Renal Flashcards
pre-renal uraemia vs acute tubular necrosis
sodium and water reabsorption
clinical response to fluid resus:
PRU > diuresis
ATN > remain oliguric
rhabdo features
raised K, PO4, CK
low Ca
diagnosing AKI
rise of creatinine 26 in 48h
rise in creatinine 50% in 7 days
oliguria 0.5ml/kg/h in 6h
alport syndrome
x linked, auto rec, auto dom or auto digenic
type IV collagen basement membrane
COL4A3, COL4A4, COL4A5
CKD, sensorineural hearing loss, lenticonus
> ACEi or ARB if proteinuria/HTN
testing for iron def in CKD patients
percentage of hypochromic RBCs
if thalassaemia trait, use transferrin sat and serum ferritin
managing anaemia in CKD patients
(occurs only when eGFR < 60)
not on dialysis:
PO iron > IV iron if required
on dialysis:
IV iron (or PO if required)
treat iron def before or in parallel with EPO
aim for rate of Hb increase 10-20 per month
maintain 100-120 Hb
monitor Hb every 2-4 weeks during induction then 1-3 months
blood transfusion if failing to respond to EPO
analgesic nephropathy
daily use of preparations containing at least 2 analgesics
reduced kidney size
papillary calcifications
CKD stages
- normal eGFR. urinary or structural abnormalities
- eGFR 60-89 and urinary or structural abnormalities
3a. eGFR 45-59 - eGFR 30-44
- eGFR 15-29
- ESRF
CKD bone mineral disorder
increased PO4 > reduced calcium
> increased PTH > bone turnover
decreased vit D > osteomalacia, reduced GI absorption of Ca
monitor Ca, PO4, PTH, ALP in patients eGFR < 30
monitor Ca, PO4, PTH, vit D in patients eGFR > 30
FGF23 normally maintains normal serum PO4 levels by reducing reabsorption and reducing vit D production
causes of nephrogenic diabetes insipidus
hypercalcaemia
hypokalaemia
lithium
renal disease
demeclocycline
x linked/dom abnormality in tubular ADH receptor
tx: bendroflumethiazide
diabetic nephropathy
chronic hyperglycaemia > glomerulosclerosis
most common cause of ESRF un UK
increased blood viscosity
> reduced flow in small capillaries
> small infarcts to glomerulus
> hypoxia and inflammation from capillary leak
stages of diabetic nephropathy
- GFR elevated by 20% and increased urinary albumin excretion rate
- GFR remains elevated due to hyperfiltration, kidneys are hypertrophied. BP and albumin excretion normal.
GBM thickening, mesangial expansion - microalbuminuria or urine ACR 3-30, BP starts rising
- established nephropathy, increasing macroproteinuria, declining GFR, most will be hypertensive, diffuse glomerular sclerosis, some have kimmelstein wilson nodules
- ESRF 7 years from stage 4
eosinophilic granulomatosis with polyangiitis renal involvement
necrotising crescenteric GN
eosinophilic interstitial nephritis
mesangial GN
focal segmental glomerulosclerosis
> haematuria, proteinuria, HTN, raised creat
50% pANCA, 90% eosinophilia
focal segmental glomerulosclerosis
podocyte injury > detach from BM
> BM exposed
> proliferation of epithelial, endothelial, mesangial cells
> cell proliferation and leak of protein into Bowmans space
> collagen deposition
> nephrotic syndrome (or asymptomatic)
tx: corticosteroids
inherited forms:
finnish congenital nephrotic syndrome
late onset auto dom FSGS
childhood onset steroid resistant FSGS
secondary causes:
HIV, CMV, parvo B19, hepC
reduced renal mass
lithium, IFNa, heroin, pamidronate, sirolimus
obesity
renal ischaemia and VTE
gitelmans
loss of NaCl cotransporter in DCT
> mimics thiazide toxicity
> hypomagnesaemia, hypokalaemia, hypocalciuria, alkalosis
tx: high salt diet, Mg and K supplements
can consider potassium sparing diuretic
indomethacin in infants/children
SLC12A3 gene auto rec
Bartters
NaKCl in ascending loop
> hypokalaemic alkalosis
commonest causes of GN
min change disease in under 15ys
IgA nephropathy (Berger’s) in white adults
FSGS in black adults
primary GN
nephrotic:
membranous
min change
FSGS
mesangiocap GN
nephritic:
IgA/Bergers
rapidly progressive
secondary GN
nephrotic:
diabetes
amyloid
hep B/B
SLE class 5, 6
nephritic:
post strep
HSP, wegeners
goodpastures
SLE class 1-4
treating GN
high dose prednisolone
IV pulsed cyclophosphamide if steroid resistant
ACEi, diuretics, statins
anticoagulants for nephrotic syndrome
goodpasture
AKA anti GBM
antibodies against alpha 3 chain of type IV collagen (in glomerular and alveolar BM)
> complement activated. C3, IgG deposits
> crescenteric GN
HLA-DR15, HLA-DRB1
not all pts have pulm involvement
tx: plasma exchange, prednisolone, cyclophosphamide
granulomatosis w/ polyangiitis
necrotising granulomatous vasculitis
small to medium vessels
> haematuria, proteinuria
> haemoptysis
> epistaxis, saddle nose, subglottic stenosis
cANCA
tx: steroids, cyclophosphamide, plasma exchange
maintenance: MTX or azathioprine, also steroids
for recurrence: steroids or rituximab or cyclophosphamide or plasma exchange
haemolytic anaemia syndrome
microangiopathic haemolytic anaemia
thrombocytopaenia
AKI
most common cause of AKI in children
90% are secondary to Ecoli O157:H7
causes:
E coli
strep pneumonia
shigella type 1
HIV, coxsackie
atypical- tacrolimus, ciclosporin, complement mutations, pregnancy, SLE
HSP triad
palpable rash
joint pain
renal and GI involvement
triggered by virus or solid tumour
IgA antibodies deposited in skin, joints, kidneys, GIT
> mild proliferative and crescenteric GN
> micro haematuria, proteinuria
most resolve without treatment
Bosniak system
used to classify malignant risk of renal cysts based on CT
I: simple
IV: malignant
II, III: indeterminant
inherited cystic renal diseases
PKD
VHL
tuberous sclerosis
Dandy Walker syndrome
PCKD
auto dom:
PKD1 chromo 16 in 80%
PKD2 chromo 4 in 15%
auto rec:
PKHD1 chromo 6 (ESRF in childhood)
tx: ACEi, tolvaptan
VHL
auto dom
chromo 3
premalignant renal cysts, clear cell renal ca
phaeochromocytomas
spinocerebellar haemangioblastomas
retinal angiomas
pancreatic cysts, islet cell tumours
tuberous sclersosis
renal cysts, angiomyolipomas
epilepsy, LDs, ASD
hamartomas, shagreen patches, ash leaf spots, adenoma sebaceum
APKD criteria
2 cysts < 30y
2 cysts bilaterally 30-59y
4 cysts bilaterally > 60y
BP targets
80 and over: 145/85
below 80: 135/85
drugs causing tubulointerstitial nephritis
rifampicin
allopurinol
methicillin, penicillin, cephalosporins
sulfonamides
furosemides, thiazides
cimetidine
amphoteracin
aspirin, NSAIDs
causes of chronic tubulointerstitial nephritis with macroscopically normal kidneys
reflux nephropathy
analgesic nephropathy
obstructive and cystic disease
presentation of interstitial nephritis
acute:
mild renal impairment
hypersensitivity (fever, arthralgia, rash, eosinophilia, raised IgE)
chronic:
HTN, anaemia, proteinuria
CKD or ESRF
RTA type 1
nephrogenic DI
salt wasting
diagnosing tubulointerstitial nephritis
biopsy
acute:
interstitial oedema
plasma cell infiltration w/ lymphocytes and monocytes
granulomatoses if sarcoid
chronic:
chronic inflammatory infiltrate
granulomatous in sarcoid and TB
extensive scarring and tubular loss
how might someone be exposed to lead?
deteriorating paint surfaces
battery manufacturing
radiator repairing
bullet firing ranges
contaminated water
toys
foetal exposure
lead is stored in bone so can provide long term storm after exposure has ended
features of lead toxicity
renal- fanconi
CVS- HTN, CAD, PAD
neurodevelopmental
lead chelation therapy
dimercaprol
succimer
sodium calcium edetate
liddle syndrome
auto dom, SCNN1B, SCNN1G
dysfunctional gain of Na channels in collecting ducts
> severe HTN, hypokalaemic metab alkalosis, reduced renin and aldosterone
HTN is not responsive to typical antihypertensives
tx: Na restriction, K supplements, amiloride or triamterene (K sparing diuretics)
causes of membranous nephropathy
HLADR3 risk factor
idiopathic
AI
hep B, C, syphilis
malignancy
gold, lithium, NSAIDs, penicillamine
post transplant, sarcoid
circulating antibodies to M type phospholipase A2 receptor PLA2R
membranous nephropathy diagnosis
nephrotic syndrome
biopsy: thick GBM, spike formation
immunofluorescence: IgG and C3 deposits in GBM
treating membranous nephropathy
can resolve spontaneously, persist or progress to renal failure
ACEi if HTN
statin if hyperlipid
furosemide/hydrochlorthiazide if oedema
steroids if medium/high risk to ESRF
causes of minimal change disease
usually idiopathic
leukaemia, hodgkins
hep B, hep C
NSAIDs
allergic reactions
immunisations
minimal change disease diagnosis
biopsy only if not responding or frequently relapsing
light microscopy: no changes
electron microscopy: podocyte effacement
managing minimal change disease
85% of children respond well to steroids
about 4-12 weeks
add ciclosporin or tacrolimus or high dose IV steroids if not responding to PO steroids in 4 weeks or if frequently relapsing
relapse: proteinuria for 3 days
treat similarly to initial episode and wean steroids once no proteinuria for 3 days, then maintenance steroids for several weeks
complications of minimal change disease
loss of antithrombin > thrombosis
loss of IgG and immunosuppressive treatment > infection and spontaneous peritonitis
relapse (75%)
renal failure (rare)
HTN
symptoms of polyarteritis nodosa
haematuria, proteinuria, AKI/CKD
subcut nodules, livedo reticularis
necrotic ulcers
HTN
ischaemic abdo pain
mononeuritis multiplex
diagnosing polyarteritis nodosa
ANCA negative
necrotising inflammation on biopsy of arteries/muscle/skin
rosary beads microaneurysms on angiography
diagnosing post strep GN
nephritic picture
low C3
recent strep infection (pharyngitis or impetigo)
biopsy: diffuse proliferative GN, global increase in cellularity, infiltration of polymorphonuclear cells
treating post strep GN
loop diuretics for oedema and HTN
ACEi or CCB second line for HTN
usually resolves spontaneously
adverse effects of immunosuppressants
ciclosporin- hirsuitism, gum hyperplasia, liver dysfunction, HTN, chronic renal allograft nephropathy
azathioprine- bone marrow suppression, esp w/ allopurinol
MMF- diarrhoea, bone marrow suppression
sirolimus- hyperlipidaemia
immunosuppression for renal transplant
tacrolimus + antimetabolite e.g. MMF + prednisolone
peritoneal dialysis
continuous amubulatory:
1.5-3L per day
effective for 3-6y
automated:
overnight
haemodialysis access
AV fistula takes 4-6 weeks to mature
temporary tunnelled vascular access catheter can be used for those who present late or with fistula complications
absolute contraindications to renal donation
pre-existing renal disease
disease of unknown aetiology (e.g. MS or sarcoid)
recent malignancy
overt IHD
renal transplant exclusion criteria
current or recent malignancy
severe comorbidity (COPD, uncontrolled IHD, extensive PVD, CVA, dementia)
active infection
AIDs with opportunistic infection
active substance misuse
uncontrolled psychiatric disease
complications of peritoneal dialysis
bacterial peritonitis- coag neg staph, gram neg bacteria, staph aureus
ultrafiltration failure- APD and polymer based solutions may help
encapsulating peritoneal sclerosis- peritoneum thickens and encases bowel
hernias, fluid leak (pleural effusion), malnutrition
CVS complications of dialysis
arrhythmia, congestive cardiomyopathy
vascular calcification
valve calcification, esp aortic
dialysis related amyloid
beta2 microglobulin increased and deposited as amyloid within carpal tunnel, joints, bones
acute vs chronic renal transplant dysfunction
acute:
first 2 weeks
fluid retention, rising BP, rapidly rising creat
> IV steroids
chronic:
after 1y
gradual rise in creat, proteinuria, resistant HTN
vascular changes, fibrosis, tubular atrophy
not responsive to increasing immunosuppression
post renal transplant non renal complications
non hodgkins, skin cancer
all other malignancies
IHD
infections esp PJP, CMV
osteoporosis
gout
new onset diabetes
vasculitis recurrence
> cotrimox is given for 1st 6 months as PJP prophylaxis
previous TB or Asian patients are given isoniazid for 1y as TB prophylaxis
indications for haemodialysis over peritoneal
abdo surgery or irremediable hernia
recurrent/persistent peritonitis
peritoneal membrane failure
age, general frailty
severe malnutrition
hypercatabolic states
chronic severe chest disease
indications for nephrectomy before transplant
pyonephrosis or any suppuration within urinary tract
massive polycystic kidneys
uncontrollable HTN
renal/urothelial malignancy
transplant rejection
hyperacute:
recipient abs against donor kidney
within minutes
acute:
acute deterioration in function assoc w/ pathological changes in graft
acute cell mediated- mononuclear infiltration
acute antibody mediated- C4d
chronic:
from 3 months
HTN, proteinuria, transplant vasculopathy
immunosuppression for transplant surgery
methylprednisolone
anti CD25 mono ab e.g. basiliximab
types of RTA1
1 (distal):
alpha cells in DCT fail to excrete H+ and absorb K+
hypokalaemic hyperchloraemic acidosis
> calculi
diabetes insipidus, salt wasting
2 (proximal):
PCT fails to reabsorb bicarb
less severe acidosis
hypokalaemic hypercholaemic acidosis
osteomalacia, rickets
3:
rare
impaired PCT bicarb resorption and DCT acid excretion
biochemical abnormalities dependent on whether PCT or DCT is predominant
4:
low or resistant to aldosterone
hyperkalaemic hyperchloraemic acidosis
CKD
causes of RTA
1:
primary
SLE, sjogren, hepatitis
tubulointerstitial disease
nephrocalcinosis
lithium, amphoteracin, toluene
2:
idiopathic
Fanconi- wilsons, fructose intolerance, sjogrens
tubulointersitial disease
tetracyclines, lead, mercury, sulfonamides, acetazolamide
4:
low renin and aldo- diabetes, NSAIDs, ciclosporin
high renin low aldo- adrenal destruction, ACEi, ARB
RTA and urinary calculi
urinary calcium excretion is increased in severe acidosis
calcium salts are more insoluble in alkaline urine
develops in distal RTA (type 1)
managing RTA
potassium citrate to alkalinise urine
PO K and HCO3 for type 1 and 2
fludrocortisone for type 4 if acidotic or hyperkalaemic
diagnosing rhabdo
CK 5x upper limit
non traumatic causes of rhabdo
thyroid storm
phaeochromocytoma
DKA
seizures
influenza A, clostridium spp
polymyositis, dermatomyositis
cocaine, amphetamines, narcotics, barbiturates, sedatives, diuretics, statins, antipsychotics, antidepressants
cyanide, mercury, copper, CO, bee stings, snake bites
DIC from rhabdo
thromboplastin released during muscle injury
> DIC
rhabdo biochemistry
5x elevated CK
raised myoglobin
raised K, Mg, PO4, urea, creat
low Ca
if DIC:
low platelets, fibrinogen, Hb
raised D dimer, PT, APTT
renal involvement of sarcoid
hypercalcaemia
granulomatous intersitial nephritis
renal involvement of systemic sclerosis
scleroderma renal crisis:
malignant HTN
rapid renal impairment
onion skin intrarenal vasculature
tx> ACEi
steroids increase risk of renal crisis
urinary tract TB
pulm infection or reactivation of miliary disease
> haematogenous spread
> seeding
long latency between primary infection and presentation
quiescent granulomas reactivate and shed bacteria in urinary tract
bladder and ureteric TB is usually secondary to renal
presentation:
repeated UTIs unresponsive to abx
nephritic syndrome if renal
bladder irritation symptoms if bladder
incontinence and incomplete urination if ureteric
investigating urinary tract TB
urine culture, TB testing, CXR
IV pyelogram- beaded appearance of ureters
CT most useful
MCU- irregular wall and decreased capacity
plain KUB
metabolic factors predisposing to stones
hypercalciuria, hyperoxaluria
hyperuricuria
cystinuria
hypocitraturia
most common sites of stone
VUJ
renal pelvis is most common site of kidney stone
causes of stones
hypercalciuria:
loop diuretics, hyperparathyroid
hyperoxaluria:
primary (rare genetic), small bowel malabsorption, increased tea or vit C intake
hyperuricuria:
excess meat (purine), ileostomy, chronic diarrhoea, myeloproliferative disease, gout
cystinuria:
auto rec condition
infection:
MAP staghorn from proteus, pseudomonas, klebsiella
when is a stone likely to pass?
ureteric: < 4mm and in lower ureter
renal: < 5mm
preventing recurrence of stones
potassium citrate if mostly calcium oxalate stone
thiazide diuretics if mostly calcium oxalate stones
surgery for stones
ureteric:
lithotripsy if < 2cm
ureteroscopy
renal:
lithotripsy if < 2cm
percutaneous nephrolithotomy
flexible ureterorenoscopy and lithotripsy for small stones in renal collecting system unsuitable for lithotripsy due to anatomy
open nephrolithotomy
nephrectomy
diagnosing UTI according to bacterial growth
at least 10^3 Ecoli or staph saprophyticus
at least 10^4 of a single organism
at least 10^5 mixed growth with one predominant organism
treating UTI in pregnant pt
nitro 7/7 (avoid if at term)
amox 7/7
cefalexin 7/7
VHL
auto dom (20% de novo mutation)
chromo 3
VHL mutation or deletion
> increased HIF, PDGF, VEGF
haemangioblastomas, phaeochromocytomas, renal cell ca, pancreatic cysts
mortality mostly due to renal cell ca and CNS tumours
types of VHL
1: low risk of phaeochromocytoma
2: phaeochromocytoma
2A low risk renal ca
2B high risk renal ca
2C only phaeochromocytoma
stages of lupus nephritis
1: immune deposits
2: mesangial proliferation
3: focal disease
4: diffuse disease
(3 and 4 require steroids + MMF +/- cyclophosphamide)
5: membranous
6: advanced sclerosis
(5 and 6 ACEi)
