Nephrotic Syndrome Flashcards
Nephrotic syndrome: what does PEAL stand for?
Proteinuria (>=3.5g/days)
Edema (Peripheral)
hypoAlbuminemia (<25 g/L)
hyperLipidemia
Define nephrotic syndrome
it’s a clinical syndrome where the glomerulus has increased permeability due to damage to the filtration barrier (mainly podocyte)
Tell me about the epi of nephrotic syndrome
Adults vs children and type of nephrotic syndrome
Most common in adults in their 40s
- specifically diabetic nephropathy
Most common type in children is minimal change disease ➔ males > females (2:1) untile adolescence
what are the three histology buckets of nephrotic syndrome?
- minimal change disease
- focal segmental glomerulosclerosis
- membranous nephropathy
What are some etiologies for nephrotic syndrome?
- diabetes
- pre-eclampsia in the 3rd trimester of pregnancy
- lupus
- multiple myeloma
- medications (NSAIDs)
- genetic mutations in podocyte proteins
why is there hypo-albuminemia in nephrotic syndrome?
what happens to calcium?
- increased permeability in the filtration barrier and loss of glomerular membrane negative charge
- albumin and other proteins can cross (albumin makes up the majority of protein content in serum)
- more albumin is excreted
*may result in hypocalcemia (total calcium, not ionized) bc most calcium is albumin bound
what is the underfill hypothesis for nephrotic syndrome?
Water is following solutes (albumin) in the urine, and body compensates by releasing ADH and pulls water from urine back → now low/diluted solute in vasculature → fluid shifts out from vasculature into third space
what s/s does the underfill hypothesis in nephrotic syndrome talk about?
all signs of fluid overload ➔ edema
pitting
dependant edema
anasarca
periorbital edema
JVP
sacral edema
why do nephrotic syndrome have hyperlipidemia?
low oncotic pressure in the vasculature (from the albumin loss) triggers liver synthesis activity to compensates ➔ increased lipoprotein synthesis ➔ hyperlipidemia
why do nephrotic syndrome have increased VTE risk?
loss of anticoagulant proteins like antithrombin III, plasminogen, and protein C and S in the urine ➔ body is in a hypercoaguable state
why do nephrotic syndrome have increased infection risk?
loss of immunoglobulins (IgG) in the urine ➔ less available to mount an immune response
what is the overfill hypothesis?
- Damage to glomeruli
- Aberrant protein filtration → [plasminogen] in the tubular fluid
- Activated into plasmin which activates sodium channels for Na+ reabsorption
- Increases salt and water retention in blood → increased BP in veins
- Hydrostatic pressure in capillaries > hydrostatic pressure in interstitial space 6. Fluid shift into interstitial space → edema
what is the key hormone for the underfill hypothesis and the key enzyme for the overfill hypothesis?
underfill: increased ADH secretion acting on tubules resulting in water retention
overfill: plasminogen activated into plasmin in the tubules resulting in salt and water retention from Na+ channel expression/activation
what are some fluid status s/s you’d see in both nephrotic and nephritic syndrome?
- Peripheral edema (edema in the legs first and then edema traveling upwards because of gravity; JVP is the exception since it is right next to the heart so it will be elevated)
- Sacral edema
- JVP
- Periorbital edema
- Anasarca
besides fluid status s/s, what else may you see in nephrotic syndrome pts?
- s/s of hyperlipidemia - xanthomas
- s/s of VTEs - calf pain, dyspnea, chest pain
- frothy urine
- s/s of underlying cause (i.e., DM, lupus - joint pains)
