%18%shift to chronic glomerulonephritis Section 2.Rapidly Progressive Glomerulonephritis(RPGN)Gist:1.pathology:crescent glomerulonephritis;2.rapidly deteriorate of renal failure is the character 3.intensified plasma replacement therapy 4.methylprednisolone impaction accompanied with CTX therapy monly turn into chronic nephritisCrescent of Rapidly progressive glomerulonephritis Section 3.chronic glomerulonephritis Hematuria,proteinuria,edema&HBp are basic manifestation.The course is slow but renal failure occur at last.【mechanism】1.Comes from AGN;2.Immune inflammation or not;【pathology】Diffused glomeruli sclerosis in late stage慢性肾小球肾炎病理肾小球纤维化，肾小管萎缩，肾间质炎症细胞浸润sclerosing glomerulonephritis【manifestation】1.Symptoms of nephritis dormant,atypical 2.HBp&its complication especially the retina change 3.Acute onset in chronic course (infection,labor,kidney-toxic drug)4.Renal failure【diagnosis&deferential diagnosis】1.Hematuria,proteinuria,edema&HBp last for more than 1 years;2.Preclude secondary or genetic nephritis;【diagnosis&deferential diagnosis】Secondary nephritis:SLE,allergic purpura,etc.Alport syndrome:bland,deafness&renal damage Other nephritis concealment nephritis;AGN:C3 dont fluctuation HBp renal damage:renal tube damage such as nocturia 【treatment】1.Goal:not eliminate urine abnormality but protect renal function;2.Control HBp actively;reduce the proteinuriaproteinuria1g/d,Bp130/80mmgh ACEI or ARB:according to GBM,they may protect renal function【treatment】3.Protein&phosphate should be limited in azotemia4.Persandin or aspirin5.Glucocortical hormone&cellular toxics should be stopped when the curative effect is not contented6.Avoiding deteriorating factors:infection,tire,pregnant&toxic drug【prognosis】1.Renal failure2.The deciding factor is pathologic type3.Correct protection&treatment are also very important Section 4.Concealment nephritisGist:1.asymptomatic hematuria (glomerular originated)&/or proteinuria;2.excludefunctional&positional proteinuria;early or recover stage of nephritis renal biopsy if necessarily;3.treatment principle:recheck regularly protect renal function excise tonsil Chinese herb