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) â GFR <15 ml/minâ 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
â 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
â˘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
ďŽ Stage 1 and 2
ďŽ Asymptomatic,
ďŽ Features of hypertension like irritibility ,
headache dizziness, palpitation, easy
fatigablity , epistaxis, blurring of vision.
16. Serum Creatinine
ď Sr creatinine is poor reflection of early renal
disease/failure
ď Damage < 60% sr creatinine still normal
ď Almost all early renal failure patients are
asymptomatic
ď SCREENING IS THEREFORE VERY
IMPORTANT
17. Estimated Glomerular Filtration rate
⢠Estimate of GFR by the Cockcroft and Gault equation
ďŽ Cockroft Gault Formula
ďŽ (140 â age) X Body Weight (Kg)/
72 X Serum Creatinine (mg/dL)
ďŽ Multiply by 0.85 for women
18. Urine Testing
ď Urine for protein
ďDipstick
ď24 hour urinary protein
ď Urine microscopic examination
ďFor RBC / Pus Cell / Cast
ď Urine for microalbuminuria
ďOn morning urine sample
ďusing strip for microalbumin
19. Targets for Screening
ď Hypertensive patients
ď Diabetic patients
ď Cardiovascular disease
ď Those on regular NSAID/Herbs
ď Renal calculi
ď Anemia of unknown aetiology
ď First and second degree relatives of ESRD
ď Autoimmune disease (SLE/RA)
ď Reduction of kidney mass(Nephrectomy
20. False +ve CKD
ď Urinary Tract Infection
ď Sepsis
ď Heart Failure
ď Strenous exercise
ď Heavy protein intake
ď Menses
21. Significance of proteinuria
ďA dominant risk factor for deterioration of
renal failure (besides HT)
ďMarker of Increased Risk for CV mortality and
morbidity (DM & non-DM)
ďźe.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
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 (contâd)Hyperkalemia (contâd)
⢠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
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 (contâd)Renal osteodystrophy (contâd)
⢠Phosphate binders (contâd)Phosphate binders (contâd)
⢠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
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 (contâd)Anemia (contâd)
⢠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(contâd)Anemia(contâd)
⢠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
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 â transplant within 36 hours of
procurement
Delay may increase ATN
Pre-transplant: Immunotherapy (IV
methylprednisolone sodium succinate,
(A âmethaPred, 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
recipientsâ 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
Things that cause kidney disease:
-Glomerulonephritis, a group of diseases that cause inflammation and damage to the kidney&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&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&apos;s immune system.
-Obstructions caused by problems like kidney stones, tumors or an enlarged prostate gland in men.
-Repeated urinary infections.
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 â 45 percent
Prerenal â 21 percent
Acute or chronic kidney disease â 13 percent (mostly due to acute tubular necrosis and prerenal disease)
Urinary tract obstruction â 10 percent (most often older men with prostatic disease)
Glomerulonephritis or vasculitis â 4 percent
Acute interstitial nephritis â 2 percent
Atheroemboli â 1 percent