dm and nephropathy Flashcards
dm nephropathy
HTN from dm
Progressively increasing proteinuria
• Progressively deteriorating kidney function
• Classic histological features
why important
- Associated morbidity and mortality
- Health care burden
- Treatment options present
summarise the increased risk of CVS with kidney disease
o Risk double in dm
o Risk worse with CKD
o With both much higher risks
where can histological changes occur
glomerular
vascular
tubointerstitial
summarise the glomerular histological changes
Mesangial expansion
– Basement membrane thickening
– Glomerulosclerosis
epidemiology of nephropathy in dm
• Type 1 DM : 20-40% after 30-40 years probably same in T2 but: Age at development of disease - die first, however survival is increasing now = more nephropathy • Racial Factors • Age at presentation • Loss due to cardiovascular morbidity
clinical features of diabetic retinopathy
progressive proteinuria - screened for this, albumin and creatinine measured from 1st diagnosis - at first signs of proteinuria give ACEi
increased BP
deranged renal function
proteinuria levels
Normal Range <30mg/24hrs • Microalbuminuric Range 30 - 300mg/24hrs • Assymptomatic Range 300 - 3000mg/24hrs • Nephrotic Range >3000mg/24hr
how do you control nephropathy
hyperglycaemia control
bp control
inhibition of RAAS
stop smoking
summarise how BP control helps nephropathy
o As renal func worse with no treatment GFR fall
o As control BP – rate of fall of GFR changes (reduces)
o So tightly control BP minute get microa to reduce the rate of fall
summarise effect of inhibition of RAAS
o Captoprim – 1st ACEi – reduce risk of renal failure
Immediately things get worse then they get better eventually
Should not be used in renal artery stenosis
They prevent end stage renal failure in pts with new microalbuminuria
o ARB – block later in pathway – reduce incidence of renal failure
mechanism of how ACEi help renal function
- ANG2 – squeeze arteriole and maintain GFR
- ACEi – ACE fall – BP fall = reduction in albuminuria, GFR will also fall a bit and creatinine will rise a bit - fine
- If renal artery stensosis because of atheroma – drop in pressure – JGA = more renin= more ACE – squeeze arteriole tight – pressure high but flow poor because afferent blocked. This push out GFR. If give ACEi – pressure fall and so GFR fall a lot possibly to 0. If want to sacrifice kidney this is a way to do it – pressure can damage other kidney. Stop peeing if stenosis – ACE CI = creatinine rocket
- As long as pt doesn’t go into pul oedema – stop ACE – pressure rise – start peeing. So if pee before breathless fine
- Measure creatine before start, if shoot up then stop ACE
does nephropathy effect all pts
no - small number dont get it
implications of renal failure
electrolyte misbalance - hyperkalaemia = arrhythmias, hyponatraemia
acidosis
fluid retention
retention of waste - small molecules (urea, creatinine, urate), phosphate, middle molecules (peptides, B2-microalbumin)
secretory failure - erythropoietin, 1,25 vit D
anaemia exacerbates tiredness
renal bone disease - aches and pains, pruritis
symptoms of renal failure
tiredness, lethargy SOB, oedema pruritis nocturia cold twitching poor appetite nausea loss of/nasty taste weight loss
consequences if no renal replacement treatment
hyperkalaemia = arrhythmias, cardiac arrest pul oedema (most common presentation) nausea, vom malnutrition/cachexia fits increasing coma death
options for renal replacement
– not cure, replace 1 long term condition for another
o Dialysis – peritoneal (home) or haemodialysis (mainly hospital based - can be done at home)
o Transplantation
