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Chronic Kidney Disease
Sachin kr. Rana(58)
Sakshi mittal(60)
Outline
• Definition
• Briefly discuss it’s epidemiology,.
• pathophysiology,
• causative factors
• Staging
• Clinical features
• Screening methods
• Investigations
• treatment
DEFINITION
Chronic Kidney Disease is defined as a slow lose
of renal function over time. This leads to a
decreased ability to remove waste products
from the body and perform homeostatic
functions.
Clinical Definition
• GFR of less than 60 ml/minute or 1.73m2
per body
surface area (normal is 125ml/min) .
• Presence of kidney damage, regardless of the cause,
for three or more months
Some important definitions
1.1.AzotemiaAzotemia - elevated blood urea nitrogen (BUN- elevated blood urea nitrogen (BUN
>28mg/dL) and creatinine (Cr>1.5mg/dL)>28mg/dL) and creatinine (Cr>1.5mg/dL)
2.2.UremiaUremia - azotemia with symptoms or signs of renal- azotemia with symptoms or signs of renal
failurefailure
3.3.End Stage Renal Disease (ESRD)End Stage Renal Disease (ESRD) – GFR <15 ml/min– GFR <15 ml/min
+ uremia requiring transplantation or dialysis+ uremia requiring transplantation or dialysis
4.4.Chronic Renal Failure (CRF)Chronic Renal Failure (CRF) - irreversible kidney- irreversible kidney
dysfunction with azotemia >3 monthsdysfunction with azotemia >3 months
5.5.Creatinine Clearance (CCr)Creatinine Clearance (CCr) - the rate of filtration of- the rate of filtration of
creatinine by the kidney (GFR marker)creatinine by the kidney (GFR marker)
6.6.Glomerular Filtration Rate (GFR)Glomerular Filtration Rate (GFR) - the total rate of- the total rate of
filtration of blood by the kidneyfiltration of blood by the kidney
Epidemiology
• CKD affects about 26 million people in the US
• Approximately 19 million adults are in the
early stages of the disease
– On the rise do to increasing prevalence of
diabetes and hypertension
• Total cost in treating ESRD in US was
approximately $40 billion in 2008
Pathophysiology
•Primary kidney disease-> decrease in nephron
no. -> adaptive change in the remaing nephrons
to maintain renal function-> hypertrophy
&vasodilation of surving nephron -> leads to
increase glomerular pressure & filteration->
over a peroid of time leads to glomerular
sclerosis ->failure of adaptive function -> further
reduction of kidney fuction
Staging of Chronic Kidney
Disease
Stage Description GFR (ml/min/1.73 m2
)
At increased risk >=90 (with CKD risk
factors)
1 Kidney damage with normal or
increased GFR
90
2 Mildly decreased GFR 60-89
3 Moderately decreased GFR 30-59
4 Severely decreased GFR 15-29
5 Renal Failure <15 (or dialysis)
Symptoms
• Hematuria
• Flank pain
• Edema
• Hypertension
• Signs of uremia
• Lethargy and fatigue
• Loss of appetite
• If asymptomatic may have elevated serum
creatinine concentration or an abnormal
urinalysis
C/F of CKD
 Stage 1 and 2
 Asymptomatic,
 Features of hypertension like irritibility ,
headache dizziness, palpitation, easy
fatigablity , epistaxis, blurring of vision.
C/F of CKD
 Stage 3 and 4
 Anemia – fatigue , weakness, loss of
concentration
 Decreasing appetite; poor nutrition
 Electrolyte Abnormalities
 Calcium: backpain, kidney stone, spasm,
mental confusion
 Sodium: high b.p, weakness ,muscle Cramps,
nausea, abd. discomfort
 Water: oedema
 potassium: weakness , fatigue , nausea
C/F of CKD
 Stage 5
 All of the above – accentuated; eventually
overt uremia
Symptoms of Uremia
Screening Methods
Serum Creatinine
Estimated glomerular filtration rate (GFR)
Urine testing :
Serum Creatinine
 Sr creatinine is poor reflection of early renal
disease/failure
 Damage < 60% sr creatinine still normal
 Almost all early renal failure patients are
asymptomatic
 SCREENING IS THEREFORE VERY
IMPORTANT
Estimated Glomerular Filtration rate
• Estimate of GFR by the Cockcroft and Gault equation
 Cockroft Gault Formula
 (140 – age) X Body Weight (Kg)/
72 X Serum Creatinine (mg/dL)
 Multiply by 0.85 for women
Urine Testing
 Urine for protein
Dipstick
24 hour urinary protein
 Urine microscopic examination
For RBC / Pus Cell / Cast
 Urine for microalbuminuria
On morning urine sample
using strip for microalbumin
Targets for Screening
 Hypertensive patients
 Diabetic patients
 Cardiovascular disease
 Those on regular NSAID/Herbs
 Renal calculi
 Anemia of unknown aetiology
 First and second degree relatives of ESRD
 Autoimmune disease (SLE/RA)
 Reduction of kidney mass(Nephrectomy
False +ve CKD
 Urinary Tract Infection
 Sepsis
 Heart Failure
 Strenous exercise
 Heavy protein intake
 Menses
Significance of proteinuria
A dominant risk factor for deterioration of
renal failure (besides HT)
Marker of Increased Risk for CV mortality and
morbidity (DM & non-DM)
e.g. Microalbuminuria is associated with a 100- 150%
increase in death rate
Chronic Kidney DiseaseChronic Kidney Disease
Diagnostic StudiesDiagnostic Studies
• TESTS INTERPRETATION
1.Urinalysis haematuria & protenuria may
indicate cause. Protenuria in-
dicate progression of ckd
2.urea&creatinine to assess stability/progresn
:compare to previous result
• TESTS INTERPRETATION
3.Electrolytes to identify hyperkalemia &
acidosis
4.calcium, to assess osteodystrophy
Phosphate,
Pth hormone
5.Albumin low : consider malnutrition,
inflamation
6.CBC ( fe , ferritin, rule out anemia
Folate, B12)
• TESTS INTERPRETATION
7.Lipid profile cvs disease risk is high in ckd
8.Glucose , HbA1c rule out diabities
9.Renal usg to exclude obstruction ,small
kidneys suggest chronicity
10.ECG if pt. is >40yrs or hyperklemic
• TESTS INTERPRETATION
11.hepatitis& if dialysis or transplant is
HIV planned
12.CXR rule out pul. Oedema , uremic
pericardial effusion
TREATMENT
Nursing ImplementationNursing Implementation
• Health promotionHealth promotion
• Identify individuals at risk for CKDIdentify individuals at risk for CKD
• History of renal diseaseHistory of renal disease
• HypertensionHypertension
• Diabetes mellitusDiabetes mellitus
• Repeated urinary tract infectionRepeated urinary tract infection
• Regular checkups and changes in urinaryRegular checkups and changes in urinary
appearance, frequency and volumeappearance, frequency and volume
should be reportedshould be reported
LIFE STYLE MODIFICATION
Nutritional therapyNutritional therapy
• Protein restrictionProtein restriction
• 0.6 to 0.8 g/kg body weight/day0.6 to 0.8 g/kg body weight/day
• Water restrictionWater restriction
• Intake depends on daily urine outputIntake depends on daily urine output
CONT.
Nutritional therapyNutritional therapy
• Sodium restrictionSodium restriction
• Diets vary from 2 to 4 g depending onDiets vary from 2 to 4 g depending on
degree of edema and hypertensiondegree of edema and hypertension
• Sodium and salt should not be equatedSodium and salt should not be equated
• Patient should be instructed to avoidPatient should be instructed to avoid
high-sodium foodshigh-sodium foods
• Salt substitutes should not be used because theySalt substitutes should not be used because they
contain potassium chloridecontain potassium chloride
CONT.
Nutritional therapyNutritional therapy
• Potassium restrictionPotassium restriction
• 2 to 4 g2 to 4 g
• High-potassium foods should beHigh-potassium foods should be
avoidedavoided
• OrangesOranges
• BananasBananas
• TomatoesTomatoes
• Green vegetablesGreen vegetables
CONT.
• Phosphate restrictionPhosphate restriction
• 1000 mg/day1000 mg/day
• Foods high in phosphateFoods high in phosphate
• Dairy products ( milk, cheese , eggs)Dairy products ( milk, cheese , eggs)
• Most foods high in phosphate are alsoMost foods high in phosphate are also
high in calciumhigh in calcium
MEDICAL THERAPY
Drug therapyDrug therapy
• HyperkalemiaHyperkalemia
• Drugs that Stablise cell membraneDrugs that Stablise cell membrane
potentialpotential
• IV 10 ml 10% calcium gluconateIV 10 ml 10% calcium gluconate
• Raises threshold for excitationRaises threshold for excitation
• Shifts potassium into cellsShifts potassium into cells
• IV insulin and glucoseIV insulin and glucose
• bicarbonatebicarbonate
• Shift potassium into cellsShift potassium into cells
• Correct acidosisCorrect acidosis
• Beta agonist - salbutamolBeta agonist - salbutamol
CONT.
Drug therapyDrug therapy
• Hyperkalemia (cont’d)Hyperkalemia (cont’d)
• Sodium polystyrene sulfonate (Kayexalate)Sodium polystyrene sulfonate (Kayexalate)
• Cation-exchange resinCation-exchange resin
• Resin in bowel exchanges potassium for sodiumResin in bowel exchanges potassium for sodium
• Evacuates potassium-rich stool from bodyEvacuates potassium-rich stool from body
• Educate patient that diarrhea may occur due toEducate patient that diarrhea may occur due to
laxative in preparationlaxative in preparation
• 3. remove potassium from body3. remove potassium from body
iv furosemide &normal salineiv furosemide &normal saline
Ion exchange resin ex: resonium oral or per rectalIon exchange resin ex: resonium oral or per rectal
dialysisdialysis
CONT.
Drug therapyDrug therapy
• Hypertension (cont’d)Hypertension (cont’d)
• Antihypertensive drugsAntihypertensive drugs
• DiureticsDiuretics
• ββ-Adrenergic blockers-Adrenergic blockers
• Calcium channel blockersCalcium channel blockers
• Angiotensin-converting enzyme (ACE)Angiotensin-converting enzyme (ACE)
inhibitorsinhibitors
• Angiotensin receptor blocker agentsAngiotensin receptor blocker agents
CONT.
Drug therapyDrug therapy
• ACIDOSIS
sodium bicarbonate supplement(1g 8 hrly)
maintain plasma bicarbonate level >22mmol/l
CONT.
Drug therapyDrug therapy
• CVS DISEASE
control of dyslipidemia.
1.Statins eg Atrovastatin, lovastatin,
rosuvastatin
2. Cholestrol absorption inhibiter- eg ezetimibe
3. Fibrates eg-finofibrate, cinofibrate
4.Bile acid sequestrum resin- eg colestyramine,
colestipol.
CONT.
Drug therapyDrug therapy
HYPERPHOSPHATEMIA
phosphate binding drugs adminstered
with foodsto prevent absorption
eg: calcium carbonate , aluminium hydroxide,
lanthanum carbonate.
CONT.
Drug therapyDrug therapy
• Renal osteodystrophyRenal osteodystrophy
• Phosphate intake restricted toPhosphate intake restricted to
<1000 mg/day<1000 mg/day
• Phosphate bindersPhosphate binders
• Calcium carbonate (Tums)Calcium carbonate (Tums)
• Bind phosphate in bowel and excretedBind phosphate in bowel and excreted
• Sevelamer hydrochloride (Renagel)Sevelamer hydrochloride (Renagel)
• Lowers cholesterol and LDLsLowers cholesterol and LDLs
CONT.
Drug therapyDrug therapy
• Renal osteodystrophy (cont’d)Renal osteodystrophy (cont’d)
• Phosphate binders (cont’d)Phosphate binders (cont’d)
• Should be administered with each mealShould be administered with each meal
• Side effect: ConstipationSide effect: Constipation
• Supplementing vitamin DSupplementing vitamin D
• Calcitriol (Rocaltrol)Calcitriol (Rocaltrol)
• Serum phosphate level must be lowered beforeSerum phosphate level must be lowered before
administering calcium or vitamin Dadministering calcium or vitamin D
CONT.
• Renal osteodystrophy (cont’d)Renal osteodystrophy (cont’d)
• Controlling secondaryControlling secondary
hyperparathyroidismhyperparathyroidism
• Calcimimetic agentsCalcimimetic agents
• Cinacalcet (Sensipar)Cinacalcet (Sensipar)
• ↑↑ Sensitivity of calcium receptors inSensitivity of calcium receptors in
parathyroid glandsparathyroid glands
• Subtotal parathyroidectomySubtotal parathyroidectomy
CONT.
Drug therapyDrug therapy
• AnemiaAnemia
• Iron supplementsIron supplements
• If plasma ferritinIf plasma ferritin <100 ng/ml<100 ng/ml
• Side effect: Gastric irritation,Side effect: Gastric irritation,
constipationconstipation
• May make stool dark in colorMay make stool dark in color
CONT.
• Anemia (cont’d)Anemia (cont’d)
• Folic acid supplementsFolic acid supplements
• Needed for RBC formationNeeded for RBC formation
• Removed by dialysisRemoved by dialysis
• Avoid blood transfusionsAvoid blood transfusions
CONT.
• Anemia(cont’d)Anemia(cont’d)
• ErythropoietinErythropoietin
• Epoetin alfa (Epogen, Procrit)Epoetin alfa (Epogen, Procrit)
• Administered IV or subcutaneouslyAdministered IV or subcutaneously
• Increased hemoglobin and hematocrit inIncreased hemoglobin and hematocrit in
2 to 3 weeks2 to 3 weeks
• Side effect: HypertensionSide effect: Hypertension
DIALYSIS
Prepared by D. ChaplinPrepared by D. Chaplin
PD Advantages and Disadvantages
Immediate initiation
Less complicated
Portable (CAPD)
Fewer dietary
restrictions
Short training time
Less cardio stress
Choice for diabetics
Bacterial/chemical
periotonitis
Protein loss
Exit site of catheter
Hyperglycemia
Surgical placement of
catheter
Multiple abdominal
surgery
Advantages Disadvantages
Prepared by D. ChaplinPrepared by D. Chaplin
Hemo Advantages & Disadvantages
Rapid fluid removal
Rapid removal of urea &
creatinine
Effective K+
removal
Less protein loss
Lower triglycerides
Home dialysis possible
Temporary access at the
bedside
Rapid fluid removal
Rapid removal of urea &
creatinine
Effective K+
removal
Less protein loss
Lower triglycerides
Home dialysis possible
Temporary access at the
bedside
Vascular access
problems
Dietary & fluid
restrictions
Heparinization
Extensive equipment
Hypotension
Added blood lost
Trained specialist
Vascular access
problems
Dietary & fluid
restrictions
Heparinization
Extensive equipment
Hypotension
Added blood lost
Trained specialist
Advantages Disadvantages
Disequalibrium Syndrome
Fluid removal and decrease in BUN during
hemodilaysis which cause changes in blood
osmolarity.These changes trigger a fluid shift from
the vascular compartment into the cells. In the brain,
this can cause cerebral edema, resulting in increase
intracranial pressure and visible signs of decreasing
level of consciousness. Symptoms: Sudden onset of
headache, nausea and vomiting, nervousness, muscle
twitching, palpitation, disorientation and seizures
Treatment: Hypertonic saline, Normal saline
Nursing Care Pre, Post Dialysis
Weigh before & after
Assess site before & after (bruit, thrill,
infection, bleeding etc.)
Medications (precautions before & after)
Vital signs before and after etc
Renal Transplant
Living and Cadaveric donors
Predialysis: obtain a dry weight free of excess fluids
and toxins
More preparation time from a living donor vs.
cadaveric – transplant within 36 hours of
procurement
Delay may increase ATN
Pre-transplant: Immunotherapy (IV
methylprednisolone sodium succinate,
(A –methaPred, Solu-Medrol), cyclosporine
(Sandimmune and azathioprine ((Imuran
Immunological Compatibility
of Donor and Recipient
Done to minimize the destruction (rejection) of the
transplanted kidney
HUMAN LEUKOCYTE ANTIGEN (HLA)
This gives you your genetic identity (twins share
identical HLA)
HLA compatibility minimizes the recognition of the
transplanted kidney as foreign tissues
Immunological Compatibility
of Donor and Recipient
Done to minimize the destruction (rejection) of the
transplanted kidney
HUMAN LEUKOCYTE ANTIGEN (HLA)
This gives you your genetic identity (twins share
identical HLA)
HLA compatibility minimizes the recognition of the
transplanted kidney as foreign tissues
Immunological Analysis
WHITE CELL CROSS MATCH (the
recipient serum is mixed with donor
lymphocytes to test for performed cytotoxic
(anti-HLA) antibodies to the potential
donor kidney
A positive cross match indicates that the
recipient has cytotoxic antibodies to the
donor and is an absolute contraindication
to transplantation
Immulogical Analysis
MIXED LYMPHOCYTE CULTURE
The donor and recipient lymphocytes are
mixed. Result = HIGH SENTIVITY, this
is contraindicated for renal
transplantation.
ABO BLOOD GROUPING
ABO blood group must be compatible
Surgery
LLQ of the abdomen outside of the
peritoneal cavity
Renal artery and vein anastomosed to
the corresponding iliac vessels
Donor ureters are tunneled into the
recipients’ bladder.
Complications Post Transplant
Rejection is a major problem
Hyperacute rejection: occurs within minutes
to hours after transplantation
Renal vessels thrombosis occurs and the
kidney dies
There is no treatment and the transplanted
kidney is removed
Complications Post Transplant
Acute Rejection: occurs 4 days to 4 months after
transplantation
It is not uncommon to have at least one rejection
episode
Episodes are usually reversible with additional
immunosuppressive therapy (Corticosteroids,
muromonab-CD3, ALG, or ATG)
Signs: increasing serum creatinine, elevated BUN,
fever, wt. gain, decrease output, increasing BP,
tenderness over the transplanted kidneys
Complications Post Transplant
Chronic Rejection: occurs over months or years and
is irreversible.
The kidney is infiltrated with large numbers of T
and B cells characteristic of an ongoing , low
grade immunological mediated injury
Gradual occlusion renal blood vessels
Signs: proteinuria, HTN, increase serum creatinine
levels
Supportive treatment, difficult to manage
Replace on transplant list
Complications Post Transplant
Infection
Hypertension
Malignancies (lip, skin,
lymphomas, cervical)
Recurrence of renal disease
Retroperiotneal bleed
Arterial stenosis
Urine leakage
SUMMARY
THANK YOU!

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best Ckd presentation1 by Dr. sachin kr rana

  • 1. Chronic Kidney Disease Sachin kr. Rana(58) Sakshi mittal(60)
  • 2. Outline • Definition • Briefly discuss it’s epidemiology,. • pathophysiology, • causative factors • Staging • Clinical features • Screening methods • Investigations • treatment
  • 3. DEFINITION Chronic Kidney Disease is defined as a slow lose of renal function over time. This leads to a decreased ability to remove waste products from the body and perform homeostatic functions.
  • 4. Clinical Definition • GFR of less than 60 ml/minute or 1.73m2 per body surface area (normal is 125ml/min) . • Presence of kidney damage, regardless of the cause, for three or more months
  • 5. Some important definitions 1.1.AzotemiaAzotemia - elevated blood urea nitrogen (BUN- elevated blood urea nitrogen (BUN >28mg/dL) and creatinine (Cr>1.5mg/dL)>28mg/dL) and creatinine (Cr>1.5mg/dL) 2.2.UremiaUremia - azotemia with symptoms or signs of renal- azotemia with symptoms or signs of renal failurefailure 3.3.End Stage Renal Disease (ESRD)End Stage Renal Disease (ESRD) – GFR <15 ml/min– GFR <15 ml/min + uremia requiring transplantation or dialysis+ uremia requiring transplantation or dialysis 4.4.Chronic Renal Failure (CRF)Chronic Renal Failure (CRF) - irreversible kidney- irreversible kidney dysfunction with azotemia >3 monthsdysfunction with azotemia >3 months 5.5.Creatinine Clearance (CCr)Creatinine Clearance (CCr) - the rate of filtration of- the rate of filtration of creatinine by the kidney (GFR marker)creatinine by the kidney (GFR marker) 6.6.Glomerular Filtration Rate (GFR)Glomerular Filtration Rate (GFR) - the total rate of- the total rate of filtration of blood by the kidneyfiltration of blood by the kidney
  • 6. Epidemiology • CKD affects about 26 million people in the US • Approximately 19 million adults are in the early stages of the disease – On the rise do to increasing prevalence of diabetes and hypertension • Total cost in treating ESRD in US was approximately $40 billion in 2008
  • 7. Pathophysiology •Primary kidney disease-> decrease in nephron no. -> adaptive change in the remaing nephrons to maintain renal function-> hypertrophy &vasodilation of surving nephron -> leads to increase glomerular pressure & filteration-> over a peroid of time leads to glomerular sclerosis ->failure of adaptive function -> further reduction of kidney fuction
  • 8.
  • 9. Staging of Chronic Kidney Disease Stage Description GFR (ml/min/1.73 m2 ) At increased risk >=90 (with CKD risk factors) 1 Kidney damage with normal or increased GFR 90 2 Mildly decreased GFR 60-89 3 Moderately decreased GFR 30-59 4 Severely decreased GFR 15-29 5 Renal Failure <15 (or dialysis)
  • 10. Symptoms • Hematuria • Flank pain • Edema • Hypertension • Signs of uremia • Lethargy and fatigue • Loss of appetite • If asymptomatic may have elevated serum creatinine concentration or an abnormal urinalysis
  • 11. C/F of CKD  Stage 1 and 2  Asymptomatic,  Features of hypertension like irritibility , headache dizziness, palpitation, easy fatigablity , epistaxis, blurring of vision.
  • 12. C/F of CKD  Stage 3 and 4  Anemia – fatigue , weakness, loss of concentration  Decreasing appetite; poor nutrition  Electrolyte Abnormalities  Calcium: backpain, kidney stone, spasm, mental confusion  Sodium: high b.p, weakness ,muscle Cramps, nausea, abd. discomfort  Water: oedema  potassium: weakness , fatigue , nausea
  • 13. C/F of CKD  Stage 5  All of the above – accentuated; eventually overt uremia
  • 15. Screening Methods Serum Creatinine Estimated glomerular filtration rate (GFR) Urine testing :
  • 16. Serum Creatinine  Sr creatinine is poor reflection of early renal disease/failure  Damage < 60% sr creatinine still normal  Almost all early renal failure patients are asymptomatic  SCREENING IS THEREFORE VERY IMPORTANT
  • 17. Estimated Glomerular Filtration rate • Estimate of GFR by the Cockcroft and Gault equation  Cockroft Gault Formula  (140 – age) X Body Weight (Kg)/ 72 X Serum Creatinine (mg/dL)  Multiply by 0.85 for women
  • 18. Urine Testing  Urine for protein Dipstick 24 hour urinary protein  Urine microscopic examination For RBC / Pus Cell / Cast  Urine for microalbuminuria On morning urine sample using strip for microalbumin
  • 19. Targets for Screening  Hypertensive patients  Diabetic patients  Cardiovascular disease  Those on regular NSAID/Herbs  Renal calculi  Anemia of unknown aetiology  First and second degree relatives of ESRD  Autoimmune disease (SLE/RA)  Reduction of kidney mass(Nephrectomy
  • 20. False +ve CKD  Urinary Tract Infection  Sepsis  Heart Failure  Strenous exercise  Heavy protein intake  Menses
  • 21. Significance of proteinuria A dominant risk factor for deterioration of renal failure (besides HT) Marker of Increased Risk for CV mortality and morbidity (DM & non-DM) e.g. Microalbuminuria is associated with a 100- 150% increase in death rate
  • 22. Chronic Kidney DiseaseChronic Kidney Disease Diagnostic StudiesDiagnostic Studies • TESTS INTERPRETATION 1.Urinalysis haematuria & protenuria may indicate cause. Protenuria in- dicate progression of ckd 2.urea&creatinine to assess stability/progresn :compare to previous result
  • 23. • TESTS INTERPRETATION 3.Electrolytes to identify hyperkalemia & acidosis 4.calcium, to assess osteodystrophy Phosphate, Pth hormone 5.Albumin low : consider malnutrition, inflamation 6.CBC ( fe , ferritin, rule out anemia Folate, B12)
  • 24. • TESTS INTERPRETATION 7.Lipid profile cvs disease risk is high in ckd 8.Glucose , HbA1c rule out diabities 9.Renal usg to exclude obstruction ,small kidneys suggest chronicity 10.ECG if pt. is >40yrs or hyperklemic
  • 25. • TESTS INTERPRETATION 11.hepatitis& if dialysis or transplant is HIV planned 12.CXR rule out pul. Oedema , uremic pericardial effusion
  • 27. Nursing ImplementationNursing Implementation • Health promotionHealth promotion • Identify individuals at risk for CKDIdentify individuals at risk for CKD • History of renal diseaseHistory of renal disease • HypertensionHypertension • Diabetes mellitusDiabetes mellitus • Repeated urinary tract infectionRepeated urinary tract infection • Regular checkups and changes in urinaryRegular checkups and changes in urinary appearance, frequency and volumeappearance, frequency and volume should be reportedshould be reported
  • 29. Nutritional therapyNutritional therapy • Protein restrictionProtein restriction • 0.6 to 0.8 g/kg body weight/day0.6 to 0.8 g/kg body weight/day • Water restrictionWater restriction • Intake depends on daily urine outputIntake depends on daily urine output
  • 30. CONT. Nutritional therapyNutritional therapy • Sodium restrictionSodium restriction • Diets vary from 2 to 4 g depending onDiets vary from 2 to 4 g depending on degree of edema and hypertensiondegree of edema and hypertension • Sodium and salt should not be equatedSodium and salt should not be equated • Patient should be instructed to avoidPatient should be instructed to avoid high-sodium foodshigh-sodium foods • Salt substitutes should not be used because theySalt substitutes should not be used because they contain potassium chloridecontain potassium chloride
  • 31. CONT. Nutritional therapyNutritional therapy • Potassium restrictionPotassium restriction • 2 to 4 g2 to 4 g • High-potassium foods should beHigh-potassium foods should be avoidedavoided • OrangesOranges • BananasBananas • TomatoesTomatoes • Green vegetablesGreen vegetables
  • 32. CONT. • Phosphate restrictionPhosphate restriction • 1000 mg/day1000 mg/day • Foods high in phosphateFoods high in phosphate • Dairy products ( milk, cheese , eggs)Dairy products ( milk, cheese , eggs) • Most foods high in phosphate are alsoMost foods high in phosphate are also high in calciumhigh in calcium
  • 33. MEDICAL THERAPY Drug therapyDrug therapy • HyperkalemiaHyperkalemia • Drugs that Stablise cell membraneDrugs that Stablise cell membrane potentialpotential • IV 10 ml 10% calcium gluconateIV 10 ml 10% calcium gluconate • Raises threshold for excitationRaises threshold for excitation • Shifts potassium into cellsShifts potassium into cells • IV insulin and glucoseIV insulin and glucose • bicarbonatebicarbonate • Shift potassium into cellsShift potassium into cells • Correct acidosisCorrect acidosis • Beta agonist - salbutamolBeta agonist - salbutamol
  • 34. CONT. Drug therapyDrug therapy • Hyperkalemia (cont’d)Hyperkalemia (cont’d) • Sodium polystyrene sulfonate (Kayexalate)Sodium polystyrene sulfonate (Kayexalate) • Cation-exchange resinCation-exchange resin • Resin in bowel exchanges potassium for sodiumResin in bowel exchanges potassium for sodium • Evacuates potassium-rich stool from bodyEvacuates potassium-rich stool from body • Educate patient that diarrhea may occur due toEducate patient that diarrhea may occur due to laxative in preparationlaxative in preparation • 3. remove potassium from body3. remove potassium from body iv furosemide &normal salineiv furosemide &normal saline Ion exchange resin ex: resonium oral or per rectalIon exchange resin ex: resonium oral or per rectal dialysisdialysis
  • 35. CONT. Drug therapyDrug therapy • Hypertension (cont’d)Hypertension (cont’d) • Antihypertensive drugsAntihypertensive drugs • DiureticsDiuretics • ββ-Adrenergic blockers-Adrenergic blockers • Calcium channel blockersCalcium channel blockers • Angiotensin-converting enzyme (ACE)Angiotensin-converting enzyme (ACE) inhibitorsinhibitors • Angiotensin receptor blocker agentsAngiotensin receptor blocker agents
  • 36. CONT. Drug therapyDrug therapy • ACIDOSIS sodium bicarbonate supplement(1g 8 hrly) maintain plasma bicarbonate level >22mmol/l
  • 37. CONT. Drug therapyDrug therapy • CVS DISEASE control of dyslipidemia. 1.Statins eg Atrovastatin, lovastatin, rosuvastatin 2. Cholestrol absorption inhibiter- eg ezetimibe 3. Fibrates eg-finofibrate, cinofibrate 4.Bile acid sequestrum resin- eg colestyramine, colestipol.
  • 38. CONT. Drug therapyDrug therapy HYPERPHOSPHATEMIA phosphate binding drugs adminstered with foodsto prevent absorption eg: calcium carbonate , aluminium hydroxide, lanthanum carbonate.
  • 39. CONT. Drug therapyDrug therapy • Renal osteodystrophyRenal osteodystrophy • Phosphate intake restricted toPhosphate intake restricted to <1000 mg/day<1000 mg/day • Phosphate bindersPhosphate binders • Calcium carbonate (Tums)Calcium carbonate (Tums) • Bind phosphate in bowel and excretedBind phosphate in bowel and excreted • Sevelamer hydrochloride (Renagel)Sevelamer hydrochloride (Renagel) • Lowers cholesterol and LDLsLowers cholesterol and LDLs
  • 40. CONT. Drug therapyDrug therapy • Renal osteodystrophy (cont’d)Renal osteodystrophy (cont’d) • Phosphate binders (cont’d)Phosphate binders (cont’d) • Should be administered with each mealShould be administered with each meal • Side effect: ConstipationSide effect: Constipation • Supplementing vitamin DSupplementing vitamin D • Calcitriol (Rocaltrol)Calcitriol (Rocaltrol) • Serum phosphate level must be lowered beforeSerum phosphate level must be lowered before administering calcium or vitamin Dadministering calcium or vitamin D
  • 41. CONT. • Renal osteodystrophy (cont’d)Renal osteodystrophy (cont’d) • Controlling secondaryControlling secondary hyperparathyroidismhyperparathyroidism • Calcimimetic agentsCalcimimetic agents • Cinacalcet (Sensipar)Cinacalcet (Sensipar) • ↑↑ Sensitivity of calcium receptors inSensitivity of calcium receptors in parathyroid glandsparathyroid glands • Subtotal parathyroidectomySubtotal parathyroidectomy
  • 42. CONT. Drug therapyDrug therapy • AnemiaAnemia • Iron supplementsIron supplements • If plasma ferritinIf plasma ferritin <100 ng/ml<100 ng/ml • Side effect: Gastric irritation,Side effect: Gastric irritation, constipationconstipation • May make stool dark in colorMay make stool dark in color
  • 43. CONT. • Anemia (cont’d)Anemia (cont’d) • Folic acid supplementsFolic acid supplements • Needed for RBC formationNeeded for RBC formation • Removed by dialysisRemoved by dialysis • Avoid blood transfusionsAvoid blood transfusions
  • 44. CONT. • Anemia(cont’d)Anemia(cont’d) • ErythropoietinErythropoietin • Epoetin alfa (Epogen, Procrit)Epoetin alfa (Epogen, Procrit) • Administered IV or subcutaneouslyAdministered IV or subcutaneously • Increased hemoglobin and hematocrit inIncreased hemoglobin and hematocrit in 2 to 3 weeks2 to 3 weeks • Side effect: HypertensionSide effect: Hypertension
  • 46.
  • 47. Prepared by D. ChaplinPrepared by D. Chaplin PD Advantages and Disadvantages Immediate initiation Less complicated Portable (CAPD) Fewer dietary restrictions Short training time Less cardio stress Choice for diabetics Bacterial/chemical periotonitis Protein loss Exit site of catheter Hyperglycemia Surgical placement of catheter Multiple abdominal surgery Advantages Disadvantages
  • 48. Prepared by D. ChaplinPrepared by D. Chaplin Hemo Advantages & Disadvantages Rapid fluid removal Rapid removal of urea & creatinine Effective K+ removal Less protein loss Lower triglycerides Home dialysis possible Temporary access at the bedside Rapid fluid removal Rapid removal of urea & creatinine Effective K+ removal Less protein loss Lower triglycerides Home dialysis possible Temporary access at the bedside Vascular access problems Dietary & fluid restrictions Heparinization Extensive equipment Hypotension Added blood lost Trained specialist Vascular access problems Dietary & fluid restrictions Heparinization Extensive equipment Hypotension Added blood lost Trained specialist Advantages Disadvantages
  • 49. Disequalibrium Syndrome Fluid removal and decrease in BUN during hemodilaysis which cause changes in blood osmolarity.These changes trigger a fluid shift from the vascular compartment into the cells. In the brain, this can cause cerebral edema, resulting in increase intracranial pressure and visible signs of decreasing level of consciousness. Symptoms: Sudden onset of headache, nausea and vomiting, nervousness, muscle twitching, palpitation, disorientation and seizures Treatment: Hypertonic saline, Normal saline
  • 50. Nursing Care Pre, Post Dialysis Weigh before & after Assess site before & after (bruit, thrill, infection, bleeding etc.) Medications (precautions before & after) Vital signs before and after etc
  • 51. Renal Transplant Living and Cadaveric donors Predialysis: obtain a dry weight free of excess fluids and toxins More preparation time from a living donor vs. cadaveric – transplant within 36 hours of procurement Delay may increase ATN Pre-transplant: Immunotherapy (IV methylprednisolone sodium succinate, (A –methaPred, Solu-Medrol), cyclosporine (Sandimmune and azathioprine ((Imuran
  • 52. Immunological Compatibility of Donor and Recipient Done to minimize the destruction (rejection) of the transplanted kidney HUMAN LEUKOCYTE ANTIGEN (HLA) This gives you your genetic identity (twins share identical HLA) HLA compatibility minimizes the recognition of the transplanted kidney as foreign tissues
  • 53. Immunological Compatibility of Donor and Recipient Done to minimize the destruction (rejection) of the transplanted kidney HUMAN LEUKOCYTE ANTIGEN (HLA) This gives you your genetic identity (twins share identical HLA) HLA compatibility minimizes the recognition of the transplanted kidney as foreign tissues
  • 54. Immunological Analysis WHITE CELL CROSS MATCH (the recipient serum is mixed with donor lymphocytes to test for performed cytotoxic (anti-HLA) antibodies to the potential donor kidney A positive cross match indicates that the recipient has cytotoxic antibodies to the donor and is an absolute contraindication to transplantation
  • 55. Immulogical Analysis MIXED LYMPHOCYTE CULTURE The donor and recipient lymphocytes are mixed. Result = HIGH SENTIVITY, this is contraindicated for renal transplantation. ABO BLOOD GROUPING ABO blood group must be compatible
  • 56. Surgery LLQ of the abdomen outside of the peritoneal cavity Renal artery and vein anastomosed to the corresponding iliac vessels Donor ureters are tunneled into the recipients’ bladder.
  • 57. Complications Post Transplant Rejection is a major problem Hyperacute rejection: occurs within minutes to hours after transplantation Renal vessels thrombosis occurs and the kidney dies There is no treatment and the transplanted kidney is removed
  • 58. Complications Post Transplant Acute Rejection: occurs 4 days to 4 months after transplantation It is not uncommon to have at least one rejection episode Episodes are usually reversible with additional immunosuppressive therapy (Corticosteroids, muromonab-CD3, ALG, or ATG) Signs: increasing serum creatinine, elevated BUN, fever, wt. gain, decrease output, increasing BP, tenderness over the transplanted kidneys
  • 59. Complications Post Transplant Chronic Rejection: occurs over months or years and is irreversible. The kidney is infiltrated with large numbers of T and B cells characteristic of an ongoing , low grade immunological mediated injury Gradual occlusion renal blood vessels Signs: proteinuria, HTN, increase serum creatinine levels Supportive treatment, difficult to manage Replace on transplant list
  • 60. Complications Post Transplant Infection Hypertension Malignancies (lip, skin, lymphomas, cervical) Recurrence of renal disease Retroperiotneal bleed Arterial stenosis Urine leakage
  • 62.

Hinweis der Redaktion

  1. Things that cause kidney disease: -Glomerulonephritis, a group of diseases that cause inflammation and damage to the kidney&amp;apos;s filtering units. These disorders are the third most common type of kidney disease. -Inherited diseases, such as polycystic kidney disease, which causes large cysts to form in the kidneys and damage the surrounding tissue. -Malformations that occur as a baby develops in its mother&amp;apos;s womb. For example, a narrowing may occur that prevents normal outflow of urine and causes urine to flow back up to the kidney. This causes infections and may damage the kidneys. -Lupus and other diseases that affect the body&amp;apos;s immune system. -Obstructions caused by problems like kidney stones, tumors or an enlarged prostate gland in men. -Repeated urinary infections.
  2. The causes of acute or chronic kidney disease are traditionally classified by that portion of the renal anatomy most affected by the disorder The two major causes of reduced renal perfusion are volume depletion and/or relative hypotension. This may result from true hypoperfusion due to bleeding, gastrointestinal, urinary, or cutaneous losses, or to effective volume depletion in heart failure, shock, or cirrhosis Various vascular diseases can also lead to kidney disease. Direct etiologies from kidney: Tubular and interstitial disease, Glomerular disease, Obstructive uropathy Acute tubular necrosis — 45 percent Prerenal — 21 percent Acute or chronic kidney disease — 13 percent (mostly due to acute tubular necrosis and prerenal disease) Urinary tract obstruction — 10 percent (most often older men with prostatic disease) Glomerulonephritis or vasculitis — 4 percent Acute interstitial nephritis — 2 percent Atheroemboli — 1 percent