Renal Flashcards
Nephrotic syndrome what is it and path
proteinuria
= low serum albumin
= which provokes Oedema
& hyperlipidemia
cause = podocyte effacement = more permeable to protein
thefor no renal impairment bc diseases of only filtration barrier (podocytes) (bc nephrin bridges between the podocyte feet are lost which usually filter proteins
normal renal fxn normal Cr
Minimal change disease (MCD), what is it
pt
ix
tx
non immune depositing nephrotic syndrome
pt: children post viral infection w nephrotic syndrome (oedema)
Ix: only finding is podocyte effacement on electron microscopy (but normal glomeruli)
tx: corticosteriods resolution and complete recovery & no recurrence is norm. if dont respond = progress to FSGS
ATN types and area
TOXIC ATN (PCT)
rhabdo (myoglobin), amphoterecin, contrast dye
ISCHAEMIC/hypoperf ATN (PCT, TA, DCT)
ATN phases
PRODROMAL
Apoptosis of epithelial cells and sloughing
= Inc Cr
OLIGURIC
Filtration impaired (cast obstructing)
hyperkalaemia (ions not filtered)
volume overload (water not filtered)
Increased urea and Cr (ratio<10)
- haemodialysis
POLYURIC
Resorption impaired (cast washed away but epithelium still dont work)
volume depleted
reduced urea and CR
tx - iv fluids n ion replace
types of AIN
pyelonepthritis
allergic nephritis
NSAID caused
Pyelonephritis fx
urgency freq and dysuria + fever and loin tenderness
WBC casts (macrophages n neutrophils)
Urine micro: gram -ve ie klebsiella Uti ones
allergic nephritis fx
Eosinophilia + fever + rash post starting new sulf med:
either duiretics or abx eg PCN, cephalo, trimeth
NSAID nephropathy
reduced prostaglandins = arteriole constriction = hypoperf –> pupillary necrosis
= haematuria
and fibrosis (may lead to urothelial ca of renal pelvis)
hypocalcaemia tx
prolonged QT = urgent iv calcium gluconate
SGLT2 inhibitor example and adverse effects
dapagliflozin
Urinary genital infection (bc glycosuria)
Fourniers gangrene
normoglycaemic ketoacidosis
inc risk of lower limb amputation: closely moniter feet
fourneiers gangrene
necrotizing faciatis of the genetalia or perineum
prenal AKI
hypovolaemia ie diarohea vomiting
renal artery stenosis
renal AKI cause
glomerulonephritis
ATN
AIN
rhabdomyolysis
tumor lysis
post renal aki
stone
bph
external compression
unknown cause of aki ix
renal tract USS in 24 hrs
hypercalaemia features
bones stones groans and psychic moans
corneal calcification
shortened QT on ecg
hypertension
young pt started on acei for htn and then has deterioation in renal function
undiagnosed bilateral renal artery stenosis
causes of CKD
htn
diabetic nephropathy
chronic pyelonephritis
chronic glomeruloneph
adult polycyctic kidney disease
renal USS in CKD why
exclude obstruction
renal size (small in ckd)
exclude polycystic kidneys
drugs in CKD to slow disease
ACEi
SGLT2 - dapafloglzin
signs of CKD on examination
oedema, pallor, uremic tinge, purpura, bruising, evidence of scratching
pericardial rub
pleaural effusion
how does haemodialysis work
Blood and dialysis fluid flow either side o f a semi permeable
membrane, molecules diffuse down their concentration gradients,
plasma biochemistry changes to become more like the dialysis fluid
peritoneal dialysis complications
Bacterial peritonitis, local infection at catheter site, constipation, failure, sclerosing peritonitis.
organ transplant rejection types
hyperacute - abo incompatible
acute - in 6 mths - T cell mediated
chronic = after 6 mths vascular changes
membranous glomerulonephritis histology
basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2
causes of membranous glomeruloneph
idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
why does nephrotic predispose to vte
loss of antithrombin 3
iga nephro vs post strep glomer
iga = 2 days post illness
post strep = 1-2weeks
FSGS causes
LM
IF
EM
idiopathic
congenital
HIV
Sickle cell
heroin
Lm = some glomeruli some sclerosis
IF = -ve (maybe igm)
EM = effacement
membrano prolif path
lm
em
if
preformed ag-ab complexes
mesnagial prolif into BM
lm = basement mem splitting/thickening
em = subendothe
if = granular igg +c3
membranous nepthro
LM
EM
IF
lm = diffuse capillary thickening
em = subepithelial deposits
IF = granular igg +c3
acute urinary retention causes
BPH
UTI
dx - Anti cholinergic, opiods, TCAs
urethral structures
constipation
calculi
acute vs chronic urinary retention
chronic typically painless
may present with overflow incontinence
larger volume of urine in bladder ie 1.5l+
acute urine retention ix
urinalysis and culure (catheterise)
FBC U&E Cr CRP
Bladder USS
acute urinary retention complication
post obstructive duireses
check hourly urine output and replace any loss with fluids
hyperkalaemia mx
10% IV ca gluconate
Dextrose 50% 50ml + 15 units insulin
oral or enema calcium resonium (remove from body)
bph tx
tamulosin (relax smooth muscle alpha 1 recep)
Finesteride (stops converstion test –>dihydrotest which is more potent to androgen tissue)
macrscopic haem causes
renal tract trauma or tumor
UTI
nephritic syndrome
renal calculi
shistosomiasis
bladder causes risks
smoking
male
paint or dye worker (aromatics)
shistosomiasis (SCC)
cyclophosphomide
bladder ca ix
cystoscopy
bipsy
TURBT
bladder ca tx
TURBT
intravesical chemo
radical cystectomy or ileal conduit
or radical radiotherapy
bladder ca spread
local - uterus, rectum, pelvic side wall
lymphatic: iliac, paraortic lymph nodes
haem - liver, lungs, bone
Lower urinary tract
storage sx
urgency / frequency / nocturia / urinary incontinence / feeling the need to
urinate again immediately after
lower urinary tract voiding sx
hesitancy / weak or intermittent urinary stream / splitting / spraying / straining
/ incomplete emptying / terminal dribbling
screening tool for lower urinary tract sx
international prostate symptoms score
causes for increased PSA
prostate ca
bph
urinary retention
DRE
UTI
anal sex
catheterisation
vigorous excersise
zone most affected in prostate cancer
peripheral zone
prostate ca mc place and type
adenocarcinoma
peripheral zone
score used for prstate cancer
how does it work
gleason grading system
sum of individual scores for two most dominant ca type
1st line ix prostate ca
multiparametric MRI
ADPKD (polycystic kidney)
mc common presenting sx
haematuria
loin pain
hypertension
types ADPKD
1 =more svere
PKD1 on chromosome 16
2 = less severe
PKD2 chromosome 4
ADPKD mx
refer nephrologist
htn mc
pain mx
tx uti
tx kidney stones
tolvaptan for some to reduce growth rate of cysts
ESRD = transplant
signs of ADPKD on examination
Palpable kidneys/abdominal mass
Hepatomegaly due to hepatic cysts
Abdominal wall hernias
These are more common in ADPKD, affecting 45% of patients
Cardiac murmur
This is due to an increased incidence of mitral valve prolapse, mitral regurgitation, aortic regurgitation and dilated aortic root in patients with ADPKD.
mc cause ckd uk
t2dm
na resabsorption where and how
Main factor determining extracellular volume
drop BP and drop NaCI @ macula densa (DCT) = renin release -> aldosterone release -› more Na/K pumps.
water reabsorption
At PCT and thin loop
Determines ECF osmolality
inc osmolality or drop in BP = ADH release
loop diuretic
eg
work and effect
use
furosemide bumetanide
inhibit na/k/2cl transporter in thick ascending limb
= massive nacl ca and k excretion
oedema - ccf, nephrotic, hypercalcaemia
thiazide diuretic
eg
work and effect
use
SE
bendroflumethiazide
inhibit Nacl cotransport in DCT
= massive nacl excretion, inc Ca resabsortion
Htn, decrenal stones, mild oedema
SE loop duiretic
hypokalaemia met alkalosis
ototoxic
hypovolameia
thiazdie se
hypokal
hyperglycaemia
inc urate (CI in gout)
casts causes:
RBC
WBC
Tubular
glomerular haematuria
interstioal nephritis or pyelonephritis
ATN
interpreting urea and Cr
isolated urea rise
= dec flow ie hypoperf/dehydration
urea and cr raised = dec filtration ie renal failure
causes of post renal disease
SNIPPIN
Stone
Neoplasm
Inflammation: stricture
Prostatic hypertrophy
Posterior urethral valves
Infection: TB, schisto
Neuro: post-op, neuropathy
diseases of renal papillae, pelvis, ureter, bladder or urethra
hyperkalaemia ecg
Peaked T waves
Flattened P waves
1 PR interval
Widened QRS
Sine-wave pattern -» VE
causes of sterile pyuria
ie wbc in urine but no bacteria
TB
treated uti
appendicitis
calculi
TIN
PCK
thin basement disease
autosomal dom
mc cause asx haematuria
persistant asx microscopic haemturia
small risk of esrf
alport syndrome gene fx
mostly x linkes
haematuria , portenuria —> progressive renal failure
Sensorineural deafness
Lens dislocation and cataracts
Retinal “flecks”
Females: haematuria only
nephritic syndrome/ acute GN fx
causes
Haematuria (macro / micro) + red cell casts
Proteinuria
oedema (esp. periorbital)
Hypertension
Oliguria and progressive renal impairment
1 . Proliferative / post-streptococcal
2. Crescentic / RPGN
complications of nephrotic syndrome
Infection: reduced lg, reduced complement activity
VTE: up to 40%
Hyperlipidaemia: 1 cholesterol and triglycerides
hyperkal tx
10ml 10% calcium gluconate
100ml 20% glucose + 10u insulin (Actrapid)
Salbutamol 5mg nebulizer
Calcium resonium 15g PO or 30g PR
Haemofiltration (usually needed if anuric)
indications for acute dialysis
- Persistent hyperkalaemia (>7mM)
- Refractory pulmonary oedema
- Symptomatic uraemia: encephalopathy, pericarditis
- Severe metabolic acidosis (pH <7.2)
- Poisoning (e.g. aspirin)
AIN/TIN
what is it and causes
Immune-mediated hypersensitivity c either drugs or other Ag acting as haptans
Drug hypersensitivity in 70%
NSAIDs
Abx: Cephs, penicillins, rifampicin, sulphonamide
Diuretics: frusemide, thiazides
Allopurinol
Cimetidine
Infections in 15% - Staphs, streps
Immune disorders - SLE, Sjogren’s
AIN/TIN
IX AND Results
1gE, eosinophilia
Dip: haematuria, proteinuria, sterile pyuria
acute urate cyrystal nephropathy what and why
tx
AKI due to urate precipitation
Usually after chemo-induced cell lysis
Rx: hydration, urinary alkalinisation
rhabdo path
Pathogenesis
Skeletal muscle breakdown
release of:
K*, PO4, urate
Myoglobin, CK
inc K and AKI
causes of rhabdo
ischaemic ie embolsim/surgery
trauma
toxins - statins, fibrates, escstacy, neuroleptics
rhabdo ix and results
Dipstick: +ve Hb, -ve RBCs
Blood: increased CK, K, P04, urate
complications of CKD
CRF HEALS
Cardiovascular disease
Renal osteodystrophy
Fluid (oedema)
HTN
Electrolyte disturbances: K, H
Anaemia
Leg restlessness
Sensory neuropathy
how does srcoidosis affect kidneys
inc ca
TIN
renal vascular disease ie bilat renal artery stenosis
ix 1st and gold
US + doppler: small kidney red flow
CT/MR angio
Renal angiography: gold standard
what is TTP
Genetic or acquired deficiency of ADAMTS13 -> giant vWF multimers
features of TTP
pentad
Adult females
Pentad:
Fever
CNS signs: confusion, seizures
MAHA
Thrombocytopenia
Renal failure
tx ttp
plasmapharesis
immunosupression
splenectomy
dom PCK mx
general:
inc water intake, dec Na, deccaffeine (may dec cyst formation)
Monitor U+E and BP
Genetic counselling
MRA screen for Berry aneurysms
med
tx HTn aggressively ie ACEi
surg
maybe helped by laprosc cyst rmova or nephrectomy
dialysis or transplant in those w ESRF (70%by 70yo)
renal englargement differentials
PHONOS
Polycystic kidneys: ADPKD, ARPKD, TS
Hypertrophy 2° to contralateral renal agenesis
Obstruction (hydronephrosis)
Neoplasia: RCC, myeloma, amyloidosis
Occlusion (renal vein thrombosis)
Systemic: early DM, amyloid
