renal failure

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Renal failure. 患儿女, 11 月。因呕吐、腹泻伴发热 9 天,无尿 5 天入院。 9 天前无诱因出现腹泻,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℃ 。给予口服抗生素治疗,三天后腹泻、呕吐次数减少,但体温仍在 38 ~ 39℃ 之间。近 5 天一直无尿。 体检: 呼吸 60 次 / 分,脉搏 120 次 / 分,血压 85/54mmHg 。 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。 - PowerPoint PPT Presentation

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  • Renal failure

  • 11959344138395 60/120/85/54mmHg 8.6mmol/L128mmol/L,100mmol/L, 1.98mmol/L2.33mmol/L, 37.12mmol/L,804.44mol/LpH7.17, PCO224.5mmHg, HCO3-8.6mmol/L, SBE -18.3mmol/LT

  • 1 IntroductionNormal function of the kidneyRenal insufficiencyCausesBasic manifestation of renal insufficiency

  • Normal function of the kidneyRemove waste product from the bodyRegulate electrolyte and acid-base balance.1.ExcretionProduce reninEPO1,25(OH)2D3 and prostaglandinsInactivate gastrinPTH.2. Endocrine

  • Renal insufficiencyDiseases Dysfunction of excretion and endocrine Symptomsand signs Edema, hypertension, oliguric, polyuria, hematuria, proteinuria, anemia, osteodystrophy.

  • Causes:1 Primary renal diseasesPrimary glomerular diseases, Primary tubular diseases, Interstitial nephritis, et al.2 Secondary renal lesionCirculatory system diseases, immunity siseases, metabolic diseases, hematopathy, et al.

  • Basic manifestation of renal insufficiency 1 Glomerular dysfunction2 Tubular dysfunction3 Endocrine dysfunction

  • 1 Glomerular dysfunctionGFRblood flownet filtration pressure Kf Glomerular permselectivity

  • 2 Tubular dysfunctionproximal tubuleRenal glycosuria, aminoaciduria, renal tubular acidosis, hypophosphatemialoop of HenleHypotonic or isotonic urine, polyuriadistal tubuleAcid-base and electrolyte disorders, polyuria

  • 3 Endocrine dysfunction ReninEndothelinsKKS disordersAA DisequilibriumEPO 1,25(OH)2D3

  • 2 Acute renal failure

    DiseasesConceptionwater intoxication,azotemia, hyperkalemia, metabolic acidosis

  • Section 1 Cause and Classification 1 causes Prerenal ~ Intrarenal ~ Postrenal ~2renallesion functional~ organic ~obstructive ~3urine volumeOliguric ~Nonoliguric ~*** Classification

  • Causes 1 Prerenal factor renal blood flow Characteristicearly stage: functional~ late stage: organic ~(2) oliguria

  • MechanismECFRBF GFRReabsorptionoliguriaImpaired homeostasis

  • Causes (1) acute tubular necrosis,ATN 2/3 acute renal ischemiaacute renal poisoning hemoglobinuria, myoglobinuria (2) renal disease

    Characteristic (1) parenchymal(2) oliguric ~nonoliguric ~2 intrarenal factor

  • Differentiation between the two RFurine functionalRF organic RFspecific gravity> 1.020 < 1.015OP(mmol/L) > 700 < 250Na(mmol/L) < 20 > 40UrCr/SrCr > 40 < 20Sediment normalManicol test urine volume urine volume Necrosis epithelial cells,RBC,casts,albuminuria

  • Causes Kidney stone, tumor, obstruction of necrosis tissueCharacteristic early stage: obstructive ~ late stage: organic ~ 3 Postrenal factor

  • MechanismObstruction of the urinary tractBowmans capsule pressureNet filtration pressureGRFOliguria, anuria

  • Section 2 Pathogenesis RBF1 Net filtration pressure BP < 60mmHg CO RBF BP (50-70mmHg) GFR (1/2 2/3) BP(40mmHg) GFR = 0Urinary obstruction intracapsular pressure

    1 Glomerular factor

  • 2renal vessels constriction RBF sympathetic nerve Shock RAS prostaglandinkallikrein - kinin syetem ANP NO

  • 3 swelling endothelial cell ischemia Na+ - K+ - ATPase free radical endothelial cellular injury 4alteration of renal hemorheology fibrinogen Blood viscosity RBC PLT WBC

    renal DIC

  • Glomerular lesion filtration surface area Glomerular permselectivity GFR

  • 2 Tubular factortuble obstruction GFRpassive backflow GFR

  • 1 1 1 + ()

  • (2) PLT GFR

    2

  • 3AngADH GFR

  • 2 1 ATP ATP Na+ - K+ - ATPase Ca2+ - ATPase

    Na+H2O Ca2+

  • 2(FR) (GSH) FR FR3GSH 4 Ca2+ A2

  • 5 ATP 6

  • Section 3 Clinical Course and manifestation1 oliguria phasedaysweeks (1)features of urine urine volumeoliguria400ml/dor anuria100ml/d S.G.1.0101.020 Na+ tubular reabsorption dysfunction urine sediment:erythrocytes, casts, proteinuriaoliguric ARF

  • (2) water toxication oliguriaCatabolism Transfuse fluidFluid retentionHypervolemic hyponatremiaCell edema

  • (3) Hyperkalemia most serious Urinary excretion of K+Tissue destructionMetabolic acidosisTransfuse non-fresh blood, high K+ diethyponatremiaexchange of K+and Na+HyperkalemiaMovement of K+ from cells into ECF

  • (4) Metabolic acidosis grogressive,difficult to correctGFR excretion of acid productionSecretion of HNH3 , reabsorption of HCO3Catabolism acid productionMetabolic acidosisHyperkalemia

  • (5) Azotemia (NPN>40 mg/dl)Excretion of protein metaboliteProtein catabolism

  • 2 diuresis phase12W Mechanism

  • manifestation polyuria>400 ml/dEarly stage Hyperkalemia, Azotemia , Metabolic acidosis Late stagedehydration, hypokalemia, hyponatremia, infection.3 recovery phase

  • Nonoliguric ARFFeaures

  • Section 4 Treatment Principle of ARF1. Treat the cause; 2. Rescue actively. .

  • 11959344138395 60/120/85/54mmHg 8.6mmol/L128mmol/L,100mmol/L, 1.98mmol/L2.33mmol/L, 37.12mmol/L,804.44mol/LpH7.17, PCO224.5mmHg, HCO3-8.6mmol/L, SBE -18.3mmol/LT

  • Chronic Renal Failureetiological factors destruct nephronDysfunction of excretion and endocrine waste product , acid-base and electrolyte disorders dysfunction of endocrine Section 1 Conception

  • Section 2 Causes of CRFRenal diseases chronic glomerulonephritis et alVascular disordersdiabetes mellitushypertensive diseasePeriarteritis nodosa, et alUrinary tract obstructionurinary calculusprostatic hyperplasia et al

  • Section 3 Clinical Course of CRFcompensatory stage Renal insufficiency stage Renal failure stage Uremia stage

  • GFRml/minBUN(mmol/L)Cr(umol/L)>50

  • Section 4 PathogenesisIntact nephron hypothesisGlomerular hyperfiltration hypothesisTrade-off hypothesisTubulointerstitial injury

  • Intact nephron hypothesis

    causesProgressive reduction in the number of nephronsDestroy nephron persistentlyRenal compensation insufficiencyRenal failure

  • Glomerular hyperfiltration hypothesisCompensatory glomerular hyperfiltration GlomerulosclerosisRenal failure

  • Trade-off hypothesisGFR(P)()(PTH)()()

  • () GFR PTH

  • renal tubule -interstitial fibrosis

  • Section 5 Changes of Function and Metabolism1 characteristics of urine volumenocturiapolyuria>2000ml/dor oliguria(
  • 1.035

    1.020

    1.012

    1.008

    1.002

  • 2 acid-base and electrolyte disorders (1)fluidpulmonary and cerebral edemaheart failuredehydration(2)NahyponatremiaHypernatremia(3) Khypokalemia or hyperkalemiaK+ diet emesisdiuretic(excrete K +)K+ oliguriaPotassium-sparing diureticacidosiscatabolism , hemolysisintake K +

  • (4) Ca P P early stage : compensationPTH late stage: nephron bone dissolveCa P Vit D calcium phosphateToxic substance damage intestinal tract intake(5) Acidosis carbonic anhydrase NH3 H+ Absorption of intestine Ca

  • 3 azotemia (NPN>28.6mmol/L)BUN is not parallel to renal functionPlasma creatinine endogenous creatinine clearance rate ----CCR=Ucr VuPcr

  • 4 renal hypertension(1) Fluid and sodium retention(2) renin(3) kininPGE2

  • 5 hemorrhagic tendencyToxic substance inhibite the function of plateletPF3

  • (1) EPO(2) bone marrow(3)bleeding(4) Erythrocyte life span(5)Fe and Folic acid deficiency6Al7 Renal anemia

  • 5 renal osteodystrophyD3

  • (2)Vit D3 (4)Al (1)P Ca and secondary hyperparathyroidism(3) acidosisbone mineral lysisdecalcification, VitD3 absorption of intestine Ca

  • GFR1,25(OH)2D3 PTH

  • End-stage renal failureuremiaARFCRFToxinIntoxicationsymptom

  • source 1. Metabolite 2. Ectogenesis toxin 3. Ectogenesis toxin metabolite 4. Normal activity materialUremia toxin

  • common urea, guanidine, amines and phenolmiddle moleculesPTHAlUremia toxin

  • change of function and metabolism

  • -

  • Treatment principle

    1treatment of the primary disease 2 dialysis therapy 3 renal transplantation

  • 35201 6104-52000ml/BP146/100mmHgHb40-70g/LRBC1.3-1.761012/L+RBCWBC5-7/HP32500-3500ml/1.01010 T37R20/P120/BP150/100mmHgRBC1.49 1012/LHb47g/LWBC9.6 109/L1.9mmol/L1.3mmol/L+RBC10-15/HpWBC0-2/Hp0-2/Hp2-3/LPX

  • parenchymal