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
aims of renal replacement treatment
maintain QOL improve symptoms correct electrolyte and acid-base status remove waste products restore fluid balance
when to start dialysis
o Don’t want to wait until people come in in an emergency = worse outcomes
conversation started with eGFR <20ml/min
education - risks of renal failure, types of RRT
establish access to chosen RRT - fistua for HD, catheter for PD, transplant assessment
o <10 – do benefits outweigh risk
o <6 and no reversible features -high risk sudden death
o Life threatening complications
benefits of dialysis
improve uraemic symptoms -tiredness, nausea, pruritis
correct fluid balance - less SOB and oedema
avoid life threatening events - severe acidosis, severe hyperkalaemia, pul oedema resistant to diuretics
risks of dialysis
dialysis related complications - infection, access related, in HD: hypotension, arrhythmias
effect work, family life and travel - QOL
doesnt help:
getting old
lack of erythropoietin - anaemia
lack of vit D - hyperparathyroidism, renal bone disease
comorbidities - SLE, dm, vascular disease
summarise haemodynamic dialysis (HD)
o Blood from fistula in wrist through dialyser (rods) and bathed by dialysate. Machine makes the dialysate by reverse osmosis water which is mixed with concentrate. Dialysate exposed to blood then goes down drain
o Hospital – 3x wk but only 4hr but 6hr recovery and transport, and hanging around waiting
o Vascular access – catheter into jug vein or arteriovenous fistula
o QOL – doesn’t invade home, limit work and travel so lose independence
summarise peritoneal dialysis
o Fluid into abdo and it drains out – uses peritoneal lining
o Slower and more gentle – done at home
o Manual bags or cycling machine – attached to person at night, useful for people who work
o Home based
o Daily and continuous
o Less haemodynamic stress
o Limited by access to peritoneum and ability to do technique – have technicians come in -less expensive than HD
o Avoids swings of HD
o Less dietary and fluid restrictions
how does renal failure affect the brain
• Neuropathy and fits because of uraemic toxins – damage nerve endings = change in brain activity – cognitive problems main issue. Reversed by dialysis. Problem with vascular dementia
