Chronic Kidney Disease Flashcards
what is orthostatic proteinuria
benign condition, high urinary protein excretion during the day associated with activity and upright posture
due to compression of LRV between aorta and SMA
what causes proteinuria
CKD after physical exercse fever pregnancy UTI nephrotic syndrome
how do you measure 24h urinary protein excretion and what does it show?
spot test for protein:creatinine ratio, shows rate of progression of kidney disease
how do you measure albumin:creatinine ratio and what else is measured alongside?
creatinine clearance
24hour urine collection
albumin is most common protein in urine
why is proteinuria considered pathological?
bc LMW proteins are normally filtered and reabsorbed by glomeruli
= high glomerular permeability
30-300mg albuminuria is pathological
what does azotaemia mean
elevation of nitrogenous metabolic waste in blood due to failure of clearance in the kidneys
what is uraemia
clinical syndrome resulting from failing kidneys and progressive azotaemia
what parts of kidney absorb what?
REFER TO CASE notes
what is CKD?
reduction in kidney function for > 3 months
eGFR of <60 on 2 seperate occasions, with 90 days between them both
evidence of kidney damage in urine, biopsy or renal tract
what direct causes are there for kidney disease?
diabetes hypertension uncontrolled glomerulonephritis polycystic kidney disease medications such as NSAID's, proton pumps and lithium UTIs auto immune disease
what are other RF for CKD?
older age, smoking, family history, low birth weight, reduced kidney mass
how does CKD present?
usually asymptomatic
or pruritus, loss of appetite, nausea, oedema, muscle cramps, peripheral neuropathy
what is the eGFR
capillaries have a high UF coefficient
pressure of blood through the glomerulus is the hydrostatic pressure
acting oppositely is the negative oncotic pressure: keeps fluid not leaving circulation
capillaries allow fluid to leak out through fenestrations = gfr
what functions does the kidney have?
- ultrafiltration/reabsorptive functions
-urine dilution
excretory functions of H+, K+, creatinine - activation of vitamin D
- renin production
-EPO production
what investigations would you do for CKD?
- eGFR (creatinine based estimate)
- ACR
- urine dip for haematuria
- renal USS
- blood tests (mentioned later)
what does a high blood creatinine mean?
poor clearance of creatinine by kidneys (this is a product of wear and tear of muscles)
when do you refer to renal specialists?
eGFR <30 urgent
30-59 routine referral if other signs eg ACR, haematuria, fall in GFR > 5ml in 1 year
immediate: malignant hypertension, hyperkalemia
urgent: proteinuria with oedema and low serum albumin
routine referral for proteinuria and urine PCR/ACR, haematuria
what blood tests would you do for CKD?
- FBC for Hb, WCC (immunosuppressed)
- calcium and phosphate
- HbA1c
- PTH can cause itch, hypercalcaemia
- immunosuppression level
- sodium bicarbonate: low indicates metabolic acidosis
- serum potassium bc CKD and ACE-I = hyperkalaemia
how do you stage CKD?
G score: based on eGFR 1 >90 2: 60-98 3a 45-59 3b 30-44 4: 15-29 5: <15
A score is based on ACR ratio
A1: <3
2: 3-30
3: >30
what are the complications of CKD?
anaemia renal bone disease CV disease peripheral neuropathy dialysis related problems
what is the management of CKD initially?
- slow progression, reduce risk of complications
- hence optimise hypertensive control and optimise diabetic control
- treat glomerulonephritis
- lifestyle changes
- low phosphate,
- atorvastatin 20mg
how to treat complications of CKD?
- oral sodium bicarbonate to treat MA
- iron supplementation and EPO to treat anaemia (may need IV bc renal patients may not absorb it properly)
- vit D to treat renal bone disease
- RRT if ESRD
how do you treat hypertension in CKD?
- ACE-I
- offered to all patients with comorbidities and ACR>30
- everyone with ACR>70
why do you get anaemia in CKD?
- kidney cells produce EPO so damage to them = reduced RBC
- IV iron, then offer EPO replacement
what is renal bone disease?
CKD mineral and bone disorder
osteomalcia, osteoporosis and osteosclerosis
what is the pathophysiology of RBD?
high serum phosphate
low active vitamin D bc kidney is meant to do this
vit D important in calcium absorption
PT glands react to low calcium and high phosphate = excrete PTH to remove phosphate
= increased osteoclast activity
= osteomalacia occurs due to increased turnover of bones without adequate calcium supply
= osteoscleorisis bc new tissue is created but not mineralised due to low calcium
how do you manage RBD?
alfacalcidol and calcitriol = active forms of vitamin D
low phosphate diet
bisphosphonates can be used to treat osteoporosis
what are the indications of renal failure?
- increasing acidosis
- increasing potassium urea and creatinine
- partial respiratory compensation
- renal failure is <15ml / min
what are the indications for dialysis?
pH <7.25 K+ >7 fluid overload creatinine >400 toxins SLIME uraemic pericarditis
haemodialysis?
filtration of blood through dialsysi machine
AV fistula created / use neck for IV line
blood passes through dialyser
fluid restriction and diet changes
what are the disadvantages of haemodialysis?
- infection, IE, stenosis at site, air embolus etc
- CI: low BP, dementia, severe HF, bleeding disorders
what is peritoneal dialysis?
- dialysis solution injected into abdominal cavity through permanent catheter
-draws waste products from blood
leave to dwell: exchange
what are the disadvantages of having peritoneal dialysis?
- constipation
- peritonitis, infection, catheter blockage
- fluid retention
- hernias
what are the contraindications of peritoneal dialysis?
- IBD, diverticulitis, abdominal abcess, pregnancy, hernias, obesity, blindness
what are the 2 types of peritoneal dialysis?
CAPD: exchange is 30 mins, dwell time is 4-8 hours
APD: dialysis machine fills and drains abdomen while patient is sleeping, 3-5 exchanges over 8 hours
how does a kidnet transplant work?
donor is transplanted into groin, renal vessels from donor connected to iliac vessels of recipient
- ureter and recipients bladder joined together
what medications do you have to take after transplantation?
cyclosporin or tacrolimus which act on t-lymphocytes and puts them to “sleep”
MMF or azathioprine
= risk of infection
what are the complications of a renal transplant?
infections: UTI and chest most common, cholecystitis etc all lifethreatening
- malignancy of kidney
what are clinical features of a failing renal transplant?
anaemic, pale, skin lesions
pulm oedema, tachypnoeic due to MA, pleural effusion
hypertension, pericardial rub
ascites
neuro: restless leg syndrome, uraemic flapping tremor, myoclonic jerks
what is the relationship between ACEI-/ARBs and CKD?
= renoprotective in CKD, including diabetics
AVOID IN AKI
ARBs reduce proteinuria
contra indicated in pregnancy
why are ACE-I contraindicated in AKI?
- angiotensin 2 inhibits efferent arteriole
but in AKI, body wants to maintain the pressure and vasoconstricts it
hence if patient is on ACE-I it cannot do this
what drugs should you avoid in renal failure?
- antibiotics
- NSAIDs
- lithium
- metformin
what is the pathophysiology of diabetic nephropathy
hyperglycaemia results in constant activation of renin, as does poor blood flow to kidney (due to hypertension etc)
efferent arteriole is vasoconstricted so increase in pressure
barotrauma = affects mesangial cells = expansion = leaky capillaries
what are the clinical findings of diabetic nephropathy
initially, increased eGFR
detectable proteinuria
microhaematuria
eventually low eGFR and decreased urine output
how do you treat diabetic nephropathy
control BP
ACE-I and diabetic meds prevent constant activation of RAAS
what is EPO
growth factor stimulating production of RBC
secreted by kidney in response to cellular hypoxia
main use of exogenous EPO is to treat anaemia associated with kidney disease
what are the side effects of EPO
accelerated hypertension bone aches flu like symptoms skin rashes pure red cell aplasia
how do osmotic diuretics work and give an example
eg mannitol
work in PCT and LOH, increase solute concentration within tubules so water retains within tubule
how do loop diuretics work and give an example
eg furosemide
work at LOH and ascending limb sympotrer, prevents chloride from being reabsorbed and hence affects sodium reabsorption so water is excreted out more too
relieves stress in heart conditions bc lowers plasma volume and hence lowers BP
How do thiazide like diuretics work and give an example
work on sodium and chloride symporter in DCT
increases excretion of sodium, potassium and water
increases reabsorption of urea in pCT
= SE is gout bc uric acid
eg hydrochlorithiazide
how do potassium sparing diuretics work and give an example
work in DCT and CD
decrease reabsorption of sodium but prevent excretion of potassium
eg amiloride
