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Nefrologia PT > Nephrolithiasis > Flashcards

Nephrolithiasis Flashcards

1
Q

dietary factors that lead to nephrolithiasis

A

low fluid intake, calcium, K
high oxalate, protein, Na, sugar drinks

hipercalciuria= droga =tiazidicos-diminuir proteina, sodio, acucar e ingesta de calcio adequada

hiperoxaluira-diminuir a ingestao de oxalato, aumentar a ingesta de calcio,evitar vitamina c- piridoxina

hiperuricosuria= evitar purinas= inibidor da xantila oxilase

hipocitraturia= citrato de k, diminuir a ingesta de proteina, aumentar ingesta de frutas e vegetais

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2
Q

Inhibitors of stone formation

A

magnesium

, citrate

, pyrophosphate→retards the crystal growth of CaP and CaOx crystals by binding to the surface of basic CaP crystals

THprotein

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3
Q

acts as both promoter and inhibitor of stone formation THProtein

A

THProtein

Tamm-Horsfall protein and uromodulin are two names for the same gene.

Casts only form in the distal tubule & collecting duct, not in the proximal tubule. What is its function?

  1. Tamm-Horsfall protein acts as a constitutive inhibitor of calcium-based stone formation. Mice deficient for Tamm-Horsfall protein show an increased tendency towards nephrolithiasis.
  2. Tamm-Horsfall protein acts to prevent urinary tract infection. There is some data that certain strains of E. coli may be bound by Tamm-Horsfall protein; once cleaved this could represent a means of eliminating the organism from the urinary tract.
  3. Mutations in Tamm-Horsfall protein cause the autosomal dominant disorder medullary cystic kidney disease type 2 (MCDK2) as well as the disorder familial juvenile hyperuricemic nephropathy (FJHN) . This is a pediatric-onset disease characterized by hyperuricemia, gout, and progressive renal failure. Interestingly it appears that the pathophysiologic mechanism here is that mutations in this gene lead to defects in protein folding and intracellular deposition of mutant Tamm-Horsfall protein.
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4
Q

metabolic processes that induce ca stone formation

A

Increase urine ca >250-300 mg/day;

Urine Uric acid > 800 mg/day

, urine oxalate > 45 mg/d

, hipocitraturia < 320 mg/day;

alterations in urine ph

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5
Q

most common metabolic abnormality in ca stone formation

A

absorptive hypercalciuria

most common cause of resoprtive hypercalciuria primary hyperparathyroidism

uso de tiazidicos se hipercalciuria >200

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6
Q

clinical conditions with hypocitraturia

A

overproduction acidosis,

underexcretion acidosis

K deficiency

excess dietary protein

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7
Q

inflammatory bowel disease, jejunoileal bypass, bariatric surgery for morbid obesity

A

enteric hyperoxaluria

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8
Q

predispose to caphos lithiasis

A

alkaline urine (pH > 6.7)

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9
Q

most impt in uric acid stones

A

low urine pH

Uric Acid crystals

Precipitate in acid urine • Pleomorphic,rhombic plates or rosettes. • Seen under polarised light • Hyperuricemia • Diabetes mellitus • Metabolic syndrome • Acute uric acid nephropathy • Chronic uratenephropathy • Familial Juvenile Hyperuricemic Nephropathy (Medullary Cystic Kidney disease

Alkalinization of urine—urine pH is most important risk factor for uric acid stones – Potassium citrate or bicarbonate – Patient follow urine pH (aim for ~6.5 or higher

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10
Q

patients with gouty arthritis and kidney stones, UA > 10 md/d, urine ua > 1000 mg/day

A

hyperuricosuria

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11
Q

Increases saturation of all stone forming elements

A

low urine volume

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12
Q

Pathophysio of uric acid stones

A

Low urine pH, volume
Hyperuricosuria

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13
Q

genetic disease caused by inactivating mutations of the subunits of a dibasic aminoacid transporter in then proximal tubule

A

cystinuria

family hx of cystinuria (> 400 mg/day vs 30 mg), staghorn calculi, hexagonal crystals on urinalysis

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14
Q

most prevalent component of kidney stones

A

calcium oxalate

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15
Q

most likely cause of nephrolithiasis in a patient with distal RTA

A

hypocitraturia

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16
Q

depressions near the papillary tips, yellow crystalline deposits in the ducts of bellini, some randall plaques

A

Calcium phosphate

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17
Q

1st kidney stone work up

A

medical hx, stone analysis, urine analysis

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18
Q

Recurrent kidney stone

A

full metabolic evaluation - serum panel, PTH, VitD if hyperCa, 24ag urine >= 2 samples Na Ca Oxalate Uric acid citrate

calcio, citrato, oxalato, sodio, creatinina,acido urico

Complete Metabolic Evaluation for Nephrolithiasis

Blood

Serum calcium (if elevated, suggests primary hyperparathyroidism or other cause of hypercalcemia)Serum electrolytes (low total CO

2

raises the possibility of distal RTA)

Urine

Urinalysis—urine pH >7 with phosphate crystals in the urine sediment suggests calcium phosphate or struvite stones (struvite stones have a typical coffin-lid appearance); hexagonal cystine crystals arediagnostic of cystinuria; other crystals (calcium, uric acid, indinavir, etc.) may suggest etiology of stones24-hour urine collection(s) for urine stone risk diagnostic profile. This test is now standardized in mostclinical laboratories, with most using a reference laboratory that provides a graphical display of results(seeFig. 20

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19
Q

indicative of minimal fluid intake

A

urine volume less than 2.5L

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20
Q

pH with increase risk of uric acid precipitation, idiopathic uric acid stone, intestinal disease and diarrhea and intestinal bypass surgery

A

less than 5.5

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21
Q

Increase risk of caphos precipitation, dRTa, primary hyperparathyroidism, alkali, ca tx

A

pH > 6.7

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22
Q

pH that indicates urinary tract infection fom urease producing bacteria

A

> 7-7.5

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23
Q

Normal UCrea

A

F: 15-20 mk
M: 20-25 mk

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24
Q

reflects dietary Na and K intake

A

24H urine Na and K

O valor obtido em mEq/24h deve ser dividido por por 17 (Já que 1 g de NaCl corresponde a 17 mEq de sódio, dividimos o resultado por 17 para obter a quantidade em gramas de NaCl consumido no dia).

3- O KDIGO (Kidney Disease Improving Global Outcomes) de Hipertensão e Doença renal crônica, recomenda a ingestão < 2g de Sódio ou 5 gramas de NaCl por dia.

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25
Q

Major cause of hypercalciuria

A

High Na intake

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26
Q

Normal Urine Na K Ca

A

Na 100 K 40-60 Ca < 250-300 mg

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27
Q

Low Mg increases risk of

A

calcium stones

(UMg <30-120 mg)

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28
Q

Higher Uphos > 1100 mg

A

calcium phosphate formation

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29
Q

hyperuricosuria, Uuric acid > 600-800

A

CaOx stones Uph > 5.5
Uric acid stones UpH <5.5

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30
Q

marker of dietary acid intake

A

sulfate

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31
Q

high ammonium/sulfate ratio

A

GI alkali loss

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32
Q

Normal Urine NH4

A

30-40 meq

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33
Q

Petsistent high Uca on a restricted diet

A

intestinal hyperabsorption of Ca

34
Q

Elevated fasting Ca/Crea (0.11 mg/100 ml or <2.7 umil/100 mg), high serum calcium, elevated pth

A

primary hyperparathyroidism

35
Q

Elevated Ca/Crea, normal serum Ca, normal or suppressed PTH

A

resoprtive hypercalciuria

36
Q

elevated Ca/Cr, normal Ca, elevated pth

A

Renal hypercalciuria

37
Q

Elevated Ca/Cr (0.2 mg/mg or 0.56 mmol/mmol) 4h Ca/Crea after 1 g oral load

A

absorptive hypercalciuria

38
Q

dumbless shaped crystals

A

calcium oxalate monohydrate

39
Q

Envelope shaped crystals

A

calcium oxalate dihydrate

40
Q

Flat shaped or wedge shaped prisms, often in rosettes

A

Calcium phosphate

41
Q

Gold standard for kidney stone diagnosis

A

noncontrast ct
un enhanced ct scan
ct stonogram

42
Q

time when surgical intervention is indicated

A

4 weeks

43
Q

average days of stone passage

A

40 days

44
Q

medical expulsive therapy

A

tansulosina, doxasozina

indicacoes-> calculo maior que 0,5 e menor q 1,0 em ureter distal

sem infeccao, sem insuf renal, sem dor

calculo menor q 1cm

expulsoiu? nova imagem 1 mes apos

45
Q

target fluid intake

A

Urine volume > 2.5L
cystinuria > 4L water intake

46
Q

Dietary mgt

A

Na < 100 meq/day
animal protein 50-60 g/day
Ca 1000-1200 mg
avoid > 1g Vit C
Fruits/vegetables

47
Q

Drug of choice hypercalciuria in caOx and Caphos stone formers

A

Thiazides 25 bid

48
Q

Tx hypocitraturia in caox and caphos, uric acid stones, cystine stones

A

20-80 meqs 3-4 doses
uric acid: pH goal > 6, cysteine pH > 7,

49
Q

inhibits caox crystal formation and growth binding with oxalate

A

Magnesium

50
Q

Treatment Ca stone formers with hyperuricosuria

A

Allopurinol 100-300 mg/d

51
Q

Struvite stones when other interventions have failed

A

acetohydroxamic acid 15 mkd

52
Q

first line therapy for uric acid stone formers

A

Urine alkalinization

53
Q

tx of choice struvite stones, impacted stone; largest stone free rate and less recurrenfe rate

A

percutaneous nephrolithotomy

54
Q

hexagonal stones- tx

A

Cystine, tiopronin

penicillamine

thiola captopril

treatment • Reduce [cystine] < 250mg/L • Increase fluid intake? – Urine output > 5 L/d • Tiopronin (“Thiola”) – Typically need at least 900 mg/d (300 mg TID) •

Continue alkalinization= bic ou citrato de k= alvo ph 7,7 7,5

RESTRICAO DE SODIO E PROTEINA ANIMAL

55
Q

coffin lid like

A

struvite

56
Q

uric acid stones are

A

pleomorphic

nao da pra ver na radiografia

57
Q

calculo de estruvita

A

são chamados de “cálculos de infecção” e são compostos por uma mistura de magnésio, amônia, fosfato e carbonato de cálcio. Alguns tipos de bactérias formam amônia, elevam o pH, deixando a urina mais alcalina e promovendo a formação de estruvita.

bacterias produtoras de urease= proteus, klebsiella,

cirurgia

58
Q

hiperoxaluria primaria

autosomal recessive condition in childhood with CaOx stones and nephrocalcinosis, frequent stone recurrence

A

disturbio do metabolismo hepatico do oxalato

demais funcoes hepatocelulares=normais

achados= osseos, coracao, tecidos e sangue

nefrolitiase, nefropatia por oxalato de calcio (nefrocalcinose) e drc

o q agrava= hipovolemia, inibidor do sraa, uso de diuretico, aumento da ingesta de OXALATO, use de antiinflamatorios alguns antibioticos

tipo1 = tx de figado e rim

tipo2 =tx renal

tipo3 =nao requer tto

autosomal recessive condition in childhood with CaOx stones and nephrocalcinosis, frequent stone recurrence

59
Q

UOxalate > 100 mg/day

A

primary hyperoxaluria

60
Q

hiperoxaluria secundaria

A

aumento da abs intestinal de oxalato= nao absorve a gorduta , normal o oxalato se liga ao calcio e sai pelas fezes, quando tem muita gordura = se liga ao calcio e deixa o oxalato livre para ser absorvido

cirurgia bariatrica

y de roux

by pass jejunoileal

doença inflamtoria intestinal

aumento da ingestao de oxalato

excesso de vitamina c

fibrose cistica /insuf pancreatica/

61
Q

hiperoxaluria

A

>0,5 enterica= calcio 1 a 2g , depende da excrecao de oxalato + agnesio 200-400mg/dia

>1,0mmol /dia = primaria= piridoxima 5-20mg/kg/dia

novas drogas oxalobacter

lumasiram /nedosiram

individuals likely to form oxalate stones due to hyperoxaluria have a relative deficiency of the gut bacterium Oxalobacter formigenes, part of the normal GI flora which naturally digest oxalate.

62
Q

hiperoxaluria

A

aumentar ingesta hidrica= >2-3L/dia

dieta com pouco oxalato

dieta pobre em gorduras

calcio normal , suplemento decalcio

colestiramina= absorve sair biliares e o oxalato

oxalobacter formigens

63
Q

calculos de indinavir

A

nao da pra ver no exame de imagem

64
Q

composicao dos calculos frequencia

A

Calcium oxalate 60

Calcium oxalate and phosphate 10

Calcium phosphate 10

Magnessium, ammonium phosphate(struvite)5-10

Uric acid5-10

Cystine1Others1

Crystalline composition of renal calculi & their frequency

65
Q

análise fisica do calculo

A

difracao do rx

espectrocopia de infravermelho

microscopia eletronica

66
Q

Urease producing bacteria are associated with the formation of?

A

Magnesium ammonium phosphate stone (Struvite).

.Struvite (magnesium ammonium phosphate) stones are typically largestones associated with urease producing bacteria and an alkaline urine4

. Ureabreakdown produces excess ammonium and hydroxyl ions, a rise in urinary pH,and a decrease in phosphate solubility thus encouraging the precipitation of insoluble magnesium ammonium phosphate

Common bacteria producing urease

Proteus

Haemophilus

Pseudomonas

Klebsiella

Yersinia

Staphylococcus epidermidis

Citrobacter, Serratia and UreaplasmaurealyciumNote: E.coli does not produce urease

67
Q

oxalato de calcio

A

Calcium oxalate dihydrate – enveloped shaped crystals

Calcium oxalate monohydrate – dumbbell, spindle shaped crystals

The mainstain of treatment of calcium oxalate stones is to increase fluid intake to reach the goal of at least 2 L of urine output per day.

A reduction in calcium excretion by a low sodium diet (80-100 meg/day) may also be suggested.

Low sodium excretion will enhance proximal sodium and calcium absorption, thereby decreasing urinary calcium excretion and stone formation.

Drug therapy can also be added depending on the cause. If there is hypercalciuria, thiazide diuretics may be helpful.

Potassium citrate can be used in cases of hypocitraturia and type 1 renal tubular acidosis.

For hyperuricosuria, treatment of choice would be allopurinol or potassium citrate.

oxalato de cálcio

aumentar ingesta hidrica

diminuir ingesta de sal

tiazidico

citrato se hipocitraturia

68
Q

Crystals

A

Presence & type of crystals is determined by urine concentration, constituents, inhibitors, pH etc4

Important drugs/toxins:

– Acyclovir (needle shaped)

– Sulphonamide antibiotics (variable, needle shaped/rosettes) –

Ethylene glycol (calcium phosphate)

– High dose Vit C (calcium oxalate)

– Methotrexate (rarely seen, variable) –

Indinavir (needle shaped)

– Phosphate laxatives (calcium phosphate

69
Q

estruvita

A

Triple phosphate crystals- estruvita

• Magnesium ammonium phosphate • Struvite • ‘Coffinlid’shapedcrystals • Seeninalkalineurine • Associatedwithinfectionwithurea-splitting organisms

70
Q

types of Stones and Cause

A

Calcium oxalate—low urine volume, low citrate, high calcium, high oxalate

  • Calcium phosphate—alkaline urine, high calcium, low urine volume, low citrate
  • Uric acid—persistently acid urine
  • Cystine—autosomal recessive disorder
  • Struvite—urease producing bacteria
71
Q

exames

A
  • Hypercalciuria – Males: > 300 mg/d – Females: > 250 mg/d – Either: > 4 mg/kg/d
  • Hyperoxaluria: > 45 mg/d • Hyperuricosuria – Males: > 800 mg/d – Females: > 750 mg/d
72
Q

epidemiologia nefrolitiase

A

Kidney stones (nephrolithiasis) will occur in 12% of men and 5% of women during their lifetime. 1 em cada dez pessoas apresentara

The major types of stones are calcium (70%-80%, oxalate more common thanphosphate), uric acid (5%-10%), cystine (<1%), and magnesium ammonium phosphate (struvite) (10%).Combined calcium/urate stones are also often seen

A patient with a calcium-containing stone episode has anoverall 50% chance of recurrence within 10 years, which is higher for men than for women. Some patients willhave many recurrent stones, leading to substantial morbidity, medical costs, and even mortality

73
Q

avaliacao do pac

A

historia clinica, ocupacao, antecedentes de litiase, antecedente familiar,

sindrome metabolica, uso de medicacoes, dieta, ingesta de sal e agua

infeccoes urinarias

74
Q

exames na uergencia

A

hemograma= ureia, creat, na , k, calcio, acido urico, pcr, urina rotina , urocultura

75
Q

analgesia

A

dipirona

paracetamol ,

aines

opioides

76
Q

abordagem urologica

A

urgencia= sepse, crise algica, recorrencia da dor, questoes de trabalho, dificuldade de manejo pos alta,solicitacao do pac, calculos ureterai >1cm

eletiva= calculos ureterais>15mm

77
Q

baixa evidencia clinica

A

escopolamina para manejo da dor

bloqueador alfa para calculo renal ou calculo menor 1 5 mm

bcc

corticoide

78
Q

dent disease

A

is a rare, X-linked inherited disease of pediatric nephrology. It can be filed under the category of “renal tubular dysfunction” and is also known as “X-linked Recessive Nephrolithiasis.”

Clinical characteristics of Dent Disease include recurrent renal stones, nephrocalcinosis, hypercalciuria, low molecular weight proteinuria, and a gradual progression to ESRD, usually within childhood.

The disease is caused by mutations in the gene CLCN5, a chloride channel present in proximal tubular cells which appears to be necessary for the processing of endosomes. It is not clear why these individuals are so predisposed to nephrolithiasis and hypercalciuria. There is no good therapy for Dent Disease, though a logical case could be made for treating with oral citrate supplementation and thiazide diuretics in an attempt to mitigate hypercalciuria and delay the nephrocalcinosis-induced renal failure as much as possible.

79
Q

dent disease

A

is a rare, X-linked inherited disease of pediatric nephrology. It can be filed under the category of “renal tubular dysfunction” and is also known as “X-linked Recessive Nephrolithiasis.”

Clinical characteristics of Dent Disease include recurrent renal stones, nephrocalcinosis, hypercalciuria, low molecular weight proteinuria, and a gradual progression to ESRD, usually within childhood.

The disease is caused by mutations in the gene CLCN5, a chloride channel present in proximal tubular cells which appears to be necessary for the processing of endosomes. It is not clear why these individuals are so predisposed to nephrolithiasis and hypercalciuria. There is no good therapy for Dent Disease, though a logical case could be made for treating with oral citrate supplementation and thiazide diuretics in an attempt to mitigate hypercalciuria and delay the nephrocalcinosis-induced renal failure as much as possible.

80
Q

drpad

A

Patients with ADPKD are predisposed to nephrolithiasis. The postulated reasons for this increased prevalence of stone disease have ranged from metabolic abnormalities (previous reports have shown an increased tendency for hyperoxaluria, hypercalciuria, hypocitraturia, hyperuricosuria, and distal RTA) to anatomic abnormalities (large, obstructing cysts and dilated tubular lumens may create a situation of tubular stasis, which predisposes to stone formation).

81
Q

rim em ferradura= fusao dos polos inferiores

A

litiase em 60%

risco de neop renal e infeccao

has renovascular

82
Q

avaliacao ambulatorial por exames

A

solicitacao de exames

: hemograma, gaso,

funcao renal, sodio, k,

calcio, fosforo, PTH, glicemia, acido urico, lipidograma e magnesio.

solicitacao de exames de urina=

urina pH , densidade / urocultura com TSA

ca u > 250-300

oxalato>40

citrato<340

acido urico >750-800

pesquisa qualitativa de cistina na urina positiva

Nefrologia PT (112 decks)

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