7- Nephritic, Nephrotic, Diabetes, Glomerulus Path Flashcards
What is glomerulonephritis
Inflammation of glomeruli
What structures of glomerulus can be damaged (4)
Capillary endothelium
Glomerular basement membrane
Mesangial cells
Podocytes
What is normally involved with glomerulonephritis
Over response from immune system
Characteristics of Nephrotic
Podocyte damage leading to glomerular charge barrier disruption so doesn’t repel proteins
Proteinuria
Oedema
Why oedema in nephrotic injury
Low albumin in plasma so less oncotic pull so fluid pools in tissue
Characteristics of Nephritic injury
Inflammation disrupting glomerular basement membrane
Haematuria
Coca cola urine
What is the triad of Nephrotic syndrome
Proteinuria >350mg/mmol
Hypoalbuminaemia
Oedema
What usually accompanies Nephrotic syndrome
High cholesterol as liver tries to compensate and make more albumin and a byproduct is cholesterol.
Other features of Nephrotic syndrome
Normal BP
Creatinine may be normal
Primary causes of Nephrotic
Minimal change disease- podocyte damage
Membranous glomerulonephritis
Focal segmental glomerulosclerosis
Secondary causes of Nephrotic
Diabetes
SLE
Amyloid
Management of Nephrotic syndrome
Diuretics- oedema
ACE-I- anti-proteinuric
Statins- Hypercholesterolaemia
Treat underlying steroid- MCD
Triad of Nephritic disease
Haematuria
Reduced GFR
Hypertension
Other features of Nephritic disease
Some proteinuria
Disruption of endothelium = inflammatory response and damage to glomerulus
Acute or rapid onset
Rapid progressive
Common causes of Nephritic
Goodpastures (Anti GMB)
Rapidly progressive GN
IgA Nephropathy (Bergers))
Post Streptococcal GN
Management
BP control - ACE-I, salt restriction
Diuretics for oedema- if adequate renal function
Immunosuppressants - disease specific- 90% remission. 1-2 weeks from start of treatment
Stop smoking- manage CV risk
Dialysis- if acute onset- short term
Commonest cause of end stage renal disease
Diabetic nephropathy
Is it a glomerulopathy or glomerulonephritis
Glomerulopathy- physical changes not due to inflammation
Pathological changes in diabetic nephropathy
Hyperfiltration Capillary hypertension Glomerular basement membrane thickening Mesangial expansion Podocyte injury Glomerular sclerosis/atherosclerosis
Why does hyperfiltration and hypertrophy occur with diabetes
Hyperglycemia causes high blood sugar which causes increase in GFR
How is glucose taken up in Kidneys
SGLT2 (Na and Glucose) Powered by Na/K ATPase
coupled with Na
Whats the max glucose that the kidneys can reuptake
10mmol then glucose in urine
What leads to RAAS activation
Low delivery of NaCl to macula densa
Lots more Na absorbed so macula densa sense low Na and activate RAAS. Vasodilation of afferent and vasoconstriction efferent = hyperfiltration
Stages
Hyperfiltration and hypertrophy- GFR increased
Latent stage- Normal albumin, GBM thickening
Microalbuminuria- Mesangial expansion, GBM thickening, podocyte change, GFR normal
Overt proteinuria- diffuse histo changes, systemic HTN, decreased GFR
ESRD
What is microalbuminuria
First clinical sign
GBM thickening and mesangial expansion
Potentially reversible
Dipstick test
Over proteinuria
GFR normal initially
Mesangial expansion and sclerosis- reduced SA for filtration
Proteinuria >300mg/day- oedema
Worsening systemic hypertension
Microvascular changes- hyalinosis of arterioles = tissue ischemia
Not reversible
What is the average decline in GFR for those with overt proteinuria
12mls/min/year
ESRD- 3-7 years
Diabetic nephropathy risk factors
Genetics, race, hypertension, hyperglycemia, age, duration of diabetes, smoking
Prevention of diabetic nephropathy
Tight glucose control- can reduce microalbuminuria
Tight blood pressure control
How would SGLT 2 inhibitors help
Prevent glucose reabsorbed and also Na = RAAS not activated = no hyperfiltration
Management of microalbuminuria and proteinuria
Inhibition of RAAS, tight BP control, CV risk management (exercise, smoking, diet), moderate protein intake
How does RAAS blockade help
Reduce glomerular hyperfiltration
Efferent more than afferent
Antiproteinuric effect more than BP reduction as it decreases the pressure forcing proteins through.
Limited by hyperkalemia in CKD as kidney no longer functioning well = reduced filtration
