Renal Flashcards
(132 cards)
1
Q
Causes of HLA-antibody creation
A
Transplants
Pregnancy
Blood transfusions
2
Q
Laboratory mechanism of HLA matching
A
Single antigen bead technology (Luminex)
3
Q
Mortality difference between ABO matched and unmatched transplants
A
NO difference
4
Q
Post transplant induction agents and MOA
A
Basiliximab - IL2R/ CD25 inhibitor (works on T cells)
Anti-thymocyte globulin- works on T cells.
5
Q
Immunosuppressive Drugs used post transplant.
A
- Steroids- Prednisolone.
- Calcineurin Inhibitors - Tacrolimus, Cyclosporin.
- Anti-metabolites - Mycophenolate, Azathioprine.
- m-TOR inhibitors - Sirolimus, everolimus.
6
Q
Transplant graft related complications
A
- Graft rejection
- Graft thrombosis
- Glomerulonephritis
- Chronic allograft nephropathy
7
Q
Most common cause of delayed graft function
A
ATN
8
Q
Management of rejection
A
T-cell medicated - Anti-thymocyte globulin, Methyl-prednisolone.
B-cell mediated - Plasmaphoresis, IVIG, Rituximab.
9
Q
Management of BK virus in transplant
A
reduce immunosuppression. NO antivirals available.
10
Q
treatment of CMV
A
Valganciclovir
11
Q
Causes of renal hypertension
A
Atherosclerotic disease Fibromuscular dysplasia Embolus Dissection Vasculitis
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
13
Q
Management of Fibromuscular Dysplasia
A
Angioplasty
14
Q
Part of nephron must susceptible to hypoperfusion/ ATN
A
proximal tubule
15
Q
Biomarkers of renal function
A
Creatinine
Urea
Cystatin C (more accurate)
16
Q
Best fluid for resus in AKI
A
Hartmann’s
17
Q
Nephrotic syndromes and symptoms
A
Syndromes: Minimal change Membranous FSGS Diabetic nephropathy Amyloid nephropathy
Symptoms:
Proteinuria
Hypoalbuminemia
Hyperlipidaemia
18
Q
Nephritic syndromes and symptoms
A
Syndromes: IgA nephropathy Post strep GN Goodpastures GN Rapidly progressive GN
Symptoms: Haematuria Proteinuria Hypertension Oliguria
19
Q
Histology in Minimal change disease
A
LM: no change:
Immunofluorescence: IgM in mesangial cells.
ECM: Effacement of podocytes.
20
Q
Histology in Membranous nephropathy
A
LM: Mesangial expansion
Immunofluorescence: IgG + C3 deposition - spike and dome
ECM: GBM thickening –> seen on silver stain.
21
Q
Histology in FSGS
A
LM: FSGS
Immunofluorescence: Nil
ECM: GBM thickening, effacement of podocytes.
22
Q
Cause for hypercoagulable state in GN
A
loss of antithrombin 3 proteins.
23
Q
Antibody for Membranous nephropathy
A
PLAR2 IgG
24
Q
Histology in Diabetic nephropathy
A
LM: Mesangial expansion w Kimmelstein-Wilson nodules.
ECM: GBM thickening
25
Histology in Amyloid nephropathy
LM: apple green amyloid seen on congo red staining.
26
Pathophysiology of IgA nephropathy
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.
27
Histology of IgA nephropathy
LM: Mesangial proliferation
Immunoflurescence: IgA and IgG deposition
EM: immune complex deposition
28
Causes of rapidly progressive (crescentic) GN and Pathophys.
1, Idiopathic
2. Anti GBM-antibodies
3. Immune complex mediated
4. 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.
29
Pathophys of Goodpastures Nephritis
GBM antibodies against alpha 3 chain in collagen (found in kidney and lung). Type 2 hypersensitivity.
Activates complement system.
30
Gene for Goodpastures
HLADR15
31
Timing of Post-strep GN from infection
6 weeks.
32
Pathophys of Post-strep GN
Type 3 hypersensitivity - Antigen-Antibody complexes stuck in GBM.
33
Pathology tests to test for recent strep infection
ANti-DNAse B + Anti-Streptolysin O test (ASOT)
34
Glomerulonephritis with
Normal C3, C4
Low C3, C4
Low C3 only
Low C4 only
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
35
Pathologic classifications of GN
1. Immune (polyclonal)
2. Pauci-immune
3. Complement mediated
4. Anti-GBM
5. Monoclonal Ig
36
Genes for ADPKD
PKD 1 - Polycystin 1 on Chromosome 16
| PKD 2 - Polycystin 2 on Chromosome 4
37
Cyst locations in PKD
```
Kidneys
Liver
Epididymis
Pancreatic
IPMN
```
38
Extra-renal manifestations of ADPKD
```
Mitral prolapse
Aortic regurgitation
Diastolic dysfunction
AF
LVH
Pericardial effusion
Aortic dissection
Diverticular disease
Hernia's
Berry aneurysm
```
39
Management of ADPKD
Aim to keep urine osmolality LOW
- Low salt
- High fluid
- Tolvaptan (ADH antagonist)
40
Hb aim in CKD
100-115.
| High EPO increased risk of CKD
41
Management of Anaemia in CKD
1. Iron transfusion
| 2. EPO (Aim 100-115)
42
Management of Acidosis in CKD
Give sodium bicarb --> Has mortality benefit!
43
Role of FGF23
Decreases Phosphate and Calcium reabsorbtion in the kidneys to lower phosphate levels.
Negatively feeds back on VitD and PTH.
44
Role of Klotho
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.
45
Role of Vit D
To increase serum Calcium and Phosphate by absorbing from GIT/bones/renal.
46
Role of PTH
To increase serum calcium. Increases renal phosphate loss. Stimulates Vit D.
47
Difference between Haemodialysis and Haemofiltration
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.
48
Complications of fistulas
Haematoma
Steal syndrome - cyanotic fingers
Aneurysm
49
What is dialysis-disequilibrium syndrome?
Change in urea level causing sudden shift in cerebral oedema - usually occurs early in dialysis.
50
What are the two types of peritoneal dialysis
1. Continuous ambulatory PD - good for slow transporters
| 2. Automatic PD - for fast transporters
51
PD dialysis efficacy test
Peritoneal equilibration test
52
Acute indications for dialysis
```
Oliguria
Severe overload/ APO
Uremic encephalopathy
Uremic pericarditis
Hyperkalaemia
Acidosis
```
53
Cause of diabetes insipidus
Mutation in Vasopressin 2 receptor.
54
Location of action in nephron of: Loop diuretics
Thick ascending limb of loop of Henle
55
Location of action in nephron of: Atrial naturetic peptide
Glomerulus - increases permeability
| Collecting duct - decreases sodium reabsorption.
56
Location of action in nephron of: Renin
DCT
57
Location of action in nephron of: PTH
DCT
58
Location of action in nephron of: Aldosterone
DCT
59
Bartter Syndrome
Defect in thick ascending limb. (Bart does a loop)
Effect is like loop diuretics.
Due to Na-K-2Cl symporter defect.
60
Gitelman Syndrome
Defect in thiazide transporter.
| Causes hypercalcaemia, hypokalaemia and hypomagnesemia
61
Liddles syndrome
Due to high amounts of sodium channel in the collecting duct. Same presentation as hyperaldosteronism (Conns) . HTN + hypernatremia. Manage with spironolactone.
62
Role of Angiotensin II Type 1 and Type 2 receptors.
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
Anion Gap equation
Na + K - (HCO3 + Cl)
64
Diabetic drug which improves prognosis in CKD
SGLT2-i
65
Management of IgA nephropathy
ACEi/ARB
66
PLAR2 is specific for which condition
IDIOPATHIC membranous nephropathy
67
Urine pH balance occurs where in the nephron
Collecting ducts due to intercalated cells.
68
Cause of metabolic alkalosis + hypokalaemia
Diuretic abuse
69
Which parameter is used to measure effective dialysis
Urea
70
Why do we used dextrose in PD?
To provide and osmotic gradient and improve ultrafiltration.
71
Most common cause of secondary minimal change disease
NSAIDS
72
1st line treatment for minimal change disease
steroids
73
Most common cause of asymptomatic microscopic haematuria in young people
IgA nephropathy
74
Management of Frusemide resistance
add Thiazide diuretic
75
Causes of NAGMA
A - Addisons
B - Bicarb loss.
C - Chloride excess
D - Diuretics (Azetazolomide)
76
Livedo reticularis + AKI + stroke
Cholesterol emboli
| Occurs 6 weeks post event (usually CAGs)
77
Renal effect of lithium
nephrogenic diabetes insipidus (interrupts ADH receptors)
78
Drug most likely to cause hyponatremia
Thiazide diuretics
79
Why does urea increase more than creatinine in dehydration
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
AKI + Abdominal pain with meals
Poly-arteritis nodosa
81
Type of stone formed in short gut?
oxalate stone
82
What part of the nephron controls renal blood flow autoregulation
afferent arteriole.
83
What is the braking phenomenon?
When there is upregulation of NaCl transporters in the DCT and collecting ducts to overcome the diuresis effect of loop diuretics.
84
ADH/Vasopressin works by
Increasing aquaporins to increase water reabsorption
85
Bacteria that you are most susceptible to in nephrotic disease
Strep Pneumonia
86
Diabetic kidney disease progression can be assessed histologically by
The degree of podocytopenia
87
Klotho expression level in CKDMBD
decreased Klotho
88
Where does aldosterone work
Principal cells in the cortical collecting duct
89
Where does atrial naturetic peptide work?
Medullary collecting ducts
90
Where is trimethoprim excreted
Proximal convoluted tubule
91
Where is phosphate reabsorbed?
Proximal tubule
92
Components of arteriorsclerosis/ vascular calcification in CKDMBD
1. Hyperphosphatemia
2. reduced Klotho
3. Impaired soft tissue calcification
93
Antibiotic for BK nephropathy
Ciprofloxacin - has some activity against BK by DNA topiramase inhibition
94
Prevention of contrast nephropathy in CKD
Give sodium bicarbonate infusion pre and post
95
Type of amyloidosis in Multiple Myeloma
AL amyloidosis
96
Type of Amyloidosis in Systemic inflammatory diseases
AA amyloidosis
97
Most common bone disease in dialysis patients
Adynamic bone disease
98
Dialysis patient with carpal tunnel and shoulder pain
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
Immunosuppression in pregnancy
Tacrolimus + Azathioprine + prednisolone
100
Side effect of Gadolinium in renal patients
Nephrogenic systemic fibrosis
101
Risk factor for post transplant lymphoproliferative disorder
EBV mismatch.
Management - reduce immunosuppression or switch to Rituximab. No role for Anti-virals.
102
Uveitis and renal failure cause
TINU syndrome - tubulointerstitial nephritis and uveitis. Occurs in young women.
103
Type of GN with highest recurrence after transplant
Primary FSGS - early recurrance
| IgA - long term recurrance
104
suPAR (soluable urokinase plasminigen activator receptor) is found in which condition
FSGS.
| suPAR binds podocyte beta3 integrin causing effacement.
105
Types of RTA
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
Most common cause of GN
Membranous
107
Most common cause of PRIMARY GN
IgA
108
Management of Membranous nephropathy
Mild to moderate - supportive only with ACEi, statins, diet, anticoagulation, diuretics for oedema.
Severe - immunosuppression with Rituximab or Pred + cyclophosphamide in rapidly progressive.
109
Causes of AIN
- TINU syndrome (AIN + uveitis)
- drugs
- infections (non-renal)
- autoimmune disease
110
Drugs causing AIN
NSAIDs, ABx, Allopurinol, Mesalazine, PPIs, Antivirals.
111
Features of scleroderma renal crisis
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
Most common cause of death in patients with CKD
cardiovascular disease
113
When to replace iron in CKD
Ferritin <500 and transferrin sats <30%
114
When in CRRT preferred over intermittent haemodialysis ?
Hypotension
115
When is intermittent haemodialysis preferred over CRRT?
Refractory hyperkalaemia
116
Role of sodium bicarb in CKD metabolic acidosis
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
Leading cause of death post kidney transplant - acute and long term.
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
Urinary losses in Fanconi's
```
HCO3
Amino acids
Phosphate
Potassium
Glucose
```
119
Contraindications to kidney transplant
```
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
Transplant work up in heavy smokers
Abstain for >1 month
| CT chest prior to rule out malignancy
121
Timing of contrast nephropathy and pathophys
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
Drugs causing ATN vs Drugs causing AIN
ATN:
- Aminoglycosides (Gent)
- Contrast
- Amphotericin
- Platinum
- Paracetamol
- Acyclovir
- Lithium
- Glycopeptides: Vancomycin
AIN:
- Abx: Penicillins, Cephalosporins, Rifampicin
- NSAIDs
- Allopurinol
- Loop diuretics: Frusemide
- Sulfur drugs
123
Which donor virus is safe for kidney transplant
Hep B - low risk of transmission + can vaccinate recipient prior.
124
Most common cause of death in heamodialysis/PD vs transplant
```
HD/PD = cardiovascular disease
Transplant = malignancy
```
125
Most common reason for withdrawal of treatment in ESRF
Psycho-social reasons
126
benefit of extended hours haemodialysis
- improved phosphate levels
| - reduced medidcation burden
127
What is dense deposit disease
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
Management of BK nephropathy
1. Reduce/cease mycophenolate/ azathioprine
2. Reduce/cease cyclosporin/ tacrolimus
3. cease prednisolone
129
Next step after positive BK PCR
Renal biopsy.
| Pt has BK viremia, need to check if they have BK nephropathy.
130
Cells seen in the urine in BK
decoy cells
131
Management of dialysis disequilibrium syndrome
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
What is Dent disease
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
