Nephrology Flashcards
ADPKD 1 and 2
Which is more common
Chrm?
ADPKD 1
Chrm 16 ADPKD 1
Chrm 4 ADPKD 2
Screening investigation of choice for ADPKD
Diagnostic criteria
<30
30-59
>60
US abdominal
two cysts, unilat or bilat <30
two cysts both kidney 30-59
four cysts in both kidneys >60
Mx ADPKD (1) on (3) conditions
Tolvaptan
IF
CKD stage 2 or 3 at start of treatment
AND
Evidence of rapidly progressing disease
AND
Company provides it with agreed discount
Features of ADPKD (6)
HTN
Recurrent UTIs
AP
Renal stones
Haematuria
CKD
Extra renal manifestations of ADPKD (4)
Liver cysts
Berry aneurysms
Mitral valve prolapse
Cysts in other places
What is Alport’s syndrome?
Inheritance
Gender
X linked dominant
Defect in gene coding for type IV collagen resulting in an abnormal GBM
M>F (more severe in male)
Features Alport’s syndrome (5)
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus (protrusion of the lens surface)
Retinitis pigmentosa
Renal biopsy for Alport’s syndrome (2)
Longitudinal splitting of lamina densa of GBM
Basket weave appearance
MDRD uses what four variables for eGFR
Age
Serum creatinine
Gender
Ethnicity
Factors which can impact the eGFR (3)
Pregnancy
Muscle mass
Eating red meat 12 hours prior to sample being taken
CKD eGFR 1-5
Classification
1 >90 with some sign of kidney damage
2 60-90
3a 45-59
3b 30-44
4 15-29
5 <15
CKD
Mineral bone disease management (4)
Reduced dietary intake of phosphate
Phosphate binders
Vitamin D
Parathyroidectomy
ACR interpretation
3-70 repeat sample
If >70 then no repeat sample needed
Must be a first pass morning urine
If >3 then clinically important proteinuria
When to refer to nephrologist for CKD? (2)
Consider if (1)
- If ACR >70 (unless caused by DM)
- If ACR >30 with persistent haematuria
Consider if
ACR 3-29 with persistent haematuria and other RF
Mx of proteinuria (2)
- ACE inhib if co-existent HTN and CKD if ACR >30
- If >70 then ACE inhib even if no raised BP
Visible haematuria
Loin pain
Proteinuria
=
Renal papillary necrosis
Post Strep GN
Which bacteria?
Typically occurs when?
Prognosis
7-14 days post group A beta haemolytic strep infection (Strep pyogenes)
Good prognosis
Post Strep GN features (6)
Young children
Proteinuria more than haematuria
HTN
Oliguria
Low C3
Raised ASO titre
IgA nephropathy features (3)
Develops 1-2 days post URTI
Young males
Macroscopic haematuria
Renal biopsy post strep GN
Granular/ starry sky
IgA nephropathy associated conditions (3)
Alcoholic cirrhosis
Coeliac
Henoch-Schonlein purpura
IgA nephropathy histology
Mesangial hypercellularity
IgA nephropathy prognosis
Markers for good prognosis (1)
Poor prognosis (5)
25% have ESRF
Frank haematuria
- Male
- proteinuria >2g/day
- HTN
- Smoking
- Hyperlipidaemia
Henoch Schonlein purpura overlaps with?
Features (4)
IgA nephropathy
Features:
1. Palpable purpuric rash over buttocks and extensor surface of arms and legs
2. AP
3. Polyarthritis
4. Features of IgA nephropathy e.g haematuria
HSP prognosis
What two things should be monitored?
How many relapse?
Self limiting
Very good prognosis
BP and urinalysis should be monitored
1/3 have a relapse
Minimal change disease
Causes (5)
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis
Difference between nephrotic and nephritic syndrome
Nephritic syndrome is a condition involving haematuria, mild to moderate proteinuria (typically less than 3.5g/L/day), hypertension, oliguria and red cell casts in the urine
Nephrotic syndrome is a condition involving the loss of significant volumes of protein via the kidneys (proteinuria) which results in hypoalbuminaemia. The definition of nephrotic syndrome includes both massive proteinuria (≥3.5 g/day) and hypoalbuminaemia (serum albumin ≤30 g/L).
Cranial versus nephrogenic DI
Cranial - decreased secretion of ADH
Nephrogenic - insensitivity to ADH
Causes of cranial DI (4)
Idiopathic
Post head injury
Pituitary surgery
Haemochromatosis
What is DIDMOAD?
the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
Causes of nephrogenic DI (4)
Genetic
Hypercalcaemia
Hypokalaemia
Lithium
Ix DI
High/low plasma osmolality high/low urine osmolality
A urine osmolality of what excludes DI
What other investigation can be done?
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
Diabetes insipidus mx (2)
Central DI can be treated with? (1)
Thiazides
Low salt/ protein diet
Desmopressin
Nephrotic syndrome examples (4)
Minimal change
Membranous GN
FSGM
Diabetic nephropaathy
Nephritic syndrome examples (3)
Rapidly progressive GN
IgA nephropathy
Alport syndrome
Most common cause of GN in children
Minimal change
Causes of transient non visible haematuria (4)
UTI
Menstruation
Vigorous exercise (settles after 3 days)
Sexual intercourse
Which drugs can cause red/orange urine? (2)
Rifampicin
Doxorubicin
How do you define persistent non visible haematuria?
Blood being present in 2 out of 3 samples tested 2-3 weeks apart
Who should be referred under the 2 week wait?
=>45yo with unexplained visible haematuria w/o UTI
OR
visible haematuria that persists after successful treatment of UTI
OR
>= 60yo with unexplained non visible haematuria AND dysuria/ raised WCC
Who should get a non urgent referral to urology regarding haematuria?
> =60yo with recurrent or persistent unexplained UTI
Minimal change prognosis
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
Minimal change mx (2)
steroids
cyclophosphamide
Minimal change
Features (3)
BP
Nephritic or nephrotic
Normotension
Nephrotic syndrome
Highly selective proteinuria
Minimal change
Renal biopsy
Light microscopy (1)
Electron microscopy (1)
normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes
