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
Goodpasture is caused by
It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen.
ARPKD Genetics
It is due to a defect in a gene located on chromosome 6 which encodes fibrocystin, a protein important for normal renal tubule development.
Monitoring for BPH other than PSA
- urinary frequency-volume chart: should be done for at least 3 days
- International Prostate Symptom Score (IPSS)
Rx of BPH
- Alpha Blocker eg: Tamsulosin, alfuzosin
- 5 alpha-reductase inhibitors e.g. finasteride: block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH
also,
- combination of 1 and 2
- if there is a mixture of storage symptoms and voiding symptoms that persist after treatment with an alpha-blocker alone, then an **antimuscarinic (anticholinergic) drug such as tolterodine or darifenacin **may be tried
- Surgery (TURP)
Adverse effects of Tamsulosin
dizziness, postural hypotension, dry mouth, depression
Adverse effects of Finasteride
erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia
Risk factors for bladder cancer:
Squamous cell
Transitional cell/Urothelial
- Risk factors for Urothelial (transitional cell) carcinoma of the bladder include:
- **Smoking: most important risk factor in western countries. **hazard ratio is around 4
- Exposure to aniline dyes: for example working in the printing and textile industry. examples are 2-naphthylamine and benzidine
- Rubber manufacture
- Cyclophosphamide - Risk factors for squamous cell carcinoma of the bladder include:
- Schistosomiasis
- Smoking
Which acute phase reactant has a role in development of IDA in CKD patients
Hepcidin
Hb Target for CKD
10-12
MDRD equation for CKD considers:
CAGE
serum creatinine
age
gender
ethnicity
Factors that may affect GFR calculation
PMR
- pregnancy
- muscle mass (e.g. amputees, body-builders)
- eating red meat 12 hours prior to the sample being taken
GFR Clock
VUR is diagnosed based on —– inv?
VUR is normally diagnosed following a micturating cystourethrogram
Thin basement membrane disease —— collagen disease
type IV collagen that causes thinning of the basement membrane
(This Basement Membrane Disease: 4 words- type 4 collagen)
First line inv for Testicular Cancer
USS
—— is elevated in Seminomas
hCG
—— is elevated in Non-seminoma
AFP and/or beta-hCG
WHO classification for SLE
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
Most common for SLE
Class IV (diffuse proliferative glomerulonephritis) is the most common and severe form
Biopsy findings of class 4 lupus
glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
if severe, the capillary wall may be thickened secondary to immune complex deposition
electron microscopy shows subendothelial immune complex deposits
granular appearance on immunofluorescence
Management of Renal Stone
Renal stones (Rule of 5,10,20)
- watchful waiting if < 5mm and asymptomatic
- 5-10mm shockwave lithotripsy
- 10-20 mm shockwave lithotripsy OR ureteroscopy
> 20 mm percutaneous nephrolithotomy
Uretic stones (Rule of 10, 20)
- < 10mm - shockwave lithotripsy +/- alpha blockers
- 10-20 mm ureteroscopy
IgA Nephropathy presents as
young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients
Hyperacute rejection is —- type hypersentivity.
cause by Ig___?
Type 2
IgG
Types of HLA and their importance
class 1 antigens: include A, B and C
Class 2 antigens: include DP,DQ and DR
when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A
Idiopathic membranous glomerulonephritis is related to ——- antibodies
Idiopathic membranous glomerulonephritis is related to anti-phospholipase A2 antibodies
Membranous GN Renal Biopsy Finding
Renal biopsy demonstrates:
electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance
Aldosterone M/A
where does it work
Spironolactone is an aldosterone antagonist which acts in the cortical collecting duct.
Causes of renal papillary necrosis
POSTCARDS:
- pyelonephritis
- obstruction of the urogenital tract
- sickle cell disease
- tuberculosis
- cirrhosis of the liver
- analgesia/alcohol abuse
- renal vein thrombosis
- diabetes mellitus
- systemic vasculitis
IVU finding of Papillary necrosis
IVU findings:
‘PAP’illary - ‘CUP’
PILLarry - ‘SPILL’
IVU - papillary necrosis with renal scarring - ‘cup & spill’
Hallmark of MAHA
Schistocytes (RBC fragments): Hallmark of MAHA.
Coombs test is +/- in MAHA?
Negative
Primary or Atypical HUS occurs due to
Primary HUS (‘atypical’) is due to complement dysregulation.
Causes of Typical/Secondary HUS
Most cases are secondary (termed ‘typical HUS’):
- classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7
‘verotoxigenic’, ‘enterohaemorrhagic’
this is the most common cause in children, accounting for over 90% of cases
- pneumococcal infection
- HIV
- rare: systemic lupus erythematosus, drugs, cancer
Renal Biopsy findings of Minimal change disease
- normal glomeruli on light microscopy
- electron microscopy shows fusion of podocytes and effacement of foot processes
Rx for steroid resistant Minimal change disease
cyclophosphamide is the next step for steroid-resistant cases
IgA Nephropathy good prognosis
markers of good prognosis: frank haematuria
IgA Nephropathy poor prognosis
- male gender
- proteinuria (especially > 2 g/day)
- hypertension
- smoking
- hyperlipidaemia
- ACE genotype DD
Conditions when there is low complement level
‘CLUMPS’
Cryoglobulinemia (Think when RF elevated)
Lupus
Membranoproliferative GN
Post Strep GN
Subacute Bacterial Endocarditis
common causes of Nephrotic Syndrome in adults
- either Membranous or focal segmental
Biopsy finding of FSGS
focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy
In a patient with hypercalciuria and renal stones, calcium excretion and stone formation can be decreased by the use of —– drugs
Thiazide diuretics
M/A of drugs used in Prostate cancer Rx
Goserelin
Bicalutamide
Cyproterone
Abiraterone
Goserelin==> GnRH agonist
Anti- Androgens: A==>B==>C
First Sythensis Blocker, then Receptor Bloker
A==> Abiraterone==> Synthesis blocker
B==>Bicalutamide==>Receptor blocker
C==>Cyproterone==> Receptor blocker
N.B. any terone, means Steroidal, so CyproTerone==> Steroidal
Bicalutamide==> Non-steroidal
HIV causes what type of kidney involvement
focal segmental glomerulosclerosis
renal biopsy
focal and segmental sclerosis and hyalinosis on light microscopy/ with focal or global capillary collapse on renal biopsy
effacement of foot processes on electron microscopy
All Biopsy findings:
Minimal change
FSGS
Minimal change
FSGS
NICE guideline for referral re hematuria
Urgent referral (i.e. within 2 weeks):
Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection
Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
Non-urgent referral;
Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection
Lab Findings for DI
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
Inv of choice for DI
Water deprivation Test
Central DI treated with
central diabetes insipidus can be treated with desmopressin
Nephrogenic DI treated with
nephrogenic diabetes insipidus
thiazides
low salt/protein diet
Drugs causing Nephrogenic DI
lithium (lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts)
demeclocycline
Which one is preferred? ACR or PCR
ACR
When should ACR be repeated
if the initial ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested.
Organ transplanted pts have an increased risk of —- cancer due to immunosuppresants
Patients who have received an organ transplant are at risk of skin cancer (particularly squamous cell carcinoma) due to long-term use of immunosuppressants, also BCC.
They should minimize sun exposure
Tac can cause
- hypertension
- hyperlipidaemia
- impaired glucose tolerance and diabetes
Indications of Plasma Exchange
Plasma exchange indications:
Gillian’s Good MATCH
- Guillain-Barre syndrome
- Goodpasture’s syndrome
- Myasthenia gravis
- ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
**- TTP/HUS - Cryoglobulinaemia
- Hyperviscosity syndrome e.g. secondary to myeloma/ HUS**
Epididymo orchitis RX
ceftriaxone 500mg intramuscularly single dose, plus doxycycline 100mg by mouth twice daily for 10-14 days
Renal Stone Types
Easy to remember: O-P-U-X
O - Oxalate
P - Phosphate
U - Urate
X - Xanthine
(OP-OPaque & UC- lUCent)
Cystine - Semi-opaque
The most common genetic mutation causing nephrogenic diabetes insipidus affects ——– ?
The most common genetic mutation causing nephrogenic diabetes insipidus affects the arginine vasopressin V2 receptor (AVPR2) on chromosome Xq28
FSGS is seen in —- drug users
Heroin
How does alcohol cause Polyuria?M/A
Alcohol bingeing can lead to ADH suppression in the posterior pituitary gland subsequently leading to polyuria
Which mutations can cause Nephrogenic DI
Nephrogenic diabetes insipidus may be caused genetic mutations:
the more common form affects the vasopression (ADH) receptor
the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
Hyperacute graft rejection is a type —- rejection
occurs due to?
due to pre-existing antibodies against ABO or HLA antigens
an example of a type II hypersensitivity reaction
Hyper acute- 2 words- therefore type 2 reaction
Acute graft failure is cell/antibody mediated?
Acute graft failure (< 6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
Fibromascular dysplasia presentation
Young female
hypertension
Asymmetric kidneys
chronic kidney disease or more acute renal failure e.g. secondary to ACE-inhibitor initiation
‘flash’ pulmonary oedema
NICE recommended drugs for overactive bladder
antimuscarinic drugs should be offered if symptoms persist. NICE recommend
- oxybutynin (immediate release)
- tolterodine (immediate release)
- Darifenacin (once daily preparation)
Daily requirement of Na, K , Water and Glucose
they suggest the following requirements per 24 hours:
Sodium - 1mmol/kg
Potassium - 1 mmol/kg
Water - 30ml/Kg
Glucose - 50-100g
Which Biochemical findings cause Nephrogenic DI
hypercalcaemia
hypokalaemia
M/A
GOserelin
Degarelix
GOserelin–> (a)GOnist
Degarelix is the opposite.
Goserelin > Go
DeGarelix > Don’t Go
Angiographic finding of FMD
FMD is more common in young women and characteristically has a ‘string of beads’ appearance on angiography.
Aldosterone vs Renin in
- RAS
- Liddle’s Syndrome
- Primary Hyperaldosteronism
plasma aldosterone/renin ratio
-BOTH high ? > renal artery stenosis
-both low ? > liddle’s syndrome (Liddle’s syndrome = L = LOW for both )
-high aldosterone and renin is low : primary hyperaldosteronism
Prevention of renal stones
Prevention of renal stones
Calcium stones:
- potassium citrate may be beneficial NICE
- thiazides diuretics (increase distal tubular calcium resorption)
Oxalate stones (OPC)
- cholestyramine reduces urinary oxalate secretion
- pyridoxine reduces urinary oxalate secretion
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
Uric acid allopUrinol, Urinary alkalinization
Goserelin should be co-prescribed with—
Anti-androgen treatment such as cyproterone acetate should be co-prescribed when starting gonadorelin analogues due to the risk of tumour flare.
Messangiocapillary GN is associated with
mesangioCapiLLary- hep C, Cryoglob, Lipodystrophy with T1 as c’s are first and T2 L is second
type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy
