Renal failure Flashcards
What is acute kidney injury
It is defined as the reversible rapid reduction of renal function (eGFR) within hours or days/weeks.
When does creatinine causes problems
when its serum levels are increased
Risk factors for developing AKI
Age >75
DIABETES
DRUGS (review newly started)
SEPSIS
Chronic kidney disease
poor fluid intake/ increase fluid loss
cardiac failure
Hx of urinary symptoms
Chronic liver disease
peripheral vascular disease
What are the commonest causes of AKI
Ischaemia to the kidneys
Sepsis
Drugs (Nephrotoxins)
above 3 are the commonest
Prostatic disease in 25% - these have very good prognosis
Pre-renal causes of AKI
these are the commonest (40-70%)
Vascular occlusion
dehydration
blood loss
sepsis
cardiac failure
Renal causes of AKI
causes 10-50% of AKI
Glomerulonephritis (commonest)
vasculitis
Acute tubular necrosis
Drugs/toxins
infection
inflammatory disease
Post-renal causes
Think from start to end
Urinary tract obstruction (Calculi)
BPH
prostatic cancer
cervical cancer
urethral stricture
meatus problems
AKI presentation
Oliguria (<500ml urine per day)
Anuria - rare and indicates obstruction
in 20% there could be normal urine output or increased (non-oliguric AKI)
what is uraemia
increased serum creatinine and urea
How would a patient with pre-renal AKI present
Hypotensive and tachycardic
with signs of hypovalaemia and postural hypotension
Confusion
can present without hypotension in patients taking NSAIDs and ACE inhibitors
Hyperkalaemia and hypocalcaemia arecommon
Dilutional hyponatraemia if patient continued to drink despite oliguria or received INAPPROPRIATE IV dextrose
signs of fluid overload –> raised JVP
peripheral oedema
CVS changes
Abdominal/flank pain
What is Dilutional hyponatraemia
Low sodium levels due to excessive fluids
When does metabolic acidosis develop in AKI
when vomiting is not controlled
or there is aspiration of gastric contents
What can you tell from a dipstick in AKI
infection +ve leukocytes and nitrates
What can you tell from a dipstick in AKI
infection +ve leukocytes and nitrates
glomerular disaese (blood+protein)
What investigations to carry in AKI
Dipstick
MC&S
U&Es for creatinine and urea
FBC
LFT
Clotting
Creatine kinase
CRP
ESR - erythrocyte sedimentation rate for inflammation
renal USS
non-contrast spiral CTKUB if obstruction suspected but not picked up by USS
CXR for pulmonary oedema
ECG in Px >40 and at risk of CVS
How to manage AKI
Establish cause and treat
If hypovalaemia is present correct with IV fluids or blood as rapidly as possible.
Stop nephrtoxic drugs
Urinary tract obstruction must be releived
correct electrolyte imbalances
nutrition - parenteral or enteral
immunosuppresion in glomereloneprhitits
renal replacement therapy (RRT) if non resolving
STOP AKI
Sepsis
Toxins - nephrtoxic drugs stop
Optimized BP
Prevent complications: hyperkalaemia, pulmonary oedaema, acidosis, pericarditis
Identify cause
What is chronic kidney disease
it is the irreversible detoriartion in eGFR over years
When death is likely without RRT it is considered as end-stage renal disease (ESRD)
x4 commoner in black ethnicity because of increased risk of HTN
CKD causes
Caused by any disease that causes destruction to the kidney
Diabetes 70%
HTN
atherosclerosis
renovascular disease
Interistial disaese
Glomerular disease
SLE
congenital and inherited 5%
idiopathic
Presentation of CKD
patients may remain asymptomatic until eGFR <30
Pallor/ Anaemia
Uraemic
Yellow
purpura, easily bruising
excoriarations
HTN
Cardiomegaly
signs of fluid overload, rasied JVP
What does an alkaline phosphate in LFT show
if increased in CKD could mean renal osteodystrophy
Investigations in CKD
FBC
U&Es - reduced Ca, increased PO
LFTs
increased PTH if CKD stage 3 or more
Urine dipstick + MC&S, albumin:creatinine or protein:creatinine
USS to check kidney size –> usually smaller in CKD
Consider renal biopsy
How to manage CKD
Identify causative factor
Antihypertensives therapy - target 130/80
stop nephrotoxic drugs
Reduction of proteinuria - proteinuria is worse as disease progresses. can use ACE or ARB. will cause small reduction in eGFR initially but continue unless eGFR reduction >20%.
Lipid lowering therapy - statins to control hypercholostreamia which is common with proteinuria
Dietary and lifestyle management - less protein intake. smoking cessation and exercise.
Maintain fluid and electrolyte imbalances
screen for complications - anaemia/osteodystrophy
Renal bone disease- control with VitD
ELSA BCD
Electrolyte imbalances
Life - diet exercise smoking
Stop nephrotoxins
ACE or ARB for proteinuria
BP 130/80
Complication screen
Vit D for renal bone disease
What is the aim in managing CKD
3 Points
preventing further renal damage, managing and limiting metabolic and cardiovascular complications, and preparing for renal replacement therapy if required
Stages of renal failure
Stage 1 with normal or high GFR (GFR > 90 mL/min)
Stage 2 Mild CKD (GFR = 60-89 mL/min)
Stage 3A Moderate CKD (GFR = 45-59 mL/min)
Stage 3B Moderate CKD (GFR = 30-44 mL/min)
Stage 4 Severe CKD (GFR = 15-29 mL/min)
Stage 5 End Stage CKD (GFR <15 mL/min)
