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Renal failure

Renal failure

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Renal failure

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  1. Renal failure

  2. §1 Introduction • Normal function of the kidney • Renal insufficiency • Causes • Basic manifestation of renal insufficiency

  3. Normal function of the kidney 1.Excretion Remove waste product from the body; Regulate electrolyte and acid-base balance. 2. Endocrine Produce renin、EPO、1,25(OH)2D3 and prostaglandins; Inactivate gastrin、PTH.

  4. Renal insufficiency Dysfunction of excretion and endocrine Diseases Symptoms and signs Edema, hypertension, oliguric, polyuria, hematuria, proteinuria, anemia, osteodystrophy.

  5. Causes: 1 Primary renal diseases Primary glomerular diseases, Primarytubulardiseases, Interstitial nephritis, et al. 2 Secondary renal lesion Circulatory system diseases, immunity siseases, metabolic diseases, hematopathy, et al.

  6. Basic manifestation of renal insufficiency • 1 Glomerular dysfunction • 2 Tubular dysfunction • 3 Endocrine dysfunction

  7. 1 Glomerular dysfunction • ①GFR • ⅰblood flow • ⅱnet filtration pressure • ⅲ Kf • ② Glomerular permselectivity

  8. 2 Tubular dysfunction ①proximal tubule Renal glycosuria, aminoaciduria, renal tubular acidosis, hypophosphatemia ②loop of Henle Hypotonic or isotonic urine, polyuria ③distaltubule Acid-base and electrolyte disorders, polyuria

  9. 3 Endocrine dysfunction ① Renin ②Endothelins ③KKS disorders ④AA Disequilibrium ⑤EPO ⑥ 1,25(OH)2D3

  10. Excretion §2 Acute renal failure Conception Diseases water intoxication,azotemia, hyperkalemia, metabolic acidosis

  11. Section 1 Cause and Classification *** Classification 1causes Prerenal ~ Intrarenal ~ Postrenal ~ 2renallesion functional~ organic~ obstructive ~ 3urine volume Oliguric ~ Nonoliguric ~

  12. 1 Prerenal factor renal blood flow Characteristic early stage: functional~ late stage: organic ~ (2) oliguria Causes

  13. Mechanism ECF↓ RBF ↓ GFR↓ Reabsorption↑ oliguria Impaired hemeostasis

  14. Causes (1) acute tubular necrosis,ATN 2/3 acute renal ischemia acute renal poisoning hemoglobinuria, myoglobinuria (2) renal disease Characteristic (1) parenchymal (2) oliguric ~ nonoliguric~ 2intrarenal factor

  15. Differentiation between the two RF urine functionalRForganic RF specific gravity> 1.020 < 1.015 OP(mmol/L) > 700 < 250 Na(mmol/L)< 20 > 40 UrCr/SrCr > 40 < 20 Sedimentnormal Manicol testurine volumeurine volume Necrosis epithelial cells,RBC,casts, albuminuria

  16. Causes Kidney stone, tumor, obstruction of necrosis tissue Characteristic early stage: obstructive ~ late stage: organic ~ 3 Postrenal factor

  17. Mechanism Bowman’s capsule pressure↑ Obstruction of the urinary tract Net filtration pressure↓ GRF↓ Oliguria, anuria

  18. Section 2 Pathogenesis 1Glomerular factor ①RBF (1) Net filtration pressure BP < 60mmHg CO RBF BP (50-70mmHg) GFR (1/2 – 2/3) BP(40mmHg) GFR = 0 Urinary obstruction intracapsular pressure

  19. (2)renal vessels constriction • RBF sympathetic nerve • Shock RAS • afferent arteriole constriction • prostaglandin • kallikrein - kinin syetem afferent arteriole constriction efferent arteriole constriction GFR ET

  20. (3) swelling endothelial cell ischemia Na+ - K+ - ATPase free radicalendothelialcellular injury (4)alteration of renal hemorheology fibrinogen Blood viscosity RBC聚集和变形能力 PLT聚集 WBC粘附、嵌顿 微血管改变 renal DIC

  21. ②Glomerular lesion filtration surface area Glomerular permselectivity GFR

  22. 2Tubular factor • ①tuble obstruction • 管型 阻塞管腔 原尿不易通过 尿量 • 管腔内压 GFR • ②passive backflow • 肾小管上皮细胞变性、坏死 原尿漏出 • 肾间质水肿 囊内压 GFR 尿量

  23. 3 renal cellular injury and its mechanism ①damaged cells (1) renal tubular cells 1)necrotic lesion tubulorrhexic lesion:可发生于各段肾小管 上皮坏死+基底膜破坏。 肾持续缺血和肾中毒均可见 nephrotoxic lesion:主要发生于近球小管 仅上皮坏死,基底膜完整。 主要见于肾中毒

  24. 2)apoptotic lesion distaltubule (2) endothelial cell Tubularischemia 髓质直小血管内皮肿胀 clot endothelial injury platelet glomerular endothelial window GFR 内皮细胞释放舒血管因子

  25. (3)mesangial cell AngⅡ、ADH Gentamicin、adenosine contraction of mesangial cells resistance of glomerular capillary filtration area GFR

  26. ②mechanism of cell injury (1) production of ATP and Na+ - K+ - ATPase hypoxia ischemia toxication Na+ - K+ - ATPase Ca2+ - ATPase [Na+]in,H2O [Ca2+]in damage of mitochondria ATP

  27. (2)free radical(FR) ischemia GSH FR clearance reperfusion FR产生 (3)GSH细胞抗氧化能力 ,膜稳定性 (4)phospholipase [Ca2+]in phospholipase A2 cell membrane injury Cellular injury

  28. (5)alteration of cell framework ischemia ATP toxication (6)apoptosis alteration of cell framework

  29. Section 3 Clinical Course and manifestation oliguric ARF 1 oliguria phase(days~weeks) (1)features of urine urine volume:oliguria(400ml/d)or anuria(100ml/d) S.G.:1.010~1.020 Na+ :tubular reabsorption dysfunction urine sediment:erythrocytes, casts, proteinuria

  30. (2) water toxication • oliguria • Catabolism ,内生水 • Transfuse fluid • ADH Hypervolemic hyponatremia Fluid retention Cell edema

  31. (3) Hyperkalemia • Urinary excretion of K+ • Tissue destruction • Metabolic acidosis • Transfuse non-fresh blood, high K+ diet • hyponatremia,exchange of K+and Na+ Movement of K+ from cells into ECF Hyperkalemia

  32. (4) Metabolic acidosisgrogressive,difficult to correct • GFR excretion of acid production • Secretion of H、NH3 , reabsorption of HCO3– • Catabolism , acid production Metabolic acidosis Hyperkalemia

  33. (5) Azotemia(NPN>40 mg/dl) • Excretion of protein metabolite • Protein catabolism 血中尿素、肌酐、尿酸等非蛋白氮 称为氮质血症

  34. 2 diuresis phase(1~2W) • Mechanism : • 肾血流量和肾小球滤过功能渐恢复; • 新生的小管上皮细胞浓缩功能低下; • 血中尿素等大量滤出,渗透性利尿; • 肾间质水肿消退,阻塞解除。

  35. manifestation: • polyuria,>400 ml/d; • Early stage: Hyperkalemia, Azotemia , Metabolic acidosis; • Late stage:dehydration, hypokalemia, hyponatremia, infection. 3 recovery phase

  36. Nonoliguric ARF Feaures: • 肾病理损害较轻:尿量不少; 氮质血症 • 肾小管功能障碍:低比重尿; 尿钠低 • 病程短,预后好,但可互相转化。

  37. Section 4 Treatment Principle of ARF 1. Treat the cause; 纠正灌流量不足;慎用肾毒药物; 利尿以解除阻塞;抗感染等 2. Rescue actively. 纠正水电紊乱; 纠正代酸; 处理高钾;控制氮质血症; 透析治疗.

  38. 患儿女,11月。因呕吐、腹泻伴发热9天,无尿3天入院。患儿女,11月。因呕吐、腹泻伴发热9天,无尿3天入院。 • 9天前无诱因出现腹泻,为黄绿色稀水便,每天3~4次,伴频繁呕吐,非喷射状,量较多;同时发热,体温最高41℃。给予口服头孢拉啶、头孢氨苄及肌注地塞米松治疗,三天后腹泻、呕吐次数减少,但体温仍在38~39℃之间,并开始咳嗽。近5天一直无尿。入院前一天门诊就诊,查胸部X线片示右下肺淡片状影,诊断支气管肺炎,静滴凯福隆1.0g及1/2张0.9%生理盐水200ml后,体温下降,但仍无尿。次日颜面及双眼睑水肿,血尿素氮33.92mmol/L,血肌酐786.76μmol/L,血钾8.6mmol/L,二氧化碳结合力5.83mmol/L, 以急性肾功能衰竭入院。患儿生后人工喂养,既往易患上呼吸道感染。

  39. 体检:呼吸60次/分,脉搏120次/分,血压85/54mmHg。营养、发育中等,昏睡状态。双眼睑及球结膜水肿,睑结膜稍苍白,口唇干裂,咽充血,颈无抵抗;呼吸深大,双肺叩清音,听诊双肺密集中、小湿啰音;心前区无隆起,心尖搏动位于左侧第4肋间左锁中线内0.5cm,未及震颤,叩诊心界不大,心率120次/分,律齐,心音低钝。腹稍隆起,未触及包块,肝脏于右肋缘下5.5cm、剑突下1.0cm,质软、缘锐。脾脏于左肋缘下1.5cm,质软无压痛;腹水征阴性;双下肢无水肿;神经系统检查未见异常。体检:呼吸60次/分,脉搏120次/分,血压85/54mmHg。营养、发育中等,昏睡状态。双眼睑及球结膜水肿,睑结膜稍苍白,口唇干裂,咽充血,颈无抵抗;呼吸深大,双肺叩清音,听诊双肺密集中、小湿啰音;心前区无隆起,心尖搏动位于左侧第4肋间左锁中线内0.5cm,未及震颤,叩诊心界不大,心率120次/分,律齐,心音低钝。腹稍隆起,未触及包块,肝脏于右肋缘下5.5cm、剑突下1.0cm,质软、缘锐。脾脏于左肋缘下1.5cm,质软无压痛;腹水征阴性;双下肢无水肿;神经系统检查未见异常。

  40. 实验室检查:Hb84g/L,红细胞3.26×1012/L,白细胞分类:杆状核0.14,分叶核0.61,单核细胞0.03,淋巴细胞0.22,血小板196×109/L;便常规正常;血钾8.6mmol/L,血钠128mmol/L,氯化物100mmol/L, 血钙1.98mmol/L,血磷2.33mmol/L,二氧化碳结合力6.73mmol/L,尿素氮37.12mmol/L,血肌酐804.44μmol/L;血气分析:pH7.17, PCO23.27kPa,HCO-38.6mmol/L, SBE-18.3mmol/L;心电图:室内传导阻滞,T波高尖。

  41. Addition:  1. The role of free radical ⑴ kinds and concept of free radical free radical: 外层轨道上含有单个不配对电子的原子、原子团和分子。

  42. oxygen free radical: O-•2 、OH • kinds of (active oxygen: 1O2、H2O2) free radical lipid free radical: L•、LO•、LOO• others: Cl•、CH3•、NO

  43. (2) mechanism of increase of oxygen free radical  ① formation of oxygen free radical nature oxidation of Hb , Adr , Cyt C O2 O ‾∙2 H2O2 OH∙ H2O H2O oxidation of enzyme : xanthine oxidase(XO) O ‾∙2 xanthine uric acid O2 O ‾∙2 Mitochondria: CoQ Cyt P450(为加单氧酶)

  44. Xanthine oxidase : Ischemia ATP [Ca2+]i xanthine xanthine dehydrogenase oxidase ADP 、AMP ② increase of adenosine、 xanthine O‾∙2 oxygen free O‾∙2 cell membrane radical LTB 4 repiratory burst O‾∙2 、OH∙ mitochondria hypoxia O‾∙2 sympathetic nervous system

  45. (3) damage action of free radical ① membrane lipid peroxidation cellular membrane permeability lipid peroxidation of membrane [Ca2+] i lipid cross-linked calcium overload inhibition of Na+-pump and Ca2+-pump [Na+] i , [Ca2+] i membrane lipid phospholipase C PGs , LTs peroxidation phospholipase D TXA2 damage of mitochondria membrane ATP

  46.   ② inhibition of protein function enzymes , channels , pump , and so on ③ destruction of nuclear acid 碱基羟化、DNA断裂 染色体畸变、细胞死亡

  47. 2 Damage mechanism of calcium overload ①phospholipase injury of cell membrane and cell organ  ②ATPas ATP ③Ca2+ + phosphate production of ATP deposition ④ [Ca2+] i XO free radical

  48. Chronic Renal Failure Section 1 Conception etiological factors destruct nephron Dysfunction of excretion and endocrine waste product , acid-base and electrolyte disorders, dysfunction ofendocrine

  49. Section 2 Causes of CRF • Renal diseases:chronic glomerulonephritis et al • Vascular disorders:diabetes mellitus、hypertensive disease、Periarteritis nodosa, et al • Urinary tract obstruction:urinary calculus、prostatic hyperplasia et al

  50. Section 3 Clinical Course of CRF • compensatory stage • Renal insufficiency stage • Renal failure stage • Uremia stage