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Renal Disease Flashcards

1
Q

Diseases of the Kidney
Classification

A

*Glomerular
*Interstitial
*Tubular

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2
Q

The two most common diseases that affect
the kidney are:

A
  1. Diabetes
    Small blood vessels of the body are injured
  2. Hypertension
    blood vessels of the kidney are damage
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3
Q

Mechanism of diabetes:

A

*may cause nerve damage which can cause difficulty in emptying the bladder.
*The pressure from the overfull bladder can cause urine backup and injure the kidneys.
*If urine remains in bladder for a long time, infection develop from growth of bacteria in urine

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4
Q

Glomerular Disease

A
  1. Majority are of immune origin
    * Mechanism:
    * Immune complexes deposits in the
    kidneys.
    * Complement components are
    activated.
    * Attraction of WBCs to the area that
    releases cytokines and enzymes that
    damage the kidneys
  2. Nonimmunologic causes include
    exposure to chemicals and toxins
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5
Q

Primary Glomerulopathies

A
  1. acute diffuse proliferative glomerulonephritis
    a. Poststreptococcal
    b. Nonpoststreptococcal
  2. Rapidly progressive (crescentic) glomerulonephritis
  3. membrane gloerulopathy
  4. lipoid nephrosis
  5. focal segmental glomerolosclerosis
  6. membranoproliferative glomerulonephritis
  7. IgA nephropathy
  8. Focal proliferative glomerulonephritis
  9. chronic glomerulonephritis
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6
Q

Acute Glomerulonephritis

A

Glomerulonephritis refers to a sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine

There are multiple types of glomerulonephritis, and one type may change into another type over time

condition may become chronic

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7
Q

Acute Poststreptococcal Glomerulonephritis

A

Caused by infection with group A streptococcus
*Streptococci form immune complexes with antibodies and deposits in glomerular membrane causing inflammation

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8
Q

Symptoms of APGN

A

fever, edema (noticeably around the
eye), fatigue, hypertension

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9
Q

APGN Laboratory diagnosis:

A

*Urinalysis findings: Marked hematuria, Proteinuria, Oliguria
*Microscopic: RBC casts, dysmorphic RBCs, hyaline & granular casts, WBCs
*Elevated ASOT is evidence that the disease is of streptococcal in origin

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10
Q

Rapidly Progressive Glomerulonephritis
(RPGN

A

Aka Crescentic Glomerulonephritis

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10
Q

Rapidly Progressive Glomerulonephritis
(RPGN

A

Accumulation of cells in Bowman’s space in the form of “crescents”

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10
Q

RPGN

A

A more serious form of acute glomerular
disease: often terminates in renal failure

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11
Q

RPGN

A

*Contains macrophages, fibroblasts and fibrin

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12
Q

RPGN

A

*Initiated by deposition of immune complex

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13
Q

RPGN

A

*Complication of another form of glomerulonephritis or an immunologic disorder

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14
Q

RPGN

A

*Lab results similar to acute glomerulonephritis but becomes more abnormal as it progresses
*Markedly elevated protein
*Very low GFR

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15
Q

Goodpasture’s Syndrome

A

Antiglomerular basement membrane
antibody (anti-GBM)

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16
Q

Goodpasture’s Syndrome or (anti-GBM)

A

presence of autoantibody to glomerular, renal
tubular, and alveolar basement membranes

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17
Q

Goodpasture’s Syndrome or (anti-GBM)

A

production follow after viral respiratory infections

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18
Q

Goodpasture’s Syndrome or (anti-GBM)

A

attachment of autoantibody to basement
membrane followed by complement activation produces capillary destruction.

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19
Q

Goodpasture’s Syndrome or (anti-GBM)

A

more likely in young males between the
ages of 18 & 35
rapidly progress to renal failure
* mortality rate may be as high as 50%

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20
Q

Wegener’s Granulomatosis

A

A Small-Vessel Vasculitis
Granuloma-producing inflammation of the small blood vessels of the kidney and respiratory system

21
Q

Wegener’s Granulomatosis

A

Laboratory Diagnosis:
* Serum antineutrophilic cytoplasmic antibody (ANCA)
* Urine: hematuria, proteinuria, RBC casts
* Elevated serum creatinine and BUN

22
Q

Henoch-Schönlein purpura

A

A Small-Vessel Vasculitis
* Vasculitis with IgA-dominant immune deposits, affecting small vessels

23
Henoch-Schönlein purpura
disease occurring primarily in children following upper respiratory infections
23
Henoch-Schönlein purpura
Clinical manifestations: * Raised, red patches on the skin * Respiratory and gastrointestinal symptoms * including blood in the sputum and stools * Renal involvement * Complete recovery in >50% of patients
24
Purpura
red or purple discolorations on the skin do not blanch on applying pressure measures 0.3–1 cm (3–10 mm) *petechiae measure less than 3 mm *ecchymoses greater than 1 cm
25
Membranous Glomerulonephritis
Predominant characteristic is a pronounced thickening of the glomerular basement membrane resulting from the deposition of IgG immune complexes
26
Membranous Glomerulonephritis Associated Disorder
*systemic lupus erythematosus *Sjögren syndrome *secondary syphilis *hepatitis B *gold and mercury treatments *malignancy *Many cases of unknown etiology *Demonstration of one of the secondary disorders through blood tests can aid in the diagnosis.
27
Membranous Glomerulonephritis
Disease progresses slowly, with possible remission Frequent development of nephrotic syndrome symptoms occurs
28
Membranoproliferative Glomerulonephritis Type 1
*Displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman’s capsule), causing thickening of the capillary walls *May progress to nephrotic syndrome
29
Membranoproliferative Glomerulonephritis Type 2
*Displays extremely dense deposits in the glomerular basement membrane. *Experience symptoms of chronic glomerulonephritis
30
Membranoproliferative Glomerulonephritis
Laboratory findings: hematuria, proteinuria, and decreased serum complement levels There appears to be an association with autoimmune disorders, infections, and malignancies
31
Chronic Glomerulonephritis
Examination of the urine reveals hematuria, proteinuria, glucosuria, many varieties of casts, including broad casts.
32
Chronic Glomerulonephritis
A markedly decreased glomerular filtration rate is present in conjunction with increased BUN and creatinine levels and electrolyte imbalance.
33
IgA Nephropathy
also known as Berger’s disease
34
IgA Nephropathy
*deposition of IgG-IgA in the glomerulus *patients have increased serum levels of IgA, maybe a result of mucosal infection
35
IgA Nephropathy
most common cause of glomerulunephritis *macroscopic hematuria
36
IgA Nephropathy
Patient may be asymptomatic for 20 years or more *But there is a gradual progression to chronic glomerulonephritis and end-stage renal disease
37
Nephrotic Syndrome
Laboratory Findings; *Urinalysis: heavy proteinuria, transient hematuria, fat-droplets *Chemistry: high cholesterol and triglycerides, low albumin
38
Nephrotic Syndrome
*circulatory disruption producing systemic shock that decrease the pressure and flow of blood to the kidney *complication of glomerulonephritis
38
Nephrotic Syndrome
Increased permeability of the glomerular membrane: facilitates the passage of HMW proteins and lipids into the urine
39
Nephrotic Syndrome
Albumin is the primary protein depleted from the circulation. *Hypoalbuminemia appears to stimulate the increased production of lipids by the liver *Depletion of immunoglobulins and coagulation factors places patients at an increased risk of infection and coagulation disorders
40
Minimal Change Disease
also known as lipid nephrosis
41
Minimal Change Disease
As the name implies, produces little cellular change in the glomerulus * Patients are usually children * etiology is unknown at this time, associated with * allergic reactions * recent immunization * possession of HLA-B12
41
Minimal Change Disease
The disorder responds well to corticosteroids, and prognosis is generally good, with frequent complete remissions
42
Focal Segmental Glomerulosclerosis
affects only certain numbers and areas of glomeruli, and the others remain normal
43
Focal Segmental Glomerulosclerosis
damaged podocytes * Immune deposits, primarily IgM and C3, are a frequent finding and can be seen in undamaged glomeruli
44
Focal Segmental Glomerulosclerosis
often seen in association with abuse of heroin and analgesics and with AIDS.
45
Alport Syndrome
inherited disorder affecting the glomerular basement membrane
46
Alport Syndrome
*Sex-linked or autosomal genetic disorder *Males are frequently more severely affected than females. *The disease is due for alteration or missing of a5 chain of IV collagen. Occurs as an alteration in the basal membrane structure that affects eyes, ears and kidneys.
47
Alport Syndrome
Clinical findings: *During respiratory infections, males before the age of six may exhibit macroscopic hematuria and continue to exhibit microscopic hematuria *Abnormalities in hearing and vision also may be present
48
Alport Syndrome
prognosis ranges from mild symptoms to persistent hematuria and renal insufficiency in later life to the nephrotic syndrome and end-stage renal disease.
49

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