Renal Flashcards
ECG changes in hypokalaemia
ST depression
flat T wave
u wave
ECG changes in hyperkalaemia
peaked T waves
where is K regulated in the kidney
collecting duct - aldosterone causes K to be exchanged for Na
causes of hyperkalaemia
medications - ACE-I, ARBs, beta blockers, trimethoprim
rhabdomyolysis
tumour lysis syndrome
renal failure
acidosis
adrenal insufficiency - CAH, addisons
management of hyperkalaemia
- insulin glucose infusion - drives K intracellulalry
- salbutamol nebuliser
- calcium resonium - eliminates K from the body
- IV calcium gluconate - stabilises myocardium
- bicarbonate - correct acidosis
causes of hypokalaemia
diarrhoea
alkalsosis
volume depletion
hyperaldosteronism e.g. conns syndrome
renal artery stensosis
renal tubular acidosis
describe the renin-angiotensin system
- liver produces angiotensinogen
- angiotensinogen -> angiotensin 1 via renin
- angiotensin 1 -> angiotensin 2 via ACE (produced in lungs + kidney)
- angiotensin 2 causes:
- increase sympathetic activity
- produce aldosterone from adrenal cortex to cause reabsorption of Na and Cl and k execretion and water retention
- arteriole vasoconstriction to increase bP
- stimulate ADH secretion from pituitary to cause water reabsorption in collecting duct
mechanism of action of loop diuretics
e.g. furosemide
block Na K 2Cl co transporter in ascending loop of henle so there is increased excretion of Na, K and Cl and wate.
side effect of loop diuretics
metabolic alkalosis - secretion of H
hypokalaemia
hyponatraemia
hypochloraemia
hypomagnesasemia
mechanism of action of thiazide diuretics
act in DCT by inhibiting sodium chloride reabsorption
weak diuretics
mechanism of action of aldosterone antagonists e.g. spironolactone
block action of aldosterone in the DCt and collecting ducts so sodium and water excretion is increased
side effects of aldosterone antagonists
metabolic acidosis
hyperkalaemia
mechanism of action of osmotic diuretics e.g. mannitol
freely filtered in the bowmans capsule and increase osmolality of the filtrate within the tubule so reduces water reabsorption.
management of indirect inguinal hernias
- incarcerated (obstruction) -> manual reduction then surgery in 2-3 days
- strangulated (obstruction and toxic) -> emergency surgery
describe nephronophthisis
polydipsia
polyuria
end stage renal disease
retinal degeneration
ocular motor aprexia
b/l small kidneys
liver abnormalities
= medullary small cystic kidney disease, AR
pathophysiology of HUS
damage to renal endothelial cells
pathophysiology of lupus nephritis
diffuse proliferative glomerulonepritis with deposits of IgM, IgG, and C3
type IV reaction
blood results of post strep glomerulonephritis
low C3, normal C4
low CH50
raised ASOT
risk factors for UTI
girls > 6 months / boys < 6 months old
constipation
spinal lesions
VUR
renal calculi
common causes of UTI
e.coli ***
klebsiella
enterococcus
proteus
presentation of UTI
dysuria
increased frequency/ urgency / nocturia / enureusis
fever
vomiting
abdo pain / flank pain
signs of sepsis
gold standard test for uTI
clean and catch mid stream urine dip and microscopy
atypical UTI features
non E.coli organism
poor urine output
septicaemia / ill child
creatine raised
failure to respond to abx within 48 hours
scans required in < 6 month old with UTI
uncomplicated: USS within 6 weeks
complicated: USS during acute infection + DMSA + MCUG
Scans required in 6 month - 3 y/o with UTI
atypical -> USS during acute infection + DMSA in 4-6 months
recurrent -> USS within 6 weeks + dmsa IN 4-6 Months
scans required > 3 y/o with UTI
Atypical -> USS during acute infection
recurrent -> USS within 6 weeks and DMSA in 4-6 months
abx treatment for UTI
<3 months = IV abx
> 3 months + well = oral nitrofurantoin or trimethoprim / PO cefalexin if pyelonephritis
>3 months and unwell -> IV co-amox
describe vesico-ureteric reflux
retrograde flow of urine from bladder into urinary tract
1% newborns
severity grades of VUR
1 - tracks into non dilated ureter
2 - tracks into renal pelvis without any dilatation
3 - mild to moderate dilatation of ureter
4 - ureteral tuberosity with pelvicalcyeal dilatation
5 - gross dilatation of ureteral torturosity with blunted fornices
causes of VUR
- primary ** - congenital, AD, short ureter
- secondary - caused by high voiding pressures in bladder e.g. posterior urethral valves, neurogenic bladder, duplex ureter, uterocele
complications of vUR
recurrent urine infections
neuropathic bladder
AKI
urinary retention
hypertension
renal failure
how is VUR picked up antenatally
bilateral hydronephrosis with oligohydramnios
which scans are required post natally for VUR
MCUG ** - contrast dye to look at passing of urine via x ray
management of VUR
- bladder training e.g. double voiding
- prophylactic abx if recurrent UTIs
- oxybutynin
- surgery at age 2-3 if severe and recurrent UTI (otherwise normally resolves by age 5)
describe posterior urethral valves
most common cause of urinary tract obstruction in boys
congenital malformation of posterior urethra where mucosa folds -> dilatation of renal tract proximal to obstruction -> hypertrophied bladder
presentation of posterior urethral valves
often diagnosed pre natally - oligohydramnios
poor urine stream and dribbling
urinary retention
frequent UTIs
renal damage and post renal failure
investigations for posterior urethral valves
MCUG ***
USS - shows hydrophrosis (dilated renal pelvis > 20mm)
U&E and egFR
management of posterior urethral valves
- suprapubic catheterisation - relieves obstruction
- surgical management with resection of valves- ablation via cystoscopy
describe the primary and secondary causes of glomerulonephritis
PRIMARY (RENAL CAUSES)
- IgA nephropathy ** - days after URTI
- post strep glomerulonephritis **
- focal segmental glomerulosclerosis
- Goodpastures disease
- membranoproloiferative glomerulonephritis - circulating antigen complexes with low complement
SECONDARY (SYSTEMIC ILLNESS CAUSES)
- lupus nephritis
- HUS
- alport syndrome
- HSP
- ANCA +VE - wegeners granulomatosis
presentation of glomerulonephrits
- macroscopic haematuria
- proteinuria
- nephrotic syndrome
- nephritic syndrome
- hypertension
what are the features of nephritic syndrome
- haematuria ‘coca coloured urine’
- reduced renal function
- oliguria
- hypertension
tests for glomerulonephritis
FBC, U&E, LFT, bone, ANCA, dsDNA
urinanalysis , PCR
complement levels
renal biopsy
renal biopsy of IgA nephropathy
deposits of igA in glomerular mesangium
most common cause and presentation of glomerulonephritis
POST GROUP A STREP INFECTION
1-2 weeks prior to throat infection / 3-6 weeks prior to skin infection
renal biopsy findings in post strep glomerulonephritis
- type 3 hypersensitivity reaction
- granular deposits of IgG and C3 in capillary loop
- sub endothelial humps
investigations of post strep glomerulonephritis
- U&E
- ASOT - high
- C3 low, C4 normal
- reduced CH50
- urine - haematuria and proteinuria and tubular casts
when is a renal biopsy indicated in glomerulonephritis
- creatinine abnromal in 6 weeks
- C3 persists low beyond 3 months
- proteinuria persists low beyond 6 months
management of post strep glomerulonephritis
- penicillin
- furosemide - can help salt and water retention
- anti hypertensives
1% develop CKD
pathophysiology of good pastures disease
anti GBM antibodies target basement membrane in kidenys and lungs (against alpha 3 chain of type IV collagen in alveolar and glomerulus)
how does goodpastures disease present
- RENAL
rapidly progressive glomerulonephritis - RESP
haemoptysis, cough, fatigue, SOB
diagnosis of goodpastures disease
anti GBM antibdoies **
30% have ANCA
renal biopsy
CT chets - b/l diffuse infiltrates in lower zones (pulmonary haemorrhage)
describe Bartter syndrome
defective reabsorption of Na, K and Cl at thick ascending loop of henle
Type 1 -4 = autosomal recessive
Type 5 = X linked recessive
type 6 - AD
blood results for Bartter syndrome
hypochloraemia
hypokalaemia
hypercalcuria
metabolic alkalosis
increased renin and aldosterone levels
normal Mg
describe Gitelman syndrome
tubular loss of Na and Cl and excess loss of K in the DCT
presentation of bartter syndrome
dysmorphic features - triangular face, protruding ears, large eyes
severe salt wasting
faltering growth
muscle cramps
nephrocalcinosis
describe pathology of HSP
igA mediated vasculitis causing small vessel inflammation
presentation of HSP
70% have renal involvement - microscopic haematuria and proteinuria
skin - purpura raised rash and oedema
arthritis
GI involvement - intussception risk
causes of nephrotic syndrome
- minimal change disease (90%)*** - fusion of podocyte foot processes
- focal segmental glomerulosclerosis (10%)- steroid resistant, strcutural damage to glomerulus
when is a biopsy indicated in HSP
proteinuria > 4 weeks
nephrotic syndrome
nephritic syndrome
HTN
macroscopic haematuria
complications and risks with nephrotic syndrome
- thrombotic risk - loss of anti-thrombin 3, protein C and S -> hypercoagulable state
risk of renal artery stenosis (macroscopic haematuria) + sinus thrombosis - infection risk
risk of pneumococcal, cellulitis and peritonitis - cholesterol - hyperlipidaemia
- hypertension
triad of nephrotic syndrome
- proteinuria >1g
- hypoalbuminaemia <25 g/L
- oedema
atypical features of nephrotic syndrome
age < 1 y/o or > 12 y/o
macroscopic haematuria
HTN
high creatinine
low C3
family hx
unresponsive to steroids
management of nephrotic syndrome
prednisolone 60mg/m2/day for 16 weeks and then 40 mg for another 4 weeks
+ penicillin
+ PPI
+ fluid monitoring
90% respond to steroids within 4 weeks
if steroid resistant after 4-6 weeks in nephrotic syndrome…
BIOPSY
to try ACE-I + tacrolimus (calcineurin inhibitor) and mycophenolate (purine synthesis modulator)
cause of haemolytic uraemic syndrome
shiga toxin producing E.coli (0157:h7 variant) ** - contaminated food/ farmyard animals , 10% risk of HUS
streptococcus
HIV
EBV
presentation of HUS
- bloody diarrhoea
- vomiting + dehydration + fever
- develop 1 week later, reduced urine output + malaise + pallor
pathology of HUS
microangiopathic haemolytic anaemia with thrombocytopenia + AKI
damage to renal endothelial cells, formation of intravascular microthrombi to cause vessel occlusion
investigations for HUS
- stool sample
- bloods - reduced platelets, anaemia, increase urea/creat (haemolytic anaemia)
- blood film - fragmented RCC
management of hUS
- IV fluids and hydration
- blood transfusions
- eculizumab (monoclonal antibody to C5)
- may require dialysis
definition of AKI
- urine volume < 0.5ml/kg/hr for 6 hours
- increase serum creatinine to 1.5 x baseline or increase by 26.5 umol/l within 48 hours
pre renal causes of AKI
- volume depletion e.g. haemorrhage, diarrhoea, DKA, burns
- 3rd space losses e.g. sepsis
- heart failure e.g. CHD, myocarditis, coarction
renal causes of AKI
- medications E.G. NSAIDs, furosemide, gentamicin, contrast dye
- acute tubular necrosis + glomerulonephritis
- congenital renal disease
- vascular - b/l renal vein thrombosis, HUS *
post renal causes of AKI
- obstruction e.g. PUV, stones, mass
- neuropathic bladder e.g. trauma, spinal tumour , transverse myelitis
causes of proteinuria
NON PATHOLOGICAL
UTI
exercise
fever
transient
postural
PATHOLOGICAL
nephrotic syndrome
glomerulonephritis
CKD
tubular interstitial disease
causes of haematuria
UTI
glomerulonephritis
stones
trauma
renal tract tumour
PKD
renal vein thrombosis
exercise induced
inheritance of PKD
most commonly autosomal dominant
chromosome 16 , PKD 1 gene
presentation of PKD
multiple renal cysts -> end stage renal disease
proteinuria
HTN
berry aneuryms in circle of willis -> SAH
features of alport syndrome
microscopic haemturia
sensorineural deafness
b/l lenticlonus
features of Potter syndrome
associated with oligohydramnios
small kidneys b/l
resp distress secondary to hypoplastic lungs
low set ears
micrognathia
beaked nose
describe type 1 renal tubular acidosis
most common type in children
inherited - mutation in ATP6VIB autosomal recessive
mutations in distal tubular transporters (H+ ATPase) causing defects in H ion secretion and causing acidosis
results in RENAL STONES
ph > 5.5 in urine
describe type 2 renal tubular acidosis
usually secondary to metabolic disease e.g. cystinosis, wilsons, galactosaemia
defect in bicarb reabsorption causing acidic urine
can lead to fanconi syndrome
describe fanconi syndrome
generalised proximal tubular disorder causing
- growth flatering
- polyuria
- rickets
usually congenital e.g. familial, cystinosis, galactosaemia
blood results of fanconi syndrome
metabolic acidosis wit normal anion gap
low phosphate
low potassium
management of renal transplant
- cross match and tissue typing
- recent serology checked for CMV, toxoplasmosis, herpes, varicella, EBV, HIV, hep, syphilis
- immunosuppressants
- infection prophylaxis - co trimoxazole
- BCG and live vaccines contraindicated
which immunosuppressants used in renal transplant
- calcineurin inhibitors e.g. tacrolimus
- anti proliferative agents e.g. azathioprine
- corticosteroids
complications with renal transplants
- Hyper acute rejection (mins-hour) - T cell mediated, circulating antibodies with MHC class antigens
- hypertension
- infection
- vascular thrombosis
- maligancny
- chronic allograft nephropathy
indications for dialysis
- severe volume overload and no response to diuretics
- severe hyperkalaemia and unresponsive to treatment
- severe symptomatic uraemia - urea >40 mmol/l, seizure
- hyponatraemia or hypernatraemia
- severe metabolic acidosis
- removal of toxins
define noctural enuresis
involuntary wetting during sleep at least twice a week in children over 5 years old
risk factors for nocturnal enuresis
family history
male sex
developmental delay
constipation
sleep apnoea
obesity
psychological stress
management of nocturnal enuresis
- good fluid intake, avoid caffeine
- toileting patterns , motivational therapy and rewards
- enuresis alarm = 1st line
for short term relief e.g. sleepovers -> desmopressin 200 micrograms for 6 months +/- anticholinergic
for detrusor instability, can try oxybutynin
describe descent of testes in utero
- testicular development starts along mesodermal ridge or posterior abdominal wall
- by 28 weeks, testes reach inguinal canal
- from 28-40 weeks, descend from inguinal canal into scrotum
- descent controlled by INSULIN LIKE 3 PEPTIDE and mullerian inhibiting factor
cause of undescended testes
- retractile = exaggerated cremasteric reflex and testes can be manipulated into scrotum (usually resolves spontaneously)
- ascending testes = shortened spermatic cord pulls testes up
- anorchia = congenital absence
- idiopathic **
- syndromes e.g. prader willi, kallmann, prune belly, laurence moon
tests if b/l undescended testes
USS abdomen and pelvis and endocrine if one not felt at 3-6 months
laparoscopy >6 months if unable to palpate both
(no surgery >18 months old)
presentation of testicular torsion
acute testicular pain (pain can improve with necrosis)
nausea and vomiting
secondary hydrocele
erythematous hemi scrotum
swollen, tender, retracted, horizontal lie
signs in testicular torsion
absent cremasteric reflex
Prehns sign = negative (lifting testes does not releive the pain - +ve in epididmytis)
management of testicular torsion
- pain relief
- urgent surgical scrotal expliration within 6 hours
if testes not viable -> resect and orchidopexy on opposite side
describe torsion of appendix of epididymis
wolffian duct remnant present in 22% testest
gradual pain in upper part of scrotum
‘blue dot’ sign
management in supportive
differentials for testicular pain
- torsion
- torsion of appendix of epidymis
- torsion of appendix of testes (hydatid of morgani)
- acute epididymo-orchitis
- trauma
- testicular tumour (gradual)
- hydrocele (normally painless, transilluminates)
3 features of hypospadias
- abnormal urethral opening - urethral meatus at ventral aspect of penis
- foreskin incomplete
- chordee- penile curvature so abnormal stream of urine
DO NOT CIRCUMCISE
describe autosomal recessive polycystic kidney disease
cysts in the collection system leading to dilatation of the ducts
cysts also in liver
blood results in gitelman syndrome
hypomagnesiumaemia **
hypokalaemia
hypocalciuria
metabolic alkalosis
types of kidney stones
- struvite (large, staghorn, radioopaque, impaired renal function)
- uTI - urate
- tumour lysis syndrome
- lesch nyhan syndrome (developmental delay) - oxalate
- excessive absorption of oxalate in the gut e.g. short gut syndrome or crohns
- pnacreatitis
- cystic fibrosis
