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BPT Flashcards > Renal > Flashcards

Renal Flashcards

1
Q

Key progression factors for kidney disease

A

Proteinuria
HTN
Hyperglycaemia
Smoking

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2
Q

Aetiology of AKI

A

Pre-renal: hypovolaemia, CCF, sepsis, ACE-i, NSAIDs, hepatorenal
Nephrotoxins, contrast, atheroembolism
Obstruction: prostatic > others

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3
Q

Classification of AKI

A

Stage 1: SCr 1.5-2x
Stage 2: SCr 2-3x
Stage 3: > 3x or dialysis

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4
Q

Definition of CKD

A

> 90 days of AKI

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5
Q

Causes of ATN

A

Ischaemic
- prolonged pre-renal
- hypotension, shock
- CCF
Sepsis
- COVID
Nephrotoxic
- Drug induced - radiocontrast, aminoglycosides, cisplastinum
- Pigment nephropathy

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6
Q

TLS features

A

Hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcaemia

Associated with lymphoproliferative and leukaemia malignancies

Management with fluids + rasburicase

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7
Q

Hepatorenal syndrome

A

3 phases
- Pre-ascitic: compensated Na+ retention
- Ascites: sodium retention, mostly DCT, urinary Na < 10
- HRS: PCT Na+ retention

Diagnosis:
- Urine Na < 10
- falling GFR
- no urine blood/protein

Rx: Stop diuretics, give fluids
Terlipressin
DIalysis then liver transplantation

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8
Q

Features of radiocontrast nephropathy

A

Acute rise in serum Cr 24-48 hours post contrast, peaks day 5-7, resolves day 14
Non-oliguric

Risk factors: heart failure, dehydration, diuretics, CKD, diabetes, myeloma

Hydration w/ normal saline has best evidence

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9
Q

Athero-embolism features

A

Livedo reticularis + AKI

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10
Q

Clinical classification of glomerulonephritis

A
  • Asymptomatic urinary abnormalities: subnephrotic range proteinuria and/or microscopic haematuria
  • Nephritis syndrome: recent onset of haematuria and proteinuria, renal impairment and salt and water retentio
  • Rapidly progressive GN: progression to renal failure over days to weeks, usually in context of nephritic presentation
  • Nephrotic syndrome: nephrotic range proteinuria, hypoalbuminaemia, hyperlipidaemia, and oedema
  • Chronic glomerulonephritis: Persistent proteinuria with/without haematuria and slowly progressive impairment of renal function
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11
Q

Histological classification of GN

A
  1. Glomerular involvement
  2. Cell involvement
  3. Changes in non cellular components of glomerulus
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12
Q

Features of minimal change disease

A

Affects mostly children
Pure nephrotic syndrome
Normal light microscopy on histology, flattened podocytes on EM

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13
Q

Management of minimal change disease

A

Responds well to steroids in children, slower responses in adulthood

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14
Q

Clinical features of focal & segmental GN

A

Proteinuria, nephrotic syndrome
Hypertension, decrease GFR +/- haematuria

Histology - focal and segmental glomerulosclerosis and hyalinosis, juxtamedullary nephrons involved firstMana

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15
Q

Management of FSGS

A

Prednisone (often shows poor response)
If necessary, PLUS other immunosuppressants (e.g., cyclosporine, tacrolimus)
RAAS inhibitors
Usually leads to ESRD if left untreated

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16
Q

Clinical features of primary membranous nephropathy

A

Proteinuria, usually nephrotic

Histology: thickened GBM
Silver stain - intramembranous Ig deposits, spikes and domes appearance
Interstitial fibrosis at later stages

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17
Q

Causes of primary membranous nephropathy

A

Primary: anti-PLA2R antibodies

Secondary:
Infections (HBV, HCV, malaria, syphilis)
Autoimmune diseases (e.g., SLE)
Tumors (e.g., lung cancer, prostate cancer)
Medications (e.g., NSAIDs, penicillamine, gold)

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18
Q

Management of primary membranous nephropathy

A

RAAS inhibitors
Prednisone (often shows poor response)
PLUS other immunosuppressants (e.g., cyclophosphamide) in severe disease
Usually leads to ESRD if left untreated

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19
Q

Role of PLA2R in membranous nephropathy

A

Differentiates primary and secondary MN
Initiate immunosuppression if high titer or rising titer

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20
Q

Clinical features of IgA nephropathy

A

Asymptomatic haematuria, often synpharyngitis
Hypertension, proteinuria, decrease GFR
M > F

Histology - mesangial hypercellularity and matrix expansion, IgA +
Interstitial damage and fibrosis, occasionally crescents

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21
Q

Poor prognostic factors of IgA nephropathy

A

Persistent proteinuria, hypertension, reduce GFR, old age, interstitial fibrosis or crescents on biopsy

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22
Q

IgA nephropathy pathophysiology

A

Increased number of defective, circulating IgA antibodies are synthesized (often triggered by mucosal infections, i.e., upper respiratory tract and gastrointestinal infections) → IgA antibodies form immune complexes that deposit in the renal mesangium → mesangial cell and complement system activation → glomerulonephritis (type III hypersensitivity reaction)

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23
Q

Management of IgA nephropathy

A

RAAS inhibition - IgA with proteinuria or HTN
SGLT-2 inhibition

Prednisone
- IgA with superimposed MCD
- IgA with proteinuria >1g/day

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24
Q

Clinical features of membranoproliferative GN

A

Proteinuria + haematuria
Reduced GFR and HTN, nephrotic

Histology: Reduplication of membrane - “wire loops”
Cellular proliferation, interstitial damage

Most commonly nephritic but can be nephrotic

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25
Q

Classification of MPGN

A

Immunoglobulin (IG)-mediated membranoproliferative glomerulonephritis (type 1 MPGN)
- Associated with SLE, monoclonal gammopathy
- Can also be idiopathic

Complement-mediated membranoproliferative glomerulonephritis (type 2 MPGN: associated with dense deposit disease (IgG antibodies that stabilize C3 convertase, i.e., C3 nephritic factor, cause a persistent complement activation, leading to a depletion of C3)
- Both associated with HBV, HCV, and cryoglobulinemia
Hereditary diseases (e.g., sickle cell disease, α1-antitrypsin deficiency)
- Drugs (e.g., heroin, α-interferon)
- Tumors (e.g., lymphoma)
- Autoimmune diseases (e.g., SLE)
- May manifest with concomitant nephrotic-range proteinuria (nephritic-nephrotic syndrome)

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26
Q

Histology of MGPN

A

IG-mediated (type 1)
- IF: subendothelial and mesangial IgG immune complex deposits with granular appearance
- ↓ Serum C3 complement levels

Complement-mediated (type 2)
- Intramembranous C3 deposits (dense deposit disease) on basement membrane
- ↓ Serum C3 complement levels

Both types: LM with H&E or PAS stain shows mesangial ingrowth, which leads to thickening and splitting of the glomerular basement membrane (tram-track appearance)

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27
Q

Management of MGPN

A

Rule out myeloma
If familial, for supportive care only
Complement mediated - consider anti-C’ Rx i.e. eculizumab
Immunemediated MPGN - consider steroid, plex or rituximab

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28
Q

Features of rapidly progressive GN/crescentic GN

A

Rapidly decline in renal failure
Haematuria, proteinuria, oliguria, HTN, reduce GFR, haemoptysis, arthralgia/myalgia/weight loss, lupus

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29
Q

Histology of RPGN

A

Crescents > 50% glomeruli, interstitial inflammation

ANCA associated vasculitis - necrosis, eosinophils, pauci-immune
Anti-GBM - linear IgG
SLE - mixed features, lots of complement and Ab

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30
Q

Management of RPGN

A

Urgent diagnosis via renal biopsy, SLE, ANCA, anti-GBM

Pulse prednisone
Cyclophosphamide or rituximab, MMG
Plasmapheresis for anti-GBM or AAV

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31
Q

Class of lupus nephritis

A

Class I - normal/minimal disease
Class II - mesangial disease
Class III - focal proliferative GN
Class IV - diffuse proliferative GN
Class V - membranous FN

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32
Q

ABO compatibility of renal transplantation

A

O to all
AB to all
Others must be matched

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33
Q

Renal transplant rejection types

A

Hyperacute
- rare and early. Untreatable.
- vascular thrombosis
- PMNs
- infarction

Acute
- common, early and treatable
- T cell mediated or antibody mediated

Chronic
- common and progressive

34
Q

Pathogenesis of antibody mediated rejection

A
  1. Alloantigen exposure
  2. Antigen presentation + T cell help
  3. B cell maturation
  4. Plasma cell - high affinity DSA
  5. Antibody mediated rejection
35
Q

Histology of chronic allograft nephropathy

A

Tubular atrophy
Interstitial fibrosis
Patchy infiltrate
Arteriolar hyalinosis
Glomerulopathy

36
Q

Site of action for acetazolamide

A

PCT

37
Q

Site of action for furosemide

A

Thick ascending loop of Henle

38
Q

Medications acting in DCT

A

Thiazide, indapamide

39
Q

Site of action for spironolactone

A

CD

40
Q

Site of action for amiloride

A

DCT, connecting tubules, CD

41
Q

Features of Bartter’s syndrome

A

NKCC2, ROMK, CIC-Kb mutation
Low potassium, low calcium
Elevated urine prostaglandin

42
Q

Features of Gittelman’s

A

NKCC1 mutation
Low potassium, high calcium
Normal urine prostaglandin

43
Q

Function of parenchymal cells

A

Make up nephrons

44
Q

Function of principal cells

A

Responsible for sodium reabsorption and potassium secretion in the kidney

45
Q

Intercalated cell in CD function

A

Alpha intercalated cell is responsible for secreting excess acid and reabsorbing base (in form of bicarbonates)

Beta intercalated cells is responsible for secreting excess base (bicarbonate) and reabsorbing acid

46
Q

Function of peritubular cells

A

Makes erythropoietin

47
Q

What cells make erythropoietin?

A

Peritubular cells

48
Q

Advantages and disadvantages of EPO

A

Advantages
- improve QOL
- improves exercise tolerance
- improves sexual function
- improves cognitive function in dialysis
- leads to regression of left ventricular hypertrophy

Disadvantages
- expensive
- hypertension
- increase peripheral resistance due to loss of hypoxia vasodilation and increased blood viscosity
- encephalopathy

49
Q

Risk factors for calciphylaxis

A

ESKD
Obesity
Diabetes
Female
Dialysis-dependence > 2 years
Repetitive skin trauma from SC injections
Elevated Ca or PO4
Primary/secondary hyperparathyroidism
Oversuppressed PTH levels
Elevated ALP
Vitamin K deficiency
Warfarin
Hepatobiliary disease
Thrombophilia
SLE
Hypoalbuminaemia
Metastatic cancer
Recurrent hypotension
Rapid weight gain
Exposure to UV light
Exposure to albuminum
Elevated FGF-23

50
Q

What medication is high risk for calciphylaxis

A

Warfarin –> vitamin K deficiency

51
Q

How does warfarin cause calciphylaxis

A

Antagonises vitamin K –> blocks MGP carboxylation –> promotes vascular smooth muscle cell transdifferentation and matrix mineralisation

52
Q

Most common cause of death in calciphylaxis

A

Sepsis due to wound infection

53
Q

Gold standard investigation for diagnosis and classification of renal osteodystrophy

A

Unexplained fractures
Persistent bone pain
Unexplained hypercalcaemia
Unexplained hypophosphataemia
Possible aluminum toxicity

54
Q

Mechanism of hyperkalaemia in ACEi/ARBs

A

Reduces aldosterone biosynthesis by interrupting RAS
Reduces effective glomerular-filtration rate

55
Q

Mechanism of hyperkalaemia from amiloride

A

Blocks Na channels of luminal membrane of principal cells

56
Q

Mechanism of hyperkalaemia from beta blockers

A

Inhibits renin secretion
Decreases cellular K uptake

57
Q

Mechanism of hyperkalaemia from cyclosporine

A

Inhibits adrenal aldosterone biosynthesis
Induces chloride channel shunt
Increases K efflux from cells

58
Q

Mechanism of hyperkalaemia from digoxin

A

Inhibits Na+/K+-ATPase

59
Q

Mechanism of hyperkalaemia from heparin

A

Inhibits adrenal aldosterone biosynthesis
Decreases number and affinity of angiotensin-II receptors

60
Q

Mechanism of hyperkalaemia from NSAIDs

A

Induces hyporeninemia hypoaldosteronism through inhibition of renal prostaglandin synthesis

61
Q

Mechanism of hyperkalaemia from spironolactone

A

Mineralocorticoid receptor antagonist (competing with aldosterone)
Inhibits adrenal aldosterone biosynthesis

62
Q

Mechanism of hyperkalaemia from succinylcholine

A

Causes potassium leakage out of cells through depolarisation of cell membranes

63
Q

Mechanism of hyperkalaemia from tacrolimus

A

Inhibits adrenal aldosterone biosynthesis
Induces chloride channel shunt
Increases K efflux from cells

64
Q

Mechanism of hyperkalaemia from trimethoprim

A

Blocks Na channels in luminal membrane of principal cells

65
Q

Mechanism of patiromer

A

Used for hyperkalaemia
Sodium-free binding polymer that exchanges calcium for potassium in GIT –> increases faecal K excretion and reduces serum K levels

Can result in low Mg and GI side effects

66
Q

Mechanism of sodium zirconium cyclosilicate

A

Used in hyperkalaemia
Potassium-selective cation exchanger

Can result in peripheral oedema and GIT side effects

67
Q

Mechanism of roxadustat

A

Reversible hypoxia-inducible factor prolyl hydroxylase inhibitor –> stimulates erythropoiesis

68
Q

Role of hypoxia-inducible factors

A

Transcription factors that regulate expression of genes in response to hypoxia

Prolyl hydroxylases (PHDs - hydroxylate HIF-a subunit, resulting in rapid proteasomal degradation) is lessened in hypoxia –> enhanced erythropoiesis

Reduces levels of hepcidin
Decreases level of total cholesterol, LDL and triglycerides

69
Q

Clinical criteria to commence erythropoiesis stimulating agents

A
  • Requires transfusion
  • Hb < 100g/L
  • Intrinsic renal disease as assessed by nephrologist
70
Q

Features of podocyte

A

Highly differentiated epithelial cell, connects to GBM

71
Q

Function of podocyte

A

Structural support of capillary loop
Major component of glomerular filtration barrier
Synthesis and repair of GBM
Production of growth factors - VEGFs, PDGFs
Immunologic function

72
Q

Most common malignancy post renal transplant

A

Non-melanotic skin cancer

73
Q

Malignancies highest risk of occurring post renal transplant

A

Lung
Colon
Liver
Lymphoma (PTLD)
Melanoma
Non-melanoma skin cancer

74
Q

Drugs cleared by haemodialysis

A

BLAST
- Barbiturate
- Lithium
- Alcohol
- Salicylates
- Theophyllines

75
Q

Risk factors associated with BK nephropathy

A
  • aggressive immunosuppressive treatment
  • older recipient age
  • female donor
  • HLA DR mismatching
76
Q

Why is gadolinium exposure avoided in significant renal impairment?

A

Risk of nephrogenic systemic fibrosis
Characterised by symmetrical skin involvement with extensive waxy thickening and hardening of extremities and torso

77
Q

Treatment of PTLD

A

Reduction of immunosuppression and monitor respond
Rituximab - induce remission

78
Q

Indications for renal biopsy

A
  • Glomerular haematuria
  • Acute on chronic kidney disease of unclear cause
  • Severely increased albuminuria
  • Transplant dysfunction or monitoring
79
Q

Features of AIN

A

Classic clinical presentation
- Fever
- Rash
- Peripheral eosinophilia

Urinary findings
- Eosinophiluria
- Leukocytes
- Erythrocytes
- Leukocyte casts

80
Q

Causes of drug-induced AIN

A

Antibiotics
NSAIDs
PPIs

81
Q

Fractional excretion percentage of phosphorus in type 2 RTA

A

> 5%

82
Q
A

BPT Flashcards (32 decks)

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