Renal Flashcards
eGFR is calculated from
Creatinine
Age
Gender
Ethnicity
When is eGFR not valid
<18
Pregnancy (because kidney function varies)
AKI
Causes of pre-renal AKI (most common cause of AKI)
hypovolaemia
haemorrhage
sepsis
renal artery occlusion
made worse by:
drugs that lower BP (ACEi, ARBs, NSAIDs, loop diuretics), HF, third spacing of fluid (severe pancreatitis)
Causes of intrinsic AKI
Glomerulonephritis
Non-ischaemic ATN - drugs, myoglobin, paraproteins
Ischaemic ATN
Interstitial nephritis e.g. due to autoimmune disease, pyelonephritis, drugs
Vascular diseases like microangiopathic haemolytic anaemias (e.g. DIC) and malignant HTN
Post-renal causes of AKI
Stones Lymphoma Genitourinary tract rumours Prostate hyperplasia Strictures Urinary retention Blocked catheter
Presentation of AKI
May be none - you can lose a lot of kidney function before symptoms show
are usually non-specific and related to the underlying disease
E.g. nausea, vomiting, diarrhoea, dehydration
Stage 1 AKI
creatinine 1.5-1.9x baseline
or
<0.5ml/kg/h for 6-12 hours
Stage 2 AKI
creatinine 2-2.9x baseline
or
urine output <0.5ml/kg/h for >12 hours
Stage 3 AKI
creatinine >3x baseline or indication for RRT or urine output <0.3ml/kg/h for >24 hours or anuria for >12 hours
Risk factors for AKI
>65 History of AKI CKD (<60ml/min/1.73m2) Renal disease DM Sepsis CT diseases HF Liver disease Use of nephrotoxic drugs Iodinated contrast use in last week
NICE say to measure serum creatinine in all adults with acute illness and one of the risk factors
Investigations for AKI
full A- E assessment
take a full history to try to determine cause
particular attention to volume status - peripheral perfusion, skin turgor, changes in urination pattern
BLOOD
- ABG/VBG for metabolic acidosis
- FBC - anaemia in CKD, leukocytosis in infection
- creatinine - compare to baseline. and repeat 48-72 hours later
- ratio of serum urea to creatinine (>20:1 supports pre-renal)
- CRP and ESR
- blood culture if sepsis
- immunology - ANCA, ANA, anti-GBM, paraprotein
- can do antistreptolysin O titre but strep infection rare now
URINE
- urinalysis
- urine culture if there is suspicion of infection on urinlaysis
- albumin:creatinine ratio
- urine osmolality
IMAGING
- renal US - dilated renal calyces suggest obstruction, sclerotic kidneys suggest CKD
- CXR if associated with HF
- ECG with hyperkalaemia
- renal vascular assessment required MRA (angiography) or renal doppler
OTHER
- do a fluid challenge - will improve rapidly in pre-renal
managment of AKI
regularly assess urine output which may require a catheter
serial U+Es daily (increase if more severe)
stop nephrotoxic drugs and alter regular prescriptions to reflect change in creatinine clearance
treat hyperkalaemia
fluid challenge - 250-500ml saline over 30 mins
repeat if still dehydrated
once replete, continue fluid at 20ml + previous hour’s urine output per hour
if overloaded, consider urgent dialysis
or, if passing urine then can give diuresis as treatment
treat sepsis
refer to renal team for opinion early
if more than one organ dysfunction –> ITU
treat metabolic acidodis
relieve obstructios
how to treat hyperkalaemia in AKI
stabilize cardiac membrane with 10ml 10% calclium gluconate
drive K into cells with 10 units actrapid in 50ml 20% glucose
beta agonists may also be used e.g. 2.5mg nebulised salbutamol
Additional: stop or adjust potassium-sparing or potassium-containing medications. Resins can reduce potassium absorption but these take hours/days to have effect
when to contact the renal team for urgent dialysis in an AKI (or ITU can also do this)
- hyperkalaemia unresponsive to medical treatment or in an oliguric patient
- pulmonary oedema unresponsive to medical treatment
- uraemic complications like pericarditis, encephalopathy
- severe metabolic acidosis (pH<7.2 or BE below -10)
- fluid overload
ECG changes in hyperkalaemia
peaked T waves prolonged PR segment loss of P wave prolonged QRS ST elevation ectopics sine wave VF systole
haematuria definition
> 5 RBCs per high power field
CKD definition
proteinuria or haematuria and/or a reduction in GFR <60ml/min/1.73m2 for more than 3 months
causes of CKD
DM - most common cause
HTN
less frequent causes
- polycystic kidney disease
- obstructive uropathy
- focal segmental glomerulosclerosis
- membranous nephropathy
- lupus nephritis
- amyloidosis
- vasculitis
- myeloma
- rapidly progressive glomerulonephritis
- nephrotoxic drugs
nephrotoxic drugs
aminoglycosides (gentamicin), ACEi, ARBs, bisphosphates, calcineurin inhibitors (ciclosporin, tacrolimus), diuretics, lithium, mesalazine (5-ASA), NSAIDs
presentation of CKD
majority are asymptomatic and diagnosed by lab studies
will start to develop non-specific symptoms at more advanced stages
fatigue due to anaemia
anorexia and nausea
oedema and raised JVP due to salt and water retention
HTN
foamy urine (proteinuria)
dyspnoea (pulmonary oedema) peripheral neuropathy due to uraemia
grading of CKD
6 GFR stages and 3 albuminuria categories
Stage 1 /G1 kidney damage with normal or increased GFR, ≥90 mL/minute/1.73m²
Stage 2 /G2 kidney damage with mild decrease in GFR, 60 to 89 mL/minute/1.73m²
Stage 3a /G3a kidney damage with moderate decrease in GFR, 45 to 59 mL/minute/1.73m²
Stage 3b /G3b kidney damage with moderate decrease in GFR, 30 to 44 mL/minute/1.73m²
Stage 4 /G4 kidney damage with severe decrease in GFR, 15 to 29 mL/minute/1.73m²
Stage 5 /G5 kidney failure (end-stage kidney disease), with GFR <15 mL/minute/1.73m²
+
A1 Normal to mildly increased <3mg/mmol
A2 Moderately increased 3-29mg/mmol
A3 Severely increased >30mg/mmol
