Renal Flashcards by Chelsea Anon

Horeshoe kidney complications

hydronephrosis
nephrolithiasis
infection
increased renal ca

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Difference between CrCl and GFR

CrCl estimates GFR
CrCl slightly overestimates as creatinine is moderately secreted by renal tubules

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Where do loop diuretics act

Ascending loop of henle
Blocks Na/K/Cl transporter

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Where to thiazide diuretics act

early DCT
blocks Na/Cl transporter

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Where is majority of Na and water reabsorped in nephron

early PCT

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Aldosterone effect on principal cells vs alpha-intercalated cells

principal cells - promotes Na and water reabsoprtion, K secretion
alpha intercalated cells - promotes K reabsorption and H secretion

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Fanconi syndrome mechanism

generlised reabsorption defect in PCT
- increased excretion of AA, glucose, HCO3, PO4

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Fanconi syndrome lab findings

metabolic acidosis (type 2 RTA)
low phosphate and K

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What can cause Fanconi syndrome?

hereditary -> wilsons, glycogen storage disease
ischaemia
multiple myeloma
drugs (tenofovir, isofosfamide, cisplatin, lead poisening)

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What is Bartter syndrome and lab findings

autosomal recessive reabsorption defect in thick ascending loop of henle
Like being on chronic loop diuretics
metabolic alkalosis, low K and high Ca

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What is Gitelman syndrome and lab findings

AR defect of NA/CL transporter in DCT
causes metabolic alkalosis, low Mg K and Ca
similar to chronic thiazide use

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What is Liddle’s syndrome and lab findings

Gain of function mutation to reduce Na channel degradation -> increased Na reabsorption
Metabolic alkalosism, low K, low aldosterone and HTN

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What is SAME (syndrome of apparent mineralocorticoid excess) pathophys

AR 11beta-HSD deficiency leads to higher cortisol (rather than cortisone) which increased mineralocorticoid activity
Caused metabolic alkalosis, low K, low aldosterone and HTN

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Actions of angiotensin 2

vasocontricts arterioles -> increase BP
contricts efferent arteriole -> increased GFR when renal blood flow low
Increases Na/H transporter activity in PCT
Secretes aldosterone -> H2O net absorption
Posterior pit to secrete ADH

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Inhibitor for RAAS

ANP and BNP -> dilates afferent arteriole increasing renal blood flow and reducing renin
promotes naturesis

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Most common cause of GN in developed countries

IgA nephropathy

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IgA nephropathy presentation

40-50% macroscopic haematuria, flank pain and fever
30-40% microscopic haematuria plus mold proteinuria
10% rapid progressive GN
Rare to have malignant HTN or AKI

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IgA nephropathy clinical associations

Cirrhosis
Coeliac disease in 1/3
Dermatitis hepatiformis
HIV
Minimal change and membranous
GPA when in remission
Small cell carcinoma
Bronchiolitis obliterans
Lymphoma
TB
IBD

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Indications for Bx in IgA nephropathy

Protein >1g
Elevated creat
New HTN
Elevation in BP above previous stable baseline

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Characteristic IF finding in immune complex GN

granular deposits of polyclonal Ig

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Predictors of outcome in IgA nephropathy

reduced GFR worse
HTN worse
degree of proteinuria most important predictor in one study

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what is considered remission in IgA nephropathy

protinuria < 1g/day

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treatment of IgA nephropathy

aim ACEi, BP control, lifestyle for 6 months
if protein >1g/day or other factors (minimal change disease, AKI, RPGN) consider immunosuppresion with glucocorticoids

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Characteristic histo findings in lupus nephritis

“full house” IF pattern
glomerular deposits that stain for IgG, IgA, IgM, C3 and C1q
seen everywhere

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therapy immunosuppression for lupus nephritis

Induction: MMF or cyclophosphamide Maintence: AZA

How to Dx infection related GN

kidney bx in those with preceeding or current infection and low C3

Most common GN in adults >50yo

pauci immune (ANCA associated)

Which ANCA is GPA

PR3

Which ANCA is MPA

MPO

Genes associated with ANCA vasculitis

MHC PRTN3 gene

SNPs associated with PR3

HLA-DP SERPINA1 PRTN3

SNP asscoiated with MPO

HLA-DQ

Most likely type of ANAC vasculitis to have replapsing renal disease

GPA and PR3

Better treatment for relapsing ANCA vasculitis renal disease

rituximab is superior to cyclophosphamide

Treatment with rituximab is better in what subgroup of ANCA vasculitis

PR3

Avacopan use in ANCA vasculitis trial findings

ADVOCATE study avacopan non-inferior but not superior to tapered pred at 26 weeks, but superior at 52 weeks for sustained remission

Bx findings in pauci immune GN best and worse outcomes

focal -> best sclerotic -> worse

Characterstic IF findigs in anti-GBM

linear deposits of IgG and frequently with C3

Histo findings of anti-GBM

severe necrotising and crescenteric pattern if active

Anti-GM antigen

alpha 3 chain of type 4 collagen

Assocations with anti-GBM

smoking and lung haemorrhage hydrocarbons alemtuzumab HLA-DR2

anti-GBM presentation

rapidly progressive GBM 40% have alveolar haemorrhage

anti-GBM treatment

PLEX steriods cytotoxic therapy (cyclophosphamide)

What can occur after transplant for alport syndrome

de novo anti-GBM

How common is relapse of anti-GBM after transplant

uncommon

Proliferative GN with monoclonal Ig deposits most common Ig deposit

IgG rarely IgA less common IgM

Most common pattern of pathology in fibrillary GN

mesangial proliferative GN in 70% IgG in all pt with C3 deposits

cryoglobulinemic GN histo findings

membranoproliferative pattern with infiltrating macrophages and PAS deposits deposits most often IgM

Can differenciate between C3GN and dense deposit disease based on what

EM findings

Pathophys difference between dense deposit disease and C3GN

Both lead to C3 convertase activity increasing C3GN -> C3 mutation so is not inhibited by factor H DDD -> C3 mutation leading to functional factor H deficiency

treatment of membranoproliferative (C3GN)

mild - supportive moderate >1.5g/day -> steriods, MMF RPGN -> steriods plus cyclophosphamide or MMF +/- eculizumab +/- PLEX refractory - eculizumab

Mutations of Bartter syndrome

NA-K-Cl type 1 ROMK T2 CIC kb type 3 barttin T4 upregulation of CaSR t5

frusemide effects on Ca

inhibits all downstream events, reduced Ca reabsorption

thiazide effect on Ca

compensatory increase in NAKCl, increases Ca reabsorption

Familial hypercalcaemia hypocaluria mutation and bloods

mutation in CaSR slightly high Ca, high or inappropriate normal PTH urinary Ca/Cr ratio <0.01 or low 24 hr urine Ca

Pathology of lithium and hypercalcaemia

damaged CaSR same as FHH 15-20% of people on lithium have high Ca

Target Hb in CKD

>100

New therapies for anaemia in CKD

hypoxia inducible factor inhibitors or stabilisers

Target for acidosis in CKD

aim HCO3 23-29 sodium bicarb issue with fluid retention

Most common causes of renovascular disease

atheroscelrotic disease 60-80% fibromuscular disease 10-20%

Difference physiologically between bilateral and unilateral renal artery stenosis

both have HTN unilateral -> normal volume, high renin bilateral -> hypervolaemia, normal renin

When is stenting beneficial in renovascular HTN

in FMD high risk atheroscleosis - recurrent flash APO, advancing renal impairment

Most common cause of KD in dialysis

in decreasing order diabetic nephropathy GN HTN

most common side effects of dialysis catheter

infection

Most common cause of death of dialysis

CVD

Mortality benefit patter in renal transplant

higher early, but lower in longer term

Causes of HLA sensitisation (difficult to match for transplant)

Previous transplant Pregnancy blood transfusions in past

Most used induction agent for transplant

Basilixumab (anti CD25 and IL2 receptor)

Most common immunosuppression regime for renal transplant

pred tacro MMF

What immunosuppressant to use for induction if high immunological risk group

ATG (rabbit thymoglobulin polyclonal Ab)

Major interactions between renal transplant immunosuppressants

cyclosporin lowers MMF levels but tacrolimus doesnt

Side effects of mTOR inhibitors

wound complications proteniuria

Most common cause of renal graft loss in early (1st year)

infection 33% cardiovascular 29% cancer 7%

Most common cause of renal graft loss in late (beyond 1st year)

cancer 29% cardiovascular 22% infection 13%

Most common cause of graft loss (due to graft failure)

early: graft thrombosis (technical) late: chronic allograft nephropathy

Most common cause of delayed graft function

native kidney ATN (decease donor 30-40%)

Causes of early graft rejection

acute rejection CNI toxicity renal artery stenosis recurrent disease in early: primary FSGS and aHUS (late more IgA)

Underlying physiology behind acute graft rejection

can be T cell mediated or Ab mediated

Treatment for acute graft rejection

t-cell mediated: IV methylpred, ATG (if steriod resistant) Ab mediated: PLEX, IVIG

Features of BK virus on Bx

intranuclear viral inclusions and SV40 staining (only in medulla)

Rule of thumb for infection post transplant

first 1 month - donor derived and nocicomal first 6 months - reactivation, oppurtunistic langer term - sommunity acquired (CMV, PJP)

Most risk profile for CMV in kidney donation

donor +ve recipient -ve

prophylaxis for CMV in renal transplant

D+R- : prophylaxis for 6 months, valgancyclovir D-R+ or D+R+ : prophylaxis for 3 months

Cancers which are higher risk in renal transplant

NHL lung colorectal

Best combo of immunosuppression in renal transplant for lowest skin cancer risk

reduced dose CNI with no MMF

most common inhereted renal disease

polycystic kidney disease

mode of inheretance PCKD

Most common mutation type PCKD

PKD1 (polycystin1) 78% PKD2 15% mostly monoalleleic complete penetrance

Which are the most severe PCKD mutations?

PKD1 worst than PKD2 if non-truncating mutation -> less severe

CNS extrarenal manifestation of PCKD

cerebral aneursyms - most in MCA 5% in younger, 20% in >60yo only screen high risk pt

hepatic manifestations of PCKD

hepatic cysts with severe PLD in 15% avoid estrogen replacement in women if liver cysts

Most common valvular disease in PCKD

MVP and AR

DIagnostic criteria for PCKD

if positive Fhx: if 15-39yo need >3 cysts, if 40-59 need 2 cysts in both kidneys if negative FHx, need bilat renal enlargement and >10 cysts in each kidney

Tolvaptin MoA

vasopressin V2 receptor antagonist

Tolvaptin use in PCKD

for every 4 years on the drug, delay dialysis for 1 year