1
Q
What are the causes of metabolic acidosis:
A
Normal anion gap (hyperchloraemic)
- GI bicarbonate loss - diarrhoea, uterosigmoidostomy, fistula
- renal tubular acidosis
- drugs e.g. acetazolamide
- ammonium chloride injection
- Addison’s
Increased anion gap
- lactate: shock, hypoxia
- ketonones: DKA, alcohol
- urate: renal failure
- acid poisoning: salicylates, methanol
2
Q
Causes of metabolic alkalosis:
A
Loss of hydrogen ions or gain of bicarbonate due to kidney or GI problems:
- vomiting/aspiration
- diuretics
- liquorice, carbenoxolone
- hypokalaemia
- primary hyperaldosteronism
- Cushing’s syndrome
- Bartter’s syndrome
- congenital adrenal hyperplasia
3
Q
Causes of respiratory acidosis:
A
- COPD
- decompensation other resp conditions
- sedatives: benzodiazepines, opiate overdose
4
Q
Causes of respiratory alkalosis:
A
- anxiety
- PE
- salicylate poisoning
- CNS disorders: stroke, SAH, encephalitis
- altitude
- pregnancy
5
Q
What causes type A lactic acidosis?
A
- sepsis
- shock
- hypoxia
- burns
6
Q
What causes type B lactic acidosis?
A
metformin
7
Q
What are the causes of acute interstitial nephritis?
A
Drugs:
- penicillin
- rifampicin
- NSAIDs
- allopurinol
- furosemide
- systemic: SLE, sarcoidosis, Sjogren’s
- infection: Hanta virus, staphylococci
8
Q
What are the features and investigations of acute interstitial nephritis?
A
- fever, rash, arthralgia
- eosinophilia (casts)
- mild renal impairment
- HTN
- sterile pyuria and white cell casts
9
Q
Pre-renal causes of AKI:
A
ischaemia: e.g. hypovolaemia secondary to diarrhoea/vomiting, renal artery stenosis etc.
10
Q
Renal causes of AKI:
A
- intrinstc damage to glomeruli, renal tubules or interstitium
e. g. toxins (drugs, contrast), GN, ATN, AIN, rhabdomyolysis, tumour lysis syndrome
11
Q
Postrenal causes of AKI:
A
obstruction to urine: e.g. stones, hydronephrosis, external compression etc.
12
Q
Risk factors of AKI:
A
- CKD
- other organ failure/chronic disease e.g. HF, liver disease, diabetes
- history of acute AKI
- nephrotoxic drugs: NSAIDs, aminoglycosides, ACEi, ARBs and diuretics in past week
- iodinated contrast agent
- > =65yo
- oliguria (<0.5ml/kg/hr)
13
Q
Symptoms and detection of AKI:
A
Symptoms:
- reduced urine output
- pulmonary and peripheral oedema
- arrhythmias (secondary to changes in K+)
- features of uraemia (e.g. pericarditis or encephalopathy)
Detection:
- creatinine increase by >=26micromol/L in 48 hours
- 50% or greater rise in serum creatinine or within 7 days
- reduced urine output <0.5ml/kg/hr for more than 6 hours
- urinalysis
- renal US within 24 hours
14
Q
Drugs which should be stopped in AKI:
A
-NSAIDs
-aminoglycosides
-ACEi
-ARB
-diuretics
(metformin, lithium, digoxin)
15
Q
How do you treat hyperkalaemia e.g. in AKI?
A
- IV calcium gluconate
- combined insulin/dextrose infusion
- nebulised salbutamol
- calcium resonium (oral or enema)
- loop diuretics
- dialysis
16
Q
Criteria for diagnosing AKI:
A
- rise in creatinine of 26micromol/L or more in 48 hours OR
- > =50% rise in creatinine over 7 days OR
- fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 in children) OR
- > =25% fall in eGFR in children/young adults in 7 days
17
Q
When do you refer AKI to a nephrologist?
A
- renal transplant
- ITU with unknown cause AKI
- vasculitis/GN/tuberointerstitial nephritis/myeloma
- AKI with no known cause
- inadequate response to treatment
- complications of AKI
- stage 3 AKI
- CKD stage 4 or 5
- qualify for renal replacement hyperkalaemia/metabolic acidosis/complications of uraemia/fluid overload (pulmonary oedema)
18
Q
How can you differentiate between acute and chronic renal failure?
A
-renal US
-most chronic have bilateral small kidneys
EXCEPT ADPKD, diabetic nephropathy, amyloidosis, HIV associated nephropathy
-chronic has hypocalcaemia due to reduced vit D
19
Q
What are the types of ADPKD?
A
Type I: -polycysitn-1 -85% of cases -chromosome 16 -presents with renal failure earlier Type II: -polycystin-2 -chromosome 4
20
Q
Features and extra renal manifestations of ADPKD:
A
- HTN
- recurrent UTIs
- abdominal pain
- renal stones
- haematuria
- CKD
- extra-renal: liver cysts, berry aneurysms (SAH), mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
- cysts in other organs: pancreas, spleen, rarely thyroid, oesophagus and ovary
21
Q
How do you manage ADPKD:
A
- tolvaptan (vasopressin receptor 3 antagonist)
- if CKD stage II or III, evidence of rapidly progressing disease
22
Q
What is Alport’s syndrome? (incl features)
A
- x-linked dominant
- defect gene coding for type IV collagen (abnormal GBM)
- more severe in males
- presents in childhood
Features:
- mircoscopic haematuria
- progressive renal failure
- bilateral sensorineural deafness
- leticonus
- retinitis pigmentosa
- renal biopsy: splitting of lamina densa
23
Q
What is Amyloidosis?
A
- extracellular deposition of insoluble fibrillar protein - amyloid
- also apolipoprotein E and heparin sulphate proteoglycans
- accumulation of amyloid fibrils - tissue/organ dysfunction
24
Q
How do you diagnose amyloidosis?
A
- congo red staining - apple-green birefringence
- serum amyloid precursor scan
- biopsy of rectal tissue
25
What is an anion gap?
(sodium+potassium) - (bicarbonate+chloride)
| normal: 8-14mmol/L
26
What is anti-GBM disease?
- Goodpasture's
- rare, small vessel vasculitis
- associated with pulmonary haemorrhage and rapidly progressive GN
- antibodies against type IV collagen
- more common in men 2:1
- HLA DR2
27
How do you test for and manage anti-GBM disease?
- renal biopsy: linear IgG deposits along BM
- increased transfer factor secondary to pulmonary haemorrhages
- manage with: plasma exchange, steroids, cyclophosphamide
28
What increases the risk of pulmonary haemorrhage in anti-GBM?
- smoking
- lower RTI
- pulmonary oedema
- inhalation of hydrocarbons
- young males
29
What is ARPKD?
- autosomal recessive version
- much less common
- defect in gene on chromosome 6 which encodes fibrocytin
- end stage renal failure in childhood
- liver involvement (portal and interlobular fibrosis)
- renal biopsy shows multiple cylindrical lesions
- diagnosis on prenatal US: abdominal masses and renal failure, consistent with Potter's syndrome secondary to oligohydramnios
30
Complications of AV fistulae?
- infection
- thrombosis (absence of bruit)
- stenosis (acute limb pain)
- steal syndrome
31
What is diabetes insipidus and what are the features and investigation?
- either deficiency of ADH (cranial) or insensitivity to ADH (nephrogenic)
- polyuria and polydipsia
- increased plasma osmolality and decreased urine osmolality
- urine osmolality >700mOsm/kg excludes DI
- water deprivation test
32
What causes cranial diabetes insipidus and what is the management?
-idiopathic
-post HI
-pituitary surgery
-craniopharyngiomas
-histiocytosis X
-DIDMOAD (Wolfram's syndrome)
-haemochromatosis
manage with desmopressin
33
What are the causes of nephrogenic diabetes insipidus and the management?
-genetic (ADH receptor or aquaporin 2 channel)
-electrolytes (hypercalcaemia and hypokalaemia)
-drugs: demeclocycline, lithium
-tubulo-interstitial disease: obstruction, sickle cell, pyelonephritis
manage with thiazides, low salt/protein diet
34
Side effects of erythropoietin therapy and indication:
```
-used for anaemia associated with CKD
can cause:
-accelerated HTN - encephalopathy and seizures
-bone aches
-flu-like
-skin rashes, urticaria
-pure red cell aplasia
-increased PCV - thrombosis
-iron deficiency secondary to increased erythropoiesis
```
35
Why might someone be unresponsive to erythropoietin therapy?
- iron deficiency
- inadequate dose
- concurrent infection/inflammation
- hyperparathyroid bone disease
- aluminium toxicity
36
What is Fanconi syndrome, features and causes?
- generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule
- polyuria, type II RTA, aminoaciduria, glycosuria, phosphaturia, osteomalacia
- causes: cystinosis, Sjogren's, multiple myeloma, nephrotic syndrome, Wilson's
37
What is fibromuscular dysplasia?
- renal artery stenosis secondary to atherosclerosis
- 90% female
- causes HTN, CKD and flash pulmonary oedema
38
Maintenance fluids:
- 25-30ml/kg/day water
- 1mmol/kg/day of potassium, sodium and chloride
- 50-100g/day of glucose to limit starvation ketosis
39
What is the risk of using large volumes of NaCl 0.9%?
increased risk of hyperchloraemic metabolic acidosis
40
In which patients is Hartmann's contraindicated?
hyperkalaemic patients
41
What is focal segmental glomerulosclerosis and the causes?
- causes nephrotic syndrome and CKD
- young adults
- idiopathic
- secondary to other renal pathology
- HIV
- heroin
- Alport's syndrome
- sickle cell
- high recurrence rate in renal transplants
42
What are the investigations and management for focal segmental glomerulosclerosis?
- renal biopsy: focal and segmental sclerosis and hyalinosis, effacement of foot processes
- manage with steroids (and immunosuppressants)
43
Causes of transient or spurious non-visible haematuria:
- UTI
- menstruation
- vigorous exercise (resolves in 3 days)
- sexual intercourse
44
Spurious causes of haematuria (red/orange urine)
- beetroot, rhubarb
- rifampicin
- doxorubicin
45
Urgen referral criteria for haematuria:
- >=45yo with unexplained visible haematuria without UTI or visible haemautria that persists after successful treatment of UTI
- >=65yo and unexplained non-visible haematuria and dysuria or increased WCC
46
Non-urgent referral criteria for haematuria:
- >=60yo with recurrent or persistent unexplained UTI
| - <40yo with normal renal function, no proteinuria and normotensive (no referral - manage in primary care)
47
Presentation of HUS:
- triad: AKI, microangiopathic haemolytic anaemia, thrombocytopaenia
- bloody diarrhoea few days after onset
- most cases secondary to:
- shiga toxin producing e-coli (STEC) O157:H7 - most common in children
- pneumococcal infection
- HIV
- rare: SLE, drugs, cancer
- primary HUS - atypical - complement dysregulation
48
Management of HUS:
- supportive e.g. dialysis, fluids, blood transfusion
- no Abx
- eculixumab - C5 inhibitor monoclonal antibody
49
What is Henoch-Schonlein Purpura and the features?
- IgA mediated small vessel vasculitis
- some overlap with IgA nephropathy (Berger's)
- usually in children following infection
- palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
- abdominal pain
- polyarthritis
- features of IgA nephropathy
- good prognosis - self-limiting
50
Treatment of HSP:
- analgesia for arthralgia
| - supportive Tx for nephropathy
51
What is IgA nephropathy, associations, pathophysiology and presentation?
- Berger's
- most common cause of GN
- associated with: alcoholic cirrhosis, coeliac disease/dermatitis herpetiformis, HSP
- mesangial deposition of IgA immune complexes, mesangial hypercellularity, positive immunofluorescence for IgA and C5
- typically young male with recurrent episodes of macroscopic haematuria following a RTI
- nephrotic range proteinuria rare
- renal failure unusual
52
IgA nephropathy vs post streptococcal:
- post strep results in low complement
- post strep main symptom proteinuria
- interval between URTI and post-strep onset (1-2 weeks)
53
Prognosis of IgA nephropathy:
- 25% ESRF
- frank haematuria - good prognosis
- male, proteinuria, HTN, smoking hyperlipidaemia, ACE genotype DD - poor prognosis
54
How does membranoproliferative GN/mesangiocapillary GN present?
- nephrotic syndrome, haematuria or proteinuria
- poor prognosis
- involves mesangium as well as BM (unlike membranous)
55
Type I membranoproliferative GN:
- 90% cases
- caused by cryoglobulinaemia, hepatitis C
- renal biopsy: sub endothelial and mesangium immune deposits of electron dense material - tram track appearance
56
Type II membranoproliferative GN:
- dense deposit disease
- caused by partial lipodystrophy and factor H deficiency
- persistent activation of alternative complement pathway
- low circulating levels of C3
- C3b nephritic factor found in 70%
- renal biopsy: intramembranous immune complex deposits with dense deposits
57
Type III membranoproliferative GN is caused by:
hepatitis B and C
58
How do you treat membranoproliferative GN?
steroids
59
Membranous GN
- most common type in adults
- presents as nephrotic syndrome or proteinuria
- renal biopsy: basement membrane thickened with sub epithelial electron dense deposits (spike and dome)
60
Causes of membranous GN:
- idiopathic: antiphospholipase A2 antibodies
- infections: hep B, malaria, syphilis
- malignancy: prostate, lung, lymphoma, leukaemia
- drugs: gold, penicillamine, NSAIDs
- autoimmune: SLE, thyroiditis, rheumatoid
61
Management of membranous GN:
- ACEi or ARB
- immunosuppression (corticosteroid and cyclophosphamide)
- consider anticoagulation
62
Prognosis of membranous GN:
1/3 spontaneous remission
1/3 remain proteinuric
1/3 ESRF
63
Minimal change disease (presentation, causes, features, biopsy, management)
- presents as nephrotic syndrome
- causes: idiopathic, drugs, Hodgkin's lymphoma, thymoma, infectious mononucleosis
- T cell and cytokine mediated damage to GBM - polyanion loss
- normotension, high selective proteinuria (albumin and transferrin leak through glomeruli)
- renal biopsy: normal glomeruli on light microscopy, fusion of podocytes and effacement of foot processes on electron microscopy
- management: majority steroid responsive or cyclophosphamide if steroid resistant (do biopsy)
64
Prognosis of minimal change disease:
- 1/3 only 1 episode
- 1/3 infrequent relapses
- 1/3 frequent relapses which stops before adulthood
65
Features of nephrotic syndrome:
- triad: proteinuria, hypoalbuminaemia, oedema
- loss of antithrombin III, protein C and S and associated increase in fibrinogen predisposes to thrombosis
- loss of thyroxine - binding globulin decreased total but not free thyroxine
66
Complications of nephrotic syndrome:
- increased risk of thromboembolism due to loss of antithrombin III and plasminogen in urine
- hyperlipidaemia - increased risk of ACS, stroke etc.
- CKD
- increased risk of infection due to urinary immunoglobulin loss
- hypocalcaemia (vita and binding protein lost in urine)
67
Sign of nephrotoxicity contrast media:
25% increase in creatinine within 3 days of intravascular administration
68
Nephrotoxicity contrast media risk factors and prevention:
- know renal impairment
- >70 yo
- dehydration
- cardiac failure
- use of nephrotoxic drugs
Prevention:
- IV 0.9% NaCl at 1ml/kg/hr of 12 hours pre- and post-op
- isotonic sodium bicarbonate
- N-acetylcysteine not effective
69
Complications of peritoneal dialysis:
- peritonitis: coagulase negative staph e.g. staph epidermis most common, also aureus
- sclerosing peritonitis
70
Post-streptococcal glomerulonephritis presentation and features:
- 7-14 days following group A beta haemolytic strep infection (usually pyogenes)
- immune complex deposition in glomeruli
- mostly young hcildren
- general headache, malaise, visible haematuria, proteinuria, oedema, HTN, oliguria, low C3 and raised ASO titre
- good prognosis
71
What does the renal biopsy show in post-streptococcal GN?
- acute diffuse proliferative GN
- endothelial proliferation with neutrophils
- electron microscopy: sub epithelial humps cause by lumpy immune complex deposits
72
Rapidly progressive glomerulonephritis causes and presentation:
- rapid loss of renal function with formation of epithelial crescents in majority of glomeruli
- causes: Good pasture's, vasculitic rash or sinusitis with Wegener's
73
Reflux nephropathy:
- chronic pyelonephritis secondary to vesico ureteric reflux
- commonest cause of chronic GN
- scanning first 5 year
- strong genetic component
- renal scars may produced increased quantities of renin - HTN
- diagnosis by micturating cystography
74
Renal artery stenosis:
- secondary to atherosclerosis (90% of renal vascular disease)
- HTN, CKD, flash pulmonary oedema
75
Renal papillary necrosis incl causes and features:
- coagulative necrosis of renal papillae due to variety of causes
- caused by: severe acute pyelonephritis, diabetic nephropathy, obstructive nephropathy, analgesic nephropathy, sickle cell anaemia
- visible haematuria, loin pain, proteinuria
76
Types of renal replacement therapy:
- haemodialysis
- peritoneal dialysis
- renal transplant
77
Haemodialysis:
- most common RTT
- most need 3 per week
- surgery to create AV fistula 8 weeks before commencing
78
Peritoneal dialysis:
- filtration within abdomen
- dialysis solution injected into abdominal cavity through a permanent catheter
- high dextrose concentration of solution draws waste products out
- 2 types: continuous ambulatory and automated peritoneal dialysis
79
Renal transplant:
- into groin and renal vessels connected to external iliac
- failing kidneys not removed
- life-long immunosuppressants
- average lifespan 10-12 years
80
Haemodialysis complications:
- site infection
- endocarditis
- stenosis at site
- hypotension
- cardiac arrhythmias
- air embolus
- anaphylactic reaction to sterilising agents
- disequilibration syndrome (cerebral oedema)
81
Peritoneal dialysis complications:
- peritonitis (staph epidermis)
- sclerosing peritonitis
- catheter infection
- catheter blockage
- constipation
- fluid retention
- hyperglycaemia
- hernias
- back pain
- malnutrition
82
Renal transplantation complications:
- DVT/PE
- opportunistic infection
- malignancies (particularly lymphoma and skin cancer)
- bone marrow suppression
- recurrence of original disease
- urinary tract obstruction
- CVD
- graft rejection
83
Hyperacute rejection of transplant:
- pre-existing Ab against ABO or HLA antigens
- type II hypersensitivity
- widespread thrombosis of graft vessels -ischaemia and necrosis
- remove graft
84
Acute graft failure of transplant:
- <6 mo
- usually mismatched HLA, cell mediated cytotoxic T cells
- or CMV infection
- may be reversible with steroids and immunosuppressants
85
Chronic graft failure of transplant:
- >6 mo
- both AB and cell mediated mechanisms cause fibrosis to transplanted kidney
- recurrence of renal disease
86
Immunosuppression in renal transplantation:
- intial: ciclosporin/tacrolimus with monoclonal Ab
- maintenance: ciclosporin/tacrolimus with MMF or sirolimus
- add steroids if more than one steroid responsive acute rejection episode
87
Rhabdomyolysis features:
- AKI with disproportionately increased creatinine
- elevated CK
- myoglobulinuria
- hypocalcaemia (myoglobin binds calcium)
- increased phosphate (from myocytes)
- hyperkalaemia (before renal failure)
- metabolic acidosis
88
Causes of rhabdomyolysis:
- seizure
- collapse/coma
- ecstacy
- crush injury
- McArdle's syndrome
- drugs: statins (especially with clarithromycin)
89
Management of rhabdomyolysis:
- IV fluids to maintain good urine output
| - urinary alkalisation sometimes used
90
Causes of sterile pyuria:
- partially treated UTI
- urethritis e.g. chlamydia
- renal tuberculosis
- renal stones
- appendicitis
- bladder/renal cell cancer
- APKD
- analgesic nephropathy
91
SLE renal complications WHO classifications:
- class I: normal kidney
- class II: mesangial glomerulonephritis
- class III: focal and segmental proliferative GN
- class IV: diffuse proliferative GN
- class V: diffuse membranous GN
- class VI: sclerosis GN
class IV most common and severe
92
What produces hyaline casts:
- Tamm Horsfall protein secreted by distal convoluted tubule
| - normal urine, exercise, fever or loop diuretics
93
What is visible in the urine in ATN?
brown granular casts
94
How does the urine appear in prerenal uraemia:
bland urinary sediment
95
What is visible in the urine with nephritic syndrome?
red cell casts
96
Symptoms of anaemia in CKD:
- tachycardia
- fatigue
- pallor
- aortic flow murmur
97
What causes anaemia in CKD:
- usually normochromic normocytic anaemia
- prediposes to left ventricular hypertrophy
- decreased erythropoietin
- reduced erythropoiesis due to toxic effects of uraemia on bone marrow
- reduced iron absorption
- anorexia/nausea due to uraemia
- reduced red cell survival
98
Management of anaemia in CKD:
- determination of iron status before erythropoiesis stimulation agents
- many patients esp haemodialysis requires IV iron
- ESAs e.g. erythropoietin and darbepoietin
99
Clinical manifestations of bone disease in CKD:
- osteitis fibrosa cystica (hyperparathyroid bone disease)
- adynamic: cellular activity decreased, may be due to over treatment with vit D
- osteomalacia
- osteoscelerosis
- osteoporosis
100
Management of bone disease in CKD:
- aim to decrease phos and PTH
- 1st line: decrease phosphate dietary intake
- phosphate binders (sevelamer, calcium based)
- vit D: alfacalcidol (does not require activation in kidneys), calcitriol
- sometimes parathyroidectomy
101
CKD stage I
- GFR greater than 90ml/min
| - some sign of kidney damage
102
CKD stage II
- 60-90ml/min
| - some sign of kidney damage
103
CKD stage IIIa and b
```
a
-45-59ml/min
-moderate reduction kidney function
b
-30-44ml/min
-moderate reduction kidney function
```
104
CKD stage IV
- 15-29ml/min
| - severe reduction in kidney function
105
CKD stage V
- less than 15ml/min
- establish kidney failure
- dialysis or kidney transplant needed
106
What can affect MDRD formula for calculating CKD stage?
- pregnancy
- muscle mass
- eating red meat 12 hours before sample
107
At what eGFR does a nephrologist need to be called?
<30ml/min
108
What ratio is used to determine proteinuria in CKD?
ACR over PCR (greater sensitivity)
109
How should a urine sample be collected for CKD?
- spot sample
- first pass morning urine
- if initial ACR 3-70mg/mmol, subsequent early morning sample (higher no repeat sample needed)
110
Which ACR values should be referred to a nephrologist?
- >=70mg/mmol unless caused by diabetes
- >=30mg/mmol with persistent haematuria (2 of 3 dipsticks) after exclusion of UTI
- 3-29mg/mmol with persistent haematuria and risk factors consider
111
Management of coexistent HTN and CKD:
- ACEi or ARB
| - ACR >70mg/mmol regardless of BP
112
Which medication which CKD patients take can lead to abdominal pain, back pain, muscle weakness etc?
- calcium binders e.g. calcium acetate
| - hypercalcaemia and vascular calcification
113
What kind of murmur can you hear with anaemia?
soft ejection systolic murmur (aortic flow murmur)
114
Maintenance fluid regime rate:
500ml 0.9% saline at 100ml/hr
115
Resuscitation fluids:
500ml 0.9% saline in 15 mins
116
What should you consider in young females who develop an AKI after taking ACEi? (string bead appearance)
fibromuscular dysplasia
117
How to distinguish primary and secondary aldosteronism:
high renin - secondary e.g. renal artery stenosis
118
Most common extra renal manifestation of ADPKD:
liver cysts
119
How do you treat nephrogenic diabetes?
chlorthiazide
120
How do you treat hypokalaemia?
- cardiac monitoring
| - 3 x 1 litre bags of 0.9% saline with 40mmol KCL per bag over 24 hours
121
What variables does the MDRD equation include?
- creatinine
- age
- gender
- ethnicity
PM Important
flashcards
Decks in class (16)
# Cards
