Renal Flashcards
Cranial causes of DI
Idiopathic Head injury Pituitary surgery Histiocytosis X Craniopharyngiomas DIDMOAD
Nephrogenic DI causes
Genetic - ADH receptor mutation (AQP mutation)
Electrolytes - hypercalcaemia, hypokalaemia
Drugs - demeclocycline, LITHIUM
Tubulointerstitial disease - obstruction, sickle cell, pyelonephritis
DI Ix
High plasma osmolality (concentrated)
Low urine osmolality (dilute)
Urine osmolality >700 excludes DI
Water deprivation test
ADPKD genes
PKD1>2 (ch16 vs 4)
One is more common and presents earlier with renal failure
ADPKD USS criteria in those with pos FHX
Two cysts ( uni or bilateral) if <30
Two cysts in both kidneys if 30-59
Four cysts in both kidneys if >60
ACR sample collection rules
First pass morning sample
If 3-70 repeat, if >70 no need to repeat
Referral to a nephrologist
ACR >70 (unless known diabetic and already appropriately treated)
ACR >30 + persistent haematuria after UTI excluded (2/3 show >1+)
Consider if ACR 3-29 plus persistent haematuria and other RFs - declining eGFR, cardiovascular disease
HTN in CKD
First line
GFR <45
ACEi - esp good in proteinuric renal disease diabetic
At this point furosemide is useful, added benefit of lowering serum K
ACEi acceptable Cr and GfR changes
GFR decrease 25%
Cr rise 30%
Bladder TCC RFs
Smoking
Aniline dyes
Rubber manufacture
Cyclophosphamide
Bladder SqCC RFs
Schistosomiasis
Calmette-Guerin (BCG Rx)
Smoking
Goodpastures/anti GBM biopsy
Linear IgG deposition
Against type IV collagen
HLA DR2 associated
Anti GBM Mx
Plasmapheresis
Steroids
Cyclo
Alports mutation
Inheritance
Demographics
Type IV collagen
X linked dominant
More severe in males
Alports features
Microscopic haematuria Progressive renal failure Bilateral sensorineural deafness Lenticonus - protrusion of lens surface into anterior chamber Retinitis pigmentosa
Alports bx results
Renal Bx result- splitting of lamina densa on EM
Features of Diabetic nephroptathy
Thickened GBM Mesangial expansion Kimmelstein-Wilson nodules Disruption of podocytes (Glycation of basement membrane of efferent arteriole -> glomerular pressure -> dilation of afferent arteriole -> further inc in pressure -> hyperfiltrarion ( inc in GFR)
Diabetic nephropathy stage 1
Hyperfiltration (inc GFR)
May be reversible
Diabetic nephropathy stage 2
Silent /latent
GFR remains elevated , not yet developed microalbiminuria
Stage 3 diabetic nephropathy
Incipient
Microalbuminuria 30-300 mg/day, dipstick neg
Diabetic nephropathy stage 4
Overt nephropathy
Histology
Persistent proteinuria - albumin excretion >300mg/day, dipstick pos
HTN
Likely present
Histology - diffuse glomerulisclerosis and focal (Kimmelstein Wilson)
Stage 5 diabetic nephropathy
ESRF - GFR < 10
Needs RRT
Renal stones - calcium oxalate
Freq
Radiolucency
40%
Opaque
Renal stones - mixed calcium oxalate, phos
Freq
Radiolucency
25%
Opaque
Renal stones - triple phosphate
Freq
Radiolucency
10%
Opaque
Renal stones - calcium phosphate
10%
Radiolucency
10%
Opaque
Renal stones- urate stones
Freq
Radiolucency
5-10%
Radiolucent
Renal stones - cystine
Freq
Radiolucency
1%
Semi opaque, ground glass
Renal stones - xanthine
Freq
Radiolucency
<1%
Radiolucent