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NARAYANA HRUDAYALAYA COLLEGE OF
NURSING
PRESENTATION ON
RENAL AMYLOIDOSIS
Presented by
Koyel Thnader
1st pcbsc
NHCON
AMYLODOSIS:
Amyloidosis is an abnormal protein
that is usually produced in the bone
marrow & can be deposited in any tissue
organ.
RENAL AMYLODOSIS:
The kidney is small &colour sectioned
surface shows loss of corticomedullary
distinction& pale,waxy transluencey.
-The amyloido deposits are seen mainly in the
glomerullar capillary
-The deposits are also present in pertibular connective
tissue producing atrophic tubules & amyloid casts in
the tubular lumina, & in the artial wall producing
luminal narrowing.
Amyloid deposits damage the kidneys and make it
harder for them to filter wastes & break down
proteins. When the kidney become too damage
they may no longer able to function well enough
too maintain health, resulting kidney faliure
TYPES:
👉 AL amyloidosis (primary amyloidosis)
👉AA amyloidosis (secondery amyloidosis)
👉Heriditary amyloidosis(Familial amyloidosis)
AL amyloidosis or primary amyloidosis :
This is the most common from that occurs when
the bone marrow produces too much certain fragment
of antibody proteins, which builds up in the blood
stream & can deposits in body tissue.
AA amyloidosis or secondary
amyloidosis :
The develops along with a chronic infection or
inflammatory disease, such as tuberculosis or
rheumatoid arthritis.
Hereditary amyloidosis or familial
amyloidosis :
This is a genetic form passed down in families
that often affects nerves & kidneys.
Pathogenesis of amyloidosis
▪️For each of these amyloidogenic "precursor protein"
- initially step in amyloid fibril formation is a misfolding
event.
◾Misfolding can result from
- proteolytic cleavage (e.g-amyloid beta protein)
- an amnio acid substitution (e.g-transthyretin [TTR]
- intrinsic properties that becomes significant only at
high serum concentration or in the presence of specific
local factors.
◾Combination of these factors often determines the
amyloidogenic potential of a particular protein.
◾Regardless of the protein or the tigger for misfolding,
the misfolded variants are highly prone to self
aggregation.
◾Self aggregation generates proto filaments that intract
to from fibrils.
◾Amyloid fibrils have a characteristics - beta pleated
sheet configuration.
-produces birefrigence under polarized light when stained
with congo red dye.
Factors that determine the organ distribution of
amyloid deposits - not well understood.
How does amyloidosis cause renal
disease :
◾Disruption of tissue architecture by amyloid deposits.
◾Amyloidogenic precursor proteins, folding
intermediates, & proto filaments have toxicites that are
independent of the amyloid deposits.
- Lack of correlation between quantity of amyloid in
tissue & organ dysfunction
- detection of amyloidogenic precursor proteins in
tissue in the absence of amyloid
- rapid improvement in makers of organ dysfunction
after treatment induced reductions in precursor protein
production.
Signs & symptoms :
Signs and symptoms of amyloidosis are not usually
experienced until the condition is advanced.
◾ Swelling in the ankles & legs
◾Severe fatigue & weakens
◾Shortness of breath
◾Numbness, tungling, or pain in the hands or feet,
especially pain in the wrist (carpal tunnel syndrome)
◾Diarrhea, possibly with blood or constipation
◾Feeling full quickly when eating & significant weight loss
Contd....
◾An enlarged tongue
◾Skin changes, such as thickening or easy brushing, &
purplish patches around the eyes
◾An irregular heart beat
◾Difficulty swallowing.
Test & diagnosis :
Diagnosis usually start with through medical history &
physical examination. The following tests can be
carried out:
◾Laboratory tests with blood & urine to analyze for
abnormal protein that can indicate amyloidosis.
◾Biopsy is done by taking a sample tissue. Sample to
check for signs of amyloidosis. The biopsy may be
taken from the patients abnormal bone marro, or
organ such as kidney. Tissue analysis can help
determine the types
◾Imaging tests is carried by taking images of the organ
affected by amyloidosis to help establish the extent of
disease.
Treatment options for amyloidosis :
Treatment of amyloidosis usually involves decreasing the
protein that forms the amyloids, whuch is carried out
depending on the organ affected. The treatment options
included
◾Use drug therapies of chemo therapy such s
corticosteroids & alkeran
◾Dialysis if the kidney are failing
◾Surgical & other procedures such as
- kidney or bone marrow transplant.
Preventive measure for
amyloidosis :
1. Those who have hereditary amyloidosis should
consider going to generic counseling to learn about the
risks of passing the condition to their children.
2.studies suggest that the following dieatry choices such
as limiting meat consumption taking fish oils
supplements & vit c may help to prevent amyloidosis in
people who are at high risk, or help slow the disease
once it has developed.
Renal amyloidosis

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Renal amyloidosis

  • 1. NARAYANA HRUDAYALAYA COLLEGE OF NURSING PRESENTATION ON RENAL AMYLOIDOSIS Presented by Koyel Thnader 1st pcbsc NHCON
  • 2. AMYLODOSIS: Amyloidosis is an abnormal protein that is usually produced in the bone marrow & can be deposited in any tissue organ.
  • 3. RENAL AMYLODOSIS: The kidney is small &colour sectioned surface shows loss of corticomedullary distinction& pale,waxy transluencey.
  • 4. -The amyloido deposits are seen mainly in the glomerullar capillary -The deposits are also present in pertibular connective tissue producing atrophic tubules & amyloid casts in the tubular lumina, & in the artial wall producing luminal narrowing.
  • 5. Amyloid deposits damage the kidneys and make it harder for them to filter wastes & break down proteins. When the kidney become too damage they may no longer able to function well enough too maintain health, resulting kidney faliure
  • 6. TYPES: 👉 AL amyloidosis (primary amyloidosis) 👉AA amyloidosis (secondery amyloidosis) 👉Heriditary amyloidosis(Familial amyloidosis)
  • 7. AL amyloidosis or primary amyloidosis : This is the most common from that occurs when the bone marrow produces too much certain fragment of antibody proteins, which builds up in the blood stream & can deposits in body tissue. AA amyloidosis or secondary amyloidosis : The develops along with a chronic infection or inflammatory disease, such as tuberculosis or rheumatoid arthritis.
  • 8. Hereditary amyloidosis or familial amyloidosis : This is a genetic form passed down in families that often affects nerves & kidneys.
  • 9. Pathogenesis of amyloidosis ▪️For each of these amyloidogenic "precursor protein" - initially step in amyloid fibril formation is a misfolding event. ◾Misfolding can result from - proteolytic cleavage (e.g-amyloid beta protein) - an amnio acid substitution (e.g-transthyretin [TTR] - intrinsic properties that becomes significant only at high serum concentration or in the presence of specific local factors.
  • 10. ◾Combination of these factors often determines the amyloidogenic potential of a particular protein. ◾Regardless of the protein or the tigger for misfolding, the misfolded variants are highly prone to self aggregation. ◾Self aggregation generates proto filaments that intract to from fibrils. ◾Amyloid fibrils have a characteristics - beta pleated sheet configuration. -produces birefrigence under polarized light when stained with congo red dye. Factors that determine the organ distribution of amyloid deposits - not well understood.
  • 11. How does amyloidosis cause renal disease : ◾Disruption of tissue architecture by amyloid deposits. ◾Amyloidogenic precursor proteins, folding intermediates, & proto filaments have toxicites that are independent of the amyloid deposits. - Lack of correlation between quantity of amyloid in tissue & organ dysfunction - detection of amyloidogenic precursor proteins in tissue in the absence of amyloid - rapid improvement in makers of organ dysfunction after treatment induced reductions in precursor protein production.
  • 12. Signs & symptoms : Signs and symptoms of amyloidosis are not usually experienced until the condition is advanced. ◾ Swelling in the ankles & legs ◾Severe fatigue & weakens ◾Shortness of breath ◾Numbness, tungling, or pain in the hands or feet, especially pain in the wrist (carpal tunnel syndrome) ◾Diarrhea, possibly with blood or constipation ◾Feeling full quickly when eating & significant weight loss
  • 13. Contd.... ◾An enlarged tongue ◾Skin changes, such as thickening or easy brushing, & purplish patches around the eyes ◾An irregular heart beat ◾Difficulty swallowing.
  • 14.
  • 15.
  • 16. Test & diagnosis : Diagnosis usually start with through medical history & physical examination. The following tests can be carried out: ◾Laboratory tests with blood & urine to analyze for abnormal protein that can indicate amyloidosis. ◾Biopsy is done by taking a sample tissue. Sample to check for signs of amyloidosis. The biopsy may be taken from the patients abnormal bone marro, or organ such as kidney. Tissue analysis can help determine the types
  • 17. ◾Imaging tests is carried by taking images of the organ affected by amyloidosis to help establish the extent of disease.
  • 18. Treatment options for amyloidosis : Treatment of amyloidosis usually involves decreasing the protein that forms the amyloids, whuch is carried out depending on the organ affected. The treatment options included ◾Use drug therapies of chemo therapy such s corticosteroids & alkeran ◾Dialysis if the kidney are failing ◾Surgical & other procedures such as - kidney or bone marrow transplant.
  • 19. Preventive measure for amyloidosis : 1. Those who have hereditary amyloidosis should consider going to generic counseling to learn about the risks of passing the condition to their children. 2.studies suggest that the following dieatry choices such as limiting meat consumption taking fish oils supplements & vit c may help to prevent amyloidosis in people who are at high risk, or help slow the disease once it has developed.