Tables Flashcards by fernanda moraes

Na transport in the tubules

PCT - 60%
LOH - 30%
DCT - 7%
CD - 2-3%

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Proximal tubule Na transporters

A: Cl/IOH, NHE3
B: NaKATPase, KCC3/4

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LOH Na transporters

A: NKCC2, ROMK, Claudin
B: NaKATPase, KCC4, ClC-NKB

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DCT Na transporters

A: NCC, NHE2, ROMK, HCO0/Cl; ENac, ROMK
B: NaKATPase, ClCK-2, Kir, KCC4

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K transport in tubules

DCT 65%
TAL 25%

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Ca transport in tubules

PCT 70% → Ca transport proximal tubule paracellular, TRPV5, V6

TAL 20% → Clauding 16, 19
DT 8%

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Mg transport tubules

PT 20%
TAL 70% paracellular 16, 19
DT 5%

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Mg transport DCT

TRPM6/7

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Phos transport proximal tubule

NaPiIIa/IIc

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Bicab reabsorption tubules

PT 80% A: NHE3, AQP1
B: NBce1, NaKATPase
TAL 15%
CD 5%

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DCT Type A intercalated cell Hco3 reabsorption

A: HKATPase, HATPase
B: kAE1, KCC4, Clc-2-K-Barttin

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DCT Type B Intercalated cell Hco3 reabsorption

A: Cl/HCO3, NDCBe, HKATPase
B: HATPase, Clc-K2, AE4

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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

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Chronic lesions in SLE

GIFT - Glomerular sclerosis, Interstitial fibrosis, fibrous crescents, tubular atrophy

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Acute lesions in SLE

Fibrinoid necrosis, cellular crescents karyorrhexis, endocapillary hypercellularity, subendothelial deposits, wireloop lesions, rupture of GBM

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Treatment of SLE Class II

proteinuria >3g, steroids + CNI

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Class 3 SLE Treatment

Corticosteroids + cyclophosphamide/MMF

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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

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Class V SLE treatment

corticosteroids + cyclophosphamide, CNI, MMF, azathioprine

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1st line initial therapy in SLE

cyclophosphamide or MMF

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Maintenance therapy in SLE

AZA or MMF

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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

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Cause of hypercalcemia: High PTH, Uca less than 100 mg/24h, FeCa < 0.01

FHH, NSHPT, Lithium

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Cause of hypercalcemia: High PTH, UCa>200 mg/24h, FeCa> 0.01

primary or tertiary hyperparathyroidism

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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: 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

Cause of hyperK: TTKG\>8

advanced kidney failure; dec ECV

HyperK: TTKG \<5, TTKG \<8 after fludrocortisone

drugs

HyperK: TTKG \<5, TTKG \> 8 after fludrocortisone, low aldosterone, low renin

DM, GN, NSaids, b-blockers

HyperK: TTKG \<5, TTKG \> 8 after fludrocortisone, low aldosterone, high renin

AI, ACE, Ketoconazole

HypoK: UrineK \< 15 mmol/day, 15 mmol/g/Crea, metabolic acidosis

GI K losses

HypoK: Urine K \< 15 mmol/day, 15 mmol/g/Crea, Normal acid base

profuse sweating

HypoK: Urine K \< 15 mmol/day, 15 mmol/g/Crea, Metabolic alkalosis

remote diuretic use, vomiting

HypoK: Urine K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, low/normal BP/volume, Metabolic acidosis

RTA

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, low/normal BP/volume, Metabolic alkalosis, UCl\>20, UCa/Crea \<0.15

Gitelman

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, low/normal BP/volume, Metabolic alkalosis, UCl\>20, UCa/Crea \> 0.20

Bartter Syndrome

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, low/normal BP/volume, Metabolic alkalosis, UCl \< 10

extrarenal losses

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, high BP/volume, Low aldosterone, normal cortisol

Liddle, licorice, AME

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, high BP/volume, low aldosterone, high cortisol

Cushing syndrome

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, high BP/volume, High aldosterone, Low Renin

PA, GRA

HypoK: Urnie K \> 15 mmol/day, 15 mmol/g/Crea, TTKG \>4, high BP/volume, high aldosterone, high renin

RAS, Malignant hypertension

Metabolic alkalosis, UCl\> 20, UK \> 30, HTN, low renin

primary hyperaldosteronism

Normal or micronodularity and B masses in Adrenal CT

idiopathic hyperaldosteronim vs GRA

Unilateral hypodense nodule \> 1 cm in Adrenal CT, \> 40 years old, with no lateralization

GRA screening

Unilateral hypodense nodule \> 1 cm in Adrenal CT, \> 40 years old, with lateralization

adrenal adenoma, primary adrenal hyperplasia

Unilateral hypodense nodule \> 1 cm in Adrenal CT \< 40

adrenal adenoma, PAH

Hyponat, hypovolemic, UNa \< 30

Extrarenal losses NAURINARIO \>30= DIURETICOS , DEFICIENCIA MINERALOCORTICOIDE

Hyponat, euvol, UNa\>30

glucocorticoid deficiency, hypothyroidism, SIADH

Hyponat, Hypervol, UNa \< 30

Nephrotic syndrome, cirrhosis, heart failure \>30 nsuf renal

Metabolic alkalosis, UCl \< 2o

nonrenal

Met alk, UCl\>20, UK \< 30 meq

laxative

Met alk, UCl\>20, UK \> 30 meq, normal BP

Barter, Gitelman, Diuretics

Met alk, UCl\>20, UK \> 30 meq, high BP, high renin, high cortisol

cushing syndrome

Met alk, UCl\>20, UK \> 30 meq, high BP, high renin, normal cortisol, high renin in renal vein

renovascular htn. JGA tumor

Met alk, UCl\>20, UK \> 30 meq, high BP, high renin, normal cortisol, normal renin in renal vein

malignant hypertension

Met alk, UCl\>20, UK \> 30 meq, high BP, low renin

primary aldosteronism, licorice

Chains involved in alport syndrome

A3.4.5

chains involved in tbmd

a3,4

a chains in anti-gbm

a3 chain

Tx of MCD

corticosteroids (pred 1 mld or 3 mkd for 4-6 weeks) cycophosphamide 2-2.5 mkd for 8 weeks cylosporine 3-5 mld tacrolimus 0.05 - 1 mld for 1-2 years MMF 500-1000 mg BID 1-2 years

Tx FSGS

prednisone \> 4-16 weeks CNI 4-6 months MMF + dexamethasone

Tx MN

IV/oral steroids + cyclophosphamimde cyclosporine/tacrolimus

MPGN Type 1

oral cyclophosphamide/MMF low dose alternate day or daily corticosteroids \< 6 months

AntiGBM tx

steroids + cyclophosphamide + plasmapharesis

Pauci Immune Tx

MPP 7 mkd then pred 1 mkd for 1st month then alternate day 4-5 months; oral pred 2 mkd; cyclophosphamide rituximab + corticosteroids + plasmapharesis maintainance: azathioprine 1-2 mkd, MMF 1 g BID, methotrexate 0.3 mk/week

Predictors of Likely failure of fluid restriction in Hyponatremia

UOsm \> 500, UNa + UK \> Serum Na, 24H Urine vol \< 1500 ml/day, Inc in serum Na \<2 in 24 hours on fluid restriction \< 1 L/day

Acute rejection Banff

Glomerular inflammation, Interstitial inflammation, Vascular inflammation, Tubulitis

Chronic rejection Banff

Interstitial fibrosis, Tubular atrophy, allograft glomerulopathy (GBM duplication), Mesangial matrix increase, Arterial fibrointimal thickening, Arterial hyalinosis, peritubular capillary

HSP Class Subtypes

Class I: Minimal alteration Class II: Pure mesangial proliferation Class IIIa: Focal \<50% crescents Class IIIb: Diffuse \< 50% crescents Class IVa: Focal 50-75% Crescents Class IVb: Diffuse 50-75% crescents Class Va: Focal \> 75% crescents Class Vb: Diffuse \> 75% crescents Class VI Membranoproliferative

RPGN Types

Type I: Anti-GBM Type II: Immune complex Type III: Pauci-immune Type IV: Type I + III Type V: Anca negative, pauci immune renal vasculitis

DM Classification

Class I: GBM thickening Class II: Mesangial expansion Class IIa: mild Class IIb: severe CLass III: Nodular sclerosis Class IV: Advanced DM sclerosis

Factors increasing risk of osmotic demyelination

Serum Na \< 105 Hypokalemia Alcoholism Malnutrition Advanced Liver Disease

simple benign cyst

Bosniak Cat I

benign with thin septa. fine rim like calcification or uniform high density less than 3 cm

Bosniak Cat II

multiple septa thick area or nodular calcification high density ctsts \> 3 cm follow up at 6-12 mos

Bosniak Cat IIF

thickened irregular walls with enhancement, dense irregular calcficiation

Bosniak Cat III

clearly malignant nephrectomy \<5-6 cm

Bosniak Cat IV

absolute contraindications to renal biopsy

uncontrolled htn bleeding diathesus cystic disease hydronephrosus uncooperative patient

Bartter Syndrome Type 1

NKCC2

Bartter Syndrome Type 2

ROMK

Bartter Syndrome Type 3

CLC-Kb

Bartter Syndrome Type IV

Bartin (B subunit of Clc-Ka and Clc-Kb

Bartter Syndrome Type V

Clc-Ka and Clc-Kb