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Nimna's Flash Cards > Renal > Flashcards

Renal Flashcards

1
Q

Causes of HLA-antibody creation

A

Transplants
Pregnancy
Blood transfusions

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2
Q

Laboratory mechanism of HLA matching

A

Single antigen bead technology (Luminex)

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3
Q

Mortality difference between ABO matched and unmatched transplants

A

NO difference

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4
Q

Post transplant induction agents and MOA

A

Basiliximab - IL2R/ CD25 inhibitor (works on T cells)

Anti-thymocyte globulin- works on T cells.

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5
Q

Immunosuppressive Drugs used post transplant.

A
  1. Steroids- Prednisolone.
  2. Calcineurin Inhibitors - Tacrolimus, Cyclosporin.
  3. Anti-metabolites - Mycophenolate, Azathioprine.
  4. m-TOR inhibitors - Sirolimus, everolimus.
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6
Q

Transplant graft related complications

A
  • Graft rejection
  • Graft thrombosis
  • Glomerulonephritis
  • Chronic allograft nephropathy
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7
Q

Most common cause of delayed graft function

A

ATN

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8
Q

Management of rejection

A

T-cell medicated - Anti-thymocyte globulin, Methyl-prednisolone.
B-cell mediated - Plasmaphoresis, IVIG, Rituximab.

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9
Q

Management of BK virus in transplant

A

reduce immunosuppression. NO antivirals available.

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10
Q

treatment of CMV

A

Valganciclovir

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11
Q

Causes of renal hypertension

A 
Atherosclerotic disease 
Fibromuscular dysplasia 
Embolus 
Dissection 
Vasculitis
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12
Q

Role of re-vascularisation in renal artery stenosis?

A

NO role. No benefit in Astral or Coral studies. Can be considered in severe disease

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13
Q

Management of Fibromuscular Dysplasia

A

Angioplasty

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14
Q

Part of nephron must susceptible to hypoperfusion/ ATN

A

proximal tubule

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15
Q

Biomarkers of renal function

A

Creatinine
Urea
Cystatin C (more accurate)

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16
Q

Best fluid for resus in AKI

A

Hartmann’s

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17
Q

Nephrotic syndromes and symptoms

A 
Syndromes: 
Minimal change 
Membranous 
FSGS 
Diabetic nephropathy 
Amyloid nephropathy

Symptoms:
Proteinuria
Hypoalbuminemia
Hyperlipidaemia

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18
Q

Nephritic syndromes and symptoms

A 
Syndromes: 
IgA nephropathy 
Post strep GN
Goodpastures GN 
Rapidly progressive GN 
Symptoms: 
Haematuria 
Proteinuria 
Hypertension 
Oliguria
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19
Q

Histology in Minimal change disease

A

LM: no change:
Immunofluorescence: IgM in mesangial cells.
ECM: Effacement of podocytes.

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20
Q

Histology in Membranous nephropathy

A

LM: Mesangial expansion
Immunofluorescence: IgG + C3 deposition - spike and dome
ECM: GBM thickening –> seen on silver stain.

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21
Q

Histology in FSGS

A

LM: FSGS
Immunofluorescence: Nil
ECM: GBM thickening, effacement of podocytes.

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22
Q

Cause for hypercoagulable state in GN

A

loss of antithrombin 3 proteins.

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23
Q

Antibody for Membranous nephropathy

A

PLAR2 IgG

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24
Q

Histology in Diabetic nephropathy

A

LM: Mesangial expansion w Kimmelstein-Wilson nodules.
ECM: GBM thickening

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25
Q

Histology in Amyloid nephropathy

A

LM: apple green amyloid seen on congo red staining.

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26
Q

Pathophysiology of IgA nephropathy

A

Abnormal IgA1 proteins are formed which are galactose deficient. Anti-glycan IgG form which lead to IgA-IgG immune complexes - leading to a type 3 hypersensitivity reaction.
IgG-IgA complexes get stuck in the mesangium causing complement activation.

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27
Q

Histology of IgA nephropathy

A

LM: Mesangial proliferation
Immunoflurescence: IgA and IgG deposition
EM: immune complex deposition

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28
Q

Causes of rapidly progressive (crescentic) GN and Pathophys.

A

1, Idiopathic

  1. Anti GBM-antibodies
  2. Immune complex mediated
  3. Pauci-immune - ANCA

Pathophys: Rents (focal gaps of the capillary wall) are induced in the glomerular capillary wall, resulting in the movement of plasma products + fibrinogen, into Bowman’s space causing fibrin formation,
activation of macrophages and T cells and the release of cytokines IL-1 and TNF-alpha and procoagulant and fibrinolytic inhibitory factors.

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29
Q

Pathophys of Goodpastures Nephritis

A

GBM antibodies against alpha 3 chain in collagen (found in kidney and lung). Type 2 hypersensitivity.
Activates complement system.

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30
Q

Gene for Goodpastures

A

HLADR15

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31
Q

Timing of Post-strep GN from infection

A

6 weeks.

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32
Q

Pathophys of Post-strep GN

A

Type 3 hypersensitivity - Antigen-Antibody complexes stuck in GBM.

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33
Q

Pathology tests to test for recent strep infection

A

ANti-DNAse B + Anti-Streptolysin O test (ASOT)

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34
Q

Glomerulonephritis with

Normal C3, C4
Low C3, C4
Low C3 only
Low C4 only

A

Normal C3, C4 - IgA, ANCA vasculitis, anti-GBM, Goodpastures. (Type 2/3 hypersensitivities)
Low C3, C4 - post strep, lupus, Hep B, C, HIV, membranoproliferative.
Low C3 only - C3 glomerulopathy
Low C4 only - Cryoglobulins

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35
Q

Pathologic classifications of GN

A
  1. Immune (polyclonal)
  2. Pauci-immune
  3. Complement mediated
  4. Anti-GBM
  5. Monoclonal Ig
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36
Q

Genes for ADPKD

A

PKD 1 - Polycystin 1 on Chromosome 16

PKD 2 - Polycystin 2 on Chromosome 4

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37
Q

Cyst locations in PKD

A 
Kidneys 
Liver 
Epididymis
Pancreatic 
IPMN
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38
Q

Extra-renal manifestations of ADPKD

A 
Mitral prolapse 
Aortic regurgitation 
Diastolic dysfunction 
AF 
LVH 
Pericardial effusion
Aortic dissection 
Diverticular disease 
Hernia's 
Berry aneurysm
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39
Q

Management of ADPKD

A

Aim to keep urine osmolality LOW

  • Low salt
  • High fluid
  • Tolvaptan (ADH antagonist)
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40
Q

Hb aim in CKD

A

100-115.

High EPO increased risk of CKD

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41
Q

Management of Anaemia in CKD

A
  1. Iron transfusion

2. EPO (Aim 100-115)

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42
Q

Management of Acidosis in CKD

A

Give sodium bicarb –> Has mortality benefit!

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43
Q

Role of FGF23

A

Decreases Phosphate and Calcium reabsorbtion in the kidneys to lower phosphate levels.
Negatively feeds back on VitD and PTH.

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44
Q

Role of Klotho

A

Produced in the Kidney
Is a transmembrane protein that works as a co-factor for FGF23.
Has anti-aging properties by reducing oxidative stress from hyperphosphatemia.

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45
Q

Role of Vit D

A

To increase serum Calcium and Phosphate by absorbing from GIT/bones/renal.

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46
Q

Role of PTH

A

To increase serum calcium. Increases renal phosphate loss. Stimulates Vit D.

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47
Q

Difference between Haemodialysis and Haemofiltration

A

Haermodialysis - the gradient is from blood to dialysate - works through both hydrostatic pressure (convection) and diffusion.

Haemofiltration - Replacement fluid is added to the blood - toxins removed through convection alone.

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48
Q

Complications of fistulas

A

Haematoma
Steal syndrome - cyanotic fingers
Aneurysm

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49
Q

What is dialysis-disequilibrium syndrome?

A

Change in urea level causing sudden shift in cerebral oedema - usually occurs early in dialysis.

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50
Q

What are the two types of peritoneal dialysis

A
  1. Continuous ambulatory PD - good for slow transporters

2. Automatic PD - for fast transporters

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51
Q

PD dialysis efficacy test

A

Peritoneal equilibration test

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52
Q

Acute indications for dialysis

A 
Oliguria 
Severe overload/ APO 
Uremic encephalopathy 
Uremic pericarditis 
Hyperkalaemia 
Acidosis
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53
Q

Cause of diabetes insipidus

A

Mutation in Vasopressin 2 receptor.

54
Q

Location of action in nephron of: Loop diuretics

A

Thick ascending limb of loop of Henle

55
Q

Location of action in nephron of: Atrial naturetic peptide

A

Glomerulus - increases permeability

Collecting duct - decreases sodium reabsorption.

56
Q

Location of action in nephron of: Renin

A

DCT

57
Q

Location of action in nephron of: PTH

A

DCT

58
Q

Location of action in nephron of: Aldosterone

A

DCT

59
Q

Bartter Syndrome

A

Defect in thick ascending limb. (Bart does a loop)
Effect is like loop diuretics.
Due to Na-K-2Cl symporter defect.

60
Q

Gitelman Syndrome

A

Defect in thiazide transporter.

Causes hypercalcaemia, hypokalaemia and hypomagnesemia

61
Q

Liddles syndrome

A

Due to high amounts of sodium channel in the collecting duct. Same presentation as hyperaldosteronism (Conns) . HTN + hypernatremia. Manage with spironolactone.

62
Q

Role of Angiotensin II Type 1 and Type 2 receptors.

A

Type 1 - decreases renal blood flow through vasoconstriction.

Type 2 - increases renal blood flow and naturesis - reduces hypertension. OPPOSITE to type 1. There is much less of this receptor.

63
Q

Anion Gap equation

A

Na + K - (HCO3 + Cl)

64
Q

Diabetic drug which improves prognosis in CKD

A

SGLT2-i

65
Q

Management of IgA nephropathy

A

ACEi/ARB

66
Q

PLAR2 is specific for which condition

A

IDIOPATHIC membranous nephropathy

67
Q

Urine pH balance occurs where in the nephron

A

Collecting ducts due to intercalated cells.

68
Q

Cause of metabolic alkalosis + hypokalaemia

A

Diuretic abuse

69
Q

Which parameter is used to measure effective dialysis

A

Urea

70
Q

Why do we used dextrose in PD?

A

To provide and osmotic gradient and improve ultrafiltration.

71
Q

Most common cause of secondary minimal change disease

A

NSAIDS

72
Q

1st line treatment for minimal change disease

A

steroids

73
Q

Most common cause of asymptomatic microscopic haematuria in young people

A

IgA nephropathy

74
Q

Management of Frusemide resistance

A

add Thiazide diuretic

75
Q

Causes of NAGMA

A

A - Addisons
B - Bicarb loss.
C - Chloride excess
D - Diuretics (Azetazolomide)

76
Q

Livedo reticularis + AKI + stroke

A

Cholesterol emboli

Occurs 6 weeks post event (usually CAGs)

77
Q

Renal effect of lithium

A

nephrogenic diabetes insipidus (interrupts ADH receptors)

78
Q

Drug most likely to cause hyponatremia

A

Thiazide diuretics

79
Q

Why does urea increase more than creatinine in dehydration

A

Urea is actively reabsorbed.

This effect is enhanced because urea transporter UT-A1 in the inner medullary collecting duct is directly sensitive to vasopressin and upregulates its expression

80
Q

AKI + Abdominal pain with meals

A

Poly-arteritis nodosa

81
Q

Type of stone formed in short gut?

A

oxalate stone

82
Q

What part of the nephron controls renal blood flow autoregulation

A

afferent arteriole.

83
Q

What is the braking phenomenon?

A

When there is upregulation of NaCl transporters in the DCT and collecting ducts to overcome the diuresis effect of loop diuretics.

84
Q

ADH/Vasopressin works by

A

Increasing aquaporins to increase water reabsorption

85
Q

Bacteria that you are most susceptible to in nephrotic disease

A

Strep Pneumonia

86
Q

Diabetic kidney disease progression can be assessed histologically by

A

The degree of podocytopenia

87
Q

Klotho expression level in CKDMBD

A

decreased Klotho

88
Q

Where does aldosterone work

A

Principal cells in the cortical collecting duct

89
Q

Where does atrial naturetic peptide work?

A

Medullary collecting ducts

90
Q

Where is trimethoprim excreted

A

Proximal convoluted tubule

91
Q

Where is phosphate reabsorbed?

A

Proximal tubule

92
Q

Components of arteriorsclerosis/ vascular calcification in CKDMBD

A
  1. Hyperphosphatemia
  2. reduced Klotho
  3. Impaired soft tissue calcification
93
Q

Antibiotic for BK nephropathy

A

Ciprofloxacin - has some activity against BK by DNA topiramase inhibition

94
Q

Prevention of contrast nephropathy in CKD

A

Give sodium bicarbonate infusion pre and post

95
Q

Type of amyloidosis in Multiple Myeloma

A

AL amyloidosis

96
Q

Type of Amyloidosis in Systemic inflammatory diseases

A

AA amyloidosis

97
Q

Most common bone disease in dialysis patients

A

Adynamic bone disease

98
Q

Dialysis patient with carpal tunnel and shoulder pain

A

Dialysis related amyloidosis - due to build up of Beta-2-microgobulin. Cystic lesions containing amyloid are seen at the end of long bones. Occurs in pts on long term dialysis (>5yrs)

99
Q

Immunosuppression in pregnancy

A

Tacrolimus + Azathioprine + prednisolone

100
Q

Side effect of Gadolinium in renal patients

A

Nephrogenic systemic fibrosis

101
Q

Risk factor for post transplant lymphoproliferative disorder

A

EBV mismatch.

Management - reduce immunosuppression or switch to Rituximab. No role for Anti-virals.

102
Q

Uveitis and renal failure cause

A

TINU syndrome - tubulointerstitial nephritis and uveitis. Occurs in young women.

103
Q

Type of GN with highest recurrence after transplant

A

Primary FSGS - early recurrance

IgA - long term recurrance

104
Q

suPAR (soluable urokinase plasminigen activator receptor) is found in which condition

A

FSGS.

suPAR binds podocyte beta3 integrin causing effacement.

105
Q

Types of RTA

A

Type 1. Distal convoluted tubule and Collecting duct. Failure of alpha intercalated cells to secrete H+ and absorb K+

Type 2. Proximal tubules. Failure of PCT to reabsorb HCO3

Type 3 - Mixed 1 and 2

Type 4 - Due to hypoaldosteronism

106
Q

Most common cause of GN

A

Membranous

107
Q

Most common cause of PRIMARY GN

A

IgA

108
Q

Management of Membranous nephropathy

A

Mild to moderate - supportive only with ACEi, statins, diet, anticoagulation, diuretics for oedema.

Severe - immunosuppression with Rituximab or Pred + cyclophosphamide in rapidly progressive.

109
Q

Causes of AIN

A
  • TINU syndrome (AIN + uveitis)
  • drugs
  • infections (non-renal)
  • autoimmune disease
110
Q

Drugs causing AIN

A

NSAIDs, ABx, Allopurinol, Mesalazine, PPIs, Antivirals.

111
Q

Features of scleroderma renal crisis

A

SRC is characterized by three major features:

  1. Abrupt onset of moderate to severe hypertension that is typically associated with an increase in plasma renin activity - often accompanied by manifestations of malignant hypertension such as hypertensive retinopathy (hemorrhages and exudates) and hypertensive encephalopathy
  2. Acute kidney injury (AKI)
  3. Urinalysis that is normal or reveals only mild proteinuria with few cells or casts - The urine sediment is usually normal.
112
Q

Most common cause of death in patients with CKD

A

cardiovascular disease

113
Q

When to replace iron in CKD

A

Ferritin <500 and transferrin sats <30%

114
Q

When in CRRT preferred over intermittent haemodialysis ?

A

Hypotension

115
Q

When is intermittent haemodialysis preferred over CRRT?

A

Refractory hyperkalaemia

116
Q

Role of sodium bicarb in CKD metabolic acidosis

A

Slowing of CKD progression

Bone health - Prevention of bone buffering.

Nutritional status - Improved nutritional status and lean body mass. Acidosis causes a catabolic state and decreases IGF1.

117
Q

Leading cause of death post kidney transplant - acute and long term.

A

Kidney - Infections are the leading cause of mortality in the early posttransplant period . Atherosclerotic cardiovascular disease continues to be the overall major cause of death after kidney transplantation.
Long term malignancy > CVD ?

118
Q

Urinary losses in Fanconi’s

A 
HCO3 
Amino acids 
Phosphate 
Potassium 
Glucose
119
Q

Contraindications to kidney transplant

A 
Untreated MM or MGUS 
AL amyloidosis 
Decompensated cirrhosis 
Severe cardiac disease/ lung disease 
Neurodegenerative conditions

Note - transplant can be done in low grade prostate cancers.

120
Q

Transplant work up in heavy smokers

A

Abstain for >1 month

CT chest prior to rule out malignancy

121
Q

Timing of contrast nephropathy and pathophys

A

Decreased eGFR with in 1 day and improvement within 3-7 days.

Pathophys - ATN from renal vasoconstriction + ATN from direct cytotoxic effect on tubular cells

122
Q

Drugs causing ATN vs Drugs causing AIN

A

ATN:

  • Aminoglycosides (Gent)
  • Contrast
  • Amphotericin
  • Platinum
  • Paracetamol
  • Acyclovir
  • Lithium
  • Glycopeptides: Vancomycin

AIN:

  • Abx: Penicillins, Cephalosporins, Rifampicin
  • NSAIDs
  • Allopurinol
  • Loop diuretics: Frusemide
  • Sulfur drugs
123
Q

Which donor virus is safe for kidney transplant

A

Hep B - low risk of transmission + can vaccinate recipient prior.

124
Q

Most common cause of death in heamodialysis/PD vs transplant

A 
HD/PD = cardiovascular disease 
Transplant = malignancy
125
Q

Most common reason for withdrawal of treatment in ESRF

A

Psycho-social reasons

126
Q

benefit of extended hours haemodialysis

A
  • improved phosphate levels

- reduced medidcation burden

127
Q

What is dense deposit disease

A

A type of membranoproliferative GN: IgG autoantibody (C3 nephritic factor) binds C3 convertase, rendering C3 resistant to inactivation; immunofluorescent staining identifies C3 around dense deposits and in mesangium.

128
Q

Management of BK nephropathy

A
  1. Reduce/cease mycophenolate/ azathioprine
  2. Reduce/cease cyclosporin/ tacrolimus
  3. cease prednisolone
129
Q

Next step after positive BK PCR

A

Renal biopsy.

Pt has BK viremia, need to check if they have BK nephropathy.

130
Q

Cells seen in the urine in BK

A

decoy cells

131
Q

Management of dialysis disequilibrium syndrome

A

initiate sodium modeling (either by engaging this feature on the dialysis machine or by changing the dialysate sodium bath). dont take the patient off dialysis.

132
Q

What is Dent disease

A

Dent’s disease: a familial proximal renal tubular syndrome with low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis, metabolic bone disease, progressive kidney failure, and a marked male predominance

Nimna's Flash Cards (15 decks)

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