chronic renal failure new.mansfans.com

8/14/2019 Chronic Renal Failure New.mansfans.com

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CHRONIC RENAL FAILURECHRONIC RENAL FAILUREBy

Mohamad A. Sobh, MD, FACPMohamad A. Sobh, MD, FACPProf. & Head of NephrologyProf. & Head of Nephrology

Urology & Nephrology Center,Urology & Nephrology Center,Mansoura University,Mansoura University,

EgyptEgypt


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Chronic kidney disease (CKD) is defined as

kidney damage or glomerular filtration rate

(GFR)


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Classification of CKD based on GFR Classification of CKD based on GFR

CKD Stage Description

1 Normal or increased GFR; some evidence of kidneydamage reflected by microalbuminuria/

proteinuria, hematuria, or histlogic changes2 Mild decrease in GFR (89-60 ml/min/1.73 m 2)

3 Moderate decrease in GFR (59-30 ml/min/1.73 m 2)

4 Severe decrease in GFR (29-15 ml/min/1.73 m2

)5 GFR


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Cockcroft-Gault formula:

eGFR (ml/min/1.73 m 2) = (140- age) x Wt

S.Cr x 77

for x 0.85

eGFR


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Chronic renal failure:Chronic renal failure:Is a progressive loss of kidney function due toIs a progressive loss of kidney function due to

progressive damage of kidney tissue by a diseaseprogressive damage of kidney tissue by a disease

involving the two kidneys, with eGFR


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INCIDENCE OF CRF IS INCREASING

Environmental pollution.Environmental pollution.

Drug abuse.Drug abuse.

Others.Others.


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1.1. Primary glomerular diseasePrimary glomerular diseaseSuch as MCGN and FSGS.Such as MCGN and FSGS.

3.3. Tubulointerstitial diseaseTubulointerstitial disease

Such as NSAIDs abuse, heavy metalsSuch as NSAIDs abuse, heavy metalshypercalcaemia, hypokalaemia.hypercalcaemia, hypokalaemia.

5.5. Renal vascular diseaseRenal vascular disease

Such as renal artery stenosis and renalSuch as renal artery stenosis and renalvein thrombosis.vein thrombosis.

7.7. Chronic pyelonephritis.Chronic pyelonephritis.

ETIOLOGY OF CHRONIC RENALFAILURE


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1.1. Chronic urinary tract obstructionChronic urinary tract obstruction

2.2. Collagen diseaseCollagen disease

Such as SLE, PAN, Rh-Such as SLE, PAN, Rh- oidoid ..

4.4. Metabolic diseaseMetabolic disease

Such as DM, amyloidosis, gout, NSAIDsSuch as DM, amyloidosis, gout, NSAIDsabuse.abuse.

ETIOLOGY OF CHRONIC RENALFAILURE


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Gross appearance:Gross appearance:

Size is decreased except in PCKD, DM,Size is decreased except in PCKD, DM,

amyloidosis, hydronephrosis.amyloidosis, hydronephrosis.

Microscopic appearance:Microscopic appearance:

Tubular atrophy,interstitial fibrosis andTubular atrophy,interstitial fibrosis and

glomerulosclerosis.glomerulosclerosis.

PATHOLOGY OF CRF


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1.1. Disturbance of water excretion.Disturbance of water excretion.2.2. Disturbance of sodium excretion.Disturbance of sodium excretion.

3.3. Disturbance of potassium excretion.Disturbance of potassium excretion.4.4. Disturbance of acid-base balance.Disturbance of acid-base balance.

5.5. Disturbance of calcium-phosphate metabolism.Disturbance of calcium-phosphate metabolism.

6.6. Retention of uraemic toxins.Retention of uraemic toxins.

7.7. Failure of renal endocrine functions.Failure of renal endocrine functions.

PATHOPHYSIOLOGY OF CRF


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Loss of the renal ability toLoss of the renal ability to concentrateconcentrate urine:urine:Occurs early in uraemia, manifest as polyuriaOccurs early in uraemia, manifest as polyuria

and nocturia. Caused by osmotic overload oand nocturia. Caused by osmotic overload othe remaining nephrons. May be dangerous.the remaining nephrons. May be dangerous.

Loss of the renal ability toLoss of the renal ability to dilutedilute urine:urine:Occurs late in ureamia. Urine specific gravityOccurs late in ureamia. Urine specific gravitynever below 1010 (osmolarity 300) i.e.never below 1010 (osmolarity 300) i.e.

iosthenuria. This could be dangerousiosthenuria. This could be dangerous

DISTURBANCE OF WATER EXCRETION


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Any of the following disorders may occur:Any of the following disorders may occur:

1.1. Dilutional hyponatraemia.Dilutional hyponatraemia.

2.2. Salt loosing nephropathy.Salt loosing nephropathy.

3.3. Salt and water retention.Salt and water retention.

4.4. Hypernatraemia?!Hypernatraemia?!

DISTURBANCE OF SODIUMEXCRETION


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Hyperkalaemia only if:Hyperkalaemia only if:

2.2. GFR < 10 ml/minGFR < 10 ml/min

3.3. Excess K loadExcess K load

4.4. Severe acidosis with volume contraction.Severe acidosis with volume contraction.

5.5. Drugs as ACEI, B-blockers, AldosteronDrugs as ACEI, B-blockers, Aldosteronantagonists.antagonists.

6.6. Hyporeninaemic hypoaldosteronism.Hyporeninaemic hypoaldosteronism.

DISTURBANCE OFPOTNSSIUM EXCRETION


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Metabolic acMetabolic ac idoido sis may occure due to:sis may occure due to:HcoHco 33 wastagewastage

Inability to secrete H+.Inability to secrete H+.

Retention of titratable acids.Retention of titratable acids.

Decreased amonia production.Decreased amonia production.

May be more severe with tubulo interstitialMay be more severe with tubulo interstitialdiseases, hypercatabolic states, and indiseases, hypercatabolic states, and inchildren.children.

May aggravate bone disease.May aggravate bone disease.

DISTURBANCE OF H+ EXCRETION


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1.1. Retention hyperphosphataemia.Retention hyperphosphataemia.

2.2. Hypocalcaemia.Hypocalcaemia.

3.3. Secondary hyperparthyrodism.Secondary hyperparthyrodism.

4.4. Bone disease and soft tissue calcification.Bone disease and soft tissue calcification.5.5. Tertiary hyperparathyroidism.Tertiary hyperparathyroidism.

DISTURBANCE OFCALCIUM-PHOSOPHATE METABOLISM


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The natureThe nature of uraemic toxins is not yet certainof uraemic toxins is not yet certain

2.2. Urea, creatinine, guanidine, phenolsUrea, creatinine, guanidine, phenols

parathormon .ect.parathormon .ect.

3.3. Middle molecules (300-2000D).Middle molecules (300-2000D).

These toxins are respponsible forThese toxins are respponsible for mostmost of theof the

uraemic symptoms.uraemic symptoms.

RETENTION OF UREAMIC TOXINS


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CLINICAL FEATURES OF CRF


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Mouth:Mouth: Tast, smell, coated tongue,Tast, smell, coated tongue,dry, ulcers, dental caries.dry, ulcers, dental caries.

Stomach:Stomach: Poor appetite, nausea, vomiting,Poor appetite, nausea, vomiting,haematemesis, gastritis, erosins,haematemesis, gastritis, erosins,

hiccough.hiccough.Intestine:Intestine: Constioption, diarrhoea, dysentry,Constioption, diarrhoea, dysentry,

bleedin .bleeding.

I- Gastrointestinal manifestations of uraemia


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Cerebral:Cerebral: Headach, drowsiness, insomniaHeadach, drowsiness, insomnia

reversal of sleep rhythm, coma.reversal of sleep rhythm, coma.Neuromuscular:Neuromuscular: Tremours, peripheral neuropathy,Tremours, peripheral neuropathy,

muscle twitches, convulsions,muscle twitches, convulsions,muscle weakness.muscle weakness.

III- Cardiovascular manifestations:III- Cardiovascular manifestations:d.d. Anaemia.Anaemia.

e.e. Bleeding tendency.Bleeding tendency.f.f. Hypertension.Hypertension.g.g. Ureamic pericarditis.Ureamic pericarditis.

h.h. Heart failure.Heart failure.

II- Neurological manifestations:


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a.a. Face is muddy, pale, puffyFace is muddy, pale, puffy

b.b. Dry skin, brusis.Dry skin, brusis.c.c. Pruritis.Pruritis.d.d. Purpura.Purpura.

e.e. Infections.Infections.V- Respiratory manifestations:V- Respiratory manifestations:g.g. Acidotic breathingAcidotic breathingh.h. Recurrent infection.Recurrent infection.i.i. Dyspnea.Dyspnea.

j. j. Pleurisy.Pleurisy.

IV- Cutaneous manifestations of uraemia:


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a.a. Ureamic retinopathy.Ureamic retinopathy.b.b. Ureamic amarousis.Ureamic amarousis.c.c. red eye.red eye.

VII- Musculo-skeletal manifestations:VII- Musculo-skeletal manifestations:e.e. Muscle fatigue, wastingMuscle fatigue, wastingf.f. Bone aches, fractures, deformity in children.Bone aches, fractures, deformity in children.

g.g. Seft tissue calcification.Seft tissue calcification.VII- Gonadal manifestations:VII- Gonadal manifestations:i.i. Decreased lipido, impotence, gynaecomastiaDecreased lipido, impotence, gynaecomastia

j. j. Infertility, menstrual disorders.Infertility, menstrual disorders.

VI- Ocular manifestations of ureamia:


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a.a. Hyperparathyoidism.Hyperparathyoidism.

b.b. Lack of EPO.Lack of EPO.c.c. Lack of active vit.D.Lack of active vit.D.d.d. Increased renin activity.Increased renin activity.e.e. Decreased testosterone.Decreased testosterone.f.f. Increased prolactin and LH.Increased prolactin and LH.

g.g. Insulin increased peripheral resistance andInsulin increased peripheral resistance andhalf life.half life.

X-X- Features of the underlying disease:Features of the underlying disease:

Such as DM, SLE, Stone disease.Such as DM, SLE, Stone disease.

IX- Endocrine disorders in uraemia:


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INVESTIGATIONS OF A CASE WITHCRF

urine:urine: Proteinuria, pyuria, casts,Proteinuria, pyuria, casts,haematuria.haematuria.

Blood:Blood: High S. creatinine, anaemia,High S. creatinine, anaemia,high uric acid, high phosphate,high uric acid, high phosphate,hypocalcaemia.hypocalcaemia.

Radiologic:Radiologic: U. S. will show decreased size andU. S. will show decreased size andincreased echogenisity.increased echogenisity.

Investi ations to dia nose the etiolo ic cause.Investigations to diagnose the etiologic cause.


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MANAGEMENT OFMANAGEMENT OF

CHRONIC RENAL FAILURECHRONIC RENAL FAILUREFour steps should be adopted forFour steps should be adopted for

proper management of patientsproper management of patients

with chronic renal failure.with chronic renal failure.


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Step 1.Step 1. Confirmation of chronicity of theConfirmation of chronicity of thekidney diseasekidney disease

This could be achieved through the following:This could be achieved through the following:

History:History: A long history of renaldisease suggests chronicityA long history of renaldisease suggests chronicitywhile absent previous history suggests acute renal failure.while absent previous history suggests acute renal failure.Kidney size as detected by ultrasonography:Kidney size as detected by ultrasonography: A smallA smallatrophic kidney favours the diagnosis of chronic renal failure,atrophic kidney favours the diagnosis of chronic renal failure,while a normal sized kidney is more in favor of acute renalwhile a normal sized kidney is more in favor of acute renalfailure.failure.Magnitude of the increase in serum creatinine inMagnitude of the increase in serum creatinine inrelation to the presenting symptoms:relation to the presenting symptoms: High serumHigh serumcreatinine with minimal symptoms is in favour of chroniccreatinine with minimal symptoms is in favour of chronicrenal disease, while relatively low serum creatinine withrenal disease, while relatively low serum creatinine withsevere symptoma is in favour of acute renal disease.severe symptoma is in favour of acute renal disease.

Hyperphosphataemia and osteodystrophy:Hyperphosphataemia and osteodystrophy: are presentare presentmore with chronic cases.more with chronic cases.Anaemia:Anaemia: Is more with chronic cases.Is more with chronic cases.Renal biopsy:Renal biopsy: extensive renal interstitial fibrosis andextensive renal interstitial fibrosis andtubular atrophy in renal biopsy are features of chronic cases.tubular atrophy in renal biopsy are features of chronic cases.

S 2 h f bl fS hi f ibl f


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Step 2.Step 2. Searching for reversible factors:Searching for reversible factors:These factors are classified as the following:These factors are classified as the following:

Pre-renal factors such as:Pre-renal factors such as: Bilateral renal artery stenosis.Bilateral renal artery stenosis.Severe cardiac failure.Severe cardiac failure.Malignant hypertensionMalignant hypertensionHypertensionHypertensionDehydration and hypovolaemia.Dehydration and hypovolaemia.

c.c. Renal factors such as:Renal factors such as:Active glomerlur diseaseActive glomerlur diseaseActive tubulo-interstitial diseaseActive tubulo-interstitial diseasePyelonephritisPyelonephritis

Postrenal factors :Postrenal factors : Causing obstruction of urine flow from both kidneys such as:Causing obstruction of urine flow from both kidneys such as:

StoneStoneStricture uretersStricture uretersEnlarged prostateEnlarged prostateBladder neck obstructionBladder neck obstruction


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tep 3.tep . onservat ve treatment o chron conservat ve treatment o c ron crenal failure:renal failure:

a.a. Dietary control:Dietary control: Protein Protein is usually restricted to 0.6-1 gm/kg/day (anis usually restricted to 0.6-1 gm/kg/day (anamount which satisfies the physiologic requirement).amount which satisfies the physiologic requirement).Fluid Fluid restriction equivalent to the patients daily fluidrestriction equivalent to the patients daily fluidloss. This equals: the sensible water loss (e.g. urine,loss. This equals: the sensible water loss (e.g. urine,vomitus and diarrhea) plus the insensible water lossvomitus and diarrhea) plus the insensible water loss(respiratory and sweat) which is about 600 ml/d in an(respiratory and sweat) which is about 600 ml/d in anadult of 70 kg. Extra 200 ml fluid should be added inadult of 70 kg. Extra 200 ml fluid should be added infebrile patient for every one degree centigrade increasefebrile patient for every one degree centigrade increasein the body temperature.in the body temperature.

Electrolytes: Electrolytes: Sodium restriction with hypertension oeSodium restriction with hypertension oeoedema and potassium restriction with severe oliguriaoedema and potassium restriction with severe oliguriaand with hyperkalaemia.and with hyperkalaemia.Calories:Calories: Patient should receive about 35 K.Patient should receive about 35 K.calories/kg/day with carbohydrate 60% of non proteincalories/kg/day with carbohydrate 60% of non proteincalories and fat 40%.calories and fat 40%.

T f b diT t t f b di


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a.a. Treatment of bone disease:Treatment of bone disease: Phosphate Binders Phosphate Binders such as aluminum hydroxide,such as aluminum hydroxide,and calcium carbonate which combine withand calcium carbonate which combine with

phosphorus in the gut and are excreted with thephosphorus in the gut and are excreted with thestool. Calcium containing compound are betterstool. Calcium containing compound are betterthan aluminum salts which could be dangerous onthan aluminum salts which could be dangerous onlong term use. Calcium carbonate may be givenlong term use. Calcium carbonate may be givenorally t.d.s. with meals in a dose of 500-1000 oraly.orally t.d.s. with meals in a dose of 500-1000 oraly. Active vitamin D Active vitamin D 1-OH vitamin D which is given1-OH vitamin D which is givenorally in a daily dose of 0.25-1.0orally in a daily dose of 0.25-1.0 g.g. Acidosis Acidosis is corrected is corrected by oral Na bicarbonateby oral Na bicarbonatesupplementation.supplementation. Parathyroidectomy Parathyroidectomy may be done for cases withmay be done for cases withtertiary hyperparathroidism. Three glands andtertiary hyperparathroidism. Three glands andpart of the fourth are remove and the remaining ispart of the fourth are remove and the remaining issimplanted subcutaneously.simplanted subcutaneously.

A iA i


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a.a. Anaemia:Anaemia:Is responsible for major part of uraemic

symptoms. The first line of treatment is by

giving proper nutrition, iron, folic acid, andvitamins especially B12. Failure to respond mayindicate repeated blood transfusion or treatmentwith recombinant human Erythropoietin. Bloodtransfusion carries the advantage of being cheapbut have disadvantage of transmitting diseases(especially HIV, HBV and HCV) beside otherrisk of blood transfusion. Erthropoietin (EPO) isgiven s.c or i.v 4000u three times weekly, itcarries the advantage of being safe and effective,but it is very expensive. The dose of EPO has tobe redjusted to maintain haemoglobin value o11-13 gm/dl.


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a.a. Symptomic treatment:Symptomic treatment: Hypertension Hypertension is controlled by hypotensive drugs.is controlled by hypotensive drugs.

Itching Itching is treated by skin soothing creams, anti-is treated by skin soothing creams, anti-histaminics, treatment of hyperphosphataemia,histaminics, treatment of hyperphosphataemia,hyper and hypocalcaemia. For severe, intractablehyper and hypocalcaemia. For severe, intractablecases, parathyroidectomy may be of help.cases, parathyroidectomy may be of help.G.I.T. manifestationsG.I.T. manifestations as vomiting could beas vomiting could becontrolled by antacids and H2-receptors blockers.controlled by antacids and H2-receptors blockers.

Failure of consevative treatment to provide theFailure of consevative treatment to provide thepatient with a reasonable quality of life is anpatient with a reasonable quality of life is anindication for renal replacement therapy, i.e.indication for renal replacement therapy, i.e.

dialysis or renal transplantation.dialysis or renal transplantation.


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Step 4.Step 4. Renal replacement TherapyRenal replacement Therapy(RRT):(RRT):

This includes dialysis (haemodialysisThis includes dialysis (haemodialysis

and peritoneal dialysis) and renaland peritoneal dialysis) and renal

transplantation. Early indication of RRTtransplantation. Early indication of RRT

and good nutritional support provideand good nutritional support provide

better response to the treatment (lessbetter response to the treatment (less

patient morbidity and mortality).patient morbidity and mortality).


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Indication for (RRT):Indication for (RRT):Failure of conservative treatment withFailure of conservative treatment withprogressive deterioration in patients generalprogressive deterioration in patients generalcondition and blood chemistry.condition and blood chemistry.Persistent nausea and vomiting.Persistent nausea and vomiting.Circulatory overload which is unresponsive toCirculatory overload which is unresponsive to

loop diuretics (e.g. frusemide).loop diuretics (e.g. frusemide).Severe motor neuropathy.Severe motor neuropathy.Uraemic encephalopathy.Uraemic encephalopathy.PericarditisPericarditisBleeding diathesis.Bleeding diathesis.Hyperkalaemia (serum K+ level > 7 mEq./liter).Hyperkalaemia (serum K+ level > 7 mEq./liter).High creatinine levels and decreased creatinineHigh creatinine levels and decreased creatinineclearance (Cr. Clearance < 10ml/min).clearance (Cr. Clearance < 10ml/min).


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Contraindications for dialysis treatment:Contraindications for dialysis treatment:

2.2. Absolute:Absolute:

Patients is refusing dialysis.Patients is refusing dialysis.

Severe extrarenal illness e.g. severeSevere extrarenal illness e.g. severe

cardiac disease, end stage liver disease,cardiac disease, end stage liver disease,severe cerebrovascular disease andsevere cerebrovascular disease andadvanced malignancy.advanced malignancy.

3.3. Relative:Relative:Severe disability or handicapping.Severe disability or handicapping.

Paraplegia or hemiplegia.Paraplegia or hemiplegia.


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DIALYSIS THERAPYDIALYSIS THERAPYDefinition:Definition:

Dialysis is a process in which the soluteDialysis is a process in which the solutecomposition of blood is altered by exposing it tocomposition of blood is altered by exposing it toa physiological solution (dialysate) across aa physiological solution (dialysate) across a

semipermeable membrane (dialysis membrane).semipermeable membrane (dialysis membrane).Solutes will move from one compartment toSolutes will move from one compartment toanother through the dialysis membrane.another through the dialysis membrane.Type of Dialysis:Type of Dialysis:There are two forms of dialysis therapy:There are two forms of dialysis therapy:

(A) Haemodialysis, and(A) Haemodialysis, and(B) Peritoneal dialysis(B) Peritoneal dialysis


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(A) Haemodialysis(A) Haemodialysis

Definition:Definition:

It is the movement of solutes and waterIt is the movement of solutes and waterfrom the patients blood across afrom the patients blood across asemipermeable membrane which is thesemipermeable membrane which is thedialyzer.dialyzer.

This is carried out via vascular accessThis is carried out via vascular access

where the blood is pumped by awhere the blood is pumped by ahaemodialysis machine into the dialzer thenhaemodialysis machine into the dialzer thenthe filtered blood returns back to the patientsthe filtered blood returns back to the patientscirculation.circulation.


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l f h d l


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Complications of haemodialysis :Complications of haemodialysis :(I) Common complications:(I) Common complications:

Hypotension:Hypotension: This is the commonestThis is the commonestcomplication and may be due to:complication and may be due to:High ultrafiltration rateHigh ultrafiltration rateDialysis solution sodium level is too lowDialysis solution sodium level is too low

Acetate-containing dialysis solution.Acetate-containing dialysis solution.Dialysis solution is too warm.Dialysis solution is too warm.Food ingestion (splanchnic vasodilatation).Food ingestion (splanchnic vasodilatation).Autonomic neuropathy (e.g. diabetic patients)Autonomic neuropathy (e.g. diabetic patients)

Diastolic dysfunctionDiastolic dysfunctionHaemorrhageHaemorrhageSepticaemiaSepticaemiaArrhythmiaArrhythmiaDialyzer reactionDialyzer reaction


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(A)(A) Muscle Cramps.Muscle Cramps.

(B)(B) Nausea and Vomiting.Nausea and Vomiting.

(C)(C) Headache.Headache.(D)(D) Chest pain and back pain.Chest pain and back pain.

(E)(E) Itching.Itching.

(F)(F) Fever and Chills.Fever and Chills.


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(II) Less Common Complications:(II) Less Common Complications:

Disequilibrium Syndrome::Disequilibrium Syndrome:: Definition: Definition: Disequilibrium syndrome is aDisequilibrium syndrome is a

set of systemic and neurologic symptoms whichset of systemic and neurologic symptoms whichare often associated with characteristic EEGare often associated with characteristic EEGfinding that can occure either during or soonfinding that can occure either during or soonafter dialysis.after dialysis.

Early manifestations include headache,Early manifestations include headache,nausea, vomiting, convulsions and may benausea, vomiting, convulsions and may becoma. In severe cases, death can occur if notcoma. In severe cases, death can occur if nottreated properly.treated properly.

lDi l i


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Dialyzer reactions:Dialyzer reactions:Type A (anaphylactic type):Type A (anaphylactic type):The manifestation of this type may be mild in theThe manifestation of this type may be mild in the

form of itching, cough, urticaria, sneezing, coryza orform of itching, cough, urticaria, sneezing, coryza orwatery eyes; or may be severe in the form of dyspnea,watery eyes; or may be severe in the form of dyspnea,chest tightness, cardiac arrest or even death.chest tightness, cardiac arrest or even death.

Treatment:Treatment:Stop dialysis immediatelyStop dialysis immediately

AntihistaminicsAntihistaminicsSteroidsSteroidsType B (Non specific type):Type B (Non specific type):The patients may complain of back pain or chestThe patients may complain of back pain or chest

pain.pain. Etiology EtiologyComplement activationComplement activationTreatment Treatment No specific treatmentNo specific treatment


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ArrhythmiasArrhythmiasArrhythmias during dialysis are common especially inArrhythmias during dialysis are common especially in

patients receiving digitalis.patients receiving digitalis.Cardiac tamponadeCardiac tamponadeUnexpected or recurrent hypotension during dialysisUnexpected or recurrent hypotension during dialysismay be sign of pericardial effusion or impendingmay be sign of pericardial effusion or impending

tamponade.tamponade.Intracranial bleeding:Intracranial bleeding:

Underlying vascular disease and hypertensionUnderlying vascular disease and hypertensioncombined with heparin administration can sometimescombined with heparin administration can sometimesresult in intracarnial bleeding.result in intracarnial bleeding.

Seizures:Seizures: This occur more often in children.This occur more often in children.Haemolysis:Haemolysis:

Acute haemolysis during dialysis may be a medicalAcute haemolysis during dialysis may be a medical

emegency.emegency.Air embolism:Air embolism: It is a potential catastrophe that can lead to death if It is a potential catastrophe that can lead to death if

not quickly detected and treated.not quickly detected and treated.


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(B) Peritoneal Dialysis (PD)(B) Peritoneal Dialysis (PD)

Definition:Definition:It is the movement of solutes and waterfrom patients blood across a semipermeable

membrane (which is the peritoneal membrane)to the dialysis solution (dialysate).This is carried out via a peritoneal

catheter which is inserted into the peritonealcavity for infusion of the dialysate which is leftto dwell then drained out via the catheter.


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Types of PD:Types of PD:


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Types of PD:Types of PD:2)2) CAPD (Continuous ambulatory peritoneal dialysis):CAPD (Continuous ambulatory peritoneal dialysis):

In which the dialysate is always present in theperitoneal cavity and is exchanged every 4-6 hours/day.This is the commonly used from of P.D worldwide.4)4) CCPD (Continuous cyclic peritoneal dialysis):CCPD (Continuous cyclic peritoneal dialysis):In which the dialysate is exchanged at bed time via acycler (P.D. machine) 3-4 times and the last exchangefluid is left in the abdomen during the daytime.

6)6) NIPD (Nocturnal intermittent peritoneal dialysis):NIPD (Nocturnal intermittent peritoneal dialysis):In which the dialysate is exchanged at bed tim via acycler 5-8 times/day and the abdomen is left dry the restof the day. This is the new trend nowadays, but it islimited because of the high cost of the cycler.TPD (Tidal peritoneal Dialysis): This is still anexperimental form of NIPD which was designed tooptimize solute clearance by leaving large volume odialysate in the peritoneal cavity throughout the dialysissession.

Indications for PD:Indications for PD:


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Indications for PD:Indications for PD:Because it provides the best rehabilitationBecause it provides the best rehabilitation

potential as it is safe and easy, it is used for allpotential as it is safe and easy, it is used for allages and all sizes of patients with end stageages and all sizes of patients with end stagerenal failure.renal failure.Specific indications for peritoneal dialysisSpecific indications for peritoneal dialysisinclude the following:include the following: 4.4. Infant and very young children.Infant and very young children.5.5. End stage renal failure patients withEnd stage renal failure patients withcardiovascular or haemodynamic instabilty.cardiovascular or haemodynamic instabilty.6.6. Haemodialysis patients with vascular accessHaemodialysis patients with vascular accessfailure (especially diabetics).failure (especially diabetics).7.7. Patients for whom vascular access can not bePatients for whom vascular access can not be

created (especially diabetics).created (especially diabetics).8.8. High risk anticoagulants.High risk anticoagulants.

9.9. Patients who desire greater freedom to travel.Patients who desire greater freedom to travel.

f


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Contraindications for PD:Contraindications for PD:Absolute:Absolute:

1.1. Extensive peritoneal fibrosisExtensive peritoneal fibrosis2.2. Pleuropertoneal leak Pleuropertoneal leak

Relative:Relative:1.1. The same as those in haemodialysisThe same as those in haemodialysis2.2. Presence of colostomy or nephrostomyPresence of colostomy or nephrostomy3.3. Recent thoracic or abdominal surgeryRecent thoracic or abdominal surgery

4.4. Inguinal or abdominal herniaInguinal or abdominal hernia5.5. BlindnessBlindness6.6. Mental retardationMental retardation

7.7. Poor motivation and compliance.Poor motivation and compliance.

C li ti f PDComplic tions of PD


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Complications of PD:Complications of PD:Mechanical:Mechanical:

Pain during inflow owing to hot dialysate orPain during inflow owing to hot dialysate orrapid jetting.rapid jetting.Pain during outflow due to ball-valve effectPain during outflow due to ball-valve effectOutflow failure due to constipation, obstructionOutflow failure due to constipation, obstruction

or malposition of the catheter.or malposition of the catheter.Pericatheter leakage because of very early usagePericatheter leakage because of very early usageof the catheterof the catheterScrotal odemaScrotal odema

Pulmonary:Pulmonary:AtelectasisAtelectasisHydrothoraxHydrothorax

Restricted chest movementRestricted chest movement


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Metabolic:Metabolic:HyperglycaemiaHyperglycaemia

HyperlipidaemiaHyperlipidaemia

Protein depletionProtein depletion

ObesityObesityInfectious and inflammatory:Infectious and inflammatory:

PeritonitisPeritonitisExit site infectionExit site infection

Tunnel infectionTunnel infection


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KIDNEY TRANSPLANTATIONKIDNEY TRANSPLANTATION

Definition:Definition:Kidney transplantation means the

treatment of chronic renal failure bysurgical implantation of a kidney that is

obtained from either healthy kidneydonor or brain stem dead cadaver.

Principle:Principle:


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Principle:Principle:Kidney transplantation is preformed by doing a unilateralnephrectomy for the donor to be implanted into thepatient with end stage renal disease The recipient.The new kidney is placed in the patients abdomen,usually in the right iliac fossa. The artery and vein areanastomosed to patients vessels (usually internal iliac)and the ureter is implanted into the bladder (Fig. 5.4)

The native kidneys are left in place, unless there is anindication to be removed e.g. uncontrollable hypertension,infection or if they are hugel enlarged.The immune system of the recipient consider thetransplanted kidney as a foreign body and tries to destroyit. This is called rejection which can be prevented by:

Pre operative immunological investigations to be surethat tissue typing of the recipient and the donor isidentical or similar and via.Post operative suppression of the recipients immunesystem by immunosuppression therapy.

I di tiIndications:


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Indications:Indications:Patients with end stage renal failure requiring renalreplacement therapy.

Contraindications:1- Patient refusal 2- Psychosis3- Age more than 60 years (relative)4- Recurrent disease, if the original kidney disease that caused

renal failure can recur in the transplanted kidney anddestroy it e.g. oxalosis.

5- Systemic disease: Some co-existing systemic diseases maycontraindicate transplantation because of their effect on thepatient's survival or because of the danger of posttransplant immunosuppression therapy. These include thefollowing:

Severe respiratory disease e.g. C.O.P .D.Severe cardiovascular disease e.g. severe left ventricular failureSevere hepatic disease e.g. liver cirrhosisCentral nervous system e.g. cerebral hemorrhage.Active peptic ulceration .MalignancyActive infection

6- Unrepairable urologic abnormalities.

Immunosuppression after transplantation:


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Immunosuppression after transplantation:Definition:Immunosuppression therapy is used after

kidney transplantation in order to modify therecipient's immune system so that rejection isprevented.

Duration:Immunosuppression therapy continues for life. Mode of action: Immunosuppression can be achieved bydifferent drugs. Each drug has a differentmechanism by which it can depressleukocytes which are responsible for the

immune response.


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Regimens: Many regimens are presentSteroids are the corner stone drug usedTriple regimen (steroids-azathioprine-cyclosporine) is the commonest regimenOther new drugs: (Prograf, Mycophenolateand Rapamycin).Polyclonal antibodies as A TG and ALG .Monoclonal antibodies as OKT3Cymeric and humanized antibodies assimulect (Novartis) and zenapax (Roche).

Complications after kidney transplantation:


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Complications after kidney transplantation: Rejections:

Hyperacute: usually occurs Immediatelypostoperative.Acute: Usually occurs days or weeks to

months postoperatively .Chronic: Usually occurs months to yearspostoperatively.

6. Complications of immunosuppression therapy: a. General complications: 1- Infection

2- Increased incidence of malignancy


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b. Complications due to individual drugs: Steroids:

hypertension, D.M., atherosclerosis, Bonedisease, GIT. bleeding and cataract.

Azathioprine: Bone marrow depression and hepaticdysfunction

Cyclosporine: Nephrotoxicity, hepatotoxicity, hypertensionand D.M.

Outcome after transplantation:


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Outcome after transplantation:The outcome of kidney transplantation iscontinuously improving with the advancesin the immunosuppressive drugs and theimmunologic assessment of donors andrecipients, technique of surgery and the

postoperative care.The current 1 year graft survival is about90-95% and 5 years survival is about 60-70%.Continuous advancement in immuno-suppressive drugs aims to an ideal drug withmaximal ability to prevent rejection and

minimal side effects.


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chronic renal failure new.mansfans.com

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