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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
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