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High yield Flashcards

1
Q

What role does dopamine have on AKI

A

NONE

  • 3 systematic reviews - concluded no benefit in treating or preventing AKI
  • potential harm - incl MI, arrhythmias and reduced intestinal blood flow
    e. g Fenoldopam - BAD
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2
Q

Treatment of severe malaria

A
  • mortality 15-25% - jaundice, severe anaemia, ARDS
  • IV artesunate - treatment of choice for severe malaria!!!
  • resistance has emerged in SE asia - single point propeller region mutation - chromosome 13
  • Severe malaria
    • ​IV artesunate 2.4mg/kg bolus IV then daily (S/e cerebellar ataxia)
    • switch to oral artemether-lumefantrine to complete 3 days
    • if not available, then do IV quinine instead of atesunate
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3
Q

Prophylaxis of malaria

A

Mefloquine - effective against both vivax and falciparum - resistance in thailand, cambodia - start 2 wks before travel, 4 weeks after reutrn, SE - GI , cardiac, neuro - psychotic episodes, safe in 2nd and 3rd trimester of pregnancy

Doxycycline - 1 day before and 4 weeks on return - contraindicated in pregnancy - SE - photosensistivity, GIT upset, OCP ineffective

Malarone - expensive, start one 1 day before, continue one week after

insufficient data on pregnancy

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4
Q

what is medullary sponge kidney and cystic kidney

A

Medullary sponge kidney - common, malformation of terminal collectiing ductos - microscopic and macro medullary cysts - generally bilateral

  • benign, but associated with nephrolithiasis and UTIs
  • majority causes sporadic then inherited

Medullary cystic kidney - misnomer - majority do not have renal cysts evident on imaging - predom a tubulo-interstitial disorder - progress to ESRD

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5
Q

define acute infective endocarditis and likely organisms

A

Short history (days) of fevers, rigors, unwell,

hypotension, embolic lesions, heart failure

– Aggressive organism eg Staphylococcus aureus

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6
Q

what is NGAL? - Neutrophil Gelatinase Associated liocalin?

A
  • originally found bound to gelatinase from human neutrophils
  • expression upregulated following ischaemia in renal prox epithelial cells
  • INCREASE in NGAL in blood probably from other organs

- INCREASE in NGAL in urine from renal tubular cells - predicts development of AKI early and sustained AKI.

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7
Q

Define PUO

A
  • Prolonged illness (2-3 weeks duration)
  • Fever (above 38.3C) on several occasions
  • No diagnosis after intelligent investigations
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8
Q

What is dengue fever?

  • spread
  • incubation?
  • serotypes?
A
  • flaviviruses - spread by mosquitoes
  • 4 serotyes - 1 to 4, incubation 3-10 days
  • four clinical syndromes - undifferentiated fever, classic fever, dengue hemorrhagic fever, dengue shock syndrome (DSS severe form)
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9
Q

what is autosomal dominant polycystic kidney disease

A
  • inherited disease

irreversible decline in kidney fn, most common cause of genetic cause of CKD - 5% sporadic, 75% fmhx

accnts for 5% of pts with ESRD on dialysis

PKD1 - chromosome 16 - polycystin 1 - more RAPID deterioration, more cysts and ESRD at age 54

PKD2 - chromosome 4 - protein polycystin 2 - more indolent decline renal fn, median age ESRD 74

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10
Q

What is the duke criteria

A

Duke Criteria (Durack) 1994

– Pathological criteria

– Clinical criteria

 2 major - microbiology - typical bugs in two bottles, persistantly positive BC with unusual organism, endocardial involvement - echo criteria and new murmur or positive serology for C.burnetti

 1 major and three minor

- 5 minor, fever over 38, vascular phenomena, immunological (osler, roth, glomnephritis), heart cond or IVDU, suggestiev microbio

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11
Q

Nephrotoxic agents that can contribute to AKI

A
  • radiocontrast
  • aminogylcosides
  • cisplatin
  • ACEI, ARBs
  • NSAIDs
  • Tacrolimus, cyclosporin
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12
Q

What antibiotics to use when resistance - carbapenems, aminoglycosides, colistinm tigecycline, fosomycin?

A
  • Carbapenems - use only if low level Resistance - double therapy
  • aminoglycosides - use only if not Resistance (amikacin> gent)
  • colistin - nephrotoxicity - complicated dosing
  • tigecycline - inappropriate for bacteraemia - large Vd, increased mortality - does not cover pseudomonas
  • fosomycin - strongest data only for UTI/prostate
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13
Q

Haematuric renal disorders - general classification

A
  • proliferation of resident glomerular cells
    • mesangial
    • epithelial
    • endothelial
  • influx of systemic inflamm cells
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14
Q

minimal change disease ?

A
  • ​not associated with progressive renal insufficiency
  • based upon histopath
  • renal biopsy normal on light micro
  • electron micro - reveals effacement flattening of podocyte foot processes
  • disruption of integrity of protein barrier - resulting in heavy proteinuria
  • 90% of cases of nephrotic syn in child less than 10, 10-15% of adult cases of nephrotic syn
  • other causes - malignancy (haem) or drugs (NSAIDs and cox2, bisphosphonates)
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15
Q

Tx for PCKD

A
  • vasopressin receptor antagonist - Tolvaptan

other novel tx

  • mTOR - rapamycin - no difference

Mx - HTN, haematuria, UTIs, calculi

extra renal - liver disease, vascular (aneurysms, valvular heart disease

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16
Q

Rhabo summary

A
  • leakage of muscle cell contents into circulation
  • myoglobin - filtered by glomerulus, enters tubular epi cells - causes toxicity through vasocons (intra renal , direct tub toxicity thru oxidative damage and tubular obstruction in distal tubules
  • precipitation of myoglobin within tubules when interacts with TAMM- HORSFALL protein, favoured by acidic urine
  • risk of AKI low when CK less than 15-20k
  • hypocal can occur due to calcium entering damaged muscle, rise in potassium

Tx - FLUIDS, some evidence for iv sodium bicarb, minimal evi for mannitol

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17
Q

Most common causes of AKI

A
  1. SEPSIS

major surgery, cardiogenic shock, hypovolemia, medications

hepatorenal syndrome, trauma, cardiopul bypass, rhabdo, obstructive uropathy

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18
Q

acquisition of which gene makes staph aureus methicillin resistant

A

SCC MEC - staph casette chromosome mec

most common is MEC A

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19
Q

what is cystic renal disease?

A
  • acquired cystic disease of kidney

multiple bilateral renal cysts

different from ADPCKD - no fam hx, small to normal sized kidneys and smooth contour

associated with renal cell cancer - no screening in AUS

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20
Q

What is chikungunya

A
  • alphavirus
  • spread by aegypti and albopictus mosquitos
  • same mosquitos that spread dengue fever
  • India, malaysia, carribbean
  • incubation 2-4 days - range 1-14 days
  • Sx FEVERS, arthralgias, rash and myalgia
  • Dx - serology and alphavirus PCR
  • 72-97% get symptomatic disease - arthritis can be debilitating - bent posture
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21
Q

Define sub acute endocarditis

A

– Long history (weeks to months) “PUO”

– Malaise, fever, night sweats, weight loss

– Immunological and embolic phenomena

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22
Q

Tx for uncomplicated malaria

A
  • First line - ARTEMETHER-LUMEFANTRINE (riamet)
    • ​4 tabs BD for 3 days, take with fatty food, >95% cure in p.falciparum, p.vivax good efficacy
  • second-line - atovaquone-proguanil (Malarone)
    • ​4 tabs daily for 3 days, slower parasite clearance than riamet
    • treatment failure reported
    • can also be used for prophylaxis
  • Third line
    • ​quinine + doxy/clinda for 7 days
      • ​mefloquine to be dropped
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23
Q

What are the common complications of endocarditis?

A
  • CCF from valvular dysfunction
  • Embolisation - risk drops after first week of abx therapy - increase if >1cm ant MV vege or S. aureus
  • Periannular extension of infection - needs valve replacement, may cause AV block (node)
  • Splenic abscess
  • Mycotic aneurysms - can occur early or late
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24
Q

What is P.falciparum

A
  • plasmodia that infects humans
  • almost all death/severe disease
  • no dormant liver stage, no late relapses
  • medical emergency - almost always chloroquine resistant
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25
Q

Simple renal cysts significance?

A
  • Generally increase in size over time

  • do not impact renal fn

no further follow up required

further f.u with CT contrast IF - septated cyst, calcifciation or cluster of cysts potentially masking solid lesion

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26
Q

What is proteinuri nephrotic disorders ?

A

nephrotic range proteinuria > 3.5g day

hypoalbuminaemia

peripheral oedema - associated with hyperlipidaemia

thrombotic disease more frequently observed

disturbance of podocyte functn or endothelial/gbm/podocyte interface

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27
Q

What is dengue haemorrhagic fever?

A
  • more common after repeated infections and in children described in first time travellers
  • 4 necessary criteria for DHF
    • ​fever or recent hx of acute fever
    • hemorrhagic manifestations
    • low platelet count - less than 100,000
    • objective evidence of leaky capillaries
      • ​elevated hematocrit 20% or more over baseline
      • low albumin
      • pleural or other effusions
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28
Q

What is cystatin C?

A
  • biomarker of AKI
  • endogenous cysteine proteinase inhibitor
  • produced at a constant rate by all nucleated cells - released into plasma
  • 99% filtered by glomeruli - no tubular secretion or reabosorption into plasma
  • after filtration –> completely absorbed in to prox tubular cells
  • hence NONE in urine
  • SO PLASMA cystatin C is good marker of GFR and Urine cystatin C is a good marker of tubular injury
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29
Q

What are the common organisms for Subacute endocarditis - top being most likely?

A
  1. Viridans strep - mutans, mitis, bovis
  2. Enterococcus
  3. HACEK group - 5% - haemophilus, acinomycetamcomitans

Others - culture neg - rare 7%, Q fever, Bartonella, coag neg staph

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30
Q

Indications for surgical treatment of IE?

A

Valve replacement indications

  • heart failure
  • paravalvular extension
  • uncontrolled infection/difficult organism
  • recurrent embolic events despite appropriate Ab - mobile vegetations above 10mm
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31
Q

What is the mechanism of action of calcimimetics (Cinacalcet)?

A

Cinacalcet directly lowers parathyroid hormone levels by increasing the sensitivity of the calcium sensing receptors to activation by extracellular calcium, resulting in the inhibition of PTH secretion

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32
Q

Treatment for viridans strep SBE ?

A

2-4 weeks IV benzylpenicillin IV 4hrly + 2 weeks IV gent (low dose)

or

ceftriaxone 2g IV for 4 weeks (outpt course)

or

benzylpenicillin as a single agent for 4 weeks

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33
Q

What is classic dengue fever?

A
  • 1st phase - abrupt onset of fevers 39-40 for 2-3 days, severe back pain, HA, retro-orbital pain, arthralgias, maculopaplular rash, metallic taste
  • 2nd phase - D-3-6, A/N/V/D, lymphadenopathy
  • 3rd phase - defervescence for 1-2days
  • 4th phase - fever recrudescence, morbilliform rash, skin desquamation
  • 5th phase: cnvalescence with prolonged lethargy
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34
Q

What is tolvaptan

A

vasopressin V2 receptor antagonist that inhibit cyst growth and decline of renal function - however only 2-3 % less increase in renal volumes - ? not widely used yet

used in PCKD

  • suppression of vasopressin release reduces second messenger systems - cAMP identified as promoters of kidney-cyst cell proliferation and luminal fluid secretion
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35
Q

what is membranous GN

A
  • Deposition of IgG and C3 along the GBM
  • IgG4 most commonly associated idiopathic membranous nephropathy
  • most commonly idiopathic - commonest cause of nephrotic syn in adults
  • malignancy responsible for 5-10percent of cases - solid tumour such as cancer of lung or colon
  • SLE - 10-20% of cases of lupus nephritis have a MN picture
  • Spontaneous remission of proteinuria occurs in 5 to 20 percent of cases
  • Partial remission (
  • incidence of end‐stage renal disease ~14 percent at 5 year
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36
Q

HIV

A

retrovirus of the lentiviridae family

human HIV-1 is genetically similar to chimp isolates

HIV 2 rare in aus, less virulent

cellular target of HIV - CD4 T cells - predominant target in all tissues

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37
Q

What are the non-immunosuppresive therapies for nephrotic syndrome?

A

used most often in cases of FSGS and membranous nephropathy - response to immuosup tx slow or partial

issues to address - proteinuria, oedema, HTN, dyslipidaemia, thrombotic risk

  • proteinuria - target BP 125/75, proteinuria > 1g/day - use ACEI or ARB, aldo antag- spiro
  • diuretics - loop, thiazides (greater anti-hypertensive effect than diuretic)
  • statins
  • pro-thrombotic - decreased levels of anti-thrombin III - urinary losses , anticoag when alb less than 20,
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38
Q

What steps should you take to prevent contrast induced AKI

A
  • pre-hydration - N/Saline (IV)
  • minimise contrast volume
  • use non-ionic contrast which is low or iso-osmolar
  • discontinue nephrotoxins (ACEI or ARB)
  • NAC (variable effect, also results in minor lowering of Creatinine) - 1200mg BD shown benefit compared to low dose
  • ? Statins - ongoing trials
  • periprocedural haemofiltration - no benefit
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39
Q

pathophysiology of AKI

A
  • reduction in kidney perfusion –> ATP depletion in renal tubular epithelial cells - causes cell death (apoptosis / necrosis)
  • prox tubular cells are susceptible - high metabolic rate 2* to ion transport, limited capacity for anaerobic glycolysis
  • endothelial injury with microvascular congestion, hypoerfusion particularly in the S3 segment of nephron - outer stripe of medulla
  • SEPSIS - cytokines and bacterial factors - binds TLR4 on tubular cells and causes cell damage through oxidative stress
  • microvascular changes - hypo-perfusion in peritubular capillaries - generation of reactive oxygen and nitrogen species
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40
Q

what is first line for gonorrohea

A
  • Ceftriaxone!!! + azithromycin and doxy to cover for chlyamdia
  • established fluoroquinolone resistance
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41
Q

Diagnosis of Malaria - The great imitator!!

A
  • FBE - haemoyltic anaemia, WCC normal/low, no eosinophilia, thrombocytopenia common
  • Thick and thin blood smear
  • antigen capture tests - rapid dx 15-20mins
  • ICT
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42
Q

What is the treatment for uncomplicated TV endocarditis/IVDU?

A

2 weeks of IV fluclox and gent has been used

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43
Q

What is the anti-relapse therapy for malaria?

A
  • Primaquine
    • ​eliminates liver forms of P vivax and ovale
    • need G6PD screen
    • total dose of primaquine received is important
    • no other alternatives
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44
Q

Clinical approach to ARF

A
  • Pre renal: hypovolemia, hypotension, CCF, aortic dissection
  • Renal - ATN, tubular injury - ischaemic, toxic - drugs causing acute tubulo-interstitial nephritis, infetions, acute GN - pauci-immune, anti-gbm
  • Post renal - obstruction - staghorn calculi, retroperitoneal fibrosis.
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45
Q

What was the SAFE study? What did it show?

A
  • was an RCT of 7000 patients

compared albumin as resus fluid vs N/Saline

  • Showed NO overall benefit in mortality or need for RRT

fluids containing synthetic colloid - HES - found to be associated with increased need for renal replacement therapy - and increased mortality

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46
Q

FSGS

A

Focal – involving some of the glomeruli

Segmental – involving a portion of the affected glomerulus

Electron microscopic findings same as MCD- Effacement of podocyte foot processes

pathogenesis - injury to the podocyte via an immune mechanism - associated with progressive renal insufficiency in 25-50% of cases

Tx - immunosupp tx for primary FSGS, no role for secondary forms

  • glucocorticoids, cyclosporin - in conj for resistant cases,
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47
Q

Glomerulonephritis classes

A

Proteinuric -nephrotic - minimal change, FSGS and membranous

Haematuric - nephritic - IgA nephropathy, SLE, Pauci-immune GN, anti GBM, post step

Both - membrano-proliferative GN - mesangio capillary GN

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48
Q

What is the treatment for enterococcal IE and side effects?

A

4-6 weeks of IV benzylpenicillin or amoxil/AMP + Gentamicin (4-6weeks)

combination of AMP with ceftriaxone may be effective

for enterococci resistant to AMP - use Vanc + Gent

SE: ototoxicity and renal failure

if E.faecalis - then replace gent with ceftriaxone - therefore Amp + Cef

49
Q

What is carbapenem resistance and where?

A
  • frequently due to carbapenemase - hydrolyse all B-lactams incl carbapenems
  • esp ppl from india, asia and hospitals in america

MUST know - New Delhi metallo- beta lactamase - does not occur in isolation, co-transmission of other resistance elements

50
Q

What is the diagnosis of dengue fever?

A

Lab findings - early neutropenia with subsequent lymphocytosis, mildly raised ALT and AST

severe disease- low platelet count - less than 100,000

elevated transaminases 3-5 of ULN

Dx - serology - 4 fold rise in antibody titre over 2 weeks

flavivirus PCI, NS1 antigen

Mx - symptomatic, supportive

51
Q

What is MERS CoV

A
  • middle eastern respiratory syndrome coronovirus
  • pt presents with pneumonia and ARDS
  • human to human transmission possible
  • consider in travelllers from middle east in the last 14 days
  • mortality rate 55%
52
Q

Treatment of AKI

A
  • Treat/remove causes/ exacerbating factors
  • fluids, renal perfusion- resus
  • mx of hyper K and acidosis
  • RRT as required - fluid overload, azotemia
  • stress ulcer prophylaxis
  • modify med dosing
53
Q

What is the sensitivity and specificity of echo for IE?

A

TTE - sensitivity less than 60%, specificty 98%

TOE - sens very high, spec very high

  • neg predictive value 99-100% in NVE, Pos PV 90%
  • PVE 86-94%, 88-100%
54
Q

What abx would you use for culture negative endocarditis?

A

Ceftriaxone 3-4 weeks + gent for 2 weeks - active against bartonella/strep/HACEK

for Bartonella endocarditis - switch to IV doxy or azithromycin + ? gent

Q fever endocarditis - doxy + plaquenil (12-18months) + RIF

55
Q

Cause of host genetic resistance to HIV

A

delta 32 mutation in CCR5 - found in 10% caucasians - heterozygous

associated with slower HIV disease progression

56
Q

Biomarkers of AKI - Are they sensitive?

A

NO - do not become abnormal until GFR reduced by 50%

  • begin to change late after injury occurs

confounding - muscle mass, age, sex, nutrition, meds (steroids)

57
Q

Causes of PUO

A
  1. infections - SBE usually viridans, TB, intra-abdominal abscess, HIV related infection
  2. connective tissue diseases - PMR, Giant cell arteritis, vasculitis (PAN), SLE, thyroiditis
  3. Malignancy - lymphoma, necrotic mets, Renal cell cancer
  4. other - drug fever, factitious

Remember role of PET scan

58
Q

What is the treatment of Staph IE?

A

4-6 weeks IV fluclox - 2g 4hrly

MRSE or MRSE - vancomycin 4-6 weeks - Rifampicin + Fusidic acid in prosthetic valve endocarditis

**TG - states if vanc resistance or intermediate - then use daptomycin or linezolid***

59
Q

Hepato renal syndrome

A
  • occurs in severe liver dysfunction - progressive oliguria with very low urinary sodium (
  • sepsis, hypovolemia due to diuretics/paracentesis
  • splanchnic circulation dilatation, intra-renal arteriolar constrction
  • POOR prognosis

Prevention - IV albumin reduces AKI after paracentesis, vasoconstriction with terlipressin (improves short term survival and renal fn)

60
Q

Who to treat with Membranous GN

A
  • Those with heavy proteinuria- Less likely to spontaneously remit
  • Those with renal dysfunction - Disease more likely to progress

Cyclophosphamide and steroid based regimens 1st line immunosppressive therapy

2nd line - cyclosporine - provided preserved GFR, rituximab

61
Q

What is the nerve supply of the bladder - emptying and filling?

A

emptying - S2-4 parasympathetic innervation via pelvic nerves mediated by M2 & M3 receptors

filling - sympathetic T11-L2 innervation via hypogastric nerve mediated by B3 receptors

Urethra - closure is via external sphincter S2-4 pudental N - somatic originating in onuf’s nucleus

closure - male bladder neck - alpha1A adrenergic

opening NOS/NO

62
Q

What stimulates the bladder empyting

A
  • sensory bladder afferents - complex suburothelial sensory network
  • myelinated Adelta fibres - 30% - mechanoreceptors mediating sense of fullness via spinobulbospinal pathway via pontine micturition centre - PMC
  • unmyelinated C fibres - 70% - normally silent, high mechanical threshold, activated by noxious stimuli eg. infection

after spinal dysfuntion - drive spinal segmental reflex pathway

63
Q

what causes ARF in terms of acute GN

A
  • pauci immune - anca associated vasculitis
  • linear IgG - anti- gbm
  • immune complex deposition - SLE, IgAN, PIGN, MPGN
64
Q

what in polycystic kidney disease genetics is associated with worse disease?

A
  • PKD1 gene on chromosome 16, encodes protein polycystin 1

more rapid deterioration in renal function

increased number of cysts

cysts at an earlier age - cf PKD-2

median age of ESRD at age 54 compared to 74 for PKD-2 on chromosone 4

65
Q

What are the sonographic criteria for the diagnosis of ADPKD in individuals with a family hx of PCKD

(remember no dx criteria in those with no family hx)

A

15-29 - 3 or more cysts - unilateral or bilateral

30-39 - 3 or more cysts unilateral or bilateral

40-59 - 2 or more cysts in each kidney

greater than 60 - 4+ cysts in each kidney

66
Q

What are the extra-renal manifestations of ADPCKD

A
  • polycystic liver disease
  • intracranial aneurysms - in 6% of pts with neg fmx, 16% with fmx
  • thoracic aortic, cervico-cephalic dissections, coronary artery aneuysms
  • valvular heart disease - mitral valve prolapse and aortic incompetence
67
Q

Prognosis of FSGS is related to ?

A

• Prognosis dependent upon

  • Severity of proteinuria
  • Degree of renal dysfunction
  • Degree of background renal damage on renal biopsy
  • Response to therapy
68
Q

What is the primary tx for FSGS

A

Glucocorticoids cornerstone of therapy

• Cyclosporin (in conjunction with glucocorticoids) in

resistant cases

  • Provided renal function is preserved
  • Other agents – less studied
  • Cyclophosphamide
  • Tacrolimus
  • Mycophenolate
  • Sirolimus
  • Rituximab
69
Q

what is the first line treatment for membranous GN

A

1) cyclophosphamide and steroid based regiments 1st line immunosuppresive therapy

alt immunosuppresive therapies

  • cyclosporine 2nd line - provided preserved eGFR

rituximab

70
Q

what is the auto-antibody found in serum of patients with idiopathic membranous nephropathy?

A

M-Type Phospholipase A2 receptor as Target antigen in idiopathic membranous nephropathy

  • apparently (anti-phospholipase A2 receptor antibodies) correlate with clinical status in idiopathic membranous nephropathy
71
Q

what calcium channel blockers possess anti-proteinuric properties?

A

the non-dihydropiridine calcium channel blockers

  • verapamil
  • diltiazem

needed to reach target blood pressure of 125/75 for nephrotic syndromes

72
Q

why do u have a pro-thrombotic state in nephrotic syndrome

A
  • decreased levels of anti-thrombin III due to urinary losses
  • increased platelet activation
  • presence of high molecular weight fibrinogen moieties in the circulation
  • additional possiblilty is that immune mediated injury in the glomerulus results in increased procoagulant activity sufficient to have a systemic effect

10-40% of cases have deep vein or renal vein thrombosis

73
Q

What are the light microscopic findings for Mesangial prolif GN / mesangio-capillary GN

A

Common to all causes

  • Mesangial hypercellularity
  • Endocapillary proliferation
  • Duplication of the glomerular basement membrane

(producing double contours)

74
Q

what causes seconday MPGN ?

A
  • usually in association with chronic infections - predominantly hep C
75
Q

what is the pathophysiology of MPGN

A

immune complex mediated

  • deposition of immune complexes in the glomeruli resulting from persistent antigenaemia
  • development of antigen-antibody complexes - chronic infectons (hep c)

Complement mediated MPGN

  • commencing and involving regulation of C3 , loss of complement regulation

independent of antigen/antibody stimulation

76
Q

What is the potential treatment of complement mediated MPGN

A

poor quality of evidence available

  • can use immunosuppressive therapy

plasma infusion

OR

non specific inhibition of complement cascade - Eculizumab - anti C5 monoclonal antibody - inhibition of C5 activation

77
Q

What suggests chronicity of renal disease?

A

Evidence suggesting chronicity:

  1. Normocytic anaemia
  2. ↑phosphate, ↓calcium, ↑PTH, osteodystrophy
  3. Small, echogenic kidneys
78
Q

What are the aims of Hb and iron in CRF

A

treat if hb less than 100 - aim for 100-120

egfr less than 60 for pbs funding

functional iron deficiency with EPO therapy - aim Tsat 20-50%, ferritin 300-500

need to give enough iron as relative functional iron deficiency

79
Q

what are the targets for ca, phos, pth in CRF pts

A

Targets: CARI guidelines

Parameter Target

PO4 0.8–1.60 mmol/L

Ca 2.1–2.4 mmol/L

[Ca x PO4]

iPTH 2–3 times the upper normal limit

80
Q

what are the agents to help treat renal bone disease?

A

* Control PO4 with phosphate binders

  • Ca Carbonate (Calsup), Sevelamer (Renagel), Lanthanum (Fosrenol)

* Use Calcitriol (Vit D3) to titrate up Ca2+

  • Measure PTH 2-3 monthly
  • PTHectomy if autonomous
  • i.e. High PTH & Ca, whilst off all Ca/Vit D agents.

* Calcimimetics eg. Cinacalcit (Sensipar)

  • Parathryroid sensitised to respond to lower ca levels.
  • Improve survival surrogotes PTH, Ca, PO4, [CaxPO4]
  • BUT – ‘Evolve’ trialno survival benefitPBS de-listing 8/15
81
Q

what are the classess of lupus nephritis

A

I Minimal mesangial LN

normal light microscopy

II Mesangial Proliferative LN

III Focal LN

IV Diffuse LN

>50% of glomeruli involved

V Pure Membranous LN

VI Advanced Sclerosing LN

≥ 90% of glomeruli

82
Q

what are some of the features seen on proliferative lupus nephritis histology

A

• Subendothelial immune deposits

/wire loops

  • Hypercellularity
  • Leukocyte infiltration
  • Fibrinoid necrosis /hyaline thrombi
  • IF- deposits of IgG,C1q,C3,IgA,IgM
83
Q

what are the agents used for induction of lupus nephritis?

A
  • steroids
    • IV methylpred x 3 pulses or pred 1mg/kg/day then wean
  • cyclophosphamide
    • improves renal remission rate, less risk of doubling Cr /ESRF
    • either IV cyclo monthly for 3-6 months then MMF or Aza
    • IV route less toxic than oral (cumulative dose accumulation - infertility )
  • mycophenolate
    • 1-3g/day in 2 divided doses
  • Rituximab
84
Q

what is the major SE of cyclophosphamide treatment?

A
  • gonadal toxicity

major infection

herpes zoster

bladder toxicity

malignancy

bone marrow suppression

cumulative dose of 14g - haemorrhagic cystitis

85
Q

how does mycophenolate work and major toxicities - relating to lupus nephritis

A
  • Inhibitor of inosine monophosphate dehydrogenase
  • Inhibits purine synthesis
  • Anti-proliferative effects on lymphocytes
  • myco is as effective as cyclophos at inducing remission
  • less major infection and minimizes gonadal toxicity
  • SE
    • ​gastrointestinal upset
    • pancyotpaenia
    • infection
    • malignancy - skin - NEEDS YEARLY SURVEILLANCE
86
Q

what agents are used for maintenance treatment in lupus nephritis

A
  • myco, aza at least as effective as cyclo with less toxicity
  • maintanence treatment for at least 2 yrs
  • ? lifelong if relapse
  • myco superior in maintaining renal response post induction and preventing relapse
87
Q

what is rituximab and what role does it have in lupus nephritis?

A
  • murine/human monoclonal antibody
  • anti-CD 20, b cell depletion
  • no benefit over standard treatment in LUNAR trial
  • however possible role in severe refractory or relapsing disease
88
Q

what is pauci-immune RPGN, ANCA + vasculitis ?

A
  • Autoantibodies reacting with myeloperoxidase(MPO) or proteinase 3 (PR3)
  • Characteristic cytoplasmic (c-ANCA) or perinuclear (p-ANCA) IF staining on ethanol fixed neutrophils.
  • Three major
    • ​wegner’s granulomatosis - 90% ANCA +, 80-90% PR3
    • microscopic polyangitis - 70% ANCA, most have MPO
    • renal limited vasculitis - most anca +, 75-80% MPO
89
Q

what is the induction treatment for pauci immune RPGN

A
  • cyclophos - 3-6 months, oral vs IV as IV smaller cumulative dose
  • steroids - iV methylpred pulse than pred in severe disease
  • in severe disease ANCA + vasculitis - plasma exchange resulted in higher rate of renal recovery
    • ​esp in severe renal failure, concurrent anti-gbm antibodies and anca pos, pul haemorrhage
90
Q

what is the maintenance therapy for pauci immune RPGN

A
  • aza verus cyclophos
  • aza for 18months shown to be as effective as cyclo to minimise relapse
  • aza more effective than mycophenolate at maintaining remission in ANCA associated vasculitis
  • rituximab - as alternative to cyclo - no difference in adverse events, as effective
91
Q

what are the ranges for microalbuminuria?

A

Urine albumin : Creatinine ratio (UACR)

males 2.5-25mg/mmol

females 3.5-35mg/mmol

Albumin excretion rate (AER)

30-300mg/ 24hrs

20-200μ g/min in timed collection

If positive then further 1-2 checks within 3

months

92
Q

what is the definition of macroalbuminuria

A

Urine albumin : Creatinine ratio (UACR)

males >25mg/mmol

females >35mg/mmol

Albumin excretion rate (AER)

>300mg/ 24hrs

>200μ g/min in timed collection

93
Q

What is atherosclerotic RAS and what part of renal aa does it involve

A
  • ARAS part of generalised atherosclerosis

common in pts with or without HT

  • typically involves the proximal 1/3rd of main renal aa

men and women age over 55

ostial/proximal renal aa

radiologically eccentric or concentric lesions - total occlusion and ischaemic atrophy

94
Q

what is fibromuscular dysplasia?

A

in women aged 30-40

mid-distal renal artery, bilateral in 60%

radiologically string of beads

can affect carotid, visceral and peripheral arteries

total occlusion and ischaemic atrophy is rare

perimedial fibroplasia can threaten, cause dissection

95
Q

What happens in the proximal tubule and what drug acts here

A

60 – 65% sodium reabsorbed

Site of HCO3 - reabsorption

All glucose and amino acids reabsorbed

Site of solute secretion

  • anions (urate, ketoacid, penicillins, cephalosporins, radiocontrast media, diuretics)
  • cations (cr, cimetidine, Li)

Target carbonic anhydrase inhibitors

• Mild metabolic acidosis

96
Q

what happens in the thick ascending limb

A
  • 25-30% of sodium reabsorption
  • concentration of medulla and counter current system
  • mg and ca transport passive
  • frusemide decreases mg absorption - less positive lumen
  • claudin 16 gene encodes for mg transport paracellular pathway
  • mutations in paracellin 1 gene - hypomagnesemia and nephrocalcinosis
97
Q

What is Bartter’s syndrome

A
  • autosomal recessive
  • normotensive
  • hypokalaemic, metabolic alkalosis
  • hypercalciuria +/- hypomg
  • increase in urine prostaglandin E
  • increase renin and aldo
  • neonatal presentation

Affects NKCC - losing sodium, cannot retain hence high renin and aldo to compensate

98
Q

What is the distal tubule responsible for and what diuretics ?

A
  • 5% of total NACL absorption
  • thiazide action - indapamide
  • mg and ca reabsorption
    • ​Mg absorption via TRPM6/M7 - this is inhibited by tacrolimus
    • 2-5% of mg absorbed
  • Thiazides
    • ​inhibit Na/CL co-transporter
    • compete for Cl site
    • decrease absorption of Na
    • increase calcium reabsorption - prevention of renal calculi
99
Q

what is gitelman’s syndrome

A
  • Autosomal recessive - disorder of NaCl transporter
  • Salt wasting
  • Normotensive, metabolic alkalosis, hypokalemia,
  • hypomagnesemia, hypocalciuria (similar thiaside)
  • Increase renin and aldosterone
  • Urine prostaglandin E normal
  • Diagnosed late childhood or adulthood
  • Musculoskeletal presentation
100
Q

what is pseudohypoaldosteronism type 2

A
  • •Autosomal dominant
  • •Hypertension 2nd /3rd decade
  • •Normal anion gap acidosis
  • •Hyperkalemia
  • •Hypercalciuria
  • •High aldosterone levels
  • •Treatment thiasides
  • •Mirror image to thiaside use
101
Q

what is the action of potassium sparing diuretics

A

Amiloride and Triamterene, High dose trimethoprim

  • close sodium channels directly
  • Amiloride used to inhibit Lithium entry into cells​

Spironolactone and Eplerenone

  • competitively antagonises aldosterone at receptor level
  • Eplerenone more specific less anti‐testosterone side effects
102
Q

what is liddle syndrome

A
  • Autosomal dominant (chromosome 16)
  • Early onset H/T + hypokalemic metabolic alkalosis
  • decreased plasma renin and aldosterone levels
  •  Increased number of Na channels
  • Mutation identified in  or  subunit of Na channel (unable to catabolise Na channel)
  • Presentation similar to apparent minerocorticoid excess (Licorice)
  • Amiloride and Triamterene, not Spironolactone used for treatment as they close the channels
103
Q

how does aldosterone and ANP act in the cortical connecting tubule

A

Fine tuning by renin angiotensin

Electronegative lumen promotes K+ and H+ excretion

Aldosterone increase number of sodium channels

increase Na reabsorption and secretion of K+

ANP binds to basolateral receptor decreases Na

channels

Li enters these cells via Na channels

104
Q

what is anion gap and causes

A
  • Anion gap Na+ ‐ (Cl‐+ HCO3)
  •  Anion gap 8‐15
  •  Measure of unmeasured anions (albumin ,Phosphate and sulphate)

 Anion gap increased

  • Decrease K+, Ca2+ or Mg2+
  • Increase anions – lactate, ethylene ketones
  • 2* to increased lactate, methanolol, alcohol, rhabdo, renal failure or ketoacidosis

 Anion gap decreased

  • Low albumin (correction .25 x albumin g/L)
  • Multiple myeloma
105
Q

what is the urine anion gap and what does it signify?

A

Urine anion gap = [Na+] + [K+] – [Cl‐]

GI causes: “neGUTive” UAG +

• Infusion ++ amounts Na Cl

 Positive anion gap

• Type 1 RTA, Type 4 RTA, renal failure

 Impaired renal acid excretion

Urinary anion gap unreliable

pH > 6.5

U Na

Toluene/lactic/ketoacidosis

106
Q

what is type 1 RTA

A
  • Distal defect —>  decreased H+ secretion
  • K+ secreted instead of H+ (hypokalemia)
  • Urine pH > 5.5
  • Hypercalciuria
  • Most acidotic of the three types of RTA
  • Renal Calculi
    • • Hypercalciuria
    • • Hypocitraturia
  • Confirmatory test –Ammonium Cl acidification
  • primary causes
    • ​idiopathic, sporadic, mutation in H+-ATPase and AE1 gene , association nerve deafness
  • secondary causes
    • autoimmune - sle, sjogrens, RA, drugs - PPI, lithium, chronic hep, renal transplant , thyroid disorders
      *
107
Q

what is type 2 RTA

A

Failure of proximal tubular reabsorption of HCO3

Acidosis is milder that in type 1 RTA (HCO3 ‐ 12‐20 mmol/L)

Urine pH varies with serum HCO3 ‐ (pH

Threshold distal reabsorption of HCO3

‐Treatment may require high dose HCO3 ‐ (10‐15 mmol/kg/day)

Often associated with generalised proximal tubule dysfunction

(Fanconi syndrome - generalised prox tube dysfunction)

Confirmatory test fractional excretion of Bicarbonate > 25%

108
Q

What is type 4 RTA

A

Aldosterone deficiency or distal tubule resistance to Aldosterone

Decrease in Na+ absorption

Decreased H+ and K+ secretion hyperkalemia and acidosis

Urine pH

Impaired ammonium production

Acquired causes - dec renin 2* to Diabetic nephro, NSAIDs, interstital nephritis, normal renin dec aldo - ACEI arb, heparin, primary adrenal response

dec response to aldo - meds - spiro, tac, sle, amloid

treatment - dietary restriction of Na and frusemide

109
Q

What is Wegner’s granulomatosis - GPA

A

granulomatous polyangitis

eponymous description of disease entity

small vessel vasculitis affecting respiratory tract vessels – nose to lungs and renal vessels

110
Q

what is goodpastures disease?

A
  • ​anti GBM antibodies cause this disease
  • mainly present with rapidly progressive disease
  • areas of necrosis and crescents
  • antibody – IgG – deposits on the basement membrane
  • always a cresenteric disease
  • combination of haemoptysis, renal failure and linear IgG deposits points to a diagnosis of good pasture’s syndrome.
  • An antibody to alpha 3 component of type IV collagen
  • More common in men
  • Bimodal distribution – peaks in 20-30 and 60-70, associated with HLA DR2
  • Ix – renal biopsy and raised transfer factor secondary to pul haemorrhage
  • Management – plasma exchange, steroids and cyclophosphamide
  • ANCA related nephropathies are associated with crescentic glomerulonephritis
111
Q

What is the main risk factor for IgAN progression? Note - IGAN is the most common cause of GN leading to ESKD in ANZ

A

PROTEINURIA!!!!!

  • degree of proteinuria - esp not responding to tx generally the strongest predictor for renal decline in glomerular diseases

interaction between BP & proteinuria

  • reflects glomerular injury

BP control still essential - generally more treatable

  • proteinuria and albuminuria is also a predictor of CV events and all cause mortality in CKD

Tx - ACEI, ARB, fish oil, glucocorticoids and cyclophosphamide

112
Q

what is the treatment of ANCA associated vasculitis than is PR3-ANCA pos, anti-gbm negative

A

so ideal treatment is cyclo IV to reduce cumulative dose,

can use rituximab as alternative

plasmapheresis is used short term in achieving dialysis independence in ANCA pos vasculitis presenting as dialysis requiring - serum Cr greater than 500

  • also in pts with pul haemorrhage or co-existing anti-GBM antibody

but u also need to use cyclophosphamide as induction therapy

113
Q

what is the first line treatment of membranous nephropathy

A
  • cyclophosphamide and prednisolone alternating monthly for 6 months
  • remember PLA2R Ab - present in 70% of idiopathic MN and negative in secondary MN

steroids alone do not work for iMN

can use for 6 or 12 months

another target for idiopathic MN is THSD7A

114
Q

what are the donor requirements for kidney transplant -

do they need to be ABO compatible

do they have a higher rate of ESKD compared to the popn

A

So

  • transplant donors are generally from a highly selected population - lower risk of ESKD
  • higher risk than healthy non donors - but absolute risk is LOW
  • cannot transplant melanomas - even past hx - as high death rates

ABOI no longer an absolute contraindication in living donor kidney Tx - generally requires antibody removal pre- TX - antibody remoal for low antibody titres

  • kidney exchange program for high titres- to avoid unsuccessful attempt at Ab removal or higher risk of early rejection
115
Q

what is the main cause of death in dialysis patients

A

1 CVD!!!!!

  1. withdrawal from dialysis - however now nearly the same as CVD
  2. infection
  3. vascular - stroke, GI bleed, bowel infarction

first few months - high risk of infections

116
Q

How does calcitriol work and SE

A
  • 1,25 OH vitamin D reduces PTH secretion - directly or indirectly via relative hypercalcaemia
  • increases GI absorption of Calcium and phosphate - unwanted SEs
  • avoid relative hypercalcaemia, hyperphosphataemia and low PTH - adynamic bone disease - vascular calcification
    *
117
Q

when is egfr most accurate - MDRD

A

for patients with CRF and egfr 15-45 mls/min

118
Q
A

► Med Misc 27 (12 decks)

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