Renal Flashcards
Causes of pre-renal AKI
hypovolaemia - D&V
Renal artery stenosis
Causes of intrinsic AKI
Glomerulonephritis
Acute tubular necrosis
Rhabdomyolysis
Tumour lysis syndrome
Causes of post-renal AKI
Kidney stone
BPH
External ureter compression
Diagnosis of AKI
rise in creatinine >= 26 in 48hrs
rise in creatinine >=50% in 7 days
fall in urine OP <= 0.5mls/kg/hr
US KUB if ?cause
Common causes CKD
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
HTN
APCKD
GFR equating to CKD
1 > 90
2 60-90
3a 45-59
3b 30-44
4 15-29
5 <15
Use of ACR
detects proteinuria
first pass morning sample
>3 = clinically signifcant
management of proteinuria in CKD
ACE inhibs (increase Cr 30% and decrease GFR 25% acceptable)
ARBs
SGLT2s
Causes of anaemia in CKD
low erythropoietin
low iron
Anorexia/nausea due to uraemia
Management of anaemia in CKD
erythropoiesis stimulating agents
PO iron (IV if not improved in 3 months)
What causes bone disease in CKD
Low vit D and high phosphate cause low Ca
Above causes secondary hyperparathyroidism
Clinical manifestations of bone disease in CKD
Osteitis fibrosa cystica
osteomalacia
osteoporosis
Management of bone disease in CKD
reduce dietary phosphate
Phosphate binders (Sevelamer)
Vit D
parathyroidectomy
Complications of AV fistulas
Infection
Thrombosis
Stenosis
Steal syndrome
Time for AV fistula to develop
6-8 weeks
Symptoms of BPH
Voiding: weak flow, straining, hesitancy, terminal dribbling, incomplete emptying
Storage: urgency, frequency, nocturia
Scoring for BPH
International Prostate Symptom Score
<7 : mild
8-10: mod
>20: severe
Management of BPH
alpha 1 antagonists e.g. tamsulosin, alfuzosin
5 Alpha reductase inhibitors e.g finasteride
TURP
MOA alpha 1 antagonists
tamsulosin, alfuzosin
decrease smooth muscle tone in prostate and bladder
SE alpha 1 antagonists
dizziness, postural hypotension, dry mouth
MOA 5 alpha reductase inhibs
finasteride
block conversion of testosterone to DHT which induces BPH
reduces size of prostate, can take 6 months to see effects
SE 5 alpha reductase inhibs
erectile dysfunction, decreased libido, ejaculation issues, gynaecomastia
Pathophysiology of PKD
cysts form, reduce function + compress other nephrons
initial compensation but when disease progresses GFR drops
Types of PKD
Autosomal dominant
PKD 1: polycystin 1 Ch 16
PKD 2: polycystin 2 Ch 4
Autosomal recessive
PKHD1: fibrocystin Ch 6
Presentation of PKD
HTN
haematuria, polyuria
abdo/flank pain
UTIs
renal stones
Extra renal manifestations of PKD
liver cysts
Berry aneurysm
mitral valve prolapse
Diagnosis of PKD
US abdo
<30 yo 2 cysts
30-59 yo 2 cysts bilaterally
>60 yo 4 cysts bilaterally
Management of PKD
Vasopressin receptor 2 antagonist (tolvaptan)
ACE/ARB
statin
RRT
Pathophysiology amyloidosis
proteins which fold incorrectly then stick together forming Beta sheet which deposits in tissues causing damage
Types of amyloidosis
AL
- plasma cell disorder, increased light chain production, leak into blood, fold incorrectly
AA
- chronic inflam causes increased serum amyloid A in blood, fold incorrectly
Examples of systemic amyloidosis
Nephrotic syndrome
Restrictive Cardiomyopathy
Investigations for amyloid
Biopsy
Congo red staining: pink
Polarised light: apple green
What is nephrotic syndrome
- proteinuria >3.5g/day
- hypoalbuminaemia <30
- hyperlipidaemia
- oedema
How does nephrotic syndrome present
- oedema: legs, face, SOB
- hyperlipidaemia: xanthelasma
- recurrent infections: immunoglobulins lost in urine
- frothy urine
- hypercoagubility: antithrombin III lost in urine, increased risk of DVT/PE
-hypocalcaemia: vit D and binding protein lost in urine
Causes of nephrotic syndrome
Minimal change
focal segmental glomerulosclerosis
membrane nephropathy
diabetic nephropath
amyloidosis
diagnosis of nephrotic syndrome
PCR >300mg/mmol
hypoalbuminaema
Management of nephrotic syndrome
steroids - pred
10/20% steroid resistant (50% more likely to go to end stage renal failure)
immunosuppressants
- diuretics
statins
prophylactic LMWH
Bladder cancer type
transitional cell
What is Calciphylaxis and how does it present
deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.
Treatment of Calciphylaxis
reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds.
What causes chronic pyelonephritis
recurrent infections lead to scarring of renal parenchyma and impaired function
Predisopising factors of chronic pyelo
obstruction (Stones)
vesicourethral reflux in kids
exam features of chronic pyelo
blunted calyx
corticomedullary scarring with atrophy of tubules
eosinophilic casts in tubules
What is diabetes insipidus
either decrease in secretion of ADH (cranial) or insensitivity to ADH (nephrogenic)
Causes of cranial DI
idiopathic
head injury
pituitary surgery
craniopharyngiomas
infiltrative (sarcoid)
causes of nephrogenic DI
genetic
hypercalcaemia
hypokalaemia
lithium
tubulo-interstitial disease: obstruction, sickle cell, pyelo
symtoms of DI
polyuria
polydypsia
investigations of DI
increased plasma osm and decreased urine osmo (if urine >700 cannot be DI)
water deprivation test
Management of DI
Cranial: desmopressin
Nephrogenic: thiazides, low salt low protein diet
Causes of epididymo-orchitis
genital: chlamydia, gonorrhoea
bladder: e.coli
Features of epididymo-orchitis
unilateral tesicular pain/swelling
*in torsion, <20yo, severe acute pain
Ix for epididymo-orchitis
STI check
MSU
Mx epididymo-orchitis
if STI: sexual health check
?organism ceftriaxone 500mg IM once + doxy 100mg BD 10-14/7
if enteric: PO quinolone (ofloxacin) 2/52
pathophysiology of minimal change disease
T cells release cytokines that flatten podocytes (effacement) so the negative charge barrier is reduced allowing albumin through
Larger proteins cannot get through = selective proteinuria
Features of minimal change disease
- nephrotic syndrome
- selective proteinuria
- renal biopsy: podocyte fusion and effacement of foot processes, normal glomeruli
Management of minimal change disease
PO cortiocosteroids -> cyclophosphamides
prognosis of minimal change disease
1/3 single episode
1/3 infrequent relapse
1/3 frequent relapse
causes of minimal change disease
mostly idiopathic
NSAIDS
Hodgkins
infective mono
causes of focal segmental glomerulosclerosis
idiopathic
secondary to renal pathology - IgA nephropathy
HIV
heroin
SSD
Pathophysiology of FSGS
damaged podocytes -> proteins through
trapped proteins/lipids in glomerulous -> hyalinosis -> sclerosis
Ix FSGS
renal biopsy -> focal and segmental sclerosis and hyalinosis
effacement of foot processes
Mx FSGS
steroids +/- immunosuppressants
causes of membranous glomerulonephritis
idiopathic
hep B, malaria, syphilis
malig: prostate, lung, lymphoma, leukaemia
SLE, rheumatoid, thyroiditis
Membranous glomerulonephritis diagnosis
nephrotic symptoms
renal biopsy: spike and dome appearance of basement membrane
Management of membranous glomerulonephritis
ACEI/ARB
cortiocosteroids= + cyclophosphamide
anticoag if high risk
Prognosis of membranous glomerulonephritis
1/3 spontaneous recovery
1/3 persistent proteinuria
1/3 ESRF
Good prognostic factors: female, young, asymptomatic
What type of tumour is Wilms
nephroblastoma
management of wilms
nephrectomy
chemo
radio
