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Nephrology Flashcards

1
Q

What is AKI?

A

A syndrome of decreased renal function
Rise in creatinine >26 umol/L within 48h
Or rise in creatinine >1.5x baseline within 7 days
Urine output <0.5mL/kg/hr for >6h

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2
Q

Staging of AKI

A

1- 1.5 x baseline creatinine within 1 week
2 x baseline
3 x baseline

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3
Q

Pre-renal causes of AKI

A 
Reduced renal perfusion
Hypovolaemia
Sepsis
HF
renal artery disease
Dehydration
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4
Q

Renal causes of AKI

A

Intrinsic renal disease
Glomerulonephritis
Vasculitis
Interstitial nephritis - secondary to medications (NSAIDs)

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5
Q

Post-renal causes of AKI

A

Obstruction to urinary outflow tract
Tumors
Clots
Calculi

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6
Q

Features of AKI

A 
Oliguria 
Fluid overload - peripherl oedema, SOB
Acidosis - kussmaul breathing 
Uraemia - malaise, lethargy, pruritis
Hyperkalaemia - chest pain, palpitations
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7
Q

Management of AKI

A

General - supportive, monitor fluid - avoid over-load and hypovolaemia. Abx if sepsis

Review medications - stop nephrotoxins
Refer to nephrology if intrinsic cause, urology if post-renal. In put and output managing

Manage complications

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8
Q

Causes of CJD

A

Diabetes
HTN
Renovascular disease
Glomerulonephritis

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9
Q

Investigations of CKD

A

Blood - u+e, urea, Hb, glucose, calcium, PTH
Urine - distick, MC&S, albumin and protein to creatinine ratio
Imaging - USS, CT - obstruction
Histology

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10
Q

Management of CKD

A

Referral to nephro
Treatment to slow progression and treat complications
Renal replacement therapy

Slow progression - target BP <140, offer ACEi
Glycaemic control
Bone protection - bisphospanates
Other - stations, CVD protection (lifestyle) urology input for obstruction, iron if anaemia
Caution drugs - NSAIDs
Renal transplant

Renal replacement therapy

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11
Q

Classification of CKD

A 
G1 - eGFR (>90)
G2 - eGFR (60-89)
G3 - eGFR (30-59)
G4 - eGFR (15-29)
G5 - eGFR (<15)
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12
Q

Signs and symptoms of CKD

A

Early stages - asymptomatic. Signs of cause - diabetes, HTN, proteinuria (glomerulonephritis)

Later stages - BROKEN PIDDLE BAGS

BP - HTN
RBCs - anaemia 
Oedema 
K+ - raised
Neurological symptoms 
Pericarditis 
Itch
Dermal darkening 
Diuresis
Lipid elevation 
Bone osease 
GI - nausea vomiting 
Skinny - weight loss
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13
Q

What is nephritic syndrome?

A

Presence of haematuria, variable proteinuria, renal impairment, and HTN

Known as glomerulonephritis
Describes the presence of an inflammatory process within the glomeruli

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14
Q

Causes of nephritic syndrome

A

Due to inflammation.
Can be due to inflammation of the small vessels within the capillary tuft or formation of anti-glomerular basement membrane autoantibodies

Immune complex deposition - deposition of immunoglobulin and complement. Typical of a systemi disease (SLE, post-strept. Glomerulonephritis, IgA nephropathy)

Small vessel vasculitis - limited or no immune deposition in the glomeruli. Instead patients have circulating ANCA (targets self-antigens leading to inflammation) - broadly 3 diseases- microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis

Anti-GBM - formation of GBM antibodies that target IV collagen in the basement membrane.

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15
Q

What is IgA nepropathy, what type of disease is it?

A

Immune complex deposition causing nephritis-type condition
Galactose deficient IgA recognised by IgG and a different IgA type - forms an immune complex that deposits in the renal mesangium

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16
Q

What is presentation of IgA nephropathy?

A

Asymptomatic non-visible haematuria or visible haematuria following an infection (typically a URTI)
Increased BP
Think of in young males, with episodic haematuria following an acute URTI

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17
Q

Diagnosis of IgA nephropathy

A

Urinalysis - haematuria and rarely proteinuria
FBC, renal function, LFTs, bone profile
Imaging - USS / CT - exclude structural symptoms

Renal biopsy is definitive

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18
Q

Treatment of IgA nephroapthy

A

Optimal supportive care, control of BP, reduction of proteinuria
Lifestyle modifications - weight loss, smoking cessation, dietary sodium restriction has shown benefits
ACEi / ARB

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19
Q

What are the 3 ANCA-associated vasculitis conditions?

A

Microscopic polyangiitis
Granulomatosis with polyangiitis (wegener’s)
Eosinophilic granulomatosis with polyangitis

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20
Q

What is granulomatosis with polyangiitis?

A

Also known as wegeners granulomatosis

Small vessel vasculitis - ANCA associated
Usually develops from an initiating event in a genetically predisposed individual

Can affect any organ system

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21
Q

Features of granulomatosis with polyangiitis

A

ELK (ENT nose throat)
ENT - sensioneural hearing loss, epistaxis, otitis, sinusitis, saddle shaped nose deformity
Lung - haemostasis
Kidney - asymptomatic haematuria, proteinuria, nephritic syndrome

Also eye symptoms- conjunctivitis, episcleritis
Also - fever, lethargy, weight loss anorexia

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22
Q

Investigations of granulomatosis with polyangiitis

A

Biopsy - of affected organ (kidney, nose)
ANCA positivity
Also - urinalysis- blood/protein
Red cell casts - suggestive of glomerulonephritis
Routine bloods - FBC, coag, u+e, crp, LFT, bone profile
Vasculitis screen - ana, complement, anti-GBM
Imaging - CXR (effusions), CT sinuses

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23
Q

Management of granulomatosis with polyangiitis

A

Immunosuppression

Induce - steroids in combination with retuximab in life-threatening

Maintenance - multiple agents - rituximab, azathioprine, methotrexate

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24
Q

Post-streptococcal glomerulonephritis presentation and management

A

1-2 weeks after infection
Myalgia, headache, haematuria, proteinuria
Supportive management

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25
What is nephrotic syndrome?
Proteinuria >3.5 g/day Hypoalbuminaemia <25g/L Oedema Hyperlipidaemia
26
Causes of nephrotic syndrome
Primary: Minimal change disease Focal segmental glomerulosclerosis Membranous nephropathy Secondary: DM Amyloidosis HIV
27
Presentation of nephrotic syndrome
``` Features of fluid overload Fatigue Poor appetite Peripheral and periorbital oedema SoB - Pleural effusions Foamy urine - protein ```
28
Diagnosis of nephrotic syndrome
Proteinuria >3.5 g/day Hypoalbuminaeamia <35 g/L Oedema
29
Complications of nephrotic syndrome
``` Thromboembolism Infection Hyperlipidaemia Hypocalcaemia Acute renal failure ```
30
What is minimal change disease?
Common childhood cause of nephrotic syndrome Characterised by podocyte fusion under electron microscopy Cause is often idiopathic but some due to drugs and malignancy and infections
31
Symptoms of minimal change disease
Nephrotix syndrome Oedema Proteinuria
32
Diagnosis of minimal change disease
Children - assumption | Adults - renal biopsy
33
Managemet of minimal change disease
Prednisolone - most recover 6-8 weeks | If dont respond - more steroids or more intensive immunosuppressives
34
What is focal segmental glomerulosclerosis?
Describes a histological lesion - focal (particular glomeruli involved) segmental (only part of glomeruli involved) Sclerosis = scarring
35
Causes of Focal segmental glomerulosclerosis
Primary secondary or genetic Primary - circulating factor that damages podocytes (spreads out which reduces effectiveness of filtration barrier) Secondary - adaptive response to injury. Cause e.g. obesity
36
Diagnosis of focal segmental glomerulonephritis
Renal biopsy | IgM deposition scarring certain segments
37
Management of focal segmental glomerulonephritis
Differentiate between primary and secondary Primary = more like minimal change disease = immunosuppressives Secondary = treat cause e.g. weight loss
38
What is Membranous nephropathy?
Most common cause of neprotic syndrome in adults Characterised by glomerular basement membrane thickening. Formation of immune deposits and subsequent thickening of the membrane Secondary causes - malignancy, autoimmune diseases, infection, gold, drugs (penicillamine)
39
Diagnosis of membranous nephropathy
``` Histological - renal biopsy Serological antibodies (anti-PLA2R) ```
40
Management of membranous nephropathy
Depends on natural history Some people may recover spontaneously Steroids / immunosuppressive for those with not irreversible disease
41
What bone problems occur in CKD?
Low vitamin D As kidneys normally excrete phosphate = high phosphate which drags calcium out of bones - resulting in osteomalacia Low calcium occurs due to lack of vitamin D Secondary hyperaparathyroidism - low calcium, high phosphate and low vitamin D
42
Management of bone disease in CKD
Reduce dietary intake of phosphate in the first line Phosphate binders Vitamin D - alfacalcidol Parathyroidectomy in some cases
43
What should be given in just about all nephrotic syndrome conditions
ACEi / ARB | Reduces proteinuria and improves prognosis
44
What is haemoyltic uraemic syndrome? Cause?
Generally seen in children Classic triad of: AKI, Microangiopathic hemolytic anaemia, thrombocytopenia Causes - most = e. Coli
45
What would suggest that symptoms are due to CKD rather than an AKI?
Small, bilateral kidneys | Hypocalcaemia
46
What is tubulointerstitial nephritis and causes
Injury to the renal tubules and interstitium Inflammation commonly due to a hypersensitivity reaction to a medication (leads to inflammation with or without AKI) Can be acute or chronic Causes - drugs (penicillin, Abx, NSAIDs)
47
Features of tubulointerstitial nephritis
``` Classic - fever, rash, eosinophilia Arthralgia Oliguria Malaise Haematuria HTN N+V ``` Associated with Abx use a lot
48
Management of tubulointerstitial nephritis
``` Supportive Stop causative agent Treat underlying cause Stop offending drug Steroids in severe cases Renal replacement - severe AKI ```
49
Causes of metabolic acidosis with normal anion gap
ABCDE Addison Bicarb loss (diarrhoea) Chloride Drugs
50
Causes of metabolic acidosis with raised anion gap
Lactate (shock, sepsis, hypoxia) Ketone- DKA Urate - renal failure Acid poisoning- salicylate, methanol
51
How long does post stept glomerulonephritis take after a URTI?
1-2 weeks (IgA nephropathy = 1-2 days
52
What is alport syndrome? Its presentation
Rare hereditary nephropathy due to mutations in genes for collagen IV Usually X-linked Affects glomerular basement membrane = nephritis Features - classic - microscopic haematuria, progressive renal failure, HTN Bilateral sensineural hearing loss Ocular defects
53
Management of alport syndrome
``` Kidney transplant for cure Lifelong nephrologist care Regular renal monitoring AcEi therapy for HTN/proteinuria Management of extra-renal disease ```
54
Management of anaemia in CKD
Determine and optimise iron status | Erthypoeitin-stimulating agents - eryhtropoetin or darbepoetin
55
Haemostasis and AKI/haematuria and proteinuria should make you think of what?
Anti-GBM (goodpastures)
56
Rash, impaired renal function, raised urinary WCC, eosinophil would make u think what?
Acute tubulointerstitial nephritis
57
Prevention of contrast-induced nephrotoxicity
1L 0.9% saline pre and post procedure
58
Rhabdomyolysis features and management
Typically a patient who has a fal or prolonged epileptic seizure found to have an acute AKI ``` Elevated creatine kinase Myoglobinuria Hypocalcaemia Elevatee phosphate Hyperkalaemia Metabolic acidosis ``` IV fluids and urinary alkalinisation
59
What is lupus nephritis?
Nephritis caused by SLE. Antibodies against nuclear components (dsDNA) Deposition of antibody complexes cause inflammation cause tissue damage
60
Investigation and management of lupus nephritis
Anti-ANA, anti-dsDNA (titres corresponds to disease severity) Clinical diagnosis Treatment - ACEi, hydroxycholoroquine for extra renal disease Higher class = immunosuppression
61
Where does furesomide act?
Ascending loop of henle | On Na/K/2Cl transporter
62
Where do thiazides act?
Distal tubule | Inhibit Na/Cl co-transporrer
63
What type of abnormality on a ABG can renal tubular acidosis cause?
Hypercholoraemic metabolic acidosis (normal anion gap)
64
What medication can help in hyperphosphataemia in patients with CKD mineral bone disease
Sevelamer | Try low phosphate diet first
65
Common complications of renal transplant
``` Surgical - bleed, thrombosis, infectionz urinary leaks, hernia Delayed graft function Rejection- acute or chronic Infection - CMV common Malignancy - skin common ```
66
Most appropriate fluids for rhabdomyolosis?
Saline (0.9%) Not heartmanns because of potassium
67
What causes a hypercoagulable state in nephrotic syndrome?
Antithrombin III
68
What would you find in urinalysis (MC&S) of interstitial nephritis?
White cell casts Microscopic haematuria Sterile pyuria

Medicine (25 decks)

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