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Chronic Renal Failure.  General introduction  Etiology  Pathogenesis  Clinical findings  Complications  Diagnosis &D.D.  Treatment Chronic Renal.

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Presentation on theme: "Chronic Renal Failure.  General introduction  Etiology  Pathogenesis  Clinical findings  Complications  Diagnosis &D.D.  Treatment Chronic Renal."— Presentation transcript:

1 Chronic Renal Failure

2  General introduction  Etiology  Pathogenesis  Clinical findings  Complications  Diagnosis &D.D.  Treatment Chronic Renal Failure

3 General introduction  1. CRF is defined as a progressive and irreversible loss of renal function. It is a serious stage of renal insufficiency.

4  Eliminate wastes and excess water  maintain water,electrolyte and acid-base balance----homeostasis  strong bone  RBC formation(erythropoietin)  control blood pressure(RAAS) General introduction

5 Renal function declines  retention of metabolite  imbalance of fluid  electrolyte and acid-base disorder  harms to other organs(almost every system) General introduction

6  CRF is artificially divided into 3 stages according to glomerular filtration rate (GFR NR 80~120ml/min ). Serum creatinine, BUN may reflect GFR in some extent. General introduction

7 stage GFR Scr BUN CM (ml/min) ( umol/L ) ( mmol/L ) ( mg/dl ) ( mg/dl ) Compensatory stage Compensatory stage diminished renal reserveAzotemia early renal failureUremia late RF end-stage RF primary  50  178(  2)  9 (  20 ) diseases  178 (  2 )  9 (  20 ) GIT symptoms < 445 ( < 5 ) <20 ( <55 ) anemia  25  445 (  5 )  20 (  55 ) uremic  10  707 symptoms

8 Etiology  Any urinary system disease that can impair the structure and function of the kidney may cause CRF.

9 Causes Primary GN Secondary nephropathy Obstructive renal diseases Chronic interstitial nephropathy Renal vascular diseases Congenital or genetic renal diseases Unknown reason

10 China  Primary CGN  Obstructive nephropathy  Diabetic nephropathy  Lupus nephritis  Hypertensive nephropathy  Policystic disease Western  Diabetic nephropathy  Hypertensive nephropathy  Primary CGN  Policystic disease Causes

11  Progressive deterioration of renal function chronic renal disease is rarely reversable and leads to progressive decline in renal function.this occur even after an inciting event has been removed.  Mechanism of uremic symptoms Pathogenesis

12  Intact nephron hypothesis  The “trade off” hypothesis  Glomerular hyperfiltration hypothesis  Tubular hypertrophy hypothesis  Others:lipid disorder,Coagulation disorder,etc. Pathogenesis Progressive deterioration of renal function

13 Pathogenesis Intact nephron hypothesis considerable amount of nephrons has been impaired,remaining nephrons still work,but reduction in renal mass leads to hypertrophy of the remaining nephrons to meet the body’s need. Unfortunately these adaptations place a burden on the remaining nephrons and leads to progressive glomerular sclerosis and interstitial fibrosis. Progressive deterioration of renal function

14 The “trade off” hypothesis Pathogenesis Progressive deterioration of renal function The “trade off” hypothesis is to be considered together with the intact nephron hypothesis,i.e,the concept that adaptations arising in chronic renal failure may control one abnormality,but only in such a way as to produce other changes characteristic of the uremic syndrome.

15 GFR Pathogenesis Progressive deterioration of renal function The “trade off” hypothesis example serum phosphate serum phosphate normal (phosphate rising corrected) PTH harmful regulation Metastatic calcification Nervous diseases Impotence Myopathy And so on

16 hypertrophy of the remaining nephrons high filtration, high perfusion and high pressure in glomeruli which will lead to glomerular sclerosis and injure the remaining nephrons. Pathogenesis Progressive deterioration of renal function  Glomerular hyperfiltration hypothesis

17 Tubular hypertrophy hypothesis although this adaptive mechanism can be beneficial in maintaining fluid, electrolyte and acid-base balance, long term consequence is perpetuation of tubular damage. Tubular hypertrophy is usually associated with increased energy expenditure and high metabolism. Pathogenesis Progressive deterioration of renal function

18 Others  lipid disorder  Coagulation disorder  etc. Pathogenesis Progressive deterioration of renal function

19 Pathogenesis Mechanism of uremic symptoms Water electrolyte disorder Acid-base imbalance Uremic toxins Uremic symptoms Uremic toxins Decreased depletion of metabolic products. Urea,creatinine,phosphate,sulphate,guanidines,products of nucleic acid metabolism(UA,cAMP…),phenol compounds,hormones(PTH…),middle molecules

20 Clinical findings  The symptoms of CRF often develop slowly and are nonspecific.Individuals can remain asymptomatic until renal failure is far- advanced.(GFR<10~15ml/min )  In any patient with renal failure,it is important to identify and correct all reversible causes. Symptoms and signs

21 Organ/system symptoms signs General fatigue weakness Sallow-appearing chronically ill Skin pruritus easy bruisability pallor ecchymoses excoriations edema xerosis ENT pale conjuctiva Pulmonary shortness of breath rales pleural effusion Cardiovascular dyspnea on exertion hypertension cardiomegaly pain on inspiration friction rub Genitourinary nocturia impotence isosthenuria Neuromuscular restless legs numbness and cramps in legs Neurologic generalized irritability stupor asterixis myoclonus and inability to concentrate peripheral neuropathy decreased libido

22 GFR years Reversible causes corrected Urinary tract infections Obstruction Extracellular volume depletion Nephrotoxins Hypertension Congestive HF Hypercalcemia Pregnancy e.t.c.

23  Urinalysis early in the course of chronic renal failure provide valuable information,but late in renal failure urinary abnormalities are less conspicuous. Clinical findings Laboratory findings

24  Proteinuria  Red cells  Casts red cell casts granular and hyaline casts large “chronic RF cast”(wax)  glycosuria Clinical findings Laboratory findings

25  The findings of small echogenic kidneys bilaterally(<10cm) by UCG supports a diagnosis of CRF;  Though normal or even large kidneys can be seen with CRF caused by adult polycystic kidney disease,DN,multiple myeloma,amyloidosis and obstructive uropathy.  Radiologic evidence of renal osteodystrophy is another helpful findings. Clinical findings imaging

26 Complications  Water,electrolyte disorder  Acid-base disorder  Cardiovascular complications  Hematologic complications  Gastrointestinal complications  Musculo-skeletal problems  Skin  Endocrine  Metabolic disorder  Immune system

27  Water retention or dehydration  hyponatremia or hypernatremia  Hyperkalemia or hypokalemia  Hypocalcemia  Hyperphosphatemia  magnesium Water,electrolyte disorder

28 Hyperkalemia  Risk of hyperkalemia (NR 3.5~5.5mmol/L) cardiac conduction system inhibition bradycardia,AVB,escape rhythm,heart arrest  Potassium balance generally remains intact in CRF until GFR is less than 10ml/min.However,certain states pose an increased risk of hyperkalemia at higher GFRs. Water,electrolyte disorder

29  Decreased potassium excretion  Acidosis.  Blood transfusion.  Increased potassium intake.  Drugs---spironolactone Hyperkalemia (normal distridution ) Water,electrolyte disorder

30 case 58ys Female,DM for 15ys,BP for 5 ys severe edema,urine output decreased for 2Ms Diagnosis: DM DN CRF(uremia) Refuse to accept dialysis Conservative treatment, symptom not released Felt weakness HR:45bpm,BP:90/40mmHg Cardiac monitor:

31  ECG:junctional escape rhythm  Serum K:6.8mmol/L,Na:125mmol/L  HCO 3 :11mmol/L Emergency!

32  Cardiac monitoring, decrease K intake  1.Correct acidosis:  2.Calcium chloride (act against the inhibition on cardiac conduction system)  3.Insulin administration with glucose  4.An orally or rectally administered ion exchange resin(sodium potassium exchange)  5.!K + >6.5mmol/L urgent dialysis Hyperkalemia Treatment

33 Acid-base disorder (death rate)  Filtration of titratable acid decreased  Tubular H + secretion decreased  NH 4 + formation decreased  Osteodystrophy  Hyperkalemia  Uremic symptoms (GIT,cardiovascular,pulmonary…)

34  Deep breath(kussmaul’s breath),bad appetite vomit,weakness,coma, HF, BP decrease  PH,CO 2 CP & HCO 3 - Acid-base disorder Treatment HCO 3 - should be maintained at 18~20mmol/l Sodium bicarbonate ivdrip or po

35 Cardiovascular complications  Hypertension  Pericarditis  Congestive heart failure  Others:atherosclerosis

36 Hypertension  Most common complication of ESRD must be properly controlled. due to  Salt and water retention  Hyperreninemic states(RAS) Cardiovascular complications

37 Treatment A. salt & water restriction (case) a mildly decreased salt diet(4~6g/d) if hypertension persists, reduced to 2g/d B. Drug therapy ACE inhibitors & ARB are the first recommendation if serum potassium and GFR permit. CCB agents,diuretics,and β-blocking agents. adjunctive drugs that are often needed reflect the difficulty of achieving and maintaining hypertensive control in these patients. Cardiovascular complications

38 28ys,female,headache for 2 months,GIT disorder Hypertension found,200/130~140mmHg, Family history:negative urine test : blood 2+, Pr 2+ ;blood test : Hb 88g/L serum test: Cr 596umol/L Kidney image:length 88mm & 92mm;echo changes Cr years hospitalization BP 200/140 BP140/90 BP138/85 Main treatment:BP control Diet & Six drugs were taken case

39 32ys, female,found hypertension in pregnancy urine Pr3+,blood 3+,gave birth after 8Ms pregnancy (infant died right after delivery) suffer ARF,got recovery,but renal lesion still exited. SCr 200umol/L,drugs taken for BP controlling. After hospitalization Ignore her desease, Drugs withdrawal 1.5 year later,back to hospital again,complained about anorexia,vomitting,fatigue,bad memory,cramp occasionally BP 170/100mmHg Tests:Hb 54g/L,BUN 55mmol/L,SCr 1002umol/L, K + 5.6mmol/L,Na + 128mmol/L,Ca mmol/L,HCO mmol/L. case

40 Failure to control BP can accelerate the progression of renal damage. Failure to control BP can accelerate the progression of renal damage.

41 Cardiovascular complications hypertension retention of fluid uremic cardiomyopathy Heart failure treatment Water & salt intake (oliguria auria) Dialysis (remove excess water) Diuretics Digoxin ACEI (is proved to be efficient)

42  retention of metabolic toxins  prolonged bleeding time; declined function of platelet and decreased amount of platelet.  Chest pain,fever,signs of poor cardiac output; a friction rub may be auscultated, X-ray,UCG  Pericarditis is an absolute indication for initiation of hemodialysis. Cardiovascular complications Pericarditis

43 Pulmonary effects  A. pulmonary edema.  B. Pneumonitis.  C. Pleuritis.  Dialysis is needed.

44 Hematologic complications  Anemia  Bleeding  WBC dysfunction

45  Normochromic and normocytic anemia  decreased erythropoietin production  Iron intake decreased  Bleeding  RBC life span shortened  BM suppression Hematologic complications anemia

46 anemia Iron, folic acid, VitB 12 BM RBC formation EPO EPO needed Spleen old RBC disrupted ingestion RBC life span 120days GIT disorder EPO decreased BM suppression RBC 80days bleeding

47  Recombinant EPO is used in patients 20~50units/kg(1000~4000u/dose) subcutaneously injection or iv. three times a week.  Iron stores must be adequate to ensure response.(folic acid,VitB 12 ) Hematologic complications Anemia treatment

48  Bleeding  Bruising,epistaxis,menorrhagia,hemorrh agic pericardial effusion.  It is mainly caused by platelet dysfunction.  Treatment:dialysis  WBC dysfunction  WBC dysfunction prone to infection Hematologic complications

49 Gastrointestinal effects  Gastrointestinal disturbances are among the earliest and most common signs of the uremic syndrome.  metabolic taste and loss of appetite; Later, nausea and intermittent vomiting, even gastrointestinal bleeding may occur. Gastritis, peptic ulcer.

50 Neuro- Muscular manifestations  Early manifestations: weakness insomnia concentration dysorder  Late :character changes,bad memory, dumps,cramp,jerk,delirium,convulsion, coma

51 osteodystrophy  Osteitis fibrosa  Osteomalacia  Osteoporosis  Osteosclerosis  Active VitD 3 deficiency  Secondary PTH  Malnutrition  others

52

53 Active VitD 3 Osteitis fibrosa myopathy µ g/d Surgery Osteomalacia Osteoporosis Osteosclerosis parathyroid osteodystrophy treatment

54 skin  Pruritus.  Yellow pigmentation.

55 Endocrine abnormalities A. Plasma renin concentration is normal or increased. B. EPO is decreased. C. 1,25-(OH) 2 VitD 3 is decreased. D. Insulin, parathyroid hormone and glucagon are increased. E. Hypogonadism.

56 Metabolic disorders  A. low temperature.  B. Abnormality of glucose metabolism.  a. Fasting blood sugar is high in some cases, because peripheral insulin resistance is increased.  b. Diabetes patients have a decrease in their insulin requirements.  C. Hyperuricemia.

57 Infection immune system  Prone to infection  Dysfunction of WBC  Lower amount of WBC  Decreased immune function

58 Diagnosis and differential diagnosis  chronic renal failure(stage)  Primary disease  Risk factors(reversible)  complications

59 CRF or not? stage? earlyazotemialate ESRD Risk factors causes complications Diagnostic route

60 Treatment  Primary diseases and risk factors.  Dietary treatment   -keto acid use  BP control  Complications  Cautious about the side effect of drugs.  Dialysis  Renal transplantation

61 Causes Primary GN Secondary nephropathy Obstructive renal diseases Chronic interstitial nephropathy Renal vascular diseases Congenital or genetic renal diseases Unknown reason

62 China  Primary CGN  Obstructive nephropathy  Diabetic nephropathy  Lupus nephritis  Hypertensive nephropathy  Policystic disease Western  Diabetic nephropathy  Hypertensive nephropathy  Primary CGN  Policystic disease Causes

63 GFR years Reversible causes corrected infections Obstruction Extracellular volume depletion Nephrotoxins Hypertension Congestive HF Hypercalcemia Pregnancy e.t.c. Risk factors Risk factors

64 Dietary treatment A. Dietary protein restriction It can decrease BUN, plasma phosphate concentration and relieve acidosis. But if protein intake is too low, malnutration may occur. Generally, dietary protein should be restricted properly when GFR is lower than 50ml/min. Pr amount : 0.6g/kg high quality Pr(animal Pr)

65  B. Diet must consist of enough calories and plenty of VitB, VitC and lactate.  C. Water and sodium must be restricted if patients have edema, HP, heat failure or oliguria;  D. potassium must be restricted when urine volume is less than 1L/d and phosphate should be restricted at azemia stage. Dietary treatment

66  -keto acid use   -keto acid can combine with nitrogen to form EAA and EAA can combine with urea to synthesize protein, so, using  - keto acid can decrease BUN.

67 BP control  Systamic BP control  Intraglomerular pressure control relieve hyperfiltration  ACEI or ARB SCr>350umol/L cautious

68 complications

69 Treatment Treatment  Dialysis GFR<10ml/min SCr>707umol/L peritoneum D, haemodialysis  Renal transplantation

70 什么是血液透析 血液透析需要每 周进行 2-3 次, 每次 3 - 5 个小时。 血液透析是利用血透机来净化血液,机器上有一个特殊 的滤器,叫做透析器,它就相当于一个人工肾脏,清除 身体里的废物和多余的水分。 血液经过一条 塑料管子被引 流到透析器里 接受净化,净 化后的血液再 通过另一条塑 料管子回流到 身体里。

71 由于一般的静脉不够粗、管壁不够厚,不能满足血透 治疗对血流量的要求,所以进行血液透析前必需手术 建立一条永久血管通路,最常用的是前臂动静脉瘘。 静脉端穿刺针动脉端穿刺针 动脉化静脉 动脉 内瘘处静脉 内瘘处动脉

72 血液透析是如何进行的? 含有废物的血 液进入透析器 透析器 经过净化的血 液输回身体里

73 什么是腹膜透析? 腹膜透析与血液透析一样可以净化血液,不同的是它 不需要使用透析机和透析器。它利用你腹部内部的一 个空腔 — 腹腔来进行透析治疗。

74 开始腹透治疗前,首先需要建立一个安全的通路来进行 换液。做一个外科小手术,把一条被称为 “ 腹透管 ” 的 柔软、可弯曲的管子插入腹腔。管子的一端留在腹腔里, 中间一段埋在皮下,另一端留在腹壁外面。你一定要保 护好这条腹透管,这就是你的生命线!

75 新的肾脏放在哪里? 原来的肾脏 移植的肾脏

76 case 58ys Female,DM for 15ys,BP for 5 ys severe edema,urine output decreased for 2Ms Diagnosis: DM DN CRF(uremia) Refuse to accept dialysis Conservative treatment, symptom not released Felt weakness HR:45bpm,BP:90/40mmHg Cardiac monitor:

77  ECG:junctional escape rythum  Serum K:6.8mmol/L,Na:125mmol/L  HCO 3 :11mmol/L Emergency!

78 Case 1: Hu fenlan, female, 68ys  Edema for 30ys, fatigue and anorexia for 2Ms  30ys ago, edema on legs was found when she was in pregnancy.10ys ago, HP was found. Nocturnal urine output has been increased for 3ys. 2Ms ago, suffered fatigue, anorexia, nausea and vomiting. Pruritus and arthralgia occurred.

79  Physical examination: p,92/min, uremic face,the cardiac dullness distending to the left, systolic murmurs heard on mitral area,percussion pain on right renal area.  Lab tests:  renal function: BUN 27.8mmol/l, CRE 766  mol/l blood gas: acidosis electrolytes: plasma Na +, k +, Cl -, Ca 2+ decreased.  x rays: left ventricle enlarged abnormalities of bone

80 Case 2: zhang tao, femal/ 34ys  Fatigue, anorexia and menorrhagia for 4Ms.  4Ms ago, felt fatigue and dizziness accompanied by menorrhagia. And then, palpitation, dyspnea, anorexia and nausea occurred gradually. One week ago, Bp 170/110mmHg, BUN 22.6mmol/l, Cre 835  mol/l.  Physical examination: the positivfindings were same as case 1.  Lab tests: plasma k + P + high, RBC and Hb low.


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