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
investigations for CKD
BLOODS
- serum creatinine for eGFR
- calcium phosphate vitamin D and PTH tests
- bicarbonate via an ABG or VBG
- lipid profile
- FBC for anaemia
- ANA for SLE, ANCA for vasculitis
- serum and urine free light chains and/or protein electrophoresis for myeloma
URINE
- urinarlysis
- albumin creatinine ratio
- urine culture to exclude infection
- electophoresis in myeloma
IMAGING
- US with LUTS
- CT-KUB for stones
- ECG because are at high risk of CVS disease
CONSIDER
- renal biopsy- useful if glomerulonephritis is supsected
management of CKD
- stop nephrotoxic drugs
- manage lifestyle factors
- assess risk of CVD
- give sources of info
- advise to avoid use of oral NSAIDs where possible
- maintain target BP with ACEi or RBS
- NICE say all people with CKD should have a statin for prevention of CKD
- K restriction in diet if hyperkalaemic
- avoid high phosphate foods - milk, egg, cheese
- vitamin D analogues (e.g. alfacalcidol)
- replace iron/B12/folate if anaemic - if still anaemic can consider recombinant human EPO
- sodium bicarb for acidosis
- diureitcs (furosemide) for oedema
stage 5 - dialysis or kidney transplant
target BP in CKD
<130/80
in diabetics or ACR >70 then <125/75
nephrotic syndrome - 4 Os
prOteinuria >3.5g/24 hours
hyperlipidaemia (O = fat)
hypOalbuminaemia <30g/L
peripheral Oedema
may also have haematuria
general treatment for nephrotic syndrome - SCAVAD
Salt +/- water restriction (be careful with this though)
treat underlying Cause
ACEi or ARBs (for HTN and proteinuria)
VTE prophylaxis ((relatively lose more antithrombotic than prothrombotic factors)
are risk of infection (variation in practice as to whether you give prophylactic Abx).
loop Diuretics for oedema
SCAVAD
nephritic syndrome 3H’s + U
HTN
haematuria (usually non-visible)
hardly any urine (oliguira)
uraemia
may also have oedema
and proteinuria but <3.5g/24 hours
nephrotic vs nephritic pathophysiology
nephrotic is a consequence of structural changes in the glomeruli in response to glomerular injury - podocytes lose foot processes
nephritic is associated with a proliferative response within the glomeruli leading to marked increase in cellularity (mesangial and endothelial proliferation and inflammatory cell infiltration)
glomerulonephritis causes that can present as both nephrotic and nephritic syndrome
membranous GN
rapidly progressive GN
post-strep GN
cause of primary nephritic syndrome
IgA nephropathy (Berger’s disease)
6 causes of secondary nephritic syndrome
post-strep GN SLE Wegener's granulomatosis/granulomatosis with polyangiitis microscopic polyangitis Henoch-Schlonlein purpura Goodpasture's syndrome
3 causes of primary nephrotic syndrome
minimal change disease
focal segmental glomerulosclerosis
membranous nephropathy
4 causes of secondary nephrotic syndrome
diabetic nephropathy
SLE
amyloidosis
hepatitis B/C
post streptococcal glomerulonephritis
almost extinct in western europe
presents 1-12 weeks after a sore throat/skin infection due to cross reaction of antibodies to group A haemolytic streptococcus
a type 3 hypersensitivity reaction
treatment is supportive
investigations for post strep glomerulonephritis
light microscopy shows proliferation of mesangial cells, immune cells
immunofluoresnce shows IgG and C3 deposits - a lumpy-bumpy complex deposition
blood shows increased C3 and anti-streptolysin O
Tetrad of Henoch-Schlonlein purpura
purpuric rash
abdominal pain
arthritis/arthralgia
glomerulonephritis
diagnosis of Henoch-Schlonlein purpura
usually clinical using the tetrad
but can be condirmed with positive immunofluroresence for IgA and C3 in skin or renal biopsy
diagnosis of granulomatosis with polyangiitis
a postitive c-ANCA test in the setting of typical otorhinolaryngeal, lung and renal involvement is suffieicnt
demonstation of necrotising vasculitits and grnaulomatous inflammation on tissue biopsy can also confirm (a negative ANCA does not exclude)
treatment of granulomatosis with polyangiitis
2 stages - remission induction and remission maintenance
IV methylprednisolone or oral prednisolone for active GPA with cylophosphamide
then remission with prednisolone for active GPA and cyclophosphamide
microscopic polyangiitis
Diagnosis: p-ANCA is positive in almost all cases. High CRP/ESR. Proteinuria and haematuria
treatment is long term prednisolone and cyclophosphamide
plasmapheresis can be helpful to acutely remove p-ANCA antibodies
goodpasture’s syndrome
caused by autoantibodies to type IV collagen - an essential part of the glomerular basement membrane
type 2 hypersensitivity reaction
treat with plasmapheresis, IV prednisolone +/- cytotoxics (cyclophosphamide)
membranous nephropathy - patholopysiology and presentation
bimodal peak in age in 20s and 60s
is caused by immune complex deposition which results in copmlement activation against glomerular BM proteins
patients typically present with oedema or HTN. May also report foamy urine or non-specific symptoms. Or could be an incidental finding on urinalysis
causes of membranous nephorpathy
2/3rds are associated with autoantibodies to phospholipase A2 receptor (are idiopathic)
other 1/3 is secondary to malignancy, rheumatoid disorders, hep B, malaria, drugs
diagnosis of membranous nephropathy
renal biopsy = diagnostic standrard
light microscopy shows thickened glomerular BM with IgG and complement deposits and thickened cappillary walls
immunofluroescence shows IgG and C3
rule of thirds with membranous nephropathy
One-third remain with MGN indefinitely, one-third remit, and one-third progress to ESRF
treatment of membranous nephropathy
Treat HTN, treat hyperlipidaemia, oedema (furosemide), steroids + cytotoxic or immunosuppressive therapy if medium or high risk of progression to ESRF
most common cause of nephrotic syndrome in children
minimal change disease (kids = minimal age, foot = minimal body part)
minimal change disease
effacement of foot processes
Onset is gradual, ranging from a few days to several weeks, and often follows a recent viral illness (suggested immune system involvement)
presents with facial or generalised oedema
treatment of minimal change disease
corticosteroids and supportive care - reducing oedema
90% of children and 80% of adults respond well – often cured after 3 months
most common cause of nephrotic syndrome in adults
focal segmental glomerulosclerosis (remember this is a primary cause of nephrotic syndrome)
causes of focal segmental glomerulosclerosis
can be primary (genetic mutations) or secondary to HIV, IV drug use (heroin), sick cell disease
investigations for focal segmental glomerulosclerosis
renal biopsy is required
light microscopy shows sclerosed lesions
antibody tests are all negative
immunofluroscence won’t show anything (might be some IgM and complement)
ECM will show GBM thickening and effacement of foot processes
management of focal segmental glomerulosclerosis
salt restriction and diuretics to reduce oedema, antihypertensives, statins, cytotoxic drugs are sometimes useful, transplant is often required (50% progress to renal failure) (steroids can be used but have an inconsistent response)
And treat underlying cause if secondary
