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
Goodpasteures
- Goodpasteures = 2 pasteures
The 2s and the Gs
Type 2 hypersensitivity
Affects 2 organs - lung + Kidney
Ab vs (type 2 x type 2) = Type 4 collagen
anti-GBM - Vs Collagen type 4 - pulmonary/glomerular BM
Px:
- Pulmonary haemorrhage - young smoker
- Biopsy - IgG deposits in linear patterns
- Increased transfer factor
RF:
- smoking
- LRTI
- pulm oedema
- inhaled hydrocarbons
- young male
IgA Nephropathy
- IgA = deposits
AKA - Bergers Dx/Mesangioprolif
Most common
Histology:
- Mesangial hypercellularity w/ +ve immunofluroensce IgA/C3
FOLOWS URTI - 1-2/7
Px:
- young male, follows URTI 1-2/7, recurrent macroscopic haematuria.
Good prognosis:
- Frank haematuria
Poor prognosis:
- Male
- Smoking
- HTN
- proteinuria
- high lipids
- ACE
Post-streptocoocal GN
PSG = THREE
3 weeks post URTI
Low C3
Lump3 - Bump3 - immune complex deposits
Type 3 hypersensitivoty
Immune complex deposition of IgM/IgG/C3
Ft:
- young child gen unweel
- LOW C3
- proteinuria
- ASO TITRE
Biopsy features:
- Acute GN - Endothelial prolif w/neutrophils
- electron microscopy –> subendothelial umps = immune complex deposits
- immunofluorescence = STARRY SKY = GRANULAR
Alports syndrome
Alports = Alfort = Al-4
Same as goodpasteures (2 organs) + can’t see or hear (2 more)
- Lungs + Kidney + eyes + Ears
remember dodgy landing X wing video on pixorize.
X - Linked dominant
Collagen type 4 defect
Eyes - cataracts/lenticonus/lens dislocation/retinopathy
- Ears - sensorineural deafness
- Kidneys - GN/haematuria
Renal biopsy - S[litting of lamina densa = basket weaves.
Minimal change dx
- THE MINIMALS
Affects kids - Minimal age
Foot = minimal body part = foot process effacement
Nepjrotic syndrome
affects CHILDREN
Causes:
- idiopathic
- Drugs - NSAID/Rifampicin
- Hodgkins lymphoma.thymoma
- infectious mononucleosis
Pathophysiology:
- T cell mediated damage to BM –> Anion loss –> electrostatic charge –> more permeable to Albumin
Ft:
- Nephrotic syndrome
- Normotension
- Selective protein loss
Inc:
- Light microscopy no change
- e- microscopy - effacement of foot processes + fusion ofpodocytes.
Mx: STEROIDS –> fx –> Cyclophoisphamade
Prognosis:
- 1/3 recover
1/3 infreq episodes
1/3 freq episodes –> stop b4 adulthood
FSGS
FSG = HIV
Px - Young adults w/ nephrotic syndrome
Causes:
- idiopathic
- secondary to IgAA/Reflux nephropathy
- HIV
- Heroin
- Alports
- SCD
- recureence risk in transplant
Biopsy finding:
- Light microscopy - focal + segmental sclerosis
- e- microscopy - foot effacement process.
Mx:
- Steroid + IS
Membranoproliferative GN
Proliferative = Fast
Prolif = fast = TRAM TRACK Px = Mixed ]
Type 1:
- majority
- causes = cryoglobulinameia/hep C
- Renal biopsy - TRAM TRACK
Type 2:
- dense deposit dx
- Causes = lipodystrophy/factor H deficiency
- Ft = low complement - C3
- Biopsy = DENSE DEPOSITS - immune complex
DB Nepropathy
Pathophysiology:
- Raised glomerualar capillary pressure –> non-enzymatic glycosylation of BM
Histology:
- BM thickening
- Capillary obliteration
- Mesangial thickening
- KW nodules
Stages:
1) Hyperfiltration - raised eGFR
2) Silent phase - no microalbuminuria
3) Incipient nephropathy microalbumin - 30 -300
4) Over nephropathy: - alb excretion >300/HTN/ KW nodules
5) ESRF
APKD
Most common inherited kidney dx.
ADPKD - Chromosome 16
APKD type 1
- 85%
- Polycystin 1
- Px earlier
APKD type 2
- 15%
- polycystin 2
Px:
- Abdo pain
- HTN
- UTI
- Aneurysmal dx
+FHx –> SCREEN
Mx: Tolvaptan - vasopressin 2
US diagnostic criteria:
- 2 cysts unilat - <30 yrs
- 2 cysts B/l - 30-60yrs
- 4 cysts B/L - >60yrs
NB: These adults tend not to be EPO Defficient –> Inflamm or mlaignancy –> suddem fall in Hb in prev stable pt as –> increase inhibition of recombinant EPO
Thin BM disease
Inherited - type 4 collagen
3 of:
- persistent haematuria
- No renal fx
- FHx - haematuria w/o renal fx.
Acute interstitial nephritis.
accounts for 25% of drug induced AKI
Causes:
- Penicillin
- Rifampicin
- NSAIDS
- Allopurinol
- Furosemide
- systems - sjrogrens/SLE/Sarcoid
infectious: - Hanta virus/staph
Ft:
- Temp/Rash/Arthralgia
- ESR
- mild renal impairment
- HTN
Inx:
- Sterile pyuria
- white casts
Histology:
- increased oedema + infiltrate of CT between renal tubule
Mx:
- Cesation +/- Steroids
Chronic interstitial nephritis.
Many causes - systemic and local
Px:
CKD/ ESRF/RTA. DB1/ Salt wasting
Renal papillary necrosis
Coagulative necrosis of renal papillae
Causes:
- severe acute pyelonephritis
- DB Nephropathy
- Obstructive nehropathy
- Analgesic nephropathy - Phenacetin/NSAIDS
- Sickle cell anaemia
Ft:
- Visable haematuria
- loin pain
- proteinuria
Q STEM - pt with chronic pain px with loin pain + CKD = Haematuria.
Reflux nephropathy
most common cause of ESKD in children
Scarring in 1st 5 years of life
Strong GENETIC component - therefore if siblings affected –> Screen
Grade 1 - 4 with increasing reflux
All children UTI - investigate - VUR
Inx - micturition cystography
Px:
- UTI in child
- Renal scar –> HTN
- Proteinuria
Mx:
GRade 1-3 self resolve
Grade >4 - surgery
Prophylactic abx if >grade 2
UTI in pregnancy
symptomatic:
- 7/7 abx - avoid Nitro if near term
- urine culture
Asx + bacteruria:
- 7/7
- urine culture
- 2nd urine culture after completeion.
Renal Stones Types
Ca Oxalate
Cystine
- Metabollic
- semi opaque
Uric Acid - Assoc with GOUT
CaPO4-
Struvite - Recurrent UTI - P.mirabilis
Diffuse proliferative GN
Post strep - in child
- Nephritix syndrome and AKI
- SLE
Goodpasteures - REMEMBER THE G
IgG
anti-GBM
AV fistula - ?time taken to develop
6-8 weeks
Cystinuria
A.R. - Chromsome 2 - defect in transport of cysteine, orthinine lysine arginine (COLA)
Recurrent renal stones = yellow + crystalline = semiopaque
Inx - cyanide - nitroprusside test
Mx:
- Hydralazine
- penicillamine
- urina alkalinisation
Membranous GN
- Need to suck some dick to become a MEMBER
Dome = street for sucking dick = Spike + Dome apperance
Who sucks dick int he street - IVDU looking to score = HEPATITIS
Most common type of GN in adults:
e- microscopy –> spike and dome appearance = thick BM + electron dense deposits
Causes:
- Idiopathic - anti-phospholipase A2
- Infection - Hep B, malaria and symphillis
- malignance - lung Ca, lymphoma, leukaemia
- Drugs - Gold, penicillamine, NSAIDs
- AI - SLE, thyroiditis, RA
Mx
- ACEI + ARB
- I.S.
- if high risk 0—> anticoah
Prognossi s= rule of 1/3
- 1/3 recover
- 1/3 persistent proteimuria
- 1/3 ESRF
HIV + renal involvement
Large kidneys FSGS Proteinuria/nephrotic syndrome Elevated urea + creatinine normotesnion
retroperitoneal fibrosis
Reidels thyroiditis inflamm AAA Sarcoidosis RT Drugs - methysergide
eGFR variables
CAGE
Cr
Age
Gendor
Ethnicity
Renal stones types
Ca Oxalate:
- pH 6
- Radio-opaque
- High calcium
- low oxalate in ureine
Cystine stones:
- Cystinuria / metabolic
- SEMI-OPAQUE
URate stones:
- Produc of pirine synthesis
- pH low
- GOUT / ileostomy
- Can be caused by malignancy
- Radio-opazue
CaPO4-:
- RTA
- pH>5.5
- RTA - type 1 + Type 2
- Radio-LUCENT
Struvite: pH<7.2 -Staghorn calculi - stones of Mg, NH3, Po4 - assoc w/ CHRONIC INFECTION
RF for stones
ehydration hyper Ca/PO4 high oxalate RTA Medullary sponge kidney Cadmium.berillyium
RF for urate stones:
- gout
- ileostomy
Drugs: - Loop diuretics steroids acetazolamide theophylline
Mx of renal stones general
NSAID - diclofenac for renal colic
Non contrast CT KUB
<5 mm - pass by itself
> 5 mm:
- SWL - CI Pregnancy - <2cm+ not preg
- Ureteroscopy - <2cm + preg
- Percut - complex staghorn
Obstruction + infection –> SURGICAL EMERGENCY
Mx of renal stones specific
Calcium:
- low protein + salt diet
- Fluid
- Thiazides
Oxalate:
- cholecystyramine
- Pyrodixine
Uric Acid:
- Allopurinol
- Urinary alkalinisation
Acute urinary retention
Pain
Px –> anuria/AKI
Inx - US
Mx: If bladder outflow obstruct –> catheter
if vesico-ureteric and above –> stent or drainage - percut
post mx – > massive diurese = temporary nephrogenic DI
Chronic urinary retention
Painless
px –> CKD/ESRF
Common complication - Na wasting/metabolic acidosis
Inx: - US –> retrograde pyelography if no obstruction identified ( VUR/post obstruct atrophy)
Causes:
Luminal = calc/clot/tumour/papillary necrosis.
Wall = neuromuscular - neuropathic bladder
External compression = multiple cause
Neuropathic bladder
Childhood most common cause:
Px:
- Upper tract dilatation –> US - no obstruction
- incontinence/reflux/infection
- assoc bowel dysfn.
Mx:
- anticholinergic
intermittent self cath
ileal conduit
Post urethral valces
Px:
- male infants
- px in 1st year of life w/ - poor stream/bladder dysfunction/failure to thrve.
Inx –> ANC US
Tx - self cath
Renal Cell Ca
Most common cell type = Clx cell
Assox:
- middle aged male
- smoking
- VHL
- Tuberous Sclerosis
Ft - Triad of:
1) Loin pain
2) Haematuria
3) Abdo mass
Other ft
- Left varicocele
- Enocrine - high PTH/high EPO. Renin/ ACTH
- 25% metastatic
- Stauffer syndrome = paraneoplastic hepatic dysfn
Mx:
- Confined - SURGERY
- High size/METS - TKI (Sonafenib)/INF-alpha/ IL-2
Wilm’s Tumour
Childhood Px - <5yrs
Ft:
- Abdo mass
- Flank pain
- Haematuria
95% = Unilat 20% Mets = lung
Assoc.
- Beckswith wiedenaan –> overgrowth syndrome - big tongue + open abdo
- WAGR - Wilms/Aniridia/ G-U/ Retardation
Mx: Nephrectomy/cryo/RT
Good prognosis - 80% cure rate
Uroethelial tumours
majority = transitional cell Ca
others - Squamous cell
RF: - Smoking - Alanine - Analgesic nephropathy -Rubber -Schistomiasis - renal cystiv dx - Renal stones (VHL) -
Bladder Ca RF
Transitional:
- Smoking
- ALANINE
- Rubber
- Cyclophosphamide
Sq Cell Ca:
- Smoking
- Schistomiasis
Amyloidosis of renal tract - Inx
Inx
- CONGO RED STAINING - APPLE GREEN BIFRINGENCE
- SAP Scan - serum amyloid precursor
- Rectal tissue biopsy
Amyloidosis of renal tract types
AL:
- Most common
- Light chain - Ig
- Ft - nephrotic syndrome/cardiac/neuro
- Mx = Mephalan –> BM transplant
AA: - Amyloid A precursor = acute phase ractant - seen in CHRONIC INFECTION - High renal dx = Tx = txunderlying
Beta-2 microglobulin
- Part og MHC
- assoc w/ pt on renal dialysis
Renal A stenosis
cokmmon causes:
Old = athersclorosis
Young female = Fibromyscylar dysplace
- US = Assymetric kidneys
- Angiography =string of beads
Px:
- HTN
- CKD/AKI
- Flash pulm oedema
- Above exac by ACEI/ARB
SLE and the Kidney
SLE –> Lupus nephritis –> Therefore req REGULAR SCREENING
WHO CLassification: - Class 1 = Normal Class 2 = Mesangial GN Type 3 = FSGN Class 4 = Diffuse prolif GN Type 5 = Diffuse membranous GN Type 6 = Sclerosing GN
Inx = Renal Biopsu
- WIRE LOOPING = endothelial/Mesangial expansio
- E- micro - Subendothelial immune deposits
- IF –> GRanular appearance
MX:
- ACEI/ARB
- Active dx –> Steroids/IS
H.U.S
see in young child - Triad of:
- AKI
- Miicroangiopathic anaemia
- Thrombocytopaenia
Causative agent - E.COLI
other causes:
- Pneumococcal
- HIV- SLE/Drugs/Ca
Inx:
- FBC
- U+E
- Stool culture
tx = supportive
- V.Sev ecoli infec –> Plasma exchnge
TTP
Abnormally large sticky multimers of vWF –> clumo
Ft:
- Triad as for HUS
- these patients have FLUCTUATING neuro signs = microemboli.
CauseS: - infection -preg - Drugs - ciclosporin/OCP/pemmocollin/Clopi - Tumours SLE - HIV
Mx:
- PLASMA EXCHANGE
- Steroid/IS
Multiple Myeloma
Mnemonics:
Ecidence of end organ damage - CRAB
M.Y.E.L.O.M.A
NEoplasm of BM
CRAB:
- Ca >11/ RFx / Anaemia / Bone dx (lytic lesion/rain drop skull)
M.Y.E.L.O.M.A
- M spike
- You better check Ca + lYtic lesion
- ESR
- Light chain/bence jones
- Ouch my bones
- myeloma nephrosis/ marrow plasmocytosis >10%
- Anaemia
Inx:
- BM biopsy –> >10% plasma cells
- IgA + IgG + Bence jones
- Skull XRAY - Raindrop skull
- MRI - radiculopathy
Diagnostic criteria 1 maj + 1 minor or 3 minor:
MAjor:
- Plasmocytoma
- > 30% plasma celss
- v.high M protein
Minor:
- 10-30% plasma cells
- minor M protein
- Osteolytic lesions
- minor level Ab
VAsculitis in Renal
Small vesse vasculitis - NO HTN :
- WG - cANCA - Saddle nose
- Churg strauss - pANCA - Astham/nasal polyp/eosinophillia
- MPA - pANCA
- Histology for all above = Necrotising GN = CRESCENT OR FOCAL PROLIF
Poly arteritis Nodosa - HTN:
- med vassel
- ANCA neg
HSP - IgA cross over
Kawasaki Dx - Child - CRASH & BURN
- Conjunctivitis - non purulent
- Rash
- adenopathy
- Strawberry togue
- HAnds + feet - erythema
- Burn = temp
Takaysau: - Lrg vessel vasculitis - claudication RAS - arotid bruit
GCS
Renal sarcoid
Px as AKI due to AIN –> HYPER CA AND HEPATO-SPLENOMEGALU
Px as CKD - due to HyperCa or CIN
Mx - steroids
- monitor serum ACE
Nephrotoxic drugs
Decrease BF:
- NSAID
- ACEI
- ARB
- Tacrolimus
- Ciclosporin
Direct toxic
- Aminoglycloside
- Amphotericin
- Cisplatin
GN:
- gold
- penicillamine
Li –> interstitial fibrosis
Most common infectign organism of PD?
Staph epididermis !!!!!
Followed by:
- stah A
- enterococcus
Rapidly progressive haematuria
HAemoptysis
URTI signs - what is it
Granulamotosis with polyangitis
Plasma exchange wjhat electrolyte is low
Hypocalcaemia
Plasma exchange is used to remove and filter a patients blood.
Citrate is used as an anticoagulant, which can bind to calcium –> hypocalcaemia
bph MX - medical
1) - alpha-1 antag
- Tamsulosin
- causes postural hypotension, dry mouth, depression
- decreas SM tone dizziness
2) 5-alpha reductase inhibitor - Finasteride
- stops T –> DHT
- reduces volume of prostate –> slow progression
- take sup to 6/12 to work
- E.D./decreased libido/ejac problems.
Drug induced AIN
Commonky allopurinol and NSAIDs
Allopurinol -, eosinophika
Note NSAIDs no eosinophiks
Mx:
A
Withdrasl of drug
(no proof for steroids, may be use din very severe)
Following Transplant immunosupression what is a common side effet
Increase in DB
Steroids heavily used in I.S.
Renal involvement in Myeloma
Cast nephropathy:
- severe renal insufficiency
- ABSENT ALBUMIN (or bery small amounts)
- Bence jones
AL. Amyloidosis:
- nephrotic syndrome
- mild. Renal. Insufficiency
- LAMBDA LIGHT CHAIN
Cryoglobunaemic glomerulonephritis:
- mild. To. Severe nephrotic sybdroe
- HAEMATURIA
Light chain deposition diseass:
- MILD disease
- KAPPA ligt chain
Amyloidosis
seen on MYELOMA AND MGUS
Other csuses:
Familal Mediterranean fever
Secondary (RA)
Apple green bifringence on congonred staining
Renal. Amyloidosis recurrs after. Transplant
Affects liver kidneys and heart
Cardiac involcemenr is the most common causs of sudden. Death
AA vs AL amyloid question features
Both are apple. Green bifringencd
AA
- related to RHEUMATOID
- chronic inflamm diseass
AL
- severe disease
Acute vs chrinic graft rejection
Acute <2 weeks:
- acute rejextion
- ATN
- CNI Toxicity
- thrombosis
- surgicla comlkciatuon
Chronic reject - >2 weekz
- chronic rejection
- chronic CNI toxicity
- obstruxt
- R. A. S
- Bk/JC virus
- recurrenc of primary dx
Acute vs chrinic graft rejection
Acute <2 weeks:
- acute rejextion
- ATN
- CNI Toxicity
- thrombosis
- surgicla comlkciatuon
Chronic reject - >2 weekz
- chronic rejection
- chronic CNI toxicity
- obstruxt
- R. A. S
- Bk/JC virus
- recurrenc of primary dx
HyperPTH vs familial hypocalciuric hypercalcaemia
Both have high serum Ca
FHH has LOW URINARY CA
Which glomerulonephritis is assoc with cance
Membranous neohritid - lung cancer
Wegners
we-C-ners
cANCA
C on stick man - effects nasopharync + lungs + kidneys
Biopsy:
- Segmental -C-rescentic necrotising GN
Poor prognosis - Renal dx
most common side effect of LT dialysis
Carpal tunnel syndrome
medullary sponge kdiney
increase risk of renal stones in pregnancy
Oain in drinking alcohol and renal. Dx
Minimal change disease
Hb aim. In CKD
110-120 g/DL
Nephritic Syndromes: PIG ARM
Post strep GN
IgA Nephropathy
Goodpastuers
Alports
RPGN
Membrano-prolif
Partial lipodystrophy - renal involvement
mesangiocapillary with C3 nephritic factor
therefore get low C3 and normal C4
Normal Anion Gap
12-18
Which vasculitis is assoc with wegners
R PGN
