renal Flashcards
haemolytic uraemic syndrome causative organism
e. coli 0157:H7
HUS triad
AKI
microangiopathic haemolytic anaemia
thrombocytopenia
rhabdomyolysis blood results: (5)
raised CK (at least x5 upper limit of normal)
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia
metabolic acidosis
how to differentiate AKI vs CKD (2)
USS - CKD have small kidneys*
hypocalcaemia (due to low vit D)
- exceptions:
- PCKD
- early diabetic nephropathy
- amyloidosis
- HIV associated nephropathy
most common cause of death for CKD pts on haemodialysis
IHD
stage 1 AKI
i. creatinine
ii. urine production
i. Increase 1.5-1.9x baseline
ii. < 0.5ml/kg/h for >6 consecutive hours
stage 2 AKI
i. creatinine
ii. urine production
i. Increase 2.0-2.9x baseline
ii.< 0.5ml/kg/h for >12 consecutive hours
stage 3 AKI
i. creatinine
ii. urine production
3 Increase > 3x baseline or >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h
most common cause of glomerulonephritis worldwide:
IgA
IgA nephropathy associated conditions:
alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura
IgA nephropathy gold standard ix
renal biopsy
IgA vs post streptococcal glomerulonephritis
IgA nephropathy
- 1-2 days post URTI
- usually young males
- macroscopic haematuria
post strp:
- 1-2 weeks post URTI
- proetinuria
- low complement
(but both have hx recent URTI and haematuria)
IgA nephropathy mgt
- conservative
- ACEi (if persisitent proteinuria or drop in renal function
- corticosteroids (if no response from ACEi or active disease i.e. falling eGFR)
post-strep glomerulopnephritis
features:
recent URTI 1-2 weeks ago
general: headache, malaise
visible haematuria
proteinuria + oedema
hypertension
oliguria
post-strep glomerulonephritis bloods:
raised anti-streptolysin O titre
low C3
how to calculate anion gap
(Na+ + K+) - (Cl- + HCO-3)
normal anion gap
10-18
metabolic acidosis with normal anion gap
(hypercholeraemic metabolic acidosis)
gastrointestinal bicarbonate loss:
prolonged diarrhoea: may also result in hypokalaemia
ureterosigmoidostomy
fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
metabolic acidosis with raised anion gap:
lactate:
- shock
-sepsis
- hypoxia
ketones:
- diabetic ketoacidosis
- alcohol
urate: renal failure
acid poisoning: salicylates, methanol
eGFR adjusted dependent on:
MDRD (modification of diet in renal disease)
CAGE
creatinine
age
gender
ethnicity
CKD classification based on eGFR
1
Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2
60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a
45-59 ml/min, a moderate reduction in kidney function
3b
30-44 ml/min, a moderate reduction in kidney function
4
15-29 ml/min, a severe reduction in kidney function
5
Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
most common cause of glomerulonephritis in children
minimal change disease
causes of minimal change disease
IDIOPATHIC
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
mono
minimal change disease mgt:
PO corticosteroids
diabetes insipidus
what is it?
condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
cranial DI causes
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis
nephrogenic DI causes
genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
diabetes insipidus ix:
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
diabetes insipidus mgt:
nephrogenic diabetes insipidus:
-thiazides
-low salt/protein diet
central diabetes insipidus can be treated with desmopressin
acute interstitial nephritis causes:
drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
acute interstitial nephritis features:
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
ix:
sterile pyuria
white cell casts
iv fluids maintenance requirements:
25-30 ml/kg/day of water
1 mmol/kg/day of potassium, sodium and chloride
50-100 g/day of glucose to limit starvation ketosis
renal a. stenosis
most common cause in:
i. <50
ii. >50
i. fibromuscular dysplasia
ii. atherosclerosis
