Vascular and glomerular disorders of kidney Flashcards
Describe the emergency mechanism of the kidneys to sustained hypotension.
Angiotensin II and III cause vasoconstriction of afferent and efferent arterioles in outer cortical nephrons to redirect bloodflow toward the medulla
Also cause prostaglandin synthesis by renal medullary interstitial cells, which counters the vasoconstrictive effects to cause vasodilation of the juxamedullary nephron afferent arterioles
This mechanism promotes blood flow to the sensitive renal medulla, and preserves the juxtamedullary nephrons which have longer LOH and better ability to concentrate urine, hence better ability to boost blood pressure
How does the rearrangement of the renal vasculature predispose to hypoxic damage?
- end arterial design means blockage of one artery can affect large portion of parenchyma even if only temporarily occluded
- large volume of blood flows through daily, increasing change of thrombi lodge
- arteriolar tone constantly changing
- blood flow is slow
What are the three mechanisms of the no-reflow phenomenon? How long must hypoxia last before this could occur?
Hypoxia of 2 + h may result in no or patchy reflow due to
- intravascular erythrocyte swelling following imbibation of plasma water
- hypoxic swelling of tubular epithelial cells, endothelial cells of glomeruli, peritubular capillaries, vasa recta
List 5 diseases that are caused or contributed to by renal hypoxia
- Renal infarction
- Renal cortical necrosis
- Ischaemic/hypoxic tubular degeneration or necrosis
- Renal medullary necrosis/papillary necrosis
- Hydronephrosis
What shape of infarct is likely to be caused by arcuate arterial occlusion? What about interlobular?
Arcuate = wedge of cortex + some medulla Interlobular = Wedge of cortex
What are the two major mechanisms for renal cortical necrosis? How is it different to renal infarct?
Either due to widespread microthrombosis and haemorrhage (DIC) due to endotoxin of bacteria
Or >2h renal hypoxia
Is thousands of tiny infarcts in the renal cortex area, rather than one large one.
Which two cell types are most susceptible in acute hypoxic nephrosis? Which part of the kidney is grossly damaged?
PCT and thick ascending LOH
Cortex is obviously damaged - may be streaky, have visible haemorrhages
What are the three most common mechanisms for renal medullary/papillary necrosis in domestic animals?
- Prolonged renal hypoperfusion/hypotension
- NSAID use
- Increased pressure in renal pelvis or other mechanism compressing vasa recta externally
What are three mechanisms for vasa recta compression that can lead to papillary necrosis?
- Obstruction of urine outflow increasing pressure in renal pelvis/calyces
- Interstitial oedema or fibrosis of inner medulla/papilla
- Amyloid deposition in the medulla
Papillary necrosis may be an incidental finding. What are three other potential consequences of renal papillary necrosis?
- Sloughing of dead tissue into the lumen which can obstruct urinary system downstream or act as nidus for calculi formation/mineralisation
- Loss of ability to concentrate urine due to loss of collecting ducts, leading to polyuria
- Inner medullary scarring can cause nephron blockage, leading to cortical scarring and eventually renal failure
Renal hydronephrosis is most commonly due to acquired obstructive lesions. List 4.
Prostatomegaly
Urinary calculi
Haemorrhagic cystitis
Caudal displacement of urinary bladder due to perineal hernia
Which two major mechanisms are at play in hydronephrosis to cause renal parenchymal damage?
- Pressure atrophy of the tubular cells
2. Compression of the vasa recta to cause infarction of renal papillary tissue
Beyond what time point can complete function of a hydronephrotic kidney not return?
> 1 - 3 weeks
What secondary disease does hydronephrosis predipose to?
Due to the urinary stasis - ascending bacterial infection and secondary pyelonephritis
Which two disease process are usually the cause of ‘nephrotic syndrome’?
Chronic glomerulonephritis
Glomerular amyloidosis
