Anatomy
Where do the kidneys lie in the abdomen?
-retroperitoneally
-extend from T12-L3
Which cells are responsible for the production of renin and EPO?
Extraglomerular mesangial cells within the juxtaglomerular apparatus
What is glomerular nephritis? And what is it caused by?
Inflammation/damage to the glomeruli/ filtration units of the kidney. Caused by:
Immune system dysfunction
Infections
Underlying medical conditions
What is nephrotic syndrome?
Loss of proteins e.g albumin primarily in the urine
Where do the renal arteries arise from?
Abdominal aorta
Name the 4 layers that encase the kidneys- from deep to superficial
- Perirenal fat
- Renal fascia
- Pararenal fat
What happens when there is low blood pressure in the body?
Renin released by JG cells. Renin catalyses the breakdown of angiotensinogen in the liver to angiotensin 1. ACE in lungs catalyses the conversion of angiotensin 1 to 2- net effect increases BP
Aldesterone release, acts on distal tubule, increases reabsorption of Na+/h20, vasoconstriction in arteriole, ADH released- increases H20 permeability/ reabsorption.
What are the clinical manifestations?
Hematuria (blood in urine), proteinuria, hypertension, decreased GFR, CKD, end-stage renal failure
Tests for nephrotic syndrome?
Urine dipstick
total protein to creatinine ratio
albumin to creatinine ratio
24 hour protein collection
Which tissue does the nephron derive from?
Metanephrous tissue bifurcates into the nephron
Name the full arterial supply chain of the kidneys?
From entering the kidneys to the glomerulus
-5 segemental arteries
-interlobar arteries
-arcuate arteries
-interlobular arteries- afferent arterioles- glomerulus
What is the countercurrent multiplier system and where is it located?
Location: loop of henle- ascending and descending limbs.
Both limbs have varying permeability to h20, creates an osmotic gradient in the renal medulla
What are the 5 steps in the process of glomerular nephritis?
Immune system activation: exacerbated, triggered by infections, autoimmune diseases, exposure to antigens. Immune system recognises the glomerular basement membrane as altered/changes mounts an immune attack
Immune complex deposition: complement activation, immune cascade response. Neutrophils/macrophages attracted to site- exacerbate damage and inflammation
Increased permeability; inflammation leads to increased permeability of glomerular capillaries. Larger molecules e.g protein passes through into urine- proteinuria
Alteration of the glomerular filtration barrier: glomerular basement membrane and podocytes maintain the barrier. Inflammation/immune complex deposition damages it- barrier more porous allows escape of RBC and proteins.
Scarring/ fibrosis: deposition of collagen and fibrosis within glomeruli- scarring can impair kidney’s ability to filter blood- decreased kidney function
Why might nephrotic syndrome cause secondary hypertension?
RAAS system may be activated because of low BP as protein is lost in urine- Na+/h20 retention/reabsorption, leads to hypertension
Where do the collecting ducts derive from?
uritary bud
(which is the budding of the mesonephric tissue which goes into the metanephric tissue, bifurcates and forms the major calyx's- further divisions (12-15) form the collecting ducts
Where does the lymphatic drainage of the kidneys drain into?
Para-aortic lymph nodes
What role do the kidneys have in the activation of Vitamin D?
Vitamin D3 cholecalciferol produced by sunlight on skin —-- liver converts Vit D3 into calcidiol—-- proximal convoluted tubule of kidney converts to calcitriol (active form)
Why is there a high risk of thrombosis in nephrotic syndrome?
protein antithrombin III lost in the blood due to podocyte (barrier) damage leads to hypercoagulative state- the renal vein will be poor in antithrombin III- high risk DVT/PE
Why does damage to the renal arteries more likely to be serious/severe?
- they are end arteries, trauma in one branch leads to ischemia and necrosis of renal paranchyma supplied by the vessel