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Renal Flashcards

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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
Classification of MPGN
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)
26
Histology of MGPN
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)
27
Management of MGPN
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
28
Features of rapidly progressive GN/crescentic GN
Rapidly decline in renal failure Haematuria, proteinuria, oliguria, HTN, reduce GFR, haemoptysis, arthralgia/myalgia/weight loss, lupus
29
Histology of RPGN
Crescents > 50% glomeruli, interstitial inflammation ANCA associated vasculitis - necrosis, eosinophils, pauci-immune Anti-GBM - linear IgG SLE - mixed features, lots of complement and Ab
30
Management of RPGN
Urgent diagnosis via renal biopsy, SLE, ANCA, anti-GBM Pulse prednisone Cyclophosphamide or rituximab, MMG Plasmapheresis for anti-GBM or AAV
31
Class of lupus nephritis
Class I - normal/minimal disease Class II - mesangial disease Class III - focal proliferative GN Class IV - diffuse proliferative GN Class V - membranous FN
32
ABO compatibility of renal transplantation
O to all AB to all Others must be matched
33
Renal transplant rejection types
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
Pathogenesis of antibody mediated rejection
1. Alloantigen exposure 2. Antigen presentation + T cell help 3. B cell maturation 4. Plasma cell - high affinity DSA 5. Antibody mediated rejection
35
Histology of chronic allograft nephropathy
Tubular atrophy Interstitial fibrosis Patchy infiltrate Arteriolar hyalinosis Glomerulopathy
36
Site of action for acetazolamide
PCT
37
Site of action for furosemide
Thick ascending loop of Henle
38
Medications acting in DCT
Thiazide, indapamide
39
Site of action for spironolactone
CD
40
Site of action for amiloride
DCT, connecting tubules, CD
41
Features of Bartter’s syndrome
NKCC2, ROMK, CIC-Kb mutation Low potassium, low calcium Elevated urine prostaglandin
42
Features of Gittelman’s
NKCC1 mutation Low potassium, high calcium Normal urine prostaglandin
43
Function of parenchymal cells
Make up nephrons
44
Function of principal cells
Responsible for sodium reabsorption and potassium secretion in the kidney
45
Intercalated cell in CD function
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
Function of peritubular cells
Makes erythropoietin
47
What cells make erythropoietin?
Peritubular cells
48
Advantages and disadvantages of EPO
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
Risk factors for calciphylaxis
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
What medication is high risk for calciphylaxis
Warfarin --> vitamin K deficiency
51
How does warfarin cause calciphylaxis
Antagonises vitamin K --> blocks MGP carboxylation --> promotes vascular smooth muscle cell transdifferentation and matrix mineralisation
52
Most common cause of death in calciphylaxis
Sepsis due to wound infection
53
Gold standard investigation for diagnosis and classification of renal osteodystrophy
Unexplained fractures Persistent bone pain Unexplained hypercalcaemia Unexplained hypophosphataemia Possible aluminum toxicity
54
Mechanism of hyperkalaemia in ACEi/ARBs
Reduces aldosterone biosynthesis by interrupting RAS Reduces effective glomerular-filtration rate
55
Mechanism of hyperkalaemia from amiloride
Blocks Na channels of luminal membrane of principal cells
56
Mechanism of hyperkalaemia from beta blockers
Inhibits renin secretion Decreases cellular K uptake
57
Mechanism of hyperkalaemia from cyclosporine
Inhibits adrenal aldosterone biosynthesis Induces chloride channel shunt Increases K efflux from cells
58
Mechanism of hyperkalaemia from digoxin
Inhibits Na+/K+-ATPase
59
Mechanism of hyperkalaemia from heparin
Inhibits adrenal aldosterone biosynthesis Decreases number and affinity of angiotensin-II receptors
60
Mechanism of hyperkalaemia from NSAIDs
Induces hyporeninemia hypoaldosteronism through inhibition of renal prostaglandin synthesis
61
Mechanism of hyperkalaemia from spironolactone
Mineralocorticoid receptor antagonist (competing with aldosterone) Inhibits adrenal aldosterone biosynthesis
62
Mechanism of hyperkalaemia from succinylcholine
Causes potassium leakage out of cells through depolarisation of cell membranes
63
Mechanism of hyperkalaemia from tacrolimus
Inhibits adrenal aldosterone biosynthesis Induces chloride channel shunt Increases K efflux from cells
64
Mechanism of hyperkalaemia from trimethoprim
Blocks Na channels in luminal membrane of principal cells
65
Mechanism of patiromer
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
Mechanism of sodium zirconium cyclosilicate
Used in hyperkalaemia Potassium-selective cation exchanger Can result in peripheral oedema and GIT side effects
67
Mechanism of roxadustat
Reversible hypoxia-inducible factor prolyl hydroxylase inhibitor --> stimulates erythropoiesis
68
Role of hypoxia-inducible factors
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
Clinical criteria to commence erythropoiesis stimulating agents
- Requires transfusion - Hb < 100g/L - Intrinsic renal disease as assessed by nephrologist
70
Features of podocyte
Highly differentiated epithelial cell, connects to GBM
71
Function of podocyte
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
Most common malignancy post renal transplant
Non-melanotic skin cancer
73
Malignancies highest risk of occurring post renal transplant
Lung Colon Liver Lymphoma (PTLD) Melanoma Non-melanoma skin cancer
74
Drugs cleared by haemodialysis
BLAST - Barbiturate - Lithium - Alcohol - Salicylates - Theophyllines
75
Risk factors associated with BK nephropathy
- aggressive immunosuppressive treatment - older recipient age - female donor - HLA DR mismatching
76
Why is gadolinium exposure avoided in significant renal impairment?
Risk of nephrogenic systemic fibrosis Characterised by symmetrical skin involvement with extensive waxy thickening and hardening of extremities and torso
77
Treatment of PTLD
Reduction of immunosuppression and monitor respond Rituximab - induce remission
78
Indications for renal biopsy
- Glomerular haematuria - Acute on chronic kidney disease of unclear cause - Severely increased albuminuria - Transplant dysfunction or monitoring
79
Features of AIN
Classic clinical presentation - Fever - Rash - Peripheral eosinophilia Urinary findings - Eosinophiluria - Leukocytes - Erythrocytes - Leukocyte casts
80
Causes of drug-induced AIN
Antibiotics NSAIDs PPIs
81
Fractional excretion percentage of phosphorus in type 2 RTA
>5%
82

BPT Flashcards (32 decks)

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