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Year 3 Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Criteria for Acute Kidney Injury

A

Any one of:
* creatinine increase by ≥ 26 μmol/L in 48 hrs
* creatinine x1.5 from baseline in 1 week
* urine output < 0.5 mL/kg/hr for 6hrs or 8 hrs in kids
* GFR decrease by 25% in children over 7 days

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2
Q

Definition of Stage 1 AKI

A

Creatinine x1.5 or urine output < 0.5 mL/kg/hr for 6 hours

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3
Q

Definition of Stage 2 AKI

A

Creatinine x2 or urine output < 0.5 mL/kg/hr for 12 hours

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4
Q

Definition of Stage 3 AKI

A

Creatinine x3 or urine output < 0.3 mL/kg/hr for 24 hours or creatinine ≥ 4 mg/dL or dialysed

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5
Q

Pathophysiology of prerenal AKI

A
  • Due to renal hypoperfusion
  • causes reduced GFR as an appropriate response to retain Na+/H2O
  • Can lead to acute tubular necrosis
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6
Q

Causes of prerenal AKI

A
  • Diarrhoea and vomiting, shock (e.g. sepsis, haemorrhage)
  • decreased cardiac output: heart failure
  • hepatorenal syndrome
  • renal artery stenosis
  • drugs: NSAIDs (constrict afferent arterioles), ACEi & ARBs (dilate efferent arterioles), diuretics (cause hypovolaemia)
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7
Q

Intrinsic causes of AKI

A
  • glomerulonephritis + rapidly progressive glomerulonephritis
  • Tubulo-interstitial disease –> Acute tubular necrosis & Acute interstitial nephritis
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8
Q

Causes of Acute Tubular Necrosis (ATN)

A

(MIRACLE)
* Myoglobin (from rhabdomyolysis)
* Ischaemia
* Radiocontrast
* Aminoglycosides
* Cisplatin
* Lithium
* Excess urate (gout)

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9
Q

Investigation for Acute Tubular Necrosis

A

Urine dipstick

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10
Q

Causes of Acute Interstitial Nephritis

A
  • Hypersensitivity reaction triggered by drugs –> NSAIDs, beta lactams, thiazides, furosemide, rifampicin, PPIs
  • Infection –> Legionella, leptspira, Group A strep, CMV
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11
Q

Investigations for Acute Interstitial Nephritis and what is shows

A
  • Urine Dipstick = Shows leukocytes, May show mild blood and proteins
  • Microscopy shows eoisinophils and eoisinophil casts
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12
Q

Definition of Rapidly Progressive Glomerulonephritis (RPGN)

A

rapid decline in kidney function - sometimes defined as a 50% decrease in GFR within 3 months - and progression to end-stage kidney disease

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13
Q

Causes of Rapidly Progressive Glomerulonephritis

A

(PIG)

Pauci-immune vasculitis (50%)
* Type 3 RPGN
* small vessel vasculitis causing aneurysms, stenosis or occlusion
* constitutional symptoms plus organ-specific signs e.g. vasculitic rash, pulmonary haemorrhage
* usually granulomatosis with polyangitis (c-ANCA) or microscopic polyangitis (p-ANCA)

Immune Complex Disease (40%)
* Type 2 RPGN, type 3 hypersensitivity
* Lupus nephritis, usually in patients with known SLE
* post-infectious GN, usually post-streptococcal
* IgA nephropathy

Anti-Glomerular Basement Membrane Disease (10%)
* Type 1 RPGN, type 2 hypersensitivity
* antibody against type 4 collagen of glomerular and alveolar basement membrane
* known as Goodpasture’s syndrome if both RPGN & pulmonary haemorrhage is present
* Biopsy shows linear IgG deposition

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14
Q

Presentation of Rapidly Progressive Glomerulonephritis

A
  • Renal features: oliguria, haematuria, proteinuria (sometimes nephrotic), oedema
  • Systemic: vomiting, fatigue, fever
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15
Q

Management of Rapidly Progressive Glomerulonephritis

A

Immunosuppression
* methylprednisolone IV + cyclophosphamide IV

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16
Q

Prognosis of Rapidly Progressive Glomerulonephritis

A

90% of RPGN progresses to end-stage kidney disease

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17
Q

Pathophysiology of post renal AKI

A

obstruction which may be intra-renal - tubules including collecting ducts - or extra-renal - renal calyces to urethral meatus

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18
Q

Causes of post-renal AKI

A
  • stones
  • catheter
  • strictures
  • prostatism
  • UTI
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19
Q

Signs and Symptoms of AKI

A

General
* oliguria
* fluid overload: pulmonary oedema (+/- orthopnea and PND), peripheral oedema
* uraemic symptoms: fatigue, nausea & vomiting, confusion

Specific
* prerenal: postural hypotension, diarrhoea & vomiting, tachycardia
* intrinsic: symptoms of systemic disease

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20
Q

Risk Factors for AKI

A
  • organ failure: CKD, liver disease (hepatorenal syndrome), HF
  • age
  • hypovolaemia and shock
  • nephrotoxic drugs (FANG): Furosemide, ACEi & ARBs, NSAIDs, Gentamicin
  • Diabetes
  • Urinary obstruction
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21
Q

Relevant investigations for an AKI

A

Urinalysis
* Dipstick
* > haematuria, albuminuria = glomerulonephritis, stones, UTI, tumour, trauma
* > WBCs = UTI, AIN
* Microscopy
* RPGN =

Bloods
* FBC: low Hb, high WBC (infection, eosinophilia in AIN), low platelets
* U&E: urea, creatinine, hyperkalaemia
* LFT: hepatorenal syndrome
* Coag: DIC in sepsis, altered clotting in CKD
* CK: rhabodomyolysis
* CRP: infection
* ABG: metabolic acidosis
* Immune markers: ANCA, anti-GBM, ANA, anti-dsDNA, RF, complement
* Serum electrophoresis
* Culture in sepsis

Imaging
* Kidney = US, abdo XR, abdo CT
* Others = ECG (hyperkalaemia), CXR (pulmonary oedema, systemic disease)

Biopsy - indications
* any suspicion of RPGN
* prolonged ATN (not recovered < 3 wks)
* no cause found for AKI

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22
Q

Management for AKI

A

Treat underlying cause
* prerenal: fluid, abx if sepsis
* intrinsic: stop causative drug, immunosuppress if RPGN
* post-renal: catheterise

Fluid balance:
* monitor fluid balance to prevent hypovolaemia or fluid overload

Referral if cause unclear or not responding to treatment:
* nephrology is intrinsic
* urology if post-renal = may use nephrostomy or stenting

Severe cases = Renal Replacement Therapy

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23
Q

How to prevent AKI in high risk patients

A
  • pause ACEi and avoid NSAIDs in diabetes or CKD patients around the time of surgery
  • For acutely ill patients getting iodinated contrast, give IV fluids
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24
Q

Complications of AKI

A
  • metabolic acidosis
  • hyperkalaemia
  • pulmonary oedema
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25
Q

Poor prognostic factors for AKI

A
  • > 50 yrs old
  • AKI that develops in hospital
  • rising urea
  • oliguria > 2 wks
  • other organ failure
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26
Q

Definition of CKD

A
  • Long term haematuria or proteinuria or…
  • GFR < 60 for > 3 months
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27
Q

Prevalance of CKD in the UK

A

10%, mainly stage 1-3

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28
Q

How is CKD staged by eGFR

A
  • Based on 2 GFR readings 3 months apart
  • Stage 1-2 also require the presence of kidney damage: persistant proteinuria or unexplained haematuria, structural disease, or GN

Stages
1. GFR>90: no impairment
2. GFR 60-89: mild impairment
3. GFR 30-59: moderate impairment, divided into 3a (45-59) and 3b (30-44)
4. GFR 15-29: severe impairment
5. GFR <15 or on dialysis: kidney failure aka end stage kidney disease

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29
Q

How is CKD staged by albumin:creatinine (ACR)

A
  • A1 mild (<3 mg/mmol)
  • A2 moderate (3-30 mg/mmol)
  • A3 severe (>30 mg/mmol)
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30
Q

Causes of CKD

A
  • Diabetes
  • Glomerulonephritis
  • Hypertension
  • PCKD
  • pyelonephritis
  • idiopathic
  • obstructive uropathy
  • renal vascular disease
  • SLE
  • amyloidosis
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31
Q

Signs and symptoms in early stages of CKD

A
  • Diabetes: proteinuria & glycosuria on dipstick
  • GN: proteinuria & haematuria on dipstick, nephrotic syndrome
  • non-renal features e.g. hypertension
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32
Q

Signs and Symptoms in later stages of CKD

A

BROKEN PIDDLE BAGS
* ↑BP: fluid retention, ↑renin
* ↓RBCs (anaemia): ↓EPO, bleeding (in part due to ↓PLT)
* Oedema: peripheral and periorbital. Pleural effusions
* K+ Elevation
* Neurological symptoms: peripheral polyneuropathy, restless legs, confusion, seizures, coma
* Pericarditis
* Itch
* Dermal darkening: skin pigmentation
* Diuresis: polyuria (especially nocturia) due to impaired urine concentration
* Lipid Elevation
* Bone disease: initially asymptomatic, later bone pain, fractures, proximal muscle weakness
* Acidosis
* GI: nausea, vomitting, diarrhoea, anorexia
* Skinny: weight loss

Commoner symptoms = fatigue, oedema, nausea, anorexia, pruritis

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33
Q

Risk Factors for CKD

A
  • Vascular: diabetes, HTN, CVD
  • Structural disease: stones, prostate enlargment
  • AKI
  • Multi-system disease with potential kidney involvement e.g. SLE
  • Family history of end-stage kidney disease
  • long term nephrotoxic drugs: NSAIDs, lithium, cyclosporin, tacrolimus
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34
Q

Investigations for CKD

A

Bloods
* FBC: normocytic ↓Hb, ↓PLT
* U+E: ↑urea, ↑creatinine, ↓/↑ Na+, ↑K+
* Monitor for ↓Ca2+, ↑PO4 and ↑PTH if GFR <30
* Glucose: check for Diabetes
* Lipids: may be elevated especially TG
* Blood gas: acidosis
* Immunological: ANA, ANCA, anti-GBM, complement
* Serum & urine protein electrophoresis for myeloma

Kidney US
* Indications: accelerated prgression, persistant haematuria, obstructive symptoms, family history of PCKD, GFR<30, pre-biopsy
* Possible findings: small kidneys, hydronephrosis, stones
* Follow up with CT if masses or cysts detected

Biospy
* Indicated if likely to affect treatment e.g. GN

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35
Q

Management of CKD in the early stages

A

Early stages about managing risk factors
* Hypertension –> 1st line = ACEi or ARB, 2nd line = CCB
* Bone protection: bisphosphonates for G1-3, vit D if deficient
* Others = statins, CVD prevention (weight loss, exercise, smoking cessation), urological intervention for obstruction
* Drug contraindications and cautions: minimise NSAIDs, avoid (tetracyclines, nitrofurantoin, lithium, metformin, radio contrast), reduce dose (beta-lactams, aminoglycosides, digoxin, atenolol, LMWH, furosemide, opioids)

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36
Q

Specific Symptomatic Treatments in CKD

A

Bone disease
* if bone disease despite vit D correction = calcitriol or alfacalcidol, which do not require renal hydroxylation
* if phosphate deficiency = dietician + offer phosphate binders

Others
* hyperkalaemia = low potassium diet
* anaemia = iron (PO, but if on dialysis = IV), recombinant EPO if anaemic despite iron repletion
* sodium bicarb if serum levels low
* fluid overload: loop diuretics, fluid restriction

Renal Replacement therapy
* considered in patients with G5 or uraemia
* options: dialysis or kidney transplant

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37
Q

Complications of CKD

A
  • CVD
  • LVH due to anaemia and HTN
  • Infection due to CKD itself, dialysis access sites, or immunosuppression post-transplant
38
Q

What are the options for Renal Replacement Therapy

A
  • haemodialysis
  • peritoneal dialysis
  • kidney transplant
39
Q

Advantages of Haemodialysis

A
  • Access can be temporary: catheter in IJV, subclavian vein, femoral vein which can then be tunneled to reduce the risk of infection
  • Permanent access is preferred though radial or brachial AV fistula
40
Q

Disadvantages of Haemodialysis

A
  • usually in hospital 3-4hrs/wk
  • risk of sepsis
  • risk of fistula failure from thrombosis, stenosis, aneurysm or infection
  • requires strict fluid and potassium restriction
  • leads to growth restriction in kids
41
Q

Advantages of peritoneal dialysis

A
  • usually done at home
  • good for kids as less growth restriction
  • less rigorous dietary and fluid restrictions than haemodialysis
42
Q

Disadvantages of peritoneal dialysis

A
  • risk or peritonitis or exit site infection, commonly staph epidermidis (safer than temp haemodialysis but not permanent haemodialysis)
  • cannot be used if there are abdominal problems, e.g. adhesions, obesity, GI disease
  • metabolic side effects: hyperglycaemia, fluid retention
43
Q

When should peritoneal dialysis be offered as first choice

A
  • age <2
  • significant co-morbidities
  • residual kidney function
44
Q

Benefits of Kidney Transplants

A
  • Improves symptoms and improves quality of life significantly more than dialysis
  • Cheaper than 1 year of dialysis
  • average survival time of organ is 10 yrs (better if living donor)
45
Q

Benefits of Living Donor Transplant over Deceased Donor Transplant

A
  • Living donor kidneys last longer than deceased donor kidneys
  • living donor kidneys work better because they are outside the recipient’s body for less time than a deceased donor
  • the patient waits less time to receive a living donor kidney transplant
  • surgery can be scheduled in advance
46
Q

What are the disadvantages of Living Donor Kidney Transplant compared to Deceased Donor

A
  • donor needs to get major surgery
  • patients may not have a living donor
47
Q

What factors need to match between patient and donor before a kidney transplant

A
  • ABO: must match
  • HLA: comprosing -A, -B, -C, and -DR. Ideally match all 8 (2 alleles each), with -DR the most important
48
Q

What types of medication does a kidney transplant patient need to be on post surgery

A

Triple Immunosuppression
* calcineurin inhibitor: tacrolimus or ciclosporin
* steroids
* antimetabolite: azathioprine or MMF

Other drugs:
* Aspirin, as CVD is the most common cause of death in transplant patients
* antimicrobial prophylaxis

49
Q

Complications of Kidney Transplant

A
  • Rejection
  • ureteric obstruction
  • renal artery stenosis
  • lymphocoele
  • infections due to immunosuppression
  • side effects of immunosuppressants
50
Q

Classification of proteinuria

A
  • normal = <30mg
  • microalbuminuria = 30 - 300 mg (not detectable on dipstick)
  • [macro]albumineua 300 - 3000 mg
  • nephrotic syndrome >3g
51
Q

Causes of modest proteinuria (<1g/day)

A
  • Tubulointerstitial disease
  • Glomerular disease
  • upper or lower UTI
  • kidney stones
  • benign causes: orthostatic proteinuria, exercise, fever, heart failure
52
Q

Causes of significant proteinuria (>1g/day)

A

Primary Glomerulonephritis
* Minimal change disease
* Focal segmental glomerulonephritis
* Membranous glomerulonephritis
* Membranoproliferativeglomerulonephritis

Secondary Glomerulonephritis
* diabetic neuropathy
* pre-eclampsia
* Autoimmune: SLE, vasculitis
* Infiltrative: amyloidosis, sarcoidosis, myeloma
* Infectious: infectious endocarditis, HBV, HCV, HIV, malaria, EBV

53
Q

Criteria for Nephrotic Syndrome

A
  • Oedema
  • Albumin <30
  • Urine PCR >350
54
Q

Presentation of Nephrotic Syndrome

A

NEPHROTIC
* Non-proliferative glomerulonephritis
* Elevated glucose
* Hyper- or hypo- tension
* Retinopathy (usually already present if diabetic)
* Oedema
* Thrombosis: liver compensates protein loss by increasing production of clotting factors, and kidney loses anti-coagulants (AT3) = DVT, PE
* Infection risk: urinary loss of IgG
* ↑ Cholesterol: compensatory liver production of lipoproteins = IHD

55
Q

Causes of Nephrotic Syndrome

A
  • Minimal Change Disease - most common form of GN in children
  • Focal segmental glomerulosclerosis - idiopathic or secondary to infection, malignancy, drugs, etc.
  • Membranous nephropathy - idiopathic or secondary to infection, malignancy, drugs, etc.
  • Amyloidosis/Myeloma/Diabetes
56
Q

Investigations for Nephrotic Syndrome

A

Urinalysis
* MC+S to exclude UTI
* Look for cell casts
* Protein electrophoresis

Bloods
* hypoalbuminaemia
* hypercholesterolaemia
* hyperglycaemia
* U+E to assess kidney function
* LFT: may show other causes of hypoalbuminaemia or fluid retention
* Coag: clotting abnormalities
* CRP: may be elevated in autoimmune disease

Investigations of Cause
* Serum IgG and electrophoresis
* Immunology: ANCA, RF, dsDNA, complement
* Microbiology: HBV, HCV, HIV

Imaging
* Kidney US is often useful, especially if there is abnormal kidney function. Needed before biospy
* CXR: pleural effusion

57
Q

Management of Nephrotic Syndrome

A
  • Proteinuria: ACEi or ARBs reduce intraglomerular pressure, reducing protein excretion
  • Oedema: salt +/- fluid restruction, and high dose loop diuretic. Weigh regularly to monitor
  • Hyperlipidaemia: statin if prolonged
  • Thrombotic risk: anticoagulation if clot occurs, but not prophylactically
  • Glomerulonephritis or autoimmune disease: immunosuppression may be needed
58
Q

Complications of Nephrotic Syndrome

A
  • Higher risk of infection
  • Venous thromboembolism
  • Progression of CKD
  • HTN
  • Hyperlipidaemia
59
Q

Presentation of Nephritic Syndrome

A
  • AKI (sometimes GFR can drop dramatically)
  • On urine dipstick: +/- blood and/or +/- protein
  • proteinuria <3.5g/24hrs
  • Hypertension
  • Some visible haematuria
60
Q

What precedes post-infectious GN

A

Weeks after Group A B-haemolytic streptococci infections
* 1-2 weeks post tonsilitis/pharyngitis
* 3-4 weeks after impetigo/cellulitis

61
Q

Who is most affected by post-infectious GN

A

Children aged 3-12 years

62
Q

Investigation findings for post-infectious GN

A
  • +ve anti-streptococcal antibodies (ASO titre)
  • Low serum C3
  • Biopsy: immune complex deposition IgG, IgM, C3
63
Q

Treatment for post-infectious GN

A
  • Usually self-limiting
  • Supportive therapy: ACEi, ARB for proteinuria & hypotension + low sodium diet
  • RRT if it proceeeds to ESRF
64
Q

Epidemiology of IgA nephropathy

A
  • most common idiopathic GN worldwide
  • occurs more in males than females
  • peak incidence in 2nd to 3rd decade of life
65
Q

Investigation findings in IgA nephropathy

A
  • Asymptomatic microhaematuria with intermittent visible haematuria
  • Increase serum IgA
  • Normal C3, C4
  • Biopsy: Mesangial immune complex deposits in glomeruli
66
Q

Treatment for IgA nephropathy

A

Supportive therapy = ACEi/ARB for proteinuria and hypertension

67
Q

Typse of small vessel vasculitis

A
  • Granulomatosis with polyangitis (GPA)
  • Microscopic polyangitis (MPA)
  • Eoisinophilic granulomatosis with polyangitis
68
Q

Symptoms in Granulomatosis
with polyangiitis
(GPA)
Symptoms in GPA

A

pulmonary & nasopharyngeal involvement - haemoptysis & nasal ulcers/polyps

69
Q

Investigation findings in Granulomatosis
with polyangiitis
(GPA)

A
  • cANCA (PR3)
  • Biopsy: segmental necrotising GN
70
Q

Treatment for Granulomatosis
with polyangiitis
(GPA)

A

Immunosuppression

71
Q

Symptoms in Microscopic
polyangiitis
(MPA)

A

usually only mild respiratory symptoms

72
Q

Investigation findings in Symptoms in Microscopic polyangitis (MPA)

A
  • p-ANCA (MPO)
  • Biopsy: segmental necrotizing GN
73
Q

Treatment for Microscopic polyangitis (MPA)

A

immunosuppresion

74
Q

Other conditions found in patients with Eosinophilic
granulomatosis with polyangiitis

A
  • Asthma
  • Allergic rhinitis
  • Purpura
  • Peripheral neuropathy
75
Q

Investigation findings in Eosinophilic
granulomatosis with polyangiitis

A
  • p-ANCA
  • Bloods: eoisinophilia
  • Biopsy: focal segmental nectrotizing GN
76
Q

Treatment for Eosinophilic
granulomatosis with polyangiitis

A

Immunosuppression

77
Q

Pathophysiology of Goodpasture Syndrome

A

Antibodies against Type IV collagen - react with pulmonary basement membrane causing pulmonary haemorrhage (haemoptysis) and can lead to RPGN

78
Q

Who gets affected by Goodpasture Syndrome

A

Two peaks
* 3rd decade of life (male>female)
* after 60 yrs (female>male)

79
Q

Investigation findings in Goodpasture Syndrome

A
  • anti-GBM antibodies
  • pulmonary infiltrates on CXR
  • Biopsy: linear deposition of IgG along basement membrane
80
Q

Treatment of Goodpasture Syndrome

A

Plasma exchange immunosuppression

81
Q

Pathophysiology of Thin Basement Membrane Disease

A

Hereditary abnormalities of Type IV collagen

82
Q

Investigation findings in Thin Basement Membrane Disease

A
  • persistent microscopic haematuria - possible intermittent visible haematuria
  • Biopsy: diffuse thinning of GBM
83
Q

Treatment of Thin Basement Membrane Disease

A
  • monitor renal function
  • supportive treatment
  • good prognosis
84
Q

Pathophysiology of Alport Syndrome

A
  • X-linked recessive (usually affects males)
  • Mutation in gene coding gor Type V collagen
85
Q

Associations with Alport Syndrome

A
  • Associated with hearing loss and abnormalities of the eyes
  • Often leads to ESRF
86
Q

Investigation findings in Alport Syndrome

A
  • persistent microscopic haematuria with intermittent visible haematuria
  • sensorineural hearing loss
  • Biopsy: splitting of GBM and alternating thickening and thinning of GBM
  • Genetic studies - family history
87
Q

Treatment of Alport Syndrome

A
  • Supportive treatment
  • renal replacement therapy
  • renal transplant - can lead to development of Goodpasture syndrome
88
Q

Associations of Lupus nephritis

A
  • complication of SLE
  • Can be nephritic or nephrotic
89
Q

Investigation findings in Lupus nephritis

A
  • ANA & anti-dsDNA +ve
  • Biopsy: 6 different classes of lupus nephritis with different presentations and slightly varying treatment options
90
Q

Treatment of Lupus nephritis

A
  • supportive therapy
  • immunosuppressive therapy based on classification/presentation

Year 3 Medicine (3 decks)

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