Tables Flashcards
Na transport in the tubules
PCT - 60%
LOH - 30%
DCT - 7%
CD - 2-3%
Proximal tubule Na transporters
A: Cl/IOH, NHE3
B: NaKATPase, KCC3/4
LOH Na transporters
A: NKCC2, ROMK, Claudin
B: NaKATPase, KCC4, ClC-NKB
DCT Na transporters
A: NCC, NHE2, ROMK, HCO0/Cl; ENac, ROMK
B: NaKATPase, ClCK-2, Kir, KCC4
K transport in tubules
DCT 65%
TAL 25%
Ca transport in tubules
PCT 70%
TAL 20%
DT 8%
Ca transport proximal tubule
paracellular, TRPV5, V6
Ca transport TAL
Clauding 16, 19
Mg transport tubules
PT 20%
TAL 70%
DT 5%
Mg transport TAL
paracellular 16, 19
Mg transport DCT
TRPM6/7
Phos transport proximal tubule
NaPiIIa/IIc
Bicab reabsorption tubules
PT 80%
TAL 15%
CD 5%
Proximal tubule HCO3
A: NHE3, AQP1
B: NBce1, NaKATPase
DCT Type A intercalated cell Hco3 reabsorption
A: HKATPase, HATPase
B: kAE1, KCC4, Clc-2-K-Barttin
DCT Type B Intercalated cell Hco3 reabsorption
A: Cl/HCO3, NDCBe, HKATPase
B: HATPase, Clc-K2, AE4
IgA: predictive of ESKD or 50% decline in GFR
Mesangial hypercellularity, tubular atrophy./interstitial fibrosis
IgA: not predictive
endocapillary hypercellularity
IgA: predictive of rate of decline in kidney function
segmental sclerosis
Chronic lesions in SLE
GIFT - Glomerular sclerosis, Interstitial fibrosis, fibrous crescents, tubular atrophy
Acute lesions in SLE
Fibrinoid necrosis, cellular crescents karyorrhexis, endocapillary hypercellularity, subendothelial deposits, wireloop lesions, rupture of GBM
Treatment of SLE Class II
proteinuria >3g, steroids + CNI
Class 3 SLE Treatment
Corticosteroids + cyclophosphamide/MMF
Class IV SLE treatment
Azathioprine 1.5-2.5 mkd
MMF 1-2 g/day
low dose steroids
or CNI if intolerant to aza and MMF
Class V SLE treatment
corticosteroids + cyclophosphamide, CNI, MMF, azathioprine
1st line initial therapy in SLE
cyclophosphamide or MMF
Maintenance therapy in SLE
AZA or MMF
Class 3 or 4 initial therapy options for cyclophosphamide
IV 0.5-1 g/m2 monthly for 6 months, 500 mg q2 weeks for 3 months, 1-1.5 mkd po 2-4 months
Cause of hypercalcemia: High PTH, Uca less than 100 mg/24h, FeCa < 0.01
FHH, NSHPT, Lithium
Cause of hypercalcemia: High PTH, UCa>200 mg/24h, FeCa> 0.01
primary or tertiary hyperparathyroidism
Cause of hyperCa: low PTH, low PTHRP, high 25(OH), high 25 (OH)2
Vitamin D overodse
Cause of hyperCa: low PTH, low PTHrP, low 25 (OH), high 25 (OH)2
Granulomatous disorders
Cause of hypercCa: low PTH, low PTHrp, low 25 (OH) and 25 (OH)2
LOH, milk alakali syndrome, immobilization, vitamin A, Drugs
Cause of hyperca: Low PTH, high PTHrP
HHM
Cause of hypoca, High crea
renal failure
Cause of hypoca: Normal Crea, Low PTH
hypoparathyroidism, low Mg, genetic
Cause of hypoca: Normal Crea, High PTH, Low Vitamin D
Vitamin D deficiency
Cause of hypoca: Normal Crea, high PTH, normal vitamin D, Normal 1, 25 (OH)2D
pseudohypoparathyroidism, Vit D dependent rickets
Cause of hypoca: Normal Crea, high PTH, normal vitamin D, High 1, 25 (OH)2D
Vit D resistant rickets