高血压英文ppt精品课件chronic renal

Chronic Renal Failure Internal Medicine Xu Xiaoqi Shanghai Second Medical Uni. 2005.10.6 Content Definition Etiology Pathogenesis of CRF Pathogenesis of uremic syndrome Clinical presentations Diagnosis Treatment Definition（ 定义定义 ） CRF is a permanent, usually progressive, diminution in renal function to a degree that has damaging consequences for the patient. It is characterized by an increasing inability of the kidney（ 肾脏 ） to maintain normal low levels of the products of protein metabolism(such as urea), normal blood pressure and hematocrit, and sodium, water, potassium, and acid-base（ 酸碱 ） balance. This occurs when glomerular（ 肾小球 ） filtration rate (GFR) is reduced by at least 50mL/min. It can be mild, moderate, or servere. End-stage renal disease (ESRD， 终末期肾病 ) is the degree of renal failure that would cause the death of the patient unless some form of RRT is initiated. n The progression of CRF leads, in the majority of instances, to end stage renal disease (ESRD) at which point renal replacement therapy is required. The rate of progression of CRF varies according to the underlying nephropathy and between individual patients. Age, gender, race, proteinuria（ 蛋 白尿 ） , lipids, hypertension, smoking. n It has been suggested that it is faster in CGN （ 慢性肾小球肾炎 ） compared with chronic interstitial nephropathies (CIN， 慢性间质性肾炎 ) or hypertensive nephrosclerosis(HNS， 高血压肾硬化 ). Proteinuria is the only continuous variable identified as an independent risk factor. CAUSES OF CHRONIC RENAL FAILURE (1) Glomerulaopathy（ 肾小球病变 ） primary glomerular disease: focal and segmental glomerulonephritis（肾 小球肾炎） membranopriliferative GN IgA nephropathy membranous nephropathy secondary glomerular disease: diabetic glomerulosclerosis（ 糖尿病肾硬化） amyloidosis,light chain disease HIV-associated nephropathy SLE（红斑狼疮） ,Wegners granulomatosis tubulointerstitial disease（ 小管间质病变 ） reflux nephropathy analgestic nephropathy obstructive nephropathy heavy metals drug hypersensitivity Hereditary diseases（ 遗传性疾病 ） autosomal dominat polycystic kidney disease medullary cystic disease Alports syndrome CAUSES OF CHRONIC RENAL FAILURE (2) n Obstructive nephropathies（ 梗阻性肾病 ） prostatic disease nephrolithiasis（ 肾结石 ） retroperitoneal fibrosis/tumor congenital n vascular disease hypertensive nephrosclerosis scleroderma vasculitis renal artery stenosis (ischemic nephropathy) CAUSES OF CHRONIC RENAL FAILURE (3) 注： 2000年全国血透病人原发病资料缺少中南、山东、北京、东北资料 2002年年底上海市尚存 3416例 慢性肾功能衰竭血透患者主要原发病因 2002年全年腹透患者中 575例慢性肾功能衰竭患者主要原发病因 Pathogenesis of chronic renal failure Pathogenesis of glomerulosclerosis Hypothesis Author(s) Glomerular hyperfiltration/hyperperfusion Hostetter and Brenner 1981 Glomerular hypertension Anderson and Brenner 1985 Nephrotoxicity of lipids Moorhead et al. 1982 Similarities with atherosclerosis EI Nahas 1988 Diamond and Kamovsky 1988 Glomerular hypertrophy Fogo and Ichikawa 1991 Nephrotoxicity of proteinuria Remuzzi and Bertani 1990 Growth factors Platelet-derived growth factor Transforming growth factor Johnson et al. 1994 Border et al. 1993 Mesangial/myofibroblast differentiation Johnson et al. 1994 Podocyte injury Kriz 1996 Figure Hypotheses for the pathogenesis of glomerusclerosis (Adapted with permission from EI Nahas) Pathogenesis of tubulo-interstitial fibrosis Hypothesis Author(s) Adaptive tubular hypermetabolism Harris and Schrier 1998 Adaptive tubular ammoniagenesis Nath and Hostetter 1985 Nephrotoxicity of lipids Moorhead et al. 1982 Nephrotoxicity of proteinuria Remuzzi and Bertani 1990 Nephrotoxicity of calcium and phosphate Alfrey 1988 Nephrotoxicity of iron Harris and Alfrey 1994 Nephrotoxicity of oxygen free radicals Nath et al. 1994 Tubular cells and fibrosis Kuncio and Neilson 1991 Tubular transdifferentation Okada, Strutz, and Nielson 1994 Figure Hypotheses for the pathogenesis of tubulo-interstitial fibrosis. (Adapted with permission from EI Nahas.) hyperperfusion GCP loss of nephron adaption of remaining nephrons glom hypertrophy liferation, focal GS, proteinuria tubu-inters. atrophy ESRD glom dis vasc dis tubu-inters dis nephroarter iolosclerosis HBP + hyperlipidemia atheroscl erosis Renovascular renal failure Ca P PTH Aquired renal cystic disease 小结 -慢性肾衰竭发病机制 n 肾小球高灌注、高压、高滤过 n 肾小管高代谢 -小管间质损伤 n 高血压 n 脂质代谢代谢异常 Pathogenesis of the uremic syndrome Uremic Toxins n Products of protein metabolism urea: 50 mmol/L sympt: malaise不适 , vomiting, bleeding, headache guanidine compounds(methylguanidine) sympt: anorexia食欲减退 ,vomiting,pruritus瘙 痒 , twitch颤动 , unconsciousness n Products of bacteria metabolism: phenol,amine,indole (uremic encephalopathy, nausea, vomiting, deterioration of renal function ) n Middle molecular weight solutes: MW 500-5000 uremic peripheral neuropathy, disorder of lipid metabolism, renal osteodystrophy, CVD n Others: aluminum, zinc Disorder of nutrition & metabolism n Catabolic metabolism分解代谢 : n Anabolic metabolism合成代谢 : n Intake: Trade-off hypothesis GFR Ca P PTH Tubule excretion of P Serum Ca parathyroid 2o hyperparathriodism Endocrine metabolic disorder n Erythropoietin n 1,25(OH)2D3 PTH n Insulin resistance 小结 尿毒症症状的发生机制 n 尿毒症毒素 n 营养与代谢失调 n 矫亡失衡学说 n 内分泌异常 Clinical Presentations Late(GFR 60 mg/dL) n cardiac failure n anemai n serositis n confusion, coma n anorexia n vomiting n peripheral neuropathy n hyperkalemia n metabolic acidosis FEATURES OF CHRONIC RENAL FAILURE Early n hypertension n proteinuria,elevated BUN or sCr n nephrotic syndrome n recurrent nephritic syndrome n gross hematuria l Gastroenterologic （胃肠道） manifestations prominent and frequently encountered anorexia nausea, vomiting,diarrhea uremic gastroenteritis peptic ulcer, bleeding unpleasant , metallic taste (uremic fetor) l Cardiovascular and pulmonary disease hypertension （高血压） congestive heart failure（充血性心衰 ） pericarditis atherosclerosis respiratory system symptoms l Hemotologic anemia （贫血） (GFR 50 No any signs and symptoms Azotemic stage 445 25-10 Obvious GI symptoms,anemia, metabolic acidosis End stage 800 1g/d 125/75 mmhg n Rx: restriction of sodium diuretic ACEI CCB Heart failure n Restriction of water and sodium n Large dose of furosemide n Vascular dilation n Digoxins n Blood purification n Correction of electrolytes and acid-base disturbance n Improvement of anemia Pericarditis n Increase dialysis frequency or time n corticosteroids n surgery Anemia n Recombinant human erythropoietin 50 u/kg tiw, iH target: Hb 100-120g/L, Hct 30-35% n Iron n Folic acid Renal osteodystrophy n Recover the imbalance of Ca, P restriction of intake phosphate binding n Vitamin D supplement n Partial parathyroidectomy fluid,electrolytes and acid-base disturbance Fluid and electrolytes water intake = urinary output + 500 ml Na intake: 3 g/d Hyperkalemia Metabolic acidosis biocarbonate 13.5 mmol/L iV Control infection Remove uremic toxins from gastrointestinal Traditional Chinese medicine Blood purification n Hemodialysis n Peritoneal dialysis Healthy Kidney Renal ReplacementPhysical Basis Location and Structure Location of the Kidneys inside of the Body Left KidneyRight Kidney Right Ureter Large Intestine Liver Lung Superior Vena Cava Heart Aorta Spleen Small Intestine Left Ureter Bladder Diseased Kidney Physical Basis of Dialysis Semipermeable Membrane Bacteria Medium sized Molecules, e.g. 2-Microglobulin Water Flow is Easily Possible Erythrocyte, Red Blood Cell Albumin, as Example of a Big Protein Molecule Electrolytes The semipermeable membrane functions similar to a fine sieve, only molecules that are small enough can pass. Healthy Kidney Renal ReplacementPhysical BasisDiseased Kidney Hemodialysis Flow Scheme Hemodialysis Blood PumpAnti-Coagulation Blood to the Patient Blood from the Patient Dialyzer Fresh Dialysate Used Dialysate Healthy Kidney Renal ReplacementPhysical BasisDiseased Kidney Hemodialysis Dialyzer Blood Inflow Dialysate Outflow Bundle of Capillaries in the Housing Dialysate Inflow Blood Outflow The dialysate flows outside of the capillaries, blood within the capillaries countercurrently. Solute Transfer across the Capillary Walls Healthy Kidney Renal ReplacementPhysical BasisDiseased Kidney Peritoneal Dialysis