Renal Diseases Flashcards
What is filtered through the glomerular capillary walls?
plasma
What does ultrafiltrate contain?
- Contains electrolytes, glucose, phosphate, urea, creatinine, peptides, low molecular weight proteins
- Do not contain proteins having a molecular weight of ≥68kd e.g. albumin and globulins
- cell free
What happens to filtrate?
is collected in Bowman’s space and enters the tubules, where its composition is modified by tightly regulated secretion and absorption of solute and fluid, until it leaves the kidney as urine.
2 factors restricting filtration of macromolecules?
- Size selective barrier of the GBM
- Strong negative ionic charges (endothelial cell, basement membrane, and epithelial cell)
- Blood proteins are negatively charged, and are repelled by the negatively charged sites in the glomerular capillary wall, thus restricting filtration
What is glomerular blood hydrostatic pressure?
it pushes water and solutes in blood plasma through the glomerular filter promoting filtration
- modified by the tone of the afferent and efferent arterioles
What is glomerular capillary oncotic pressure?
blood flowing into the glomerulus contains plasma proteins and blood cells that displace water content of the blood
- as water outside the capillaries seeks to equalize with the water inside the capillaries through osmosis
Filtration is modified by?
- the rate of glomerular plasma flow
- the hydrostatic pressure within Bowman’s space
- the permeability of the glomerular capillary wall
Classification of causes of nephrotic syndrome?
- primary
- secondary
- idiopathic
Primary causes of NS?
- Minimal change disease (the most common)
- Focal segmental glomerulosclerosis
- Membranoproliferative glomerulonephritis
- C3 glomerulopathy
- Membranous nephropathy
Secondary causes of NS?
- Vasculitides (SLE, HSP)
- malignancy [lymphoma and leukemia]
- infections [hepatitis, HIV, and malaria]
- Hereditary mutations - protein components of the glomerular filtration apparatus
Idiopathic causes of NS?
Henoch-Schönlein Purpura
Pathophysiology of NS?
- Increased permeability of the glomerular capillary wall
- Massive proteinuria and hypoalbuminemia
Biopsy results in NS?
extensive effacement of podocyte foot processes
Pathogenesis of oedema in nephrotic syndrome?
- urinary protein loss
- hypoalbuminemia
- decrease in plasma oncotic pressure
- transudation of fluid from the intravascular compartment
- decrease in intravascular volume (stimulating antidiuretic hormone release causing the leading to oedema)
- decrease in renal perfusion pressure
- activation of renin-angiotensin-aldosterone system
- stimulation of tubular reabsorption of sodium
- OEDEMA
Role of antidiuretic hormone in pathogenesis of oedema in NS?
causes the kidneys to release less water, decreasing the amount of urine produced
Role of renin-angiotensin-aldosterone system in pathogenesis of oedema in NS?
- increasing sodium reabsorption
- increasing water reabsorption
- increasing vascular tone (degree to which blood vessels narrow or constrict)
What is the underfill hypothesis?
- loss of protein
- reduced intravascular volume
- increased secretion of vasopressin and atrial natriuretic factor - along with aldosterone
- result in increased sodium and water retention by the tubules
Note: Sodium and water retention therefore occur as a consequence of intravascular volume depletion
What is the overfill hypothesis in NS?
primary sodium retention, with subsequent volume expansion and leakage of excess fluid into the interstitium