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RACP short cards > Nephrology COPY > Flashcards

Nephrology COPY Flashcards

1
Q

Gaddolinium contrast load in CKD

A

Causes Nephrogenic Systemic Fibrosis

Symmetrical skin involvement with waxy, thickened and hardening of extremities and torso

Can have fibrosis of deeper structures such as lung, heart, fascia, muscles

CD34 + fibrocytes

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2
Q

HLA sub-typing and risk of rejection

A

Complement Dependent Cytotoxicity (CDC) - Highest risk if Positive (holds most weight on decision!)

Flow

Virtual - Lowest risk if positive

Most important HLA group is HLA DQ

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3
Q

Induction therapies in Renal transplant

A

Basilixumab - Bind IL2 recetor to inhibit CD25 on T cells

Anti-Thymboglobulin (ATG) - Rabbit Thymoglobulin Ab - Mechanisms; Antibody dependent cell mediated cytotoxicity & complement dependent cytotoxicity

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4
Q

Most common treatment regime in renal transplant

A
  • Basilixumab
  • Prednisolone
  • Tacrolimus
  • Mycophenolate
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5
Q

MOA Tacrolimus

A

Calcineurin inhibitor; inhibit activation of NFAT (Nuclear Factor activated T cells) and reduce trascription of cytokines including IL2

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6
Q

MOA mTORi

A

i.e. Everolimus, Sirolimus

Binds FK receptor to inhibit mTOR (mammalian target of rapamycin) and arrest the T cell cycle to prevent proliferation (arrest of cell cycle at G1) -> which would normally be stimulated by IL2

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7
Q

Tacrolimus side effects

A

“TACROLIMUS”

Tremor
Alopecia
Cardiovascular - HTN
Renal insufficiency
Oncological risk - skin cancers
Lipid elevation
Insulin dependent diabetes (depletion not resistance)
Magnesium wasting
Uric acid elevation
Seizures

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8
Q

Cyclosporin Side effects

A

Gum Hypertrophy
Hirsutism

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9
Q

Mycophenolate MOA

A

Pro-drug of Mycophenolic Acid. Inhibits Inosine-5- Monophosphate dehydrogenase (IMPDH) to reduce purine synthesis (Guanine) and cell replication of T and B cells

Side effects are diarrhoea and BM suppression (within 6 months)

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10
Q

Types of renal transplant rejection

A

T- Cell (Donar APC: Host T cell)-> treat with pulse methyl pred +/- thymoglobulin and increase maintenance therapy.

Antibody mediated (Host APC: Host T cell) -> requires IVIG or PLEX +/- Rituximab. C4D+

Mixed

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11
Q

CMV prophylaxis indications

A

D + / R - = 6 months
D - / R + = 3 months
D - / R - = no prophylaxis unless

Oral Valganciclovir

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12
Q

CMV treatment

A

Double dose of prophylaxis with PO Valganciclovir or IV Ganciclovir, cautiously reduce immunosuppression, switch to mTORi, if resistance - Foscarnet or Cidofivor (but nephrotoxic!)

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13
Q

Immunosuppressant with low risk skin cancer

A

mTORi (Everolimus, Sirolimus) - if skin cancer -> change AZA to mTORi

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14
Q

BK Virus

A

Polyoma virus
Post transplant nephropathy

Risk factors; female, HLA mismatch, Older age, immunosuppression

Ix;
- SV 40 stain shows intracellular inclusions on biopsy
- BK Virus PCR (100% of patients!), should be screened at 12 months
- Viral load

Rx with reduction in immunosuppression, Cidofovir, Ciprofloxacin

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15
Q

RIFLE Criteria

A

for AKI (injury within 7 days);
Risk - 1.5 x Cr, UO < 0.5ml/hr/kg for 6 hours
Injury - 2 x Cr, UO < 0.5ml/kg/hr for 12 hours
Failure - 3 x Cr, UO < 0.3ml/kg/hr for 24 hours, anuria for 12 hours
Loss - Persistent renal failure for 4 weeks
ESRD

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16
Q

Management AKI; Type fluid, BP target, Dialysis commencement time

A
  • Resuscitation with N.Saline - Albumin had increased mortality
  • Aim MAP 65mmHg
  • Dialysis - NO benefit with early dialysis < 48 hours
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17
Q

Rx contrast induced nephropathy

A

IVH, no benefit from other therapies

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18
Q

Rhabdomyolysis in AKI

A
  • Dehydration with renal hypoperfusion
  • Increased water resorption with precipitation of tubular casts
  • Cast nephropathy

= Tubular ischaemia due to casts and hypoperfusion

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19
Q

Secondary causes of minimal change disease

A

Presents as acute onset Nephrotic Syndrome, with effacement of foot podocytes on light microscopy

  • NSAIDs
  • Lithium
  • Lymphoma
  • Thymoma
  • Infection
  • Atopy
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20
Q

Membranous Nephropathy

A

Nephrotic syndrome

“S”
Staining PLA2R
Subepithelial immune deposition
SLE
Screen for malignancy

Rx with observation +/- ACE or ARB for proteinuria. Immunosuppression if not resolved > 12 months

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21
Q

Secondary causes Membranous Nephropathy

A

Malignancy
SLE

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22
Q

Causes of FSGN

A
  • Genetic predisposition - APOL1 gene in young Africans
  • SuPAR (soluble urokinase-dupe plasminogen activator)
  • Shear stress - HTN, prematurity, Obesity, single kidney
  • Drugs - Lithium, Pomidronate, IFN, heroin
  • HIV
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23
Q

Biopsy findings FSGN

A

Focal segmental sclerosis in < 50% glomerulus

24
Q

IgA GN pathophysiology

A

Nephritic disease
Defect in IgA1-secreting cells forming an IgA that creates immune complexes with mesengial cells
Post-infectious
Worse prognosis if > 1g protein/day

25
Q

Types of Lupus Nephritis

A

“No Man Faces Diffuse Menstrual Situations”

  1. Normal - conservative Mngmt + ACE/ARB
  2. Mesingial - conservative Mngmt + ACE/ARB
  3. Focal Proliferative - Medical Mngmt
  4. Diffuse - Medical Mngmt
  5. membranous - Medical Mngmt
  6. Sclerosing - requires preparation for dialysis
26
Q

Indications for renal biopsy in SLE

A

If proteinuria > 0.5g/day

27
Q

Management Lupus nephritis

A

For Class 3-5

Induction - Steroids (Methyl pred or pred) + Mycophenolate or cyclophosphamide

Maintenance - Mycophenolate or Azathioprine

Resistant - consider Rituximab

28
Q

Pathognomonic features: Minimal Change Disease

A
  • Nephrotic syndrome
  • Young
  • Podocyte effacement on light microscopy
  • Due to; Thymoma, Lymphoma, Atopy, NSAIDs, Lithium
29
Q

Pathognomonic features: Membranous

A

Nephrotic syndrome
Old -> middle age
PLA2R serology & staining at subepithelium
Causes: Malignancy & SLE

30
Q

Pathognomonic features: Focal Segmental GN

A

Nephrotic syndrome
< 50% sclerosis on biopsy
Associated with APOL1 gene commonly in Africans
Due to:
- Shear stress; Obesity, HTN, Solo Kidney
- SuPAR
- Lithium, HIV, Pamidronate, IFN Heroin

31
Q

Pathognomonic features: IgA nephropathy

A

Nephritic Syndrome
2-4 weeks post-URTI
IgA-1 and complement deposits in mesengium

32
Q

Pathognomonic features: MPGN

A

Rapid Nephritic/nephrotic syndrome
Associated with Hep C, Chronic infection and Cryoglobulins
Type 1 - Immune complex deposits (IgG and C3)
Type 2 - Complement deposits (C3 only - dense deposit disease)
Tram Tracking with immune deposition on Biopsy

33
Q

Anti-GBM target

A

Alpha 3 chain of type 4 collagen

34
Q

Risk factors Anti-GBM

A
  • Male
  • HLADR2
  • Alemtuzumab use
  • Hydrocarbons
  • Influenzae A
  • Smoking
35
Q

Lipid changes with Nephrotic syndrome

A
  • Unchanged HDL
  • Increased LDL
  • Increased TAGs
  • Increased Lipprotein A
36
Q

Common associations hypercoaguable state of nephrotic syndrome

A
  • Most commonly due to membranous nephropathy
  • Renal Vein thrombosis most common site
  • Proportional to hypoalbuminaemia
37
Q

Management of Membranous Nephropathy

A

DO NOT USE STEROIDS ALONE - no evidence
- Observe for 6 - 12 months
- Immunosuppression w calceinerin inhibitors in combination with prednisolone
- Anticoagulation (given highest risk prothrombotic state with renal vein thrombosis)

38
Q

Pathognomonic features: Anti- GBM GN

A
  • Anti- GBM +
  • Linear IgG staining
  • HLA DR2
  • Use Alemtuzumab
  • Hydrocarbon exposure
  • Pulmonary-renal syndrome
39
Q

Diagnosis Polycystic Kidney Disease

A

Positive FHx;
On USS
- > 3 cysts/total < 40 years age
- > 2 cysts/kidney 40-60 years
- > 4 cysts/kidney > 60 years
On MRI
> 10 cysts by age 40
If no cysts by 18 years of age, diagnosis unlikely

Negative FHx;
On USS
Enlarged kidneys, with > 10 cysts/kidney

40
Q

PCKD inheritance

A

Autosomal Dominant, point mutations, with complete penetrance;

  • PKCD type 1 - Polycystin -1 on Chromosome 16 (severe), ESKD by 50’s
  • PKCD type 2 - Polycystin-2 on chromosome 4 (less severe), milder - ESKD by 70’s

*Non-truncated genes have milder phenotype (40%)
*Variant of autosomal recessive but often causes fetal death

41
Q

Worse prognosis in PCKD

A
  • Truncated, PKD1 mutation
  • Male (but polycystic liver disease more common in women)
  • Obesity
  • HTN
  • Degree Proteinuria
  • Larger kidney size
  • FHx ESRD < 55
  • Earlier onset symptoms
42
Q

Extra-renal manifestations of PCKD

A
  • Liver cysts - most severe in women due to oestrogen
  • Pancreatic cysts
  • Brain Aneurysms
  • Aortic Aneurysm
  • Valvular pathologies - most often mitral valve prolapse and AR
  • Seminal Vesicle cysts
  • Diverticular disease
  • Hernias
43
Q

Tolvapton

A

Vasopressin 2 receptor antagonist
Used in PCKD to reduce cyst size
causes hypotonic urine
Aim Urine Osmo < 280

44
Q

Dialysis Disequilibrium Syndrome

A

Aggressive dialysis causing cerebral oedema.
Decrease in Urea in blood post-dialysis but persistent Urea in brain therefore osmotic shift of fluid across BBB

45
Q

Kt/V

A

Clearance of Urea in the context of time on Dialysis

46
Q

ANP

A

Released from atria with stretch
Atrial Natriuretic peptide - decreases extracellular fluid volume by increasing GFR through dilation afferent arteriole and inhibition of Na resorption at ENAC and Na/K+ channels. inhibits Renin.

47
Q

Types of Vasopressin receptors

A

V1 - smooth and cardiac muscle
V2 - thick ascending LOH, DCT, medullary & cortical collecting duct (target for Talvaptan)
V3 - anterior pituitary - releases ACTH, prolactin

48
Q

Carbonic Anhydrase inhibitors

A

Act at proximal convoluted tubule - Inhibit HCO3- resorption, leading to decreased activity of Na/H+ exchange and more to more urinary Na having a weak diuretic effect

I.e. Acetazolamide and Topiramate

Will cause a metabolic acidosis (Type 2 renal tubular acidosis)

49
Q

Sites of Na resorption Kidney

A

65% PCT
25% Thick ascending LOH
5% DCT
3% Cortical collecting duct
1% Medullary collecting duct

50
Q

Bartter Syndrome

A

Autosomal recessive
Ineffective Na/K/Cl transporter at LOH - mimicking loop diuretics
- Young children with growth and mental delays
- Interrupts gradient for Mg, Ca
- Low volume leads to hyperaldosteronism & increased Na uptake with H+ secretion.
- Increased renin with high prostaglandins

Leads to
- Low K
- Low H+ with metabolic alkalosis
- Low Mg
- Low Ca

Treat with NSAIDs to block prostaglandin production. Replace electrolytes

51
Q

Gitelman Syndrome

A

Autosomal recessive
Interrupts Na/Cl- transporter at DCT to mimic thiazide diuretics
Presents in adulthood with polyuria and craps
Interrupts the electrochemical gradient of Mg resorption causing hypomagnesium

52
Q

Type 1 RTA

A
  • Loss of H+ ATPase at collecting duct
  • Increased retention H+ with metabolic acidosis
  • Decreased Na+/H+ exchange, leading to overactivity of Na+/K+ exchange and hypoklaemia
  • Hypercalcaemia as Ca drawn from bones to buffer H+, but consequence of reduced renal reabsorption calcium leading to Nephrocalcinosis

Electrolyte disturbances
- NAGMA
- Hypokalemia, urine pH > 5.5
- Hypercalcaemia

Rx with HCO3- which will increase urine pH and drive H+ excretion, reduces need for Na+/K+ exchange and decreasing hypokalaemia

Causes - Autoimmune conditions - Sjogrens, RA

53
Q

Type 2 RTA

A

Decreased capacity to resorb HCO3- at proximal tubule resulting in increased K+ secretion at DCT as compensatory mechanism

Electrolyte disturbance
- Hypokalaemia - made worse with BiCarb Rx given ++ renal wasting
- Serum bicarb 12-20
- Lower urine pH
- Can occur with other defects including impaired resorption of phosphate, glucose, uric acid and amnio acids

Due to Fanconi’s syndrome, monoclonal gammopathies, Tenofovir

54
Q

Type 3 RTA

A

Combination of Type 1 and 2

55
Q

Type 4 RTA

A

Hyperkalemia NOT hypokalaemia as with other RTA. Can be secondary to Heparin
Due to hypoaldosteronism
Rx Fludrocortisone (has mineralocorticoid activity)

56
Q

Causes of Type 4 RTA

A

NSAIDs
Calcineurin inhibitors - i.e Tacrolimus
Chronic interstitial nephritis
DM nephropathy
Acute GN
Heparin -> which has a toxic effect on adrenal glomerulosa cells
Primary adrenal insufficiency/Addisons disease
Ang2 inhibitors
Potassium sparing diuretics

57
Q

CMV treatment

A

Double dose of prophylaxis with PO Valganciclovir or IV Ganciclovir, cautiously reduce immunosuppression, switch to mTORi, if resistance - Foscarnet or Cidofivor (but nephrotoxic!)

RACP short cards (30 decks)

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