Renal Flashcards
(90 cards)
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
2
Q
Definition of Stage 1 AKI
A
Creatinine x1.5 or urine output < 0.5 mL/kg/hr for 6 hours
3
Q
Definition of Stage 2 AKI
A
Creatinine x2 or urine output < 0.5 mL/kg/hr for 12 hours
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
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
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)
7
Q
Intrinsic causes of AKI
A
- glomerulonephritis + rapidly progressive glomerulonephritis
- Tubulo-interstitial disease –> Acute tubular necrosis & Acute interstitial nephritis
8
Q
Causes of Acute Tubular Necrosis (ATN)
A
(MIRACLE)
* Myoglobin (from rhabdomyolysis)
* Ischaemia
* Radiocontrast
* Aminoglycosides
* Cisplatin
* Lithium
* Excess urate (gout)
9
Q
Investigation for Acute Tubular Necrosis
A
Urine dipstick
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
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
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
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
14
Q
Presentation of Rapidly Progressive Glomerulonephritis
A
- Renal features: oliguria, haematuria, proteinuria (sometimes nephrotic), oedema
- Systemic: vomiting, fatigue, fever
15
Q
Management of Rapidly Progressive Glomerulonephritis
A
Immunosuppression
* methylprednisolone IV + cyclophosphamide IV
16
Q
Prognosis of Rapidly Progressive Glomerulonephritis
A
90% of RPGN progresses to end-stage kidney disease
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
18
Q
Causes of post-renal AKI
A
- stones
- catheter
- strictures
- prostatism
- UTI
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
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
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
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
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
24
Q
Complications of AKI
A
- metabolic acidosis
- hyperkalaemia
- pulmonary oedema
25
Poor prognostic factors for AKI
* >50 yrs old
* AKI that develops in hospital
* rising urea
* oliguria > 2 wks
* other organ failure
26
Definition of CKD
* Long term haematuria or proteinuria or...
* GFR < 60 for > 3 months
27
Prevalance of CKD in the UK
10%, mainly stage 1-3
28
How is CKD staged by eGFR
* 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
29
How is CKD staged by albumin:creatinine (ACR)
* A1 mild (<3 mg/mmol)
* A2 moderate (3-30 mg/mmol)
* A3 severe (>30 mg/mmol)
30
Causes of CKD
* Diabetes
* Glomerulonephritis
* Hypertension
* PCKD
* pyelonephritis
* idiopathic
* obstructive uropathy
* renal vascular disease
* SLE
* amyloidosis
31
Signs and symptoms in early stages of CKD
* Diabetes: proteinuria & glycosuria on dipstick
* GN: proteinuria & haematuria on dipstick, nephrotic syndrome
* non-renal features e.g. hypertension
32
Signs and Symptoms in later stages of CKD
BROKEN PIDDLE BAGS
* ↑**B**P: fluid retention, ↑renin
* ↓**R**BCs (anaemia): ↓EPO, bleeding (in part due to ↓PLT)
* **O**edema: peripheral and periorbital. Pleural effusions
* **K**+ **E**levation
* **N**eurological symptoms: peripheral polyneuropathy, restless legs, confusion, seizures, coma
* **P**ericarditis
* **I**tch
* **D**ermal darkening: skin pigmentation
* **D**iuresis: polyuria (especially nocturia) due to impaired urine concentration
* **L**ipid **E**levation
* **B**one disease: initially asymptomatic, later bone pain, fractures, proximal muscle weakness
* **A**cidosis
* **G**I: nausea, vomitting, diarrhoea, anorexia
* **S**kinny: weight loss
Commoner symptoms = fatigue, oedema, nausea, anorexia, pruritis
33
Risk Factors for CKD
* 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
34
Investigations for CKD
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
35
Management of CKD in the early stages
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)
36
Specific Symptomatic Treatments in CKD
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
37
Complications of CKD
* CVD
* LVH due to anaemia and HTN
* Infection due to CKD itself, dialysis access sites, or immunosuppression post-transplant
38
What are the options for Renal Replacement Therapy
* haemodialysis
* peritoneal dialysis
* kidney transplant
39
Advantages of Haemodialysis
* 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
Disadvantages of Haemodialysis
* 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
Advantages of peritoneal dialysis
* usually done at home
* good for kids as less growth restriction
* less rigorous dietary and fluid restrictions than haemodialysis
42
Disadvantages of peritoneal dialysis
* 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
When should peritoneal dialysis be offered as first choice
* age <2
* significant co-morbidities
* residual kidney function
44
Benefits of Kidney Transplants
* 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
Benefits of Living Donor Transplant over Deceased Donor Transplant
* 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
What are the disadvantages of Living Donor Kidney Transplant compared to Deceased Donor
* donor needs to get major surgery
* patients may not have a living donor
47
What factors need to match between patient and donor before a kidney transplant
* ABO: must match
* HLA: comprosing -A, -B, -C, and -DR. Ideally match all 8 (2 alleles each), with -DR the most important
48
What types of medication does a kidney transplant patient need to be on post surgery
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
Complications of Kidney Transplant
* Rejection
* ureteric obstruction
* renal artery stenosis
* lymphocoele
* infections due to immunosuppression
* side effects of immunosuppressants
50
Classification of proteinuria
* normal = <30mg
* microalbuminuria = 30 - 300 mg (not detectable on dipstick)
* [macro]albumineua 300 - 3000 mg
* nephrotic syndrome >3g
51
Causes of modest proteinuria (<1g/day)
* Tubulointerstitial disease
* Glomerular disease
* upper or lower UTI
* kidney stones
* benign causes: orthostatic proteinuria, exercise, fever, heart failure
52
Causes of significant proteinuria (>1g/day)
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
Criteria for Nephrotic Syndrome
* Oedema
* Albumin <30
* Urine PCR >350
54
Presentation of Nephrotic Syndrome
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
Causes of Nephrotic Syndrome
* 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
Investigations for Nephrotic Syndrome
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
Management of Nephrotic Syndrome
* 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
Complications of Nephrotic Syndrome
* Higher risk of infection
* Venous thromboembolism
* Progression of CKD
* HTN
* Hyperlipidaemia
59
Presentation of Nephritic Syndrome
* AKI (sometimes GFR can drop dramatically)
* On urine dipstick: +/- blood and/or +/- protein
* proteinuria <3.5g/24hrs
* Hypertension
* Some visible haematuria
60
What precedes post-infectious GN
Weeks after Group A B-haemolytic streptococci infections
* 1-2 weeks post tonsilitis/pharyngitis
* 3-4 weeks after impetigo/cellulitis
61
Who is most affected by post-infectious GN
Children aged 3-12 years
62
Investigation findings for post-infectious GN
* +ve anti-streptococcal antibodies (ASO titre)
* Low serum C3
* Biopsy: immune complex deposition IgG, IgM, C3
63
Treatment for post-infectious GN
* Usually self-limiting
* Supportive therapy: ACEi, ARB for proteinuria & hypotension + low sodium diet
* RRT if it proceeeds to ESRF
64
Epidemiology of IgA nephropathy
* most common idiopathic GN worldwide
* occurs more in males than females
* peak incidence in 2nd to 3rd decade of life
65
Investigation findings in IgA nephropathy
* Asymptomatic microhaematuria with intermittent visible haematuria
* Increase serum IgA
* Normal C3, C4
* Biopsy: Mesangial immune complex deposits in glomeruli
66
Treatment for IgA nephropathy
Supportive therapy = ACEi/ARB for proteinuria and hypertension
67
Typse of small vessel vasculitis
* Granulomatosis with polyangitis (GPA)
* Microscopic polyangitis (MPA)
* Eoisinophilic granulomatosis with polyangitis
68
Symptoms in Granulomatosis
with polyangiitis
(GPA)
Symptoms in GPA
pulmonary & nasopharyngeal involvement - haemoptysis & nasal ulcers/polyps
69
Investigation findings in Granulomatosis
with polyangiitis
(GPA)
* cANCA (PR3)
* Biopsy: segmental necrotising GN
70
Treatment for Granulomatosis
with polyangiitis
(GPA)
Immunosuppression
71
Symptoms in Microscopic
polyangiitis
(MPA)
usually only mild respiratory symptoms
72
Investigation findings in Symptoms in Microscopic polyangitis (MPA)
* p-ANCA (MPO)
* Biopsy: segmental necrotizing GN
73
Treatment for Microscopic polyangitis (MPA)
immunosuppresion
74
Other conditions found in patients with Eosinophilic
granulomatosis with polyangiitis
* Asthma
* Allergic rhinitis
* Purpura
* Peripheral neuropathy
75
Investigation findings in Eosinophilic
granulomatosis with polyangiitis
* p-ANCA
* Bloods: eoisinophilia
* Biopsy: focal segmental nectrotizing GN
76
Treatment for Eosinophilic
granulomatosis with polyangiitis
Immunosuppression
77
Pathophysiology of Goodpasture Syndrome
Antibodies against Type IV collagen - react with pulmonary basement membrane causing pulmonary haemorrhage (haemoptysis) and can lead to RPGN
78
Who gets affected by Goodpasture Syndrome
Two peaks
* 3rd decade of life (male>female)
* after 60 yrs (female>male)
79
Investigation findings in Goodpasture Syndrome
* anti-GBM antibodies
* pulmonary infiltrates on CXR
* Biopsy: linear deposition of IgG along basement membrane
80
Treatment of Goodpasture Syndrome
Plasma exchange immunosuppression
81
Pathophysiology of Thin Basement Membrane Disease
Hereditary abnormalities of Type IV collagen
82
Investigation findings in Thin Basement Membrane Disease
* persistent microscopic haematuria - possible intermittent visible haematuria
* Biopsy: diffuse thinning of GBM
83
Treatment of Thin Basement Membrane Disease
* monitor renal function
* supportive treatment
* good prognosis
84
Pathophysiology of Alport Syndrome
* X-linked recessive (usually affects males)
* Mutation in gene coding gor Type V collagen
85
Associations with Alport Syndrome
* Associated with hearing loss and abnormalities of the eyes
* Often leads to ESRF
86
Investigation findings in Alport Syndrome
* 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
Treatment of Alport Syndrome
* Supportive treatment
* renal replacement therapy
* renal transplant - can lead to development of Goodpasture syndrome
88
Associations of Lupus nephritis
* complication of SLE
* Can be nephritic or nephrotic
89
Investigation findings in Lupus nephritis
* ANA & anti-dsDNA +ve
* Biopsy: 6 different classes of lupus nephritis with different presentations and slightly varying treatment options
90
Treatment of Lupus nephritis
* supportive therapy
* immunosuppressive therapy based on classification/presentation
