Flashcards in Glomerular Pathology and Clinical Presentations of Kidney Disease Deck (52)
What are the 4 renal cortical 'compartments'?
What are the 3 parts of the filtering mechanism?
(Pathology can occur in any one of these)
What are the effects if the filter gets blocked?
What is nephrotic syndrome?
Loss of significant amounts of protein
Decreased oncotic pressure - oedema
What is nephritic syndrome?
Blockage of the glomerulus
Decreased GFR - AKI
Go into renal failure
Often haematuria and hypertension
If a patient presents with nephrotic syndrome, what is the likely site of injury?
What are the common primary causes of nephrotic syndrome?
Minimal change glomerulonephritis
Focal segmental glomerulosclerosis (FSGS)
What are the common secondary causes of nephrotic syndrome?
Describe minimal change glomerulonephritis
Incidence reduces with increasing age
Heavy proteinuria/nephrotic syndrome
Responds to steroids
Usually no progression to renal failure
Glomerulus looks normal under a microscope - need electron
An unknown circulating factor damages the podocytes
Less responsive to steroids
Circulating factor damages podocytes
Progressive to renal failure - dialysis needed
Describe membranous glomerulonephritis
Commonest cause of nephrotic syndrome in adults
Rule of thirds:
1/3 get better
1/3 stay the same
1/3 go onto end stage renal failure
Immune complex deposited - antigen attaches to podocytes then lots of IgG binds
Probably autoimmune but may be secondary
Describe the long term effects of diabetes mellitus on the kidneys
Kidneys get more and more leaky - progressive renal failure
Mesangial sclerosis - nodules that are easy to pick up histologically
Basement membrane thickening
Describe IgA nephropathy
Can occur at any age
Classically presents with haematuria
Relationship with mucosal infections
Variable histological features and course
A significant proportion progress to renal failure
No effective treatment
What are the 2 extremes of hereditary nephropathies?
Thin GBM nephropathy and benign familial nephropathy
Describe thin GBM nephropathy
Describe Alport syndrome
Abnormal collage IV
Associated with deafness
Abnormal appearing GBM
Progresses to renal failure
'Basket weaving' abnormally split
Describe Goodpasture syndrome
Anti GBM disease
Relatively uncommon but clinically important
Rapidly progressive - acute onset of severe nephritic syndrome
Difficult to reverse
Association with pulmonary haemorrhage (high BP)
Autoantibody to collage IV in BM
What is the treatment for Goodpasture syndrome?
Plasmaphoresis (give donor plasma to get rid of the autoantibody)
Group of systemic disorders
No immune complex or antibody deposition
Association with anti-neutrophil cytoplasmic antibody (ANCA)
Treatable if caught early
Are kidney diseases painful?
How do many kidney diseases present?
What is acidotic breathing?
Trying to compensate for acidosis by blowing off more CO2
If patients say they are tired all the time, what investigations should be done?
Kidney function tests
What is uraemic syndrome?
Acute kidney injury
Low platelet count
How much extra water do you have to retain before getting peripheral oedema?
What are some consequences of tubular dysfunction?
Impaired concentrating ability - increased frequency and nocturia
Hormonal complications - metabolic bone disease because cannot activates vit D, anaemia due to lack of EPO and hypertension due to increased renin
Why do we usually urinate less frequently at night?
Urine is diurnally regulated
Concentrated more at night
Why might glycosuria present with tubular dysfunction?
Tubular disease causes a lower tubular threshold for glucose
Therefore may excrete glucose even when plasma glucose levels are normal
Who should be screened for kidney disease?
Urinary tract obstruction
Systemic disease (myeloma, lupus etc)