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Medicine > Nephrology > Flashcards

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
Q

What is nephrotic syndrome?

A

Proteinuria >3.5 g/day
Hypoalbuminaemia <25g/L
Oedema
Hyperlipidaemia

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26
Q

Causes of nephrotic syndrome

A

Primary:
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy

Secondary:
DM
Amyloidosis
HIV

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27
Q

Presentation of nephrotic syndrome

A 
Features of fluid overload 
Fatigue 
Poor appetite 
Peripheral and periorbital oedema
SoB - Pleural effusions 
Foamy urine - protein
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28
Q

Diagnosis of nephrotic syndrome

A

Proteinuria >3.5 g/day
Hypoalbuminaeamia <35 g/L
Oedema

29
Q

Complications of nephrotic syndrome

A 
Thromboembolism 
Infection 
Hyperlipidaemia 
Hypocalcaemia
Acute renal failure
30
Q

What is minimal change disease?

A

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
Q

Symptoms of minimal change disease

A

Nephrotix syndrome
Oedema
Proteinuria

32
Q

Diagnosis of minimal change disease

A

Children - assumption

Adults - renal biopsy

33
Q

Managemet of minimal change disease

A

Prednisolone - most recover 6-8 weeks

If dont respond - more steroids or more intensive immunosuppressives

34
Q

What is focal segmental glomerulosclerosis?

A

Describes a histological lesion - focal (particular glomeruli involved) segmental (only part of glomeruli involved)
Sclerosis = scarring

35
Q

Causes of Focal segmental glomerulosclerosis

A

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
Q

Diagnosis of focal segmental glomerulonephritis

A

Renal biopsy

IgM deposition scarring certain segments

37
Q

Management of focal segmental glomerulonephritis

A

Differentiate between primary and secondary
Primary = more like minimal change disease = immunosuppressives
Secondary = treat cause e.g. weight loss

38
Q

What is Membranous nephropathy?

A

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
Q

Diagnosis of membranous nephropathy

A 
Histological - renal biopsy 
Serological antibodies (anti-PLA2R)
40
Q

Management of membranous nephropathy

A

Depends on natural history
Some people may recover spontaneously
Steroids / immunosuppressive for those with not irreversible disease

41
Q

What bone problems occur in CKD?

A

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
Q

Management of bone disease in CKD

A

Reduce dietary intake of phosphate in the first line
Phosphate binders
Vitamin D - alfacalcidol
Parathyroidectomy in some cases

43
Q

What should be given in just about all nephrotic syndrome conditions

A

ACEi / ARB

Reduces proteinuria and improves prognosis

44
Q

What is haemoyltic uraemic syndrome? Cause?

A

Generally seen in children
Classic triad of: AKI, Microangiopathic hemolytic anaemia, thrombocytopenia

Causes - most = e. Coli

45
Q

What would suggest that symptoms are due to CKD rather than an AKI?

A

Small, bilateral kidneys

Hypocalcaemia

46
Q

What is tubulointerstitial nephritis and causes

A

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
Q

Features of tubulointerstitial nephritis

A 
Classic - fever, rash, eosinophilia
Arthralgia
Oliguria
Malaise
Haematuria
HTN
N+V

Associated with Abx use a lot

48
Q

Management of tubulointerstitial nephritis

A 
Supportive 
Stop causative agent 
Treat underlying cause 
Stop offending drug 
Steroids in severe cases
Renal replacement - severe AKI
49
Q

Causes of metabolic acidosis with normal anion gap

A

ABCDE

Addison
Bicarb loss (diarrhoea)
Chloride
Drugs

50
Q

Causes of metabolic acidosis with raised anion gap

A

Lactate (shock, sepsis, hypoxia)
Ketone- DKA
Urate - renal failure
Acid poisoning- salicylate, methanol

51
Q

How long does post stept glomerulonephritis take after a URTI?

A

1-2 weeks (IgA nephropathy = 1-2 days

52
Q

What is alport syndrome? Its presentation

A

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
Q

Management of alport syndrome

A 
Kidney transplant for cure
Lifelong nephrologist care 
Regular renal monitoring 
AcEi therapy for HTN/proteinuria
Management of extra-renal disease
54
Q

Management of anaemia in CKD

A

Determine and optimise iron status

Erthypoeitin-stimulating agents - eryhtropoetin or darbepoetin

55
Q

Haemostasis and AKI/haematuria and proteinuria should make you think of what?

A

Anti-GBM (goodpastures)

56
Q

Rash, impaired renal function, raised urinary WCC, eosinophil would make u think what?

A

Acute tubulointerstitial nephritis

57
Q

Prevention of contrast-induced nephrotoxicity

A

1L 0.9% saline pre and post procedure

58
Q

Rhabdomyolysis features and management

A

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
Q

What is lupus nephritis?

A

Nephritis caused by SLE.
Antibodies against nuclear components (dsDNA)
Deposition of antibody complexes cause inflammation cause tissue damage

60
Q

Investigation and management of lupus nephritis

A

Anti-ANA,
anti-dsDNA (titres corresponds to disease severity)
Clinical diagnosis

Treatment - ACEi, hydroxycholoroquine for extra renal disease
Higher class = immunosuppression

61
Q

Where does furesomide act?

A

Ascending loop of henle

On Na/K/2Cl transporter

62
Q

Where do thiazides act?

A

Distal tubule

Inhibit Na/Cl co-transporrer

63
Q

What type of abnormality on a ABG can renal tubular acidosis cause?

A

Hypercholoraemic metabolic acidosis (normal anion gap)

64
Q

What medication can help in hyperphosphataemia in patients with CKD mineral bone disease

A

Sevelamer

Try low phosphate diet first

65
Q

Common complications of renal transplant

A 
Surgical - bleed, thrombosis, infectionz urinary leaks, hernia 
Delayed graft function 
Rejection- acute or chronic 
Infection - CMV common
Malignancy - skin common
66
Q

Most appropriate fluids for rhabdomyolosis?

A

Saline (0.9%)

Not heartmanns because of potassium

67
Q

What causes a hypercoagulable state in nephrotic syndrome?

A

Antithrombin III

68
Q

What would you find in urinalysis (MC&S) of interstitial nephritis?

A

White cell casts
Microscopic haematuria
Sterile pyuria

Medicine (25 decks)

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