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PRESENTED BY:RAKHI PANWAR
BSN 2nd YEAR
LUPUS NEPHRITIS AND
INTERSTITIAL
NEPHRITIS
LUPUS NEPHRITIS
CONTENT:
• Risk factor
• Pathophysiology
• Clinical manifestation
• Complication
• Diagnostic evaluation
• Nursing management
• Prevention
• Introduction to lupus
nephritis
• Lupus or SLE
• Meaning and
Definition
• Classification/stage
• Etiology and causes
INTRODUCTION
• Lupus nehritis : One of the most serious
manifestations of Systemic lupus erythematosus or
SLE
• Approximately 10 to 30% of patient with lupus
nephritis progress to end stage renal disease
(ESRD)
• May require hemodialysis or renal transplantation
if ESRD occur.
LUPUS OR SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE) :
SLE Or systemic lupus erythematosus or
lupus is a autoimmune condition that causes
inflammation.
Body system affected : Joints, Skin, Lungs,
Heart,Kidneys, Brains,blood system .
MEANING/ DEFINITION :
LUPUS NEPHRITIS
•Lupus: systemic lupus erythematosus and
• nephritis: nephron :greek word, meaning
kidney and itis: inflammation
•Lupus nephritis is the inflammation of
kidney due to systemic lupus erythematosus
which is an autoimmune disease.
CLASSIFICATION AND
STAGES OF LUPUS
NEPHRTIS :
(ACCORDING TO WHO)
•Class 1: minimal mesangial glomerulonephritis
•class 2: mesangial proliferative lupus
nephritis
•class 3: focus glomerulonephritis
•class 4: diffuse proliferative nephritis
•class 5: membranous glomerulonephritis
•class 6: advanced Sclerosing lupus nephritis
ETIOLOGY AND CAUSES :
•Idiopathic
•Genetic predisposition
RISK FACTOR :
•GENDER: men are More at risk than women .
•AGE: It can occur at any age and time;
however cases are noted in people aged
between 15 and 45 years.
•ETHNICITY: Occur more frequently in
Asian, african-american and hispanics.
PATHOPHYSIOLOGY
• In a patient with lupus, process of phagocytosis is
too slow or performed incorrectly.
• Apoptic bodies are not consumed properly
• Bodies breakdown and leak out material into body
• Nuclear material(DNA) is present in apoptic bodies
and enters into extracellular matrix/space and
detected by immune system (as a foreign invader)
• Immune system creates antibody against it to attack nuclear
antigen
• Formation of immune complex takes place
• Immune complex deposition gets deposited in glomeruli of
kidney or basement membrane of Capillaries.
• Activation of complement system(type 3 hypersensitivity or
immune complex mediated hypersensitivity results in
• Neutrophile Infiltration,vasodilation and edema also activate
intrinsic pathway of coagulation system and microthrombi
form ; tissue ischmia and necrosis (fibrinoid necrosis).
CLINICAL
MANIFESTATIONS
NEPHROTIC SYNDROME
• Proteinuria(>3g/day )
• Hypoalbuminia (maitain and regulates oncotic
pressure )
• Edema
• Hyperlipidemia
NEPHRITIC SYNDROME :
• BUN increases
• GFR decrease
• Hematuria
• Oliguria
• Hypertension
FOAMY URINE
WEIGHT GAIN
MALAR RASH
EDEMA & SWELLING
HIGH BLOOD PRESSURE
•High creatinine level in blood
•Fever
• Nocturia
•Joint pain
•Muscle pain
DIAGNOSTIC EVALUATION :
•History
•Physical examination
•Urinalysis
•CBC
•Complement test (protein C3 nd C4) low
count
•Positive antinuclear antibody
•Positive anti-dsDNA
•High ESR.
•High C-reactive protein
•High serum cholesterol
•Low serum albumin
•High serum TAG
•Hematuria
•Anemia
•Low eGFR
•Low creatinine clearance
•High serum creatinine
• Kidney biopsy
• Ultrasound scan of kidney
• IOTHALAMATE CLEARANCE TEST: This is
done When kidney does not filter in correct way this
test is also use to assess the speed of Kidney
filtration more accurately. The test involve Injection
of radioactive iothalamate in blood then test the
duration how quickly it is excreted in urine.
COMPLICATION:
•Acute renal failure
•Chronic renal failure
MEDICAL MANAGEMENT :
The goal of management is :
•to decrease occurrence of flares,
•to Protects organs, joints and tissues from
damage, and
•to improve quality of live.
•Reduce symptoms or make symptoms
disappear (remission)
• Keep the disease from getting worse
•Maintain remission
•Avoid the need for dialysis or a kidney
transplant
-Belimumab:to decrease B Cell activity.
Drug regimens prescribed for lupus
nephritis include:
• mycophenolate mofetil (MMF),
cyclophosphamide + corticosteroids, and
the
immunesuppressant azathioprine with co
rticos-teroids.
• immunosuppressive drugs were better
than corticosteroids for renal outcomes
•MMF is safer than cyclophosphamide
with corticosteroids, with less chance
of causing ovarian failure, immune
problems or hair loss. It also works
better than azathioprine with
corticosteroids for maintenance
therapy.
•Hydroxichloroquine : Basic treatment
NURSING MANAGEMENT :
NURSING ASSESSMENT:
•Assess fluid status (daily weight monitoring ,
intake and output ,skin turgor, distension of
neck veins)
•Assess dietary/nutritional pattern (Diet
history , food preferences)
• Assess for edema (ankles, arm, feet, face,
eyes etc.)
NURSING DIAGNOSIS,
GOAL
AND
NURSING
INTERVENTION:
1.Acute pain related to disease condition
GOAL:To reduce the level of pain
in client
NURSING INTERVENTION:
• Provide comfortable position to the client.
• Assess the location, characteristics, Onset,duration,
frequency,quality(sharp, dull) And severity(By using
pain scale eg wong baker pain scale) of pain via
assessment.
• Perform history assessment of pain(effectiveness of
Previous pain management etc)
• Determine factors that alleviate pain.
• Administered analgesics .
1. Excess Fluid Volume Related to fluid
accumulation And decreased kidney
function.
GOAL :To reduce fluid volume in client
NURSING INTERVENTION:
• Daily weight monitoring of pt.
• Monitor intake output chart of patient
• Monitor vital signs(BP for Hypertension)
• Assess for edema (site,degree,type)
• Limiting the sodium intakes
• Limit the intake of fluid and water
• Administer diuretics as prescribed
PATIENT
TEACHING:
•Sodium restriction along with fluid restriction .
•Low fat diet (due to hyperlipidemia ) per MD
order.
•Low protein diet
•Avoid high potassium fruits and vegetables.
•Monitoring Phosphate intakes
•Educate patient about SLE.
INTERSTITIAL
NEPHRITIS
INTRODUCTION :
•Interstitial nephritis, also known as
tubulointerstitial nephritis, is
inflammation of the area of kidney
known as the interstitium, which consists
of a collection of cells, extracellular
matrix and fluid surrounding the renal
tubule.
DEFINITION:
•Interstitial nephritis is a kidney
disorder in which the spaces between
the kidney tubules become swollen
(inflamed). This can cause problems
with the way your kidneys work.
TYPES OF
TUBULOINTERSTITIAL
NEPHRITIS:
(A). ACUTE INTERSTISTIAL NEPHRITIS:
Has a rapid clinical onset and is characterized
histologically by interstitial edema, often
accompanied by leukocytic infiltration of the
interstitium or tubules and tubular injury.
(B). CHRONIC INTERSTITIAL
NEPHRITIS
There is infiltration with predominantly
mononuclear leukocytes, prominent interstitial
fibrosis,and widespread tubular atrophy.
ACUTE
• Edema
• Eosionphil
• Neutrophils
CHRONIC
• Fibrosis
• Tubular atrophy
CAUSES:
• INFECTIONS :
-acute/chronic bacterial pyelonephritis
-other infections(virus,bacteria)
• TOXINS
-drugs
-analgesics
-heavy metals(lead,cadmium)
• METABOLIC DISEASES:
-urate nephropathy (uric acid nephropathy)
-hypercalcemic nephropathy
-hypokalemic nephropathy
-oxalate nephropathy
• IMMUNOLOGIC RXN:
-lupus
-sjogren syndrome
• CHRONIC URINARY TRACT OBSTRUCTION
PATHOPHYSIOLOGY:
CLINICAL
MANIFESTATIONS :
CLASSIC TRIAD
OF SYMPTOMS :
1.Rash
2.Joint pain and
3.Increased
eosinophils in
blood
•Nausea
•Vomiting
•Anorexia
•Weight loss
•Pain with urination
•Flank pain
• BUN increases
• GFR decrease
• Non-oliguric AKI
• Hypertension (rare)
• Salt wasting
• Impaired ability to concentrate urine
(diluted urine)
• Diminished ability to excrete acids
(metabolic acidosis
DIAGNOSTIC
EVALUATION:
•Health history
•Physical examination
The health care provider will perform a
physical exam. This may reveal:
•High blood pressure
Common tests include:
•Blood chemistry
•BUN and blood creatinine levels
•Complete blood count
•Kidney biopsy
•Kidney ultrasound
•Urinalysis
MEDICAL
MANAGEMENT :
The goal of management is :
•Reduce symptoms
• Keep the disease from getting worse
•Avoid the need for dialysis or a kidney
transplant
•Removal of drug causing Condition
•cyclophosmide And Cyclosporine
(steroids)
• Immunosuppressive Therapy
• Kidney Transplant
• Dialysis
• corticosteroids
NURSING
MANAGEMENT:
NURSING ASSESSMENT:
• Assess vital signs (BP)
• Monitor intake output chart
• Assess for electrolyte imbalance
• Assess site and location of pain
• History of urine colour, frequency etc .
• Daily weight monitoring
• Assess for skin rashes
NURSING DIAGNOSIS,
GOAL
AND
NURSING
INTERVENTION:
1. Deficit fluid volume related to vomiting.
GOAL: To maintain adequate fluid status
NURSING INTERVENTION:
• Monitor vital sign (especially BP and HR).
• Assess skin turgor and oral mucous membrane for
sign of dehydration .
• Assess Alteration in mentation/sensorium
(Confusion, slowed response)
• Monitor intake output chart .
• Apply cold/hot application to reduce client’s body
temperature.
• Provide plenty of fluid to rehydration therapy.
1. Imbalanced nutrition pattern less than
body requirement related to anorexia.
GOAL: To achieve adequate nutritional
status.
NURSING INTERVENTION:
• Assess for the possible cause of Decreased
appetite Or GI discomforts.
• Monitor vital signs, intake output chart, body
weight,serum albumin.
• Provide diet consider patients like and dislikes
as far as possible.
• Provide frequent oral hygiene.
• Administered parenteral feeding as required.
PATIENT TEACHING:
• Stay well hydrated and increase (2500-3000ml )intake of
fluids .
• Restrict the use of over the counter medications.
• Restrict rich souce of oxalic acid (in oxalate
nephropathy)
• Restrict high protein diet (impaired kidney function)
Lupus and interstitial nephritis.pptx

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Lupus and interstitial nephritis.pptx

  • 1. PRESENTED BY:RAKHI PANWAR BSN 2nd YEAR LUPUS NEPHRITIS AND INTERSTITIAL NEPHRITIS
  • 3. • Risk factor • Pathophysiology • Clinical manifestation • Complication • Diagnostic evaluation • Nursing management • Prevention • Introduction to lupus nephritis • Lupus or SLE • Meaning and Definition • Classification/stage • Etiology and causes
  • 4. INTRODUCTION • Lupus nehritis : One of the most serious manifestations of Systemic lupus erythematosus or SLE • Approximately 10 to 30% of patient with lupus nephritis progress to end stage renal disease (ESRD) • May require hemodialysis or renal transplantation if ESRD occur.
  • 5.
  • 6. LUPUS OR SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) : SLE Or systemic lupus erythematosus or lupus is a autoimmune condition that causes inflammation. Body system affected : Joints, Skin, Lungs, Heart,Kidneys, Brains,blood system .
  • 7. MEANING/ DEFINITION : LUPUS NEPHRITIS •Lupus: systemic lupus erythematosus and • nephritis: nephron :greek word, meaning kidney and itis: inflammation •Lupus nephritis is the inflammation of kidney due to systemic lupus erythematosus which is an autoimmune disease.
  • 8. CLASSIFICATION AND STAGES OF LUPUS NEPHRTIS : (ACCORDING TO WHO)
  • 9. •Class 1: minimal mesangial glomerulonephritis •class 2: mesangial proliferative lupus nephritis •class 3: focus glomerulonephritis •class 4: diffuse proliferative nephritis •class 5: membranous glomerulonephritis •class 6: advanced Sclerosing lupus nephritis
  • 10. ETIOLOGY AND CAUSES : •Idiopathic •Genetic predisposition
  • 11. RISK FACTOR : •GENDER: men are More at risk than women . •AGE: It can occur at any age and time; however cases are noted in people aged between 15 and 45 years. •ETHNICITY: Occur more frequently in Asian, african-american and hispanics.
  • 12.
  • 13.
  • 15. • In a patient with lupus, process of phagocytosis is too slow or performed incorrectly. • Apoptic bodies are not consumed properly • Bodies breakdown and leak out material into body • Nuclear material(DNA) is present in apoptic bodies and enters into extracellular matrix/space and detected by immune system (as a foreign invader)
  • 16. • Immune system creates antibody against it to attack nuclear antigen • Formation of immune complex takes place • Immune complex deposition gets deposited in glomeruli of kidney or basement membrane of Capillaries. • Activation of complement system(type 3 hypersensitivity or immune complex mediated hypersensitivity results in • Neutrophile Infiltration,vasodilation and edema also activate intrinsic pathway of coagulation system and microthrombi form ; tissue ischmia and necrosis (fibrinoid necrosis).
  • 18. NEPHROTIC SYNDROME • Proteinuria(>3g/day ) • Hypoalbuminia (maitain and regulates oncotic pressure ) • Edema • Hyperlipidemia
  • 19. NEPHRITIC SYNDROME : • BUN increases • GFR decrease • Hematuria • Oliguria • Hypertension
  • 25. •High creatinine level in blood •Fever • Nocturia •Joint pain •Muscle pain
  • 26. DIAGNOSTIC EVALUATION : •History •Physical examination •Urinalysis •CBC •Complement test (protein C3 nd C4) low count
  • 27. •Positive antinuclear antibody •Positive anti-dsDNA •High ESR. •High C-reactive protein •High serum cholesterol •Low serum albumin •High serum TAG
  • 28. •Hematuria •Anemia •Low eGFR •Low creatinine clearance •High serum creatinine
  • 29.
  • 30. • Kidney biopsy • Ultrasound scan of kidney • IOTHALAMATE CLEARANCE TEST: This is done When kidney does not filter in correct way this test is also use to assess the speed of Kidney filtration more accurately. The test involve Injection of radioactive iothalamate in blood then test the duration how quickly it is excreted in urine.
  • 32. MEDICAL MANAGEMENT : The goal of management is : •to decrease occurrence of flares, •to Protects organs, joints and tissues from damage, and •to improve quality of live.
  • 33. •Reduce symptoms or make symptoms disappear (remission) • Keep the disease from getting worse •Maintain remission •Avoid the need for dialysis or a kidney transplant -Belimumab:to decrease B Cell activity.
  • 34. Drug regimens prescribed for lupus nephritis include: • mycophenolate mofetil (MMF), cyclophosphamide + corticosteroids, and the immunesuppressant azathioprine with co rticos-teroids. • immunosuppressive drugs were better than corticosteroids for renal outcomes
  • 35. •MMF is safer than cyclophosphamide with corticosteroids, with less chance of causing ovarian failure, immune problems or hair loss. It also works better than azathioprine with corticosteroids for maintenance therapy. •Hydroxichloroquine : Basic treatment
  • 36. NURSING MANAGEMENT : NURSING ASSESSMENT: •Assess fluid status (daily weight monitoring , intake and output ,skin turgor, distension of neck veins) •Assess dietary/nutritional pattern (Diet history , food preferences)
  • 37. • Assess for edema (ankles, arm, feet, face, eyes etc.)
  • 39. 1.Acute pain related to disease condition GOAL:To reduce the level of pain in client NURSING INTERVENTION:
  • 40. • Provide comfortable position to the client. • Assess the location, characteristics, Onset,duration, frequency,quality(sharp, dull) And severity(By using pain scale eg wong baker pain scale) of pain via assessment. • Perform history assessment of pain(effectiveness of Previous pain management etc) • Determine factors that alleviate pain. • Administered analgesics .
  • 41. 1. Excess Fluid Volume Related to fluid accumulation And decreased kidney function. GOAL :To reduce fluid volume in client
  • 42. NURSING INTERVENTION: • Daily weight monitoring of pt. • Monitor intake output chart of patient • Monitor vital signs(BP for Hypertension) • Assess for edema (site,degree,type) • Limiting the sodium intakes • Limit the intake of fluid and water • Administer diuretics as prescribed
  • 44. •Sodium restriction along with fluid restriction . •Low fat diet (due to hyperlipidemia ) per MD order. •Low protein diet •Avoid high potassium fruits and vegetables. •Monitoring Phosphate intakes •Educate patient about SLE.
  • 46. INTRODUCTION : •Interstitial nephritis, also known as tubulointerstitial nephritis, is inflammation of the area of kidney known as the interstitium, which consists of a collection of cells, extracellular matrix and fluid surrounding the renal tubule.
  • 47.
  • 48. DEFINITION: •Interstitial nephritis is a kidney disorder in which the spaces between the kidney tubules become swollen (inflamed). This can cause problems with the way your kidneys work.
  • 49. TYPES OF TUBULOINTERSTITIAL NEPHRITIS: (A). ACUTE INTERSTISTIAL NEPHRITIS: Has a rapid clinical onset and is characterized histologically by interstitial edema, often accompanied by leukocytic infiltration of the interstitium or tubules and tubular injury.
  • 50. (B). CHRONIC INTERSTITIAL NEPHRITIS There is infiltration with predominantly mononuclear leukocytes, prominent interstitial fibrosis,and widespread tubular atrophy. ACUTE • Edema • Eosionphil • Neutrophils CHRONIC • Fibrosis • Tubular atrophy
  • 51. CAUSES: • INFECTIONS : -acute/chronic bacterial pyelonephritis -other infections(virus,bacteria) • TOXINS -drugs -analgesics -heavy metals(lead,cadmium)
  • 52. • METABOLIC DISEASES: -urate nephropathy (uric acid nephropathy) -hypercalcemic nephropathy -hypokalemic nephropathy -oxalate nephropathy • IMMUNOLOGIC RXN: -lupus -sjogren syndrome • CHRONIC URINARY TRACT OBSTRUCTION
  • 54.
  • 56. CLASSIC TRIAD OF SYMPTOMS : 1.Rash 2.Joint pain and 3.Increased eosinophils in blood •Nausea •Vomiting •Anorexia •Weight loss •Pain with urination •Flank pain
  • 57. • BUN increases • GFR decrease • Non-oliguric AKI • Hypertension (rare) • Salt wasting
  • 58. • Impaired ability to concentrate urine (diluted urine) • Diminished ability to excrete acids (metabolic acidosis
  • 59.
  • 61. •Health history •Physical examination The health care provider will perform a physical exam. This may reveal: •High blood pressure
  • 62. Common tests include: •Blood chemistry •BUN and blood creatinine levels •Complete blood count •Kidney biopsy •Kidney ultrasound •Urinalysis
  • 63. MEDICAL MANAGEMENT : The goal of management is : •Reduce symptoms • Keep the disease from getting worse •Avoid the need for dialysis or a kidney transplant
  • 64. •Removal of drug causing Condition •cyclophosmide And Cyclosporine (steroids) • Immunosuppressive Therapy • Kidney Transplant • Dialysis • corticosteroids
  • 66. NURSING ASSESSMENT: • Assess vital signs (BP) • Monitor intake output chart • Assess for electrolyte imbalance • Assess site and location of pain • History of urine colour, frequency etc . • Daily weight monitoring • Assess for skin rashes
  • 68. 1. Deficit fluid volume related to vomiting. GOAL: To maintain adequate fluid status NURSING INTERVENTION:
  • 69. • Monitor vital sign (especially BP and HR). • Assess skin turgor and oral mucous membrane for sign of dehydration . • Assess Alteration in mentation/sensorium (Confusion, slowed response) • Monitor intake output chart . • Apply cold/hot application to reduce client’s body temperature. • Provide plenty of fluid to rehydration therapy.
  • 70. 1. Imbalanced nutrition pattern less than body requirement related to anorexia. GOAL: To achieve adequate nutritional status. NURSING INTERVENTION:
  • 71. • Assess for the possible cause of Decreased appetite Or GI discomforts. • Monitor vital signs, intake output chart, body weight,serum albumin. • Provide diet consider patients like and dislikes as far as possible. • Provide frequent oral hygiene. • Administered parenteral feeding as required.
  • 72. PATIENT TEACHING: • Stay well hydrated and increase (2500-3000ml )intake of fluids . • Restrict the use of over the counter medications. • Restrict rich souce of oxalic acid (in oxalate nephropathy) • Restrict high protein diet (impaired kidney function)