Intrinsic Renal Failure (exam2) Flashcards
Intrinsic causes of Renal Failure are up to what percentage
50%
The sites of damage for Intrinsic Renal Failure
Glomeruli, the interstitium, and or tubules
Most common cause of Intrinsic Renal Failure
Acute Tubular Necrosis (ATN)
-disease is secondary to ischemia or nephrotoxins
Nephrotic / Nephritic
Nephrotic think lots of protein loss. With Nephritic think lots of blood loss. So with nephritic think more of an inflammation process
ATN the BUN:Cr ratio is usually what
<20:1
what is ATN
Acute tubular necrosis
- Acute damage to tubule epithelium of nephron
What percentage of Intrinsic AKI is from ATN
85% of cases
Two main causes of ATN
Ischemia & Nephrotoxin Exposure
GFR is increased or decreased in Ischemic Tubular injury
Decreased
How does Pre-Renal evolve into Intrinsic AKI
Because of Decreased or inadequate renal blood flow leading to hypoxic kidney cells and death of cells
Third leading cause of inpt Toxic tubular injuy comes from?
Radiologic contrast dye
Iatrogenic - happened by medical providers
Endogenous causes of toxic Tubular injury
Heme-containing proteins (myoglobin, hemoglobin)
heme- containing proteins, bence jones proteins, gout… etc.
Clinical presentation of ATN
Generally nonspecific signs and symptoms of Acute Renal Failure
They can include
- Anorexia
- Nausea/Vomiting
- Delirium
- weakness/fatigue
- HTN
- Coma/ seizures.
Diagnostic evaluation of ATN
- Elevated BUN and Creatinine, Decreased GFT
- usually BUN:Cr rat.- <20:1
- Muddy brown sediment visible granular casts in Microscopic evaluation of Urinalysis
What electrolyte imbalances are often present with pts suffering from ATN
Hyperkalemia and Hyperphosphatemia
Urinary output of ATN
Variable
Renal absorption of sodium is often _______ . with ATN
impaired
- this results in and increased FEna - greater than or equal to 2%
increased sodium in urine
Tx of ATN
Remove the offending agent (if applicable)
Avoid volume overloading
Diuretics (if fluid overload)
Dialysis- may be included if life-threatening electrolyte abnormality.
Average maintenance phase of ATN is
1-3 wks
True or false - A nephrologists must be involved in all cases with ATN
True
What is Acute interstitial Nephritis
An inflammatory disorder of renal interstitium
What is the cause of Acute Iterstitial Nephritis in over 70% of cases
Drugs
Most common drugs that cause Acute Interstitial Nephritis
Penicillins, Cephalosporins, Sulfonamides, NSAID’s, PPIs, Rifampin, Phenytoin, and Allopurinol
Clinical presentations of Acute interstitial Nephritis
classic picture is that of a previously healthy pt developing suden renal dysfunction after starting a new medication (sometimes starting the new drug can cause a delay
Common Clinical presentation of Acute Interstitial Nephritsi
Fever- (80$)
Transient maculopapular rash(25-50%)
Flank pain d/t renal capsule distension
Myalgias and Arthralgias
Acute Interstitial Nephritis
Diagnostic EValuation
Elevated BUN and Creatinine
Decreased GFR
hematuria is common
Modest proteinuria
WBC’s present in urine in >95% of cases
WBC casts
CBC shows eosinophilia
True or false- renal imaging is helpful for Acute Interstitial Nephritis
False- not helpful
Renal Biopsy is or is not required for a definitirve diagnosis of Acute interstitial nephritis
Is =)
Treatment of Acute Interstitial Nephritis
Discontinue offending medication
Supportive care
1/3 pts require temporary dialysis
Corticosteroids
Most pts recover from acute interstitial Nephritis within?
a few weeks to months
Glomerulonephritis (GN) is comprised of what process
An inflammatory process involving primarily the glomerulus
what other structures can be effected by Glomerulonephritis
Renal vasculature
interstitium
tubular epithelium
Glomerulonephritis is relatively an uncommon cause of AKI corresponding to what percentage?
about 5%
What damage can occur due to Glomerular inflammation
Damage to the glomerular basement membrane or capillary endothelium
What is often the causation of the inflammatory process of Glomerulonephritis
Antigen-antibody complex formation and deposition
Where do complexes or antibodies become trapped to cause the inflammation during the filtration with GN
the glomerulus
what increases the risk / poorer prognosis with GN
The more glomeruli that are involved
Infection-related GN
Sequela of group A beta-hemolytic Strep or Staph Aureus infection
Clinical presentation of infection-related GN
Tea colored urine
Edema (common around mouth)
Oliguria
HTN
What titer may be elevated for weeks in Infection-related GN
Antistreptolysin O (ASO)
Most kids will recover spontaneously, or will not recover from Infection-related GN
recover spontaneously
What percentage of Adults never fully recover from Infection-Related GN
30-70% of affected adults
What is the other name for IgA Nephropathy
Berger’s Disease
Pathophys of IgA Nephropathy
Deposition of IgA immune complexes in the glomeruli, causing structural damage
What is the initial presentation of IgA Nephropathy
episode of hematuria
Hallmark of Burger’s Disase
2-6 days of Hematuria
Confirmation of IgA Nephropathy
Renal Biopsy
- IgA deposition on immunohistology
Tx of Burger’s
Teat the HTN with ACE or ARB
What percentage of Burger’s disease suffering pts will have recurrent episodes
50%
-typically this leads to progressive, chronic loss of renal function and CKD
What is HSP
Henoch-Schonlein Purpura
Hsp is not only kidney disease but…
An acute systemic immune-mediated small vessel vasculitis
What is the population that HSP effects mostly
Children less than 10 years of age
Clinical presentation and course of Henoch-Schonlein Purpura
Children present with hematuria, and large purple purpura on lower extremities
Arthralgias, abd pain, and proteinuria
Generally self-limited resolving in 94% of pts within 4 weeks
Membranoproliferative GN is due to
deposition of immune-complex and or complement factors
What are the effects of Membranoproliferative GN
Mesangial cell proliferation and capillary wall remodeling
Common population of Membranoproliferative GN
Children and young adults
Clinical presentation of Membranoproliferative GN
Most commonly presents as nephrotic syndrome
May present with recurrent gross hematuria
Diagnosis of Membranoproliferative GN requires what
Renal Biopsy
TX of Membranoproliferative GN
Corticosteroids and cyclophosphamide
if pts develop antibodies against the glomerular basement membrane (GBM) they have what disease
Anti-GBM Antibody Disease
because of tissue similarity in capillaries in the lung Anti-GBM antibodies may also do what
affect the Lungs and cause Hemorrhage
The anti-GBM antibody disease GN has also been known as what
Goodpasture’s syndrome
Pts with Anti-GBM antibody disease GN can present how
with glomerulonephritis alone or with glomerulonephritis and hemoptysis together
Diagnosis of anti-GBM GN
Made with anti-GBM antibodies testing
TX for Anti-GBM GN
Plasma exchange, chemotherapy drugs, steroids
Lupus Nephritis GN is secondary to what disease
Systemic Lupus Erythematosus (SLE)
what percentage of Lupus pts suffer from Lupus Nephritis GN
about 50%
What is the pathogenisis of Lupus Nephritis
Antinuclear antibodies (ANA) form immune complexes and cause inflammation and glomerular damage
Diagnostic Criteria of Lupus Nephritis
Lupus, plus one or more of the following
Persistent proteinuria
Cellular casts
RBCs and or WBCs consistently in urine
Indication of Renal biopsy is appropriate in all Lupus pts with evidence of nephritis
True
Tx of Lupus Nephritis depends on the severity of the disease but can include
High-dose corticosteroids which often are used to treat the autoimmune condition.
ACE or ARB should be started as well
Rapidly Progressing GN’s Clinical presentation
can be any of the glomerular conditions: not specific disease process.
What is the range that loss of renal function occurs in Rapidly Progressing GN
Days to weeks
Pts might have presentation of what in Rapidly progressing GN
Edema
Proteinuria
Hypertension
RBC casts
What is Characteristic of RPGN
Crescent Formations on Renal Biopsy
RPGN is represented by what percentage of GN
roughly 20 percent
what is the Diagnostic Evaluation for a Glomerulonephritis (GN)
- Serum Creatinine can rise over days to months
- UA showing hematuria and proteinuria
- UA microscopy will show cellular elements, such as RBCs, RBC casts and occasional WBCs
What are characteristic of GN
RBCs and RBC casts
Treatment of GN
Depends on underlying condition causing glomerulonephritis the treatment may consist of
- High dose steroids
- Cytotoxic Agents like cyclophosphamide
- Plamsa Exchange (Goodpasture’s )
True or False - Although complex Glomerulonephritis does not need a Nephrologist involved with every pt case immediately
False- because of the complexity Nephrologists should be involved immediately. PC PA’s should not attempt to manage these cases on their own .
