Renal Flashcards
A 5-year-old boy presents with a short history of facial oedema that has now progressed to total body swelling involving the face, abdomen, scrotum, and feet. Other symptoms include nausea, vomiting, and abdominal pain. The parents report that the child had a viral illness with fever a few days before the development of the swelling. On examination, he has facial oedema, ascites, scrotal oedema, and pitting oedema of both legs up to the knees.
minimal change nephropathy
A 42-year-old white man with no previous medical history presents to his primary care physician with progressively increasing oedema of both lower extremities. There is no family history of renal failure. The patient has pitting pedal oedema. Urinalysis reveals marked proteinuria (3+).
FSGS
A 48-year-old man presents to his family doctor with a recent lower-extremity swelling that is gradually worsening. Over the last few weeks, he has also noticed puffiness under his eyes. A urinalysis demonstrates significant proteinuria, and a 24-hour urine collection confirms proteinuria of 12 g. He has no history of diabetes, macroscopic haematuria, or hypertension.
membranous nephropathy
A 50-year-old man with a 15-year history of type 2 diabetes presents with oedema, fatigue, and impaired sensation in the lower extremities. He is found to have proteinuria, a reduced eGFR, anaemia, background diabetic retinopathy, and peripheral neuropathy
diabetic nephropathy
A 23-year-old white man with an unremarkable past medical history presents to the clinic for a routine physical examination including a urine analysis required for his job. This shows invisible haematuria and mild proteinuria. The physical examination reveals no significant abnormal findings
IgA nephropathy, berger’s
A 41-year-old woman is discharged from hospital following a diagnosis of community-acquired pneumonia, to be managed at home on amoxicillin. A day later she returns to the emergency department with a low-grade fever, widespread erythematous rash and pain throughout her joints and lower back, with her initial bloods showing a significantly elevated creatinine.
AIN
A 20-year-old woman presents with a 5-day history of painless light brown coloured urine. She has experienced 3 episodes of this over the 5 days. There is no dyspareunia, urgency or pain elsewhere. As of now, she is afebrile though she alludes to being ill with a respiratory infection around three weeks ago.
post strep GN
A concerned mother attends your GP surgery with her 7-year-old son. She is very concerned as she reports that ‘there is blood in his urine.’ Urine dipstick is ++++ for blood with no leukocytes, nitrates or protein. The boy reports that he first noticed the haematuria this morning. Physical examination is unremarkable, with normal heart and lung sounds and a soft non-tender abdomen. He is afebrile and does not have any symptoms of a urinary tract infection. His past medical history is unremarkable but his mother reports that he recently had a cold 2 days prior and has had several colds over the past year.
IgA nephropathy
5 causes of nephrotic syndrome
primary glomerular disease
- minimal change
- FSGS
- membranous nephropathy
systemic
- diabetes
- amyloidosis
nephritic syndrome causes
- post-strep glomerulonephritis
small vessel vasculitis
anti GBM disease
iga nephropathy
causes of crescenteric nephritis or RPGN
- SVV small vessel vasculitis
- SLE
- anti GBM good pasture’s
- aggressive phase of other inflammatory nephritis
acute intersitial nephritis causes AIN
Allergic
- drug
- autoimmune
Infective
-Toxic- noxious
chronic interstitial nephritis causes
- AIN where the cause continues
- in assoc. with glomerulonephritis
- allergic/ immune- sarcoidosis, autoimmune-sjorgen
- infective
- toxic Ig light chains, heavy metals, Li
- development/ congenital - reflex nephropathy and renal dysplasias
- inhertied- metabolic, nephrocalcinosis
- ischaemia/ papillary necrosis- sickle cell, analgesic nephropathy
haematuria causes
UTI stones tumours prostate gland disease -glomerulonephritis schistosomiasis
- not haematuria
- menstruation
- dyes in food
- transient haematuria from strenuous exercise
- if on warfarin more likely to get more significant
signs of glomerulonephritis
haematuria proteinuria one of blood pressure oedema
visible haematuria management
-exclude menstruation/ UTI
check BP, renal function
refer to urology for USS/ CT renal tracts/ cystoscopy
persistent non visible haematuria diagnosis
need 2 out of 3 positive dipsticks
exclude menstruation and UTI
persistent non visible haematuria and normal renal function and BP but over 40
refer to urology
persistent non visible haematuria and normal renal function and BP but under 40 and symptomatic
refer to urology
persistent non visisble haematuria and normal renal function and BP but under 40 and not symptomatic
keep under observation
-annual urinalysis and renal function and BP check
persistent non visible haematuria and abnormal renal function and BP
refer to renal
persistent non visible haematuria and fhx of renal disease or evidence of systemic disease
refer to renal
inx options for haematuria
-hx
-urinalysis
-urine culture
-urine microscopy
BP
-renal function
-urine ACR
all patients >40 and persistent non visible haematuria get cystoscopy and imaging along with visible haematuria patients
who to send to renal for haematuria
- hx of fhx of renal disease
- evidence of systemic disease
- abnormal BP or renal function
what is loin pain haematuria syndrome
-name given to the syndrome in which people suffer loin or flank pain and have blood in their urine, in whom no other cause is found
types of oedema
-localised
generalised- ascites, pleural effusion, facial - can with increased severity be in the genitalia and abdomen
inx for oedema
hx and exam
urinalysis
bloods- labumin
4 mechanisms of oedema
increased ECF
increased hydrostatic pressure
increased capillary permeability
lowered oncotic pressure
what can cause increased ECF
- sodium retention by kidneys renal failure
- heart failure
- nephrotic syndrome- low albumin
- liver failure
signs of general increased in hydrostatic pressure
-venous pressure is high in heart or renal failure
raised JVP
nephrotic syndrome - except get a normal JVP as intravascualr deplete
signs of local increased in hydrostatic pressure and cause
-venous pressure will be raised by DVT or venous insufficiency or by extrinsic obstruction such as pregnancy or tumour
-non pitting localised oedema- lymphoedema
also some infections, malignancy and radiation
causes of increased capillary permeability
infection
sepsis
protein leaks into the interstuitium which reduces the oncotic pressure gradient so draws fluid out
lowered oncotic pressure of blood
- low serum albumin due to reduced synthesis or increased loss
- assoc. with avid sodium retention by the kidneys
- liver failure is reduced synthesis
- nephrotic syndrome- increased loss of proteins
- malnutrition reduced synthesis
hold onto fluid
management of oedema
diuretics
salt and fluid restriction depending
compression
unilateral leg oedema suggests
a mechanical problem
oedema with hyponatraemia suggest
whole body sodium is increased but water is increased more - hypervolaemic hyponatraemia so needs restriction of water and salt but caution diuretics
proteinuria what does it signify
renal disease
-protein in the urine always comes from the kidney
three main causes of proteinuria
-glomerular disease
increased protein production
low reabsorption at proximal tubule
main causes of proteinuria
- nephrotic syndrome
- glomerular disease -glomerulonephritis, diabetes
- CKD
- autoimmune- lupus, goodpasture
- urine infection
- systemic- congestive heart failure, eclampsia
- dehydration
- htn
less important causes of proteinuria
-fever
strenuous exercise
absent in the morning but occurs in the later in the day-orthostatic proteinuria
occurs only during a urine infection
inx proteinuria
-dipstick urine
indication for further inx of proteinuria
-proteinuria >100
haematuria- think glomerulonephritis
-raised serum creatnine/ low eGFR
-HTN
-symptoms of systemic disease eg vasculitis such as rash, arthralgia
-previous hx or fhx suggesting significant renal disease
further inx for proteinuria
quantify proteinuria creatinine
urine albumin creatinine ratio
uss of kidneys
consider referral renal biopsy
what is assoc, to proteinuria
cardiovascular disease
quantification of proteinuria inx
-PCR or ACR urine
what is normal protein loss in urine
about 0.3g/day
but virtually no albumin
management of low level proteinuria
-absence of heavy proteinuria <1g day, haematuria, HTN, renal function, symptoms: monitor urine test and renal function at 6 month intervals
> 1g consider renal biopsy
see flow chart
voiding symptoms
persistent dribbling intermittent stream straining hesitancy poor flow bladder outflow obstruction double voiding
storage symptoms
frequency
urgency
nocturia
incontinence
end stage renal failure symptoms
-thirst twitching pallor fatigue nausea vomiting bone pain breathlessness pigmentation coma confusion
causes of haematuria
-cysts
-tumours
-vascular malofrmations
-glomerular disease
0interstitial disease
-infection
-cancer
-stones
-trauma
-clotting disorders
-excerise
malnutrition
def of oliguria
<400
anuria def
<100
causes of oliguria/ anuria
urinary obstruction eg prostate, tumour, stone
lack of renal perfusion- aortic dissection
RPGN
AKI stage 1 is
creatinine >1.5-1.9
urine <0.5 for >6 hours
AKI stage 2
creatinine 2-2.9
urine <0.5 for 12 hours
AKI stage 3
> 3 creatinine
urine <0.3 for 24 hrs or anuric 12 hours
how do NSAIDs act at as predisposing drugs to AKI
NSAIDS inhibit prostaglandin production which inhibits the dilatation of the afferent arteriole
which is aimed at increasing glomerular pressure
how do ACEi act as predisposing drugs to AKI
ACEi inhibit angiotensin II production which prevents constriction of the efferent arteriole
which is aimed at increasing glomerular pressure
causes of AKI
usually multifactorial
-dehydration- SEVERE hypovolaemia
pre-existing renal damage
predisposing drugs
overall get decreased glomerular pressure that is required for proper filtration
predisposing drugs to AKI
-ACEi NSAID aminoglycosides diuretics IV contrast
classification of AKI
-pre-renal
renal
post-renal
pre renal causes for AKI
- circulation- systemic and local (RAS)
- bp
- cardiac ouput
- sepsis
- fluid balance reduced
- reduced arterial circualtion
- intrarenal microcirculation
- blood loss
- dehydration
- vascular occlusion
inx for AKI
- renal u and e
2, urinalysis - renal USS
INX findings for pre-renal AKI
urine osmolality increases
sodium urine decreases- hold onto sodium
serum urea: creatinine increases
intrinisc renal AKI causes
- ATN acute tubular necrosis-prolonged pre-renal
- inflammation: glomerulonephritis, interstitial nephritis, pyelonephritis
- vascular- renal vein thrombosis, cholesterol emboli, renal infarction, malignant hypertension, recent angiography
Acute tubular necrosis pathology
-get an injury to the tubule which leads later to necrosis of the tubule and fibrosis
intrinisic renal AKI inx findings
urine osmolality decreased
urine sodium increased- loose sodium
post-renal AKI causes
- neurological
- stones, crystals blocking
- kidneys, bladder
approach to the patient with oliguria
- is it real- check bladder recordings?
- check circulation
- fluid balance
- drug chart
- previous result and hx
- uss and dipstick
elevated creatinine diff dx
- aki
- ckd
- aki on background of ckd
KDIGO criteria for AKI 3
- increase in serum creatinine by >26.5 micromol within 48 hours
- increase in serum creatinine by >1.5 x baseline within the prior seven days
- urine volume <0.5ml/kg for >6 hours
what suggest a dx of AKI rather than CKD
- normal kidney size on USS
- normal haemoglobin (RBC half life 120 days so wont be acute presentation)
- normal PTH (also takes time to develop)
if in doubt assume AKI and inx promptly
pre renal AKI clinical features
-hypotensive, tachycardic, poor peripheral perfusion, delayed CRT, postural hypotension
management of pre-renal AKI
-fluid resus will work providing tubules intact
acute tubular necrosis causes
- when hypotension is very severe or prolonged, ATN may develop due to ischaemic injury
- prolonged pre-renal goes onto develop ATN
which is when urinary sodium begins to increase and osmolality decrease as can no longer absorb sodium and water back through tubules
also toxic causes
- drugs- aminoglycosides, cisplatin, tenofovir, methotrexate, iodinated contrast
- rhabdomyolysis
- myeloma light chains
- crystals
management of ATN
- fluid resuscitiation aggressive and early
- once ATN has developed fluid resus alone will not be enough as kidney tubules take time to regenerate
mortality ATN
50% due to assoc. organ failure
Anti GBM immunofluorescence presentation
ribbon pattern
immune complex deposition disease presentation
immunofluorescence
granular or starry sky pattern
vasculitis immunofluorescence presentation
negative
causes of RPGN
-vasculitis
anti GBM
post-infectious glomerulonephritis
post renal AKI causes
-obstruction
to flow in renal tract- NEEDS TO BE BILATERAL
-Most likely benign prostatic hypertrophy
-also tumours, external compression
presentaton of post-renal AKI
-anuria
or
-polyuria
systematic approach to patient with AKI
- is the AKI renal- check renal function
- could it be pre-renal failure
- access circualtory state eg BP,JVP, mucous membranes, check fluid balance, check medications eg any new medications - could it be post-renal
-bladder palpable?
-person at high risk eg male >60, hx of bladder cancer, loin pain, visible haematuria
order USS scan - could it be an intrinsic renal cause
Toxic ATN
AIN-eosinophilic count and leucocytes
glomerulonephritis- blood and protein
management of established AKI
-drug chart stop nephrotoxic drugs
-fluids
control intake of fluid, resus, match sodium loss, no potassium initially
-hyperkalaemia management
-acidosis give sodium bicarb if pH<7
-diet: low protein and phosphate
-prevent infection
-consider PPI reduce risk Upper GI bleeds
-treat obstruction if needed
others
-dialysis
what drugs need stopping in AKI
-NSAID
-AceI
-AMINOGLYCOSIDES
-ARB
diuretics
metformin
lithium
digoxin
indications in AKI for dialysis8
- dangerous hyperkalaemia
- pulmonary oedema
- severe symptoms or complications
- poor biochemical results and unlikely to recover function quickly
- pericarditis
- neurological signs eg uraemic encephalopathy
- need for high fluid intake eg for nutrition during oliguria
- to enable nutrition
dialysis of choice for AKI
haemodialysis
why is there a polyuric phase after AKI
-excess electrolytes and fluid retained during AKI but also because the tubules are recovering from injury so are less responsive to ADH/ ang so dont appropriately retain salt and water
management of after AKI Fluid
-rough guide is to ensure total fluid is equal to urinary volume from the day before
unless signs of overload
may also need to supplement bicarb, potassium
prognosis of AKI after
- full recover
- acute on chronic disease
- AKI to ESRD
what do people with AKI die of 4
- hyperkalaemia
- pulmonary oedema
- uraemia
- infection
long term risks of aki
- recover often incomplete
- long term increased risk of ESRF
- poor outcomes are more likely with increasing severity and duration of the insult
biopsy sign of ATN
vacuolation
rf for aki
chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over
CKD stages
1 >90 2 60-90 3 30-60 4 15-30 5 <15
eGFR variables
cage Creatinine age gender ethnicity
dx of CKD
eGFR of <60 on at least 2 occasions 90 days apart
abnormalities of kidney function or structure present for more than 3 months
irereversible deterioration of renal function
main causes of CKD
diabetes mellitus interstitial disease glomerular disease hypertension systemic inflammatory disease renovascular disease cogenital and inherited unknown
clinical features CKD
<15 gfr -tired breathless renal anaemia pruuritus anorexia weight loss n and v
risk factors for developing ESRD
-severity proteinuria haematuria high BP young age
inx
blood tests urinalysis and proteinuria ACR HEPATitis testing renal USS CT/ MRI angiography
referral CKD to nephrologist
- eGFR <30
- rapid deterioration >25% from past yr
- significant proteinuria unless known to be due to diabetes ACR >70
- ACR >30 with non visible haemturia
- HTN that remains poorly controlled despite 4 medications
- suspicion of renal involvement in multisystem disease
AKI def
1.5 x baseline 7days
cr 26.5 in 48hrs
0.5 urine for 6hrs ?
when to refer to renal unit -immediate
suspect acute renal failure oliguria obstruction ARF on CRF severe new renal failure
cause ckd 4-5
often multifactorial diabetes and renal artery stenosis inflammation eg glomerulonephritis circulatory obstruction inherited eg pkd
management CKD 3
-assess- features, urinalysis, medication, PMH
-monitoring: aim to keep BP <140/90
management of CVD- stain
refer for specialist
-proteinuria
haematuria
rapid deteriorating renal function
young age
fhx of renal failure
poorly controlled HTN
CKD managemenet
-BP control <130/80 if albuminuria ACEi if proteinuria bicarbonate for acidosis dietary avoid potassium salt restriction avoid high protein diet
complications of CKD
-HTN potassium acidosis anaemia renal osteodystrophy CVD risk malnutrition
acidosis rx in ckd
sodium bicarb
avoid too much protein
anaemia of ckd is
normochromic normocytic anaemia
make sure from renal and not another cause
anaemia pathology CKD
recombinant EPO
IV iron
-definiciency of EPO
decreased response to EPO, toxic effect of uraemia, reduced RBC survival
renal osteodystrophy pathology
low vitamin D
high PTH- high phosphate levels stimualte PTH
decreased calcium absortion
osteoclastic bone resporption
rx of renal bone disease
phosphate binders eg calcium carbonate
calcitriol alfacalcidol
drugs to stop taking on sick days
ACEi ARB NSAID diuretics metformin
indications for dialysis
fluid overload- acute pulmonary oedema hyperkalaemia uraemia-encephalopathy metabolic acidosis bleeding diathesis
ESRD options
conservative treatments
dialysis
types of dialysis
hospital haemodialysis home haemodialysis peritoneal dialysis -continuous ambulatory peritoneal automated peritoneal dialysis
haemodialysis preparation
-anticoagulation
-vascular access
monitoring
SE haemodialysis
hypotension muscle cramps bacteraemia hypotension cardiac arrhythymias haemorrhage air embolism dialyser pulmonary oedema sepsis
types of haemodialysis
haemofiltration-mostly AKI
haemodiafiltration- haemodialysis and ultrafiltration
continuous ambulatory peritoneal dialysis
-4 x 2L fluid exchanges dialy
4-6 hrs with a gap overnight
each bag takes 30-60 minutes
automated peritoneal dialysis
overnight 8-9hrs as sleep
disadvantages of peritoneal dialysis
peritoneal infection peritonitis catheter site exit infection ultrafiltration failure sclerosing pertinoitis
contraindication to PD
major abdo surgery peritoneal adhesions inguinal hernias severe respiratory compromise inability to perform the technique safely and hygenically
sclerosing peritonitis is
major complication of PD usually by staph epidermidis or bowel organism
-abdo pain, fever, cloudy PD
antibiotics needed
ESRD definition
implies a level of renal function at which death is likely within weeks or months
symptoms
immunosuppression for transplant
triple therapy
- MMF mycophenalate mofetil or azathioprine
- tacrolimus or cyclosporine
- relatively low dose prednisolone
risks of immunosuppression therapy for transplant
- increased SCC risk
- cardio toxicity
- renal failure nephrotoxicity
rejection from transplant
5 days to 2 weeks
- give high dose steroids
- tubulointerstitial inflammatory infiltrates
what is hyper-acute rejection
minutes to hours
due to pre-existing antibodies
HLA type 1 antigens
type II reaction
complication of transplant
- ischaemia reperfusion injury- interruption of blood supply, build up toxicities, organ damage
- delayed graft function- more common cadaveric so may need dialysis initially - oliguric after transplant
- technical problems
- acute rejection
<6 months post-transplant
signs and symptoms of infection
mismatched HLA
rise in creatinine - chronic rejection >6 months both antibody and cell mediaated mechanism cause fibrosis or due to recurrence of original disease
- infections- CMV especially
- CMV
- anastomosis damage or infection
- arterial thrombosis
- cardiac event at transplantation
immunosuppression risks
BK virus transplant
also called polyomavirus only causes problems in transplant most people who carry it have no symptoms biopsy Blood PCR testing urine cells attacks transplant
balance risk of developing this on immunosuppression
-reduce immunosuppressive drugs
AIN causes
allergic
NSAID, PPI, antibiotics-penicillin, allopurinol, furosemide
immune-autoimmune -TINU syndrome-tubulointerstitial nephritis and uveitis -AIN only sjorgen syndrome sarcoidosis transplant rejection
infective
toxic- drugs most common
inx for AIN
-eosinophilia leucocytes drug induced generalised signs of drug hypersensitivity white cell cast sterile urine biopsy shows inflammation
management AIN
withdrawal of drug
high dose steroids
treat cause
chronic interstitial nephritis is
renal dysfunction with firbosis and infiltration of the renal parenchyma by lymphocytes, plasma cells and macrophages
cause chronic interstitial nephritis
-persistent AIN
glomerulonephritis
immune
-sarcoidosis, sjorgen ,chronic transplant rejection, SLE
myeloma-bence jones protein -cast nephropathy
posions eg lead poisoning
drugs eg gentamicin, chemo, tenofovir, all drugs from AIN, lithium, ciclosporin, tacrolimus
infection
inherited
-VUR, renal dysplasias, wilson disease, sickle cell
metabolic- hypokalaemia, calcium phosphate crystals
unknown sometimes especially Asian race in UK
cast nephropathy causes
-form casts seen in
loop diuretics, myeloma
fanconi syndrome is
renal glycosuria in normal blood sugars
damage to proximal tubules
crystals form in proximal tubules
excess glucose, uric acid,phosphates being excreted
signs of CIN
HTN small kidneys CKD impaired concentration abilities sodium and water deplete
CIN management
supportive
correct acidosis and hyperkalaemia
renal replacement therapy if irreversible renal damage has occurred
ATN causes
- prolonged pre-renal aki
- severe infection- v.low BP
- toxicity
- myeloma
- crystals
- rhabdomyolysis
nephrotic to nephritis
minimal change
FSGS
Membranous nephropathy
diabetic nephropathy
MCGN
Post strep
vasculitis
GBM
nephrotic syndrome triad
heavy proteinuria >3.5g/24hrs
hypoalbuminuria <30g/l
peripheral oedema formation - due to avid sodium and fluid retention by the kidneys
cause nephrotic
damage to podocyte or non inflammatory architectyal alterations of the glomerulus
minimal change disease
normal glomeruli on micoroscopy can get podocyte foot process effacement most common cause children in adults assoc. to NSAID nand hodgkin high dose steroids
FSGS focal segmental golmeruli sclerosis
focal scarring idiopathic, HIV, reflux nephropathy, obesity primary= idiopathic- treat with steroids secondary- gradual onset, causal, ACEi variable response to steroids may progress to renal failure tends to be younger people
membranous nephropathy
usually idiopathic, some drugs, rarely malignancy
more common elderly
1/3 progress to renal failure
thickened glomerular capillary walls and basement membrane
basememnt membrane spikes on silver staining
immune complex deposition
often primary in adults and secondary in children
amyloidosis
early manifestation often
amyloid protein depositis
more common elderly
SLE
usually young women
management nephrotic syndrome
diet control salt intake
diuretics often loop
-careful and stop if signs of increasing creatinine or hypovolaemia
ACEI anticoagulation statin infection steroids and PPI
nephrotic oedema 2 main factors
sodium retention directly by renal
secondary sodium retention in which the low plasma oncotic pressure due to hypoalbuminaemia promotes the movement of fluid from the vascular space into the interstitium
complications of nephrotic syndrome
susceptibility to infection increased risk DVT high cholesterol hypercoaguability protein malnutrition hypovolaemia AKI
nephritic syndrome presentation
haematuria- often non visible
hypertension
reduction in renal function
pathology nephritic syndrome
inflammation in the glomeruli which damages and disrupts the glomerular basement membrane GBM, allowing red blood cells to enter the urinary space
allows RBC to enter into the urinary space
increased permeability
RPGN presentations
- post strep- ASOT, c3, c4
- anti GBM
- small vessel vasculitis - ANCA
- lupus- ds DNA ANA c3 c4
mild glomerulonephritis presentations
- IgA nephropathy IgA and HSP
- mesangiocapillary glomerulonephritis MCGN- c3, c4 hiv, hep b, ANA dsDNA
- Alport syndrome -genetic screening, hearing test
RPGN crescenteric nephritis
severe and rapid nephritic syndrome
exhibits many cellular “crescents”
presentation
- non visible haematuria
- severe nephritic syndrome
- acute onset of haematuria, HTN, oedema
- pulmonary haemorrhages good pastures
- systemic features vasculitis
main causes of RPGN
post strep
vasculitis
anti GBM
Lupus
treatment of RPGN
pulse methylprednisolone then daily oral prednisolone
IV cyclphosphamide or rituximab
plasmapharesis
IgA nephropathy
common disease most common worlwide often slowly evolving over decades can occur as HSP IgA deposited in the mesangium of glomeruli
post- strep GN
-10-14 days after strep throat fluid retention hypertension oedema haematuria reduced GFR diffuse proliferation of cells on renal biopsy
small vessel vasculitis
usually assoc. with antibodies to neutrophil granule enzyme ANCA
other systemic features
-microscopic polyangiitis
wegner disease
if severe can cause crescenteric nephritis
MCGN mesangiocapillary glomerulonpehritis
either
can be caused by persistent infection or other diseases or occur alone
IgA presentation
-most common asymptomatic visible haematuria dark brown urine discomfort in kidneys rarely sa nephrotic syndrome hypertension young male occurs with or a few days after resp infection
diagnosis of IgA nephropathy
hx of passing blood at same time as infection
urinalysis blood
bloods= raised IgA
renal biopsy- immune deposits
management of IgA nephropathy
- ACEi
- Steroids if haematuria and either renal dysfunction, proteinuria
- fish oil
- immunosuppression- cyclophosphamide, cyclosporin -most not needed
- 1/3 develop CKD and need dialysis and some need transplant
prognosis Iga NEPHROPATHY
1/3 devlop chronic kd
vasculitis pathology
ANCA antibodies to neutrophil cytoplasmic antigens, granule enzymes such as myeloperoxidase
presentation of 2 main small vessel vasculitis
- wegner granulomatosis with polyanggitis-sinusitis
- MPA microscopic polyangiitis -kidney, gut and skin
- HSP; children, abdo pain, rash, haematuria, weakness
dx of SVV
ANCA positive
antibodies to myeloperoxidase
biopsy
presentation of SVV
systemically unwell
renal
RPGN
pulmonary haemorrhage, rash
management of SVV
-cyclophosphamide, steroids and plasma exchange
post strep GN
asymptoamtic microscopic haematuria full blown acute nephritic- headahce, malaise light brown urine children oedema gross haematuria and HTN usually 1-3 weeks after strep throat
inx for post-strep GN
in children -urinalysis serology antibodies renal function no biopsy
biopsy signs of post strep GN
diffuse GN
starry night
neutrophils
deposition of IgG and c2
diff dx for post-strep GN
need to consider if lasts beyond 2 weeks
membranoproliferative GN -lasts longer
IgA nephropathy -shorter time interval
management post -strep GN
supportive
minimal change disease
often hx of recent viral illness oedematous puffy child facial oedema, abdominal and scrotum HTN is rare can have nausea and vomiting
diagnosis of MCD
dont biopsy in children-trial steroids first
biopsy appears normal on light microscopy
on electron microscopy can see podocyte foot processes
causes of MCD
-infectious 90% cause unknown allergic reaction asoc. to other disease drugs eg ibuprofen hodgkin's
prognosis MCD
1/3 frequent relapse
1/3infrequent relapse
1/3 only one episode
management MCD
give high dose of prednisolone
if dont respond
-wrong disease or
-need a combination of treatment
relapsing MCD treatment
cylophosphamide 8-12 week course of drug can prevent relapses for many months or years
in patients with frequent relapses
cyclosporin
tacrolimus
FSGS pathology
2 types
diseases that damage the glomeruli in small areas and leave scarring = secondary FSGS
primary FSGS= occurs without any known reason- idiopathic
biopsy of FSGS shows
only some / focal areas of glomeruli show scarring
assoc. to primary FSGS
WEST AFRICA
apoliprotein 1
secondary FSGS causes
-presents with more modest proteinuria than primary
- HUS
- cholesterol emboli
- toxins
- genetic
- HIV, severe obesity
presentation of FSGS
nephrotic
all ages
sometimes responds to steroid treatmnet- not always
kidney function can be abnormal
can cause complete kidney destruction and need dialysis
can come back after transplantation
diff dx FSGS
can be mistaken for MCD if biopsy taken of a normal part of glomeruli
primary FSGS treatment
steroids
secondary FSGS treatment
depends on cause
ACEI to prevent progression
membranous nephropathy pathology
in membranous nephropathy the filtering layer becomes thickened and there is a protein leak into the urine
- attack on the cells within the glomerulus that make the GBM known as podocytes
- most common cause of nephrotic syndrome in caucasian adults
- antibodies attack podocytes
causes of membranous nephropathy
-2/3 idiopathic (anti PLA2)
-arthritis lupus
drugs pencillamine, gold, captopril
cancer
infections hepatitis
toxins eg mercury, formaldehyde
histology of membranous nephropathy
thickened GBM
subepithelial spikes
PLA2
presentation of membranous nephropathy
asymptomatic
proteinuria
peripheral oedema
hypercoaguable state
prognosis membranous nephropathy
5-15% remission
30-40% partial remission
25% disease will progress and cause slow loss of function , lead to ESRF
factors that increase the chance of loss of kidney function
male >50 high proteinuria kidney biopsy scarring BP not well controlled kidney function abnormal at dx hepatitis - known cause cant be cured
management membranous nephropathy
-monitoring steroids -immunosuppressive cyclophosphamide, cyclosporin bp treatment diuretics
mesangiocapillary glomerulonephritis pathology
pattern of injury seen on renal biopsy characterised by an increase in mesangial cellularity with thickening of glomerular capillary walls
presentation MCGN
nephrotic or nephritis
types of MCGN
1st= deposition of IG into glomeruli, assoc. to chronic infections 2nd= deposition of complement into glomeruli , assoc. inherited or acquired abnormalities in complement pathway, dense deposit disease
treatment of MCGN
immunoglobulin type eg MMF, cyclophosphamide
complement type eg eculizumab
lupus markers
ANA
anti DS DNA
management of Lupus
MMF cyclophosphamide azathioprine cytotoxic agents anti B cell antibodies rituximab
thiazides side effects
hyponatraemia
hypocalciuria
hypokalaemia
action thiazides
inhibit reabsorption of NaCl in tubules
loop diuretics action
inhibit reabsorption of NaCL in loop henle
spironalactone
aldosterone antagonist
inhibits sodium potassium exhange
SE of loop diuretics
hypercalciuria hyponatraemia hypokalaemia hypomagnesia ototoxic
Ace inhibitors side effects
hypotension dry cough rash hyperkalaemia renal dysfunction
calcium channel side effects
constipation in verapamil
bradycardia
drugs to avoid in renal failure
ACEi ARB gentamicin nitrofurantoin NSAID opiates heparin LMWH use UFH vancomycin
alport syndrome pathology
defect in type 4 collagen
GBM deteriorates with time leading to progressive loss of glomeruli often with deafness
rare
loss of alport protein- autoimmune
histology alport
basket weaving
thick and thin GBM
presentation of alport
male renal problems sensorineural hearing loss women only get partial symptoms if carriers x-linked worse in me
thin GBM disease
often runs in families
benign familial haematuria
thin GBM
some also carry one copy of alport protein gene mutation
benign familial haematuria
-inherited cause for blood appearing in urine
often related to Thin GBM
nail patella syndrome
-poorly formed nails
2. patella missing
3. elbows often dont straighten properly
4. iliac horns
5. scolitosis
6. abnormality GBM
7. glaucoma
autosomal dominant
get nephrotic syndrome
LMX1B-collagen
good pasture’s disease is
an autoimmune condition in which there can be severe inflammation affecting kidneys and lungs
antibodies develop against the a3 chain of type 4 collagen
young patients
anti GBM presentation
-haematuria nephritic renal failure RPGN can get more severe features signs of kidney failure lung haemorrhages dry cough and minor breathlessness haemoptysis
diagnosis anti GBM
early symptoms often vague
biopsy
anti GBM antibodies
check for ANCA
management AntiGBM
steroids
cyclphosphamide
plasma exchange
DIABETIC NEPHROPATHY
late microvascular complication of diabetes mellitus
typically appears more than 20yrs type 1 dm
most already have diabetic retinopathy and neuropathy
phases of diabetic nephropathy
phase1= hyperfiltration
-elevated GFR
hypertension
microalbuminuria
phase 2= over diabetic neuropathy -overt proteinuria dipstick test positive BP can start to lose dip at night GFR starts to go back to normal
phase 3= incipient nephropathy
htn
proteinuria
npehortic syndrome
phase 4
progressive renal failure
CKD
histo features of diabetic nephropathy
mesangial expansion in glomerulus
slit diaphragm break down and protein leak
kimmelstiel- nodules of matrix
arterio hyalinolysis
risk factors diabetic nephropathy
poor diabetic control
duration of diabetes
presence of retinopathy and other microvascular complications
fhx susceptibility to HTN
diagnosis of diabetic nephropathy
ACR urine albumin creatinine ratio more sensitive
GFR renal function
if atypical then renal biopsy might be considered aka rapid onset not indicating diabetic nephropathy
prevention of diabetic nephropathy
blood sugars control
bp control
ACEI for proteinuria
diet protein restrict
management diabetic nephropathy no proteinuria
monitoring aim BP <130/80 hba1c <7 diet advice stop smoking
management diabetic nephropathy proteinuria
close monitoring monitor urine protein aim BP <125/75 further BP drugs cholesterol ACEI
who needs a renal biopsy for diabetic with kidney problems
- Type 1dm <10 yrs failing kidneys
- rapid progression proteinuria
- rapid deterioration renal function
- absence retinopathy
- presence severe haematuria
- additional systemic symptoms such as weight loss
polycycstic kidney disease presentation
abdominal pain early satiety palpable mass urinary tract infection haematuria hypertension asymptomatic initially renal failure
PKD pathology
autosomal dominant inherited
50% with PKD1 progresss to ESRD
PKD2 tends to be milder
dx PKD
-USS
cyts not detectable till in 20s
so cant use for screening in teens
can also be hepatic cysts
MRI
berry aneurysm if fhx of them sudden death or high risk job
renal function
can be fairly normal till late stage
management pkd
tolvaptan
ADH vasopressin V2 receptor antagonist
slows rate of growth of cyst and GFR loss
risk of dehydration due to polyuria
50% dialysis and renal transplant
complications of PKD
- hepatic cysts= hepatomegaly
- diverticulosis
- berry aneurysms- subarachnoid haemorrhages
- ovarian cysts
- mitral valve prolapse
- kidney stones
infantile PKD pathology
autosomal recessive rare different gene PKHD1 gene fibrocystin also cysts in liver pulmonary fibrosis severe illness
alport syndrome pathology
x-linked young men recessive women as carriers get a lesser disease due to lyonisation get inactivation in some cells collagen 4 absent or normal
histology alport
basket weave
presentation alport
deafness sensorineural
eye involvement -lenticonus of lens
progressive haematuria, proteinuria then renal failure in teens
management alport
acei limit progression
renal anaemia is
normochromic normocytic anaemia
due to deficiency in EPO
management of renal anaemia
look for contributing causes- dont assume renal
need to ensure IRON replete before giving EPO
erythropoiesis stimulating agents 2-3 injections a week
IV iron
se of EPO treatment
HTN encephalopathy bone aches urticaria pure red cell aplasia- antibodies develop
haemoglobin target for renal anaemia
100-110
avoid predisposing to thrombosis
renal artery stenosis pathology
arteriosclerosis of renal arteries
reduction in renal perfusion pressure activates the RAS system
increase in angII
vasoconstriction and increased aldosterone so retain sodium
global renal ischaemia leads to shrinkage of kidney
> 70% stenosis haemodynamically significant effects
most common cause secondary HTN
main cause of RAS in young patients
fibromuscular dysplasia
-uncommon
-hypertrophy of the media which narrows artery
more often women <50
distal main renal artery or the intra-renal branches
presentation of RAS
usually HTN
classic but rare presentation is with recurrent episodes of sudden flashing lights
flash pulmonary oedema-usually at night
RAS is more likely if
severe HTN asymmetrical kidneys flash pulmonary oedema peripheral vascular disease of lower limbs renal impairment renal function has deteriorated on ACEi
inx RAS
dipstick blood- hypokalaemia secondary aldosteronism increased renin MRI/ CT angiography USS RENAL ARTERIOGRAPHY GOLD STANDARD
Management RAS
-fibromuscular dysplasia patients often resond to balloon dilatation
1st line
-medical therapy
2nd line
interventions
angioplasty - balloon
indications for management angioplasty RAS
young <40 BP intractable flash pulmonary oedema malignant HTN deteriorating renal function
what is ischaemic nephropathy
CKD that results from RAS
acute renal infarction
sudden occlusion of the renal arteries
loin pain, non visible haematuria
severe HTN
can be caused by thrombosis of a renal artery or thromboemboli from a distant source
thrombotic microangiopathy pathology
diseases are assoc. with platelet thromboses in small blood vessels
damage to endothelium
plateelt thromboses in small vessels
causes of thrombotic microangiopathy
HUS TTP DIC malignancy systemic sclerosis PET
diagnosis
BLood film
- microangiopathic haemolytic anaemia MAHA
- schistocytes= fragments of RBC
blood
raised LDH
elevated unconjugated bilirubin
thrombocytopaenia
thrombotic thrombocytopaenia purpura pathology
haematological, CNS and renal pathology
-autoimmune disorder against antibodies to ADAMTS-13
this is involved in regulating platelet aggregation
low serum ADAMTS 13
USUALLY helps to break down vWF larger versions
so get abnormal build up of large vWF
presentation of TTP
-MAHA thrombocytopaenia purpura neurological manifestations fever renal disease AKI schistocytes on blood film petechiae lower abdominal pain fatigue typiclaly female
causes of TTP
post infection pregnancy drugs- ciclopsorin, OCP, penicillin, clopidogrel tumours SLE HIV
inx findings for TTP
thrombocytopaenia renal failure anaemia schistocytes direct coomb's test will be negative low ADAMTS13
management TTP
plasma exchange therapy and steroids
capacuzimab
HUS haemolytic uraemic syndrome pathology
typical
-blood diarrhoea in children from E.coli toxin
shiga toxin causes endothelial damage which causes platelet activation and clumping
-activates GB3 receptors
-these then destroy red blood cells as they get damaged passing through- MAHA
atypical
-to do with complement dysregulation
chronic disease both children and adult
HUS presentation
anaemia thrombocytopaenia AKI schistocytes typical often children with bloody diarrhoea
other causes of HUS
pneumococcal infection
HIV
SLE
atypical
CTD
Drugs eg quinine, cytotoxic
malignancy
management HUS
typical
supportive only
dialysis if severe renal failure
in those with fhx atypical HUS may benefit from complement inhibitors
plasma exchange
ECULIZUMAB for atypical types
DIC management
haemostasis
replace clotting factors
cholesterol emboli presentation
renal impairment haematuria proteinuria sometimes eosinophilia vasculitis can be ischaemic toes
patient undergoes cardiac arteriiography then gets renal failure
suspect cholesterol emboli
myeloma and renal pathology
hypercalcaemia
free light chains can be toxic to tubular cells and cause cast nephropathy and acute tubular necrosis
myeloma and renal presentations
- cast nephropathy
- fanconi syndrome- uric and phosphate … all excreted
- amyloidosis nephrotic
- monoclonal immunoglobulin deposition disease
- hypercalcaemia
3 main causes of amyloidosis
- AL amyloid due to light chains eg from myeloma
- ALL amyloid due to proteins in chronic infection or inflammation eg rheymatoid
- diabetes amyloid
HIV nephropathy presentation
collapsing FSGS
Proteinuria, nephrotic, progressive renal imapirment
responds to HAART if treated early enough
sodium risks
up too fast= cerebral pontine myelinolysis
low too fast= cerebral oedema
hypernatraemia causes
-reduced water intake eg coma, depression
-increased losses -hypovolaemic
increased loss via gut, skin, tract
-iatrogenic salt administration
-diabetes insipidus
features hypernatraemia
thirst oliguria concentrated urine weakness nausea loss of appetitie reduced cerebral function
inx findings hypernatraemia
increased plasma urea
management hypernatraemia
oral replacement
-water normal
-5% dextrose and .9% saline if severe
5% dextrose if mild
hypontaraemia causes
euvolaemic SIADH primary polydipsia hypothyroidism beer potomania poor diet intake of sodium
hypervolaemic
excess water exceeds excess sodium
cardiac liver or renal failure
RAAS
hypovolaemic large electrolyte losses Addison diuretic vomiting diarrhoea GI cerebral salt waste syndrome
clinical features of hyponatraemia
often asympatomatic acute <48hrs chronic >48hrs oedema confusion drowsy n and v seizure chovstek and trosseau
chronic hyponatraemia >48hrs
hypovolaemic give 0.9% saline
euvolaemic: fluid restrict, tolvaptan, vasopressin siadh
hypervolaemic: fluid and salt restrict,
acute hyponatraemia <48hrs rx
if also signs of cerebral oedema
need to restore rapidly using hypertonic sodium chloride 1.8%
drugs causing hyponatraemia
thiazide nsaid, antibiotics, PPI SIADH drugs: antidp, antipsychotics, carbarmazepine, anti cancer, opioids, MDMA Venlafaxine MDMA
hyperkalaemia causes
increased intake tissue breakdown- rhabdomyoloysis hyperglycaemia and acidosis cause relase addison spironalactone impaired excretion AKI and CKD drugs
signs of hyperkalaemia
rare
asymptomatic
progressive muscle weakness
ECG changes hyperkalaemia
- tented t waves
- loss of p waves
- wide QRS
- sine waves
treatment hyperkalaemia
- give IV calcium gluconate to stabilise the membrane
2.IV glucose and insulin
50ml 50% and 5units actrapid - salbutamol
- sodium bicarbonate
- IV fluids
- dialysis
- potassium biding resins -calcium resonium
- loop diuretics
hypokalaemia causes
<3.5 loss of potassium from the GI tract eg vomiting shift into cells eg insulin endocrine eg hyperaldosteronism drugs decreased intake increased excretion eg cushing excessive liquorice RTA
clinical features low K
asymptomatic
lethargy
muscle weakness
in chronic can get noctyria, polyuria, polydipsia
inx
ECG flatten and inversion t waves
can often seem normal potassium as not measuring intracellular
management hypokalaemia
give KCL IV
rich diet
potassium bicarb if acidosis
hypercalacaemia ssymptoms
stones bones throans psychiatric overtones moans
management high calcium
IV 0.9% saline IV bisphosphonates steroids calcitonin calcimimetics parathyroidectomy
