Renal Flashcards
Contrast nephrectomy
occurs 2-5 days after administration
RF:
- Known CKD
- AGE
- Dehydration
- Hfx
- NEphrotoxicss
ACEI - ?renal A stenosis
Fall in eGDR of 25% or rise in Cr of 30%
Gosrelin MOA
GnRH Agonist –> neg feedback to ant pituitary
persistent non-visible haematuria def
Blood + 2/3 samples taken 2-3 weeks apart
Post tranplant infection
CMV - CMV PCR
Testicular Ca - types
95% germ cell –> divided into seminoma and non seminomas
Non germ cell = Leydig and sarcomas.
peak incidence for teratoma = 25 yrs
peak incidence for seminoma = 35 yrs
Testicular Ca - RF
Infertility cryptorchidism Fhx Klinefelter's mumps orchitis
Testicula Ca features
Painless lump
Hydrocele
gynaecomastia
Seminoma - hCG
AFP/LDH elevated in most
Diagnosis = US
TEsticular Ca Mx
Orchidectomy
chemo/RT
Semioma 5yr survivval >teratoma
95%:85%
Site of action of diuretics
Loop:
- Furosemide - TAL - NA-K+-Cl
- Bumetande
Thiazide:
- Distal tubule - Na-CL
Aldostenerone angtag:
- Spironolactone
- Distal tubule/Collectinf duct - Na/K+
- ANP = anti aldisteribe
Proteinuria
microalbuminuria = 30-250 of Alb or UACR >5mg
non renal causes of high protein:
- Temp
- Ex
- Skin dz
- LUTI
Orthostatic proteinuria:
- Raised protein after standing for long time - disappears afte recumbence - early a.m. = N
Renal angiography complicaion
Nephrogenic systemic fibrosis = similar to scleroderma
Renal tubular acidosis
Type 1:
- Distal
- Poor H+ excretion
- URinary pH >5.3 - alkaline
- HYPOKALAEMIA
- Complication: Nephrocalcinosis/Renal stines
- Causes: idiopathic/SLE/Sjrogrens/amphoterecin/analgesic neohropathy
Type 2: - Proximal - NaHCO3- rabs fx Urine pH normal - HYPOKALAEMIA - Causes: idiopathic/fanconi syndrome/ Wilsons's dx/cystinosis/tetracycline/carbonic anhydrase inhib
Typ 4:
- Low aldosterone –> Dont form NH3+
- HYPERKALAEMIA
- Causes: Hpoaldosteronism/DB
Fanconi syndrome
General reabsorptive disporder of procimal tubule
Rype 2 RTA
glycosuria, Amino-aciduria, polyuria, phsphateuria
Causes:
- Cystinosis
- Sjrogrens
- MM
- Wilson’s
- Nephrotic syndrome
Hypokalaemia causes
w/HTN
- Cushings
- Conns
- Liddles
- 11-beta-hydroxyas deficiency
w/o HTN
- Diuretics
- GI loss
- RTA
- Barters
- Giltemanns
Liddles/barters/gitelman - what are they
Liddle:
- Xs Na Reabs
- These NA channels = amiloride sensitice
- HTN + Hypokalaemia
- Mx: Na restrict/ K+ replace/ Amiloride
Barters:
- A.D.
- Defect in Cl- channel of NA- K - CL transporter
- low BP/hyper reninuria
- Tx = K+ replace +/- NSADS
Gitelmans:
- Similar to BArters
- A.R.
- Px later in life:
- Low K+/ Mg/ H+/ Ca
- Mx: Mg + K replace
AKI KDIGO Classification
Satge 1:
- Cr - >26 mmol or rise of =/> 1.5-1.9x BL
- UO - <0.5 ml/kg/6hr
Stage 2:
- Cr: >2 - 2.9x
- UO: <0.5 ml/kg/>24hr
Stage 3:
- Cr: >3x or >354 mmol
- On RRT
- UO <0.3/kg/24hr or Anuria for/12 hrs
Drugs to stop in AKI
Stop as worsens AKI
- NSAIDS
- ACEI/ARBS
- aminoglycloside
- Diuretics
Stop as increase toxic:
- metformin
- Dig
- Li
ATN
Causes
- Renal ischaemia
- Toxins - Aminoglycloside/Myoglobin (Rhabdomyolysis)
Ft
- High urea/cr/K+
- MUDDY BROW CASTS
Histopathology
- Tubular epithelial necrosis
- these necrotic cells can block tubules
- thos can cause tubular dilation
Phases
- Oliguric
- Polyuric
- Recovery
ATN Vs Pre-renal uraemia
Think about pre-renal ureamia - HOLDING on to Na + urea
Urinary NA:
- ATN>30
- PU - <20
Na Secretion:
- ATN >%
- PU <1%
Urea excretion:
- ATN >35%
PU <35%
URine:plasma OSm:
- PU >1.5
ATN <1.1
Urine:
- ATN - muddy brown cast
- PU - bland sediment
Indications for emergecy dialyss
- Hyperkalia > 6.5
- URaemia - pericarditis/encephalopathy
- pH <7.1
- Resistant fluid overload
Rhadbomyolysis
Causes:
- Seizure
- Long lie
- Traumatic –> IVDU
- Ecstasy
- Crush injury
- McArdles
- Statins - combo with clarithromycin
Mx:
- IVI
- URinary alkalinisation
RF for Contrast nephropathy
RF:
- high contrast lad
- multiple doses
- Age
- CKD
- Hypovolaemia
- Dehydration
- Myeloma
- hyper Ca
- Hyperuricaemia
CKD
Stage 1 - eGF>90
- Req abnoral U+E or proteinuria
Stage 2: 60-90: req abnormal U+E or proteinuria - no anaemia - no MBD - may have HTN
Stage 3a = 45-59 and 3b = 30-44
- Most commonly have HTN]
- largest group
- 3b –> anaemia/MBD
Stage 4: 15-30:
- HTN +++
- PO4-
Stage 5: <15
- RRT
Anaemia of CKD - causes
dmaged kidney produce less EPO
URaemia + Toxin build up –> decrease EPO production
Nausea/anorexia
Decreased Fe absorption
BLood loss - fragile capillaries - GI
Reduced RBC survival
anaemia - CKD MX
EPO stimulating agents:
- EPO/darbopoeitin
- target = 10 - 12 g/l
- Ensure Fe Replac
- only use when deemed likely to benefit from QOL and physical fn
Resistance to EPO:
- Low Fe
- Occult GI blood loss
- Al toxicity
- hyper PTH
- sepsis/chronic inflamm
- pure red cell aplasia
S.e:
- Accelerated HTN/Encephalopathy
- Flu-like
- Bone aches
- thrombosis
- Pure red cell aplasia = Ab vs exog/endo EP
CKD HTN
ACEI + ARB = 1st line
eGFR <30-45 consider furosemide
CKD - PRoteinuria
UACR used :
Early am spot test 3-7 –> rpt –> >3 –> confirms
>70 - doesnt need repeat
Freq monitoring - per yr - SEE NOTES
Referral to nephrologist:
- UACR >70
- UACR >30 + persistent haematuria (xcl UTI)
- UACR >3 + persistent haematuria + 2 other R F(renal fn/CVD)
CKD - MBD - Histological findings at bone biopsy
OSteomalacia = low vit D
Hyper PTH bone dx = OSteoperosis + OSteitis fibrosa cystia ( Subperiosrteal eroisons in radial border of phalanges)
OSteoperosis = malnurised + high PTH
Osteosclerosis - RUGGER JERSE SPINE
Adynamic bone dx –> low urnober
Aluminium bone dx - rre now as AL agents not used
CKD - MBD mx:
1) low dietary PO4-
2) PO4- Binders
- Sevelamer - Non Ca based –> decreases uric Acid + improves lipids
- Ca based –> S.e. hyper Ca + vascular calc
- Al based - no longer used
3) Vit D replace - alpha -calcidol.calcitriol
4) PTH-ectomy
HD vs PD - When to choose HD
- recent abdo surgery
- recurrent peritnitis
- severe recurrent illness
- resp dx - stenting
- frail
- peritoneal mebrane/ ultrafiltration faiure
- too poor renal fn
- sev malnutrition –> lots of protein lost in efluent..
PD complications
BActerial peritonitis
- Staph epidermis - most common —> Staph A/G-
- rpt episodes –> HD
Ultrafiltration fx
Pt = high transporter of glucose
Encapsulating peritoneal scelrosis:
- Recurrent peritonitis or LT PD _-> Peritoneum thickens and encases bowel –> UF/ Bowel obstruct / Malnutritiom
Haemodialysis
usually vasc access via elective fistula
can use tunelled catheter in emergencies:
- Late px w/sev uraemia
- Fistula complication
- higher infection risk
- OBstruction risk
Lt complications
IHD
LVH/dilated cardiomyopaty
vacular calcification
calvular dx
pyrophosphate arthropathy –> pseudogout/gout
Contraindications to Renal transplant
Recurrent/ malignancy (<2yrs)
Severe comorbidity
Graft rejection
Hyperacute:
- Mins - hrs
- mottled dusky skin
- preformed Ab vs Donor HLA class 1
- Types 2 hypersensitivity
- mx = remove graft
Acute graft rejection:
- <6/12
- T cell mediated
- mismatch HLA or CMV
- Mx - Steroid/IS
Chronic graft rejection:
- > 6/12
- Ab & Cell mediated –> fibrosis
- Recurrence of original dx - MCGN>IgA>FSGN
Acute graft dysfn causes
ATN of graft
Stenosis:
- Uncontrolled HTN –> angioplasty
thrombosis
- if arterial –> sudden anuria –> immed surgery
- Venous –> pain + swelling + oliguria –> graft loss.
urine leakage
- Decreased UP / high Cr/ fever –> US revision
infection/lymphocele –> drain
chronic graft dysfn
Chronic renal allograft nephropathy:
- immunological and non-immune cuases
- Develop –> proteinuria + graft dysfn
- Mx - controlled HTN/low proteinuria –> ACEI / ARB
Recurrence of primary dx
polyomavirus infection:
- BK/JC virus
- Decrease MMF
Renla transplant I.S - example regimes
initial: Ciclosporin/Tacrolimus w/Mab
Maintenance: Ciclosporin/tacrolimus w/ MMF or sirolimus
+ steroid if >1 steroid responsive acute rejection
Renal transplant I.S. - medicaqtions
Ciclosporin
- Calcineurin Inhibitor
Tacrolimus
- Stop B/T cell
- s.e. - GI/BM supression
Sirolimus:
- IL-2 inhib –> stop T cell prolif
- s.e. Hyperlipidsaemia
Mab:
- Il-2 inhibitors
Monitoring:
- CV dx
- Renal Fx
- Malignancy
Nephritic
- Rapidly progressive GN
- IgA Nephropathy
- Alports
I= eye = things you can see - H’s:
- HTN
- HAematuria
- HArdly pee - Oliguria
Nephrotic syndromes
nephr-O-tic
- minimal changed - Minimal Age
- membranous GN - Suck some dick to become a MEMBER of the club
- FSGS - FSG - HIV
- Amyloidosis
- DB nepropathy
-O-:
pr-O-teinuria
hyp-O-albuminaemia
Fat chick with big belly - hyperlipidaemia
Mixed nephrotic/nephritic
Triad:
1) Proteinuria - >3g/day
2) Hypoalbuminaemia - <30g/L
3) Oedema
- Diffuse prolif GN
- Membranoproliferaive GN - Proliferative = fast
- post-strep GN
Rapidly progressive GN
- Rapidly “crescenteric” GN
Crescents = look like loops = LUPUS or DIFFLUPUS (Diffuse prolif)
- Loop wire lesions
Rapid onset –> AKI
HTN
Histology - glomeruli full of crescent cells.
Mx:
- plasma exchange - Steroid/IS