Nephrology Gap Flashcards
Raised Anion Gap Metabolic Acidsis
MUDPILES
M Methanol
U Uraemia
D Diabetic ketoacidosis
P Paracetamol
I Isoniazid
L Lactic acid- shock, sepsis, hypoxia
E Ethanol
S Salicylates
also alcohol
Addisons disease causes what type of metabolic abnormality
Normal ANion Gap Metabolic Acidosis
Urine OSM in Acute Tubular Necrosis is —–?
<350 mOsm
(> 500 in pre renal uremia)
Prerenal uraemia - kidneys hold on to sodium to preserve volume
Drugs causing AIN
The Pt with AF needed PRN meds.
Allopurinol
Furosemide
Penicillin
Rifampicin
NSAIDs
Biochemical findings of of AIN
- eosinophilia
- mild renal impairment
Investigations
**- sterile pyuria
- white cell casts
**
Renal Artery stenosis causes pre/renal/post renal AKI?
Pre-Renal
Causes of Intrinsic AKI
- glomerulonephritis
- acute tubular necrosis (ATN)
- acute interstitial nephritis (AIN), respectively
- rhabdomyolysis
- tumour lysis syndrome
Dx criteria for AKI
a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
Drugs that Should be stopped in AKI as may worsen renal function
NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
* Aminoglycosides
* ACE inhibitors
* Angiotensin II receptor antagonists
* Diuretics
Drugs that May have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)
- Metformin
- Lithium
- Digoxin
ADPKD Genetics
Type 1: Chromosome 16
Type 2: Chromosose 4
Two disease loci have been identified, PKD1 and PKD2, which code for polycystin-1 and polycystin-2 respectively
Management of ADPKD
tolvaptan (vasopressin receptor 2 antagonist) may be an option
ADPKD is treated if :
- they have chronic kidney disease stage 2 or 3 at the start of treatment
- there is evidence of rapidly progressing disease and
- the company provides it with the discount agreed in the patient access scheme.
Extra-renal manifestations
Extra-renal manifestations
liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
Commonest extra-renal manifestation of ADPKD
Liver cyst
Alport Presentation
- microscopic haematuria > progressive renal failure
- bilateral sensorineural deafness
- lenticonus: protrusion of the lens surface into the anterior chamber, retinitis pigmentosa
it’s like being on an Airport (similar to ALPORT) in a Plane
- wearing the eye mask so you can’t see
- the toilet is always crowded so you can’t pee
- and you’ve got them ear plugs in while you sleep
Alports Genetics
- X-linked dominant pattern
- It is due to a defect in the gene which codes for type IV - collagen resulting in an abnormal glomerular-basement membrane (GBM).
Renal Biopsy FInding of Alport
characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance
Types of Amyloidosis
AA amyloidosis
AL amyloidosis
Beta 2 microglobulin amyloidosis
Dx of Amyloidosis
Congo red staining: apple-green birefringence
serum amyloid precursor (SAP) scan
biopsy of skin, rectal mucosa, or abdominal fat
Normal ANion Gap
N A R M A L — G=
N Normal anion gap,
A Acetazolamide ,
R Renal tubular acidosis,
M mmonium chloride injections,
A addison disease
GI loss bicarbonate
Anti GBM Renal Biopsy
renal biopsy: linear IgG deposits along the basement membrane
Rx of Goodpasture
plasma exchange (plasmapheresis)
steroids
cyclophosphamide
Goodpasture associated with HLA—?
HLADR2