Acute Kidney Injury Flashcards
Is GN a lifestyle disease?
No. Patients are usually young and healthy.
What is the treatment for GN and what are the side effects?
Immunosuppressants. Highly toxic. Treatments can be long.
What are the most common types of GN?
- diabetic nephropathy
- IgA nephropathy
- minimal change disease
- FSGS
What percentage of ESRD is caused by GN?
Around 25%.
Outline the progression of GN taxonomy.
- started based on clinical features
- then categorized based on histologic patterns
- then categorized based on etiology
What are the two broad groups of GN?
Nephrotic syndrome - due to isolated injury to the filtration barrier
Nephritic syndrome - due to diffuse inflammation in the glomerulus
Name four main features of nephrotic syndrome.
- proteinuria (>3.5g/d)
- hypoalbuminemia
- hypercholesterolemia
- peripheral edema
- decreased renal function
Name the 7 main complications of nephrotic syndrome.
Hypoalbuminemia
- due to urinary loss and decreased production
Peripheral edema
- due to low oncotic pressure and some filtered substances trigger Na reabsorption
Hypercholesterolemia
- low oncotic pressure induces hepatic production
Hypercoagulability and venous thromboembolism
- due to urinary losses of anticoagulant proteins and increased production of procoagulant proteins
Infection
- due to urinary losses of immunoglobulins
AKI
- due to heavy proteinuria, fluid shifts causing intravascular volume depletion and interstitial edema in the kidney
Lipiduria
- due to high amount getting into urine
- you get fatty casts
What are the three most common causes of idiopathic nephrotic syndrome?
Minimal change disease, focal segmented glomerulosclerosis (FSGS), and membrane nephropathy (MN)
Describe minimal change disease and how it normally presents.
Glomerulus looks normal on LM, but EM reveals diffuse foot process effacement.
Tends to present with sudden onset peripheral edema over several weeks.
In what populations do you find minimal change disease?
Bimodal distribution. You find it in young and older adults (>60 years).
How is minimal change disease typically treated?
Steroids. 75% respond rapidly to treatment with steroids. Good renal prognosis in this case.
Do all types of GN require a kidney biopsy for diagnosis?
Yes
how do you think this works?
Just like this
I think you are silly
but why
What does FSGS do to the glomerulus?
Focal = less than 50% of glomeruli Segmental = only portion of each glomerulus is involved. Sclerosis = scarring
So, scarring on portions of less than 50% of the glomeruli
Is FSGS more common in child or adulthood?
Adulthood
Does MCD or FSGS have a worse prognosis?
FSGS. Doesn’t respond as well to steroids and has a higher progression to ESRD (50% at 5 years)
What is the most common cause of nephrotic syndrome in caucasians and in what ages is it most common?
Membranous nephropathy. Most common in those >40 years.
80% of MN patients present with ______________
High grade proteinuria. (risk of VTE is quite high)
Describe how membranous nephropathy works and what is the most common target antigen.
It’s an organ specific autoimmune disease with Ab’s targeting antigens on the podocytes.
Activates complement and induces GBM/podocyte damage.
70% may be the phospholipase A2 receptor.
Describe your workup for nephrotic syndrome including quantifying the severity of the disease and ruling out common secondary causes.
Quantify: - creatinine and eGFR - albumin, cholesterol profile - 24 hour urine test for protein, ACR and PCR - urinalysis and microscopy Rule out secondary: - Infection: HIV, HBV, HCV serology - Hematologic malignancy: SPEP, UPEP - Autoimmune disease: ANA, C3, C4, ESR - Fasting blood sugar
BIOPSY to do next tests.
What does nephritic syndrome cause?
Influx of inflammatory cells in the glomerulus leads to:
- damage to filtration barrier causing proteinuria, but less severe than nephrotic
- full breaks in barrier allows RBCs into urine
- reduced kidney function in earlier course of disease
- salt retention and hypertension with more moderate edema
What are the key findings that point to nephritic?
Hematuria and active urine (dysmorphic RBC and RBC casts)
What is rapidly progressing GN (RPGN)?
Nephritic syndrome with rapidly declining renal functions over several weeks.
What is your general approach to nephritic syndrome?
Look at pattern of immunoglobulin staining on biopsy:
Pauci-immune (no immunoglobulin) - ANCA vasculitis Linear staining - Anti-GBM Ab disease - Goodpasture's disease Granular (immune-complex) - lupus, autoimmune disease, IgA nephropathy etc.
What is ANCA and what is the average age of onset?
“Anti-Neutrophil Cytoplasmic Antibodies”
- Ab targeting proteins from the cytoplasm of neutrophils
- Multi organ disease with severe presentation with rapid progression to renal failure
- average age is 55-70 years
What are the two target antigens we can easily test for regarding ANCA?
cytoplasmic-ANCA = proteinase 3 perinuclear-ANCA = myeloperoxidase (MPO)
Do you need ANCA to have ANCA vasculitis?
No. 10% of ANCA vasculitis patients are ANCA negative.
What is ANCA vasculitis and how severe is it?
Vessel inflammation typically due to ANCA
- used to be 80-90% mortality before immunosuppressives
- current mortality is about 20-25%
- death is usually due to immunosuppression complications
What are some body systems affected by ANCA vasculitis?
Nervous system, eyes, skin/joints, ENT, lungs, general symptoms, heart, kidney
How does ANCA vasculitis present histologically in the glomerulus?
Fibrinoid necrosis (massive breaks in GBM) and cellular crescents (hypercellularity in Bowman’s space compresses glomerulus)
What is lupus nephritis?
Granular nephritic syndrome. Auto-immune disease affecting any organ in the body.
What is mortality of lupus nephritis (SLE) and does it depend on race?
2x that of general population and risk is higher in blacks, hispanics and asians.
Risk of dying is 3x higher in SLE with nephritis vs without nephritis.
