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Chronic Renal Failure
General introduction Etiology Pathogenesis Clinical findings Complications Diagnosis &D.D. Treatment
Chronic Renal Failure
General introduction
1. CRF is defined as a progressive and irreversible loss of renal function. It is a serious stage of renal insufficiency.
Eliminate wastes and excess water
maintain water,electrolyte and
acid-base balance----homeostasis
strong bone
RBC formation(erythropoietin)
control blood pressure(RAAS)
General introduction
Renal function declines retention of metabolite imbalance of fluid electrolyte and acid-base disorder harms to other organs(almost
every system)
General introduction
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
stage GFR Scr BUN CM
(ml/min) ( umol/L ) ( mmol/L ) ( mg/dl ) ( mg/dl )
CompensatoryCompensatory stagestage diminished renal reserve
AzotemiaAzotemiaearly renal failure
UremiaUremialate RF
end-stage RF
primary
50 178(2) 9 ( 20 ) diseases
25-50 178 ( 2 ) 9 ( 20 ) GIT symptoms
< 445 ( < 5 ) <20 ( <55 ) anemia
25 445 ( 5 ) 20 ( 55 ) uremic
10 707 symptoms
Etiology
Any urinary system disease that can impair the structure and function of the kidney may cause CRF.
Causes
Primary GNPrimary GNSecondary nephropathy Secondary nephropathy Obstructive renal diseasesObstructive renal diseasesChronic interstitial nephropathyChronic interstitial nephropathyRenal vascular diseasesRenal vascular diseasesCongenital or genetic renal diseasesCongenital or genetic renal diseasesUnknown reasonUnknown reason
China Primary CGN Obstructive nephropat
hy Diabetic nephropathy Lupus nephritis Hypertensive nephrop
athy Policystic disease
Western Diabetic nephropathy Hypertensive nephrop
athy Primary CGN Policystic disease
Causes
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
Intact nephron hypothesis The “trade off” hypothesis Glomerular hyperfiltration hypothesis Tubular hypertrophy hypothesis Others:lipid disorder,Coagulation disor
der,etc.
PathogenesisProgressive deterioration of renal function
Pathogenesis
Intact nephron hypothesis considerable amount of nephrons has b
een 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
The “trade off” hypothesis
PathogenesisProgressive 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.
GFR
PathogenesisProgressive 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
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.
PathogenesisProgressive deterioration of renal function
Glomerular hyperfiltration hypothesis
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.
PathogenesisProgressive deterioration of renal function
Others lipid disorder Coagulation disorder etc.
PathogenesisProgressive deterioration of renal function
PathogenesisMechanism 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
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
Organ/system symptoms signs
General fatigue weakness Sallow-appearing chronically illSkin 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 isosthenuriaNeuromuscular restless legs numbness
and cramps in legsNeurologic generalized irritability stupor asterixis myoclonus
and inability to concentrate peripheral neuropathy
decreased libido
GFR
years
Reversible causes
corrected
Urinary tract infections
Obstruction
Extracellular volume depletion
Nephrotoxins
Hypertension
Congestive HF
Hypercalcemia
Pregnancy
e.t.c.
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
Proteinuria Red cells Casts red cell casts
granular and hyaline casts
large “chronic RF cast”(wax) glycosuria
Clinical findings Laboratory findings
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
Complications Water,electrolyte disorder Acid-base disorder Cardiovascular complications Hematologic complications Gastrointestinal complications Musculo-skeletal problems Skin Endocrine Metabolic disorder Immune system
Water retention or dehydration hyponatremia or hypernatremia Hyperkalemia or hypokalemia Hypocalcemia Hyperphosphatemia magnesium
Water,electrolyte disorder
Hyperkalemia Risk of hyperkalemia (NR 3.5~5.5mmol/L) cardiac conduction system inhibition bradycardia,AVB,escape rhythm,heart arre
st
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
Decreased potassium excretion Acidosis. Blood transfusion. Increased potassium intake. Drugs---spironolactone
Hyperkalemia (normal distridution )
Water,electrolyte disorder
case58ys 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:
ECG:junctional escape rhythm Serum K:6.8mmol/L,Na:125mmol/L HCO3:11mmol/L
Emergency!Emergency!
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 Hyperkalemia TreatmentTreatment
Acid-base disorder Acid-base disorder (death rate)(death rate)
Filtration of titratable acid decreased Tubular H+ secretion decreased NH4
+ formation decreased
Osteodystrophy Hyperkalemia Uremic symptoms(GIT,cardiovascular,pulm
onary…)
Deep breath(kussmaul’s breath),bad appetite vomit ,weakness,coma, HF, BP decrease
PH ,CO2CP & HCO3-
Acid-base disorderAcid-base disorder
TreatmentHCO3
- should be maintained at 18~20mmol/l
Sodium bicarbonate ivdrip or po
Cardiovascular complicationsCardiovascular complications
Hypertension Pericarditis Congestive heart failure Others:atherosclerosis
Hypertension Most common complication of ESRD m
ust be properly controlled.
due to Salt and water retention Hyperreninemic states(RAS)
Cardiovascular complicationsCardiovascular complications
TreatmentA.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 complicationsCardiovascular complications
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 changesCr
600
400
200
2 yearshospitalization
BP 200/140
BP140/90
BP138/85
Main treatment:BP control
Diet & Six drugs were takencase
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 hospitalizationIgnore her desease, Drugs withdrawal 1.5 year later,back to hospital again,complained ab
out 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,Ca2+ 1.7mmol/L,HCO3
- 12mmol/L.
case
Failure to control BP can Failure to control BP can accelerate the progression of accelerate the progression of renal damage.renal damage.
Cardiovascular complications hypertension
retention of fluid
uremic cardiomyopathy
Heart failure
treatment Water & salt intake (oliguria auria)
Dialysis(remove excess water)
Diuretics
DigoxinACEI (is proved to be efficient)
retention of metabolic toxins prolonged bleeding time; declined functio
n 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 complicationsPericarditis
Pulmonary effectsPulmonary effects
A. pulmonary edema. B. Pneumonitis. C. Pleuritis. Dialysis is needed.
Hematologic Hematologic complicationscomplications
Anemia
Bleeding
WBC dysfunction
Normochromic and normocytic anemia
decreased erythropoietin production Iron intake decreased Bleeding RBC life span shortened BM suppression
Hematologic Hematologic complicationscomplicationsanemiaanemia
Hematologic Hematologic complicationscomplicationsanemiaanemia
Iron, folic acid, VitB12
BM RBC formation
EPOEPO needed
Spleen old RBC disrupted
ingestion
RBC life span 120days
GIT disorder
EPO decreased
BM suppression
RBC 80days
bleeding
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,VitB12)
Hematologic Hematologic complicationscomplicationsAnemia treatment Anemia treatment
BleedingBleeding Bruising,epistaxis,menorrhagia,hemorrh
agic pericardial effusion. It is mainly caused by platelet dysfunctio
n. Treatment:dialysis
WBC dysfunction WBC dysfunction prone to infection
Hematologic Hematologic complicationscomplications
Gastrointestinal effectsGastrointestinal 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.
Neuro-Neuro-MuscularMuscular manifestations manifestations
Early manifestations: weakness insomnia concentration dysorder
Late :character changes,bad memory, dumps,cramp,jerk,delirium,convulsion, coma
osteodystrophyosteodystrophy
Osteitis fibrosa Osteomalacia Osteoporosis Osteosclerosis
Active VitD3 deficiency
Secondary PTH Malnutrition others
Active VitD3 Osteitis fibrosa myopathy
0.25-1.0µg/d
Surgery Osteomalacia Osteoporosis
Osteosclerosis
parathyroid
osteodystrophyosteodystrophytreatmenttreatment
skinskin Pruritus. Yellow pigmentation.
Endocrine abnormalitiesEndocrine abnormalitiesA. Plasma renin concentration is normal or
increased.
B. EPO is decreased.
C. 1,25-(OH)2VitD3 is decreased.
D. Insulin, parathyroid hormone and glucagon are increased.
E. Hypogonadism.
Metabolic disordersMetabolic 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.
Infection immune system Infection immune system
Prone to infection
Dysfunction of WBC Lower amount of WBC Decreased immune function
Diagnosis Diagnosis and differential diagnosisand differential diagnosis
chronic renal failure(stage) chronic renal failure(stage) Primary diseasePrimary disease Risk factors(reversible)Risk factors(reversible) complicationscomplications
CRF or not?
stage?
early azotemia late ESRD
Risk factors
causes
complications
Diagnostic routeDiagnostic route
TreatmentTreatment Primary diseases and risk factors. Dietary treatment -keto acid use BP control Complications Cautious about the side effect of drugs. Dialysis Renal transplantation
Causes
Primary GNPrimary GNSecondary nephropathy Secondary nephropathy Obstructive renal diseasesObstructive renal diseasesChronic interstitial nephropathyChronic interstitial nephropathyRenal vascular diseasesRenal vascular diseasesCongenital or genetic renal diseasesCongenital or genetic renal diseasesUnknown reasonUnknown reason
China Primary CGN Obstructive nephropat
hy Diabetic nephropathy Lupus nephritis Hypertensive nephrop
athy Policystic disease
Western Diabetic nephropathy Hypertensive nephrop
athy Primary CGN Policystic disease
Causes
GFR
years
Reversible causes
corrected
infections
Obstruction
Extracellular volume depletion
Nephrotoxins
Hypertension
Congestive HF
Hypercalcemia
Pregnancy
e.t.c.
Risk factorsRisk factors
Dietary treatmentDietary 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)
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 treatmentDietary treatment
-keto acid use-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.
BP controlBP control
Systamic BP control Intraglomerular pressure control
relieve hyperfiltration ACEI or ARB
SCr>350umol/L cautious
complicationscomplications
TreatmentTreatment
Dialysis
GFR<10ml/min
SCr>707umol/L
peritoneum D, haemodialysis
Renal transplantation
什么是血液透析什么是血液透析
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。
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
血液透析是如何进行的?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
什么是腹膜透析?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。
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!
新的肾脏放在哪里?新的肾脏放在哪里?
原来的肾脏移植的肾脏
case58ys 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:
ECG:junctional escape rythum Serum K:6.8mmol/L,Na:125mmol/L HCO3:11mmol/L
Emergency!Emergency!
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.
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 766mol/l
blood gas: acidosis electrolytes: plasma Na+, k+, Cl-, Ca2+ decr
eased. x rays: left ventricle enlarged abnormalities of bone
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.