Documentos de Académico
Documentos de Profesional
Documentos de Cultura
BUBRENO-MOKRANOG
SUSTAVA
angiotenzinogen
angiotenzinogen
renin renin
angiot. I angiot. I
ACE
ACE
angiot. II angiot. II
NaCl/H2o NaCl/H2o
reapsorpcija reapsorpcija
vazokonstrikcija
aldosteron vazokonstrikcija
aldosteron
JGL stanice
Macula densa
Aferentna
arteriola Eferentna arteriola
Baroreceptorski mehanizam: tlak u af.arterioli simpatika stimulacija- Macula densa mehanizam- detekcija koncentracije NaCl u
inhibira otputanje renina iz JG stanica 1 adrenergikih receptora- distalnom kanaliu potie luenje renina
(crvene strelice); otputanje renina (zelene strelice);
tlaka u af.arteriolipotie otputanje renina (zelene strelice) koncentracija NaCl inhibira luenje renina
(zelene strelice) (crvene strelice)
PRERENALNI POREMEAJI BUBRENE
FUNKCIJE
To se postie itakoer oputanjem aferentne arteriole ali i stezanjem
Prerenalnom
eferentne zatajenju bubrega (uzrokovanog poremeajima sustavnog
arteriole
krvotoka) obino prethodi faza pre-prerenalnog zatajivanja bubrega
Oputanje aferentne arteriole se deava autoregulacijom (miogeni refleks i
To je kompenzirana
tubuloglomerularna faza prerenalnog
povratna sprega) zatajivanja u kojoj su odrane
temeljne funkcije bubrega(filtracija, ekskrecija, koncentracija urina)=u njoj
seStezanje eferentne
vri regulacija na arteriole
3 osnovneserazine:
deava pomou lokalno stvorenog
angiotenzina II preko renina i u manjim koncentracijama noradrenalina.
1. Mijenjanje veliine bubrene frakcije
Na teminutnog volumena
naine se poveava srca
kapilarni
tlak u glomerulima to poveava
2. Promjenom
frakciju GF frakcije GF
3. Promjenom frakcije 3. Promjena
tubularne frakcije soli
reapsorpcije
i vode tubularne reapsorpcije
soli i vode
PRERENALNI POREMEAJI BUBRENE
FUNKCIJE
Prerenalnom
Prilikom zatajenju
poveanja bubregatlaka
kapilarnog (uzrokovanog
u poremeajima sistemnog
krvotoka) obino
glomerulima prethodi
poveava faza pre-prerenalnog
se i frakcija filtracije zatajivanja bubrega
To je kompenzirana
Pritom faza prerenalnog
se filtrira uglavnom tekuina bez zatajivanja
proteina, u kojoj su odrane
temeljne
pa funkcije bubrega(filtracija,
koloidno-osmotski ekskrecija, koncentracija urina)=u njoj
tlak u krvi u peritubularnim
se vri regulacija
kapilarama raste, na
a...3 osnovne razine:
Kapilarni tlak u tim1.istim peritubularnim
Mijenjanje veliine bubrene frakcije
kapilarama pada zbog stezanja
minutnogeferentne arteriole
volumena srca
Sve to dovodi do vee reapsorpcije vode i soli
2. Promjenom frakcije GF
3. Promjenom frakcije tubularne reapsorpcije soli
i vode
Nadmai li se kapacitet te filtracijske priuve, pre-prerenalno
zatajenje prelazi u PRERENALNO ZATAJENJE.
GF se poinje smanjivati zbog :
nemogunosti daljnje dilatacije aferentne arteriole i konstrikcije
eferentne arteriole
U odrasla ovjeka bubreni autoregulacijski mehanizmi mogu
kompenzirati smanjenje arteriskog tlaka do oko 80 mmHg
Sve promjene u pre-prerenalnom zatajenju su reverzibilne ako
se normalizira srani min.volumen i arterijski tlak.
U teim cirkulacijskim poremeajima aktivira se simpatikus jo jae i dodatno se
stvara angiotenzin II koji sada sve jae stee aferentnu arteriolu
Smanjuje se GF i zadravaju se duikovi spojevi u krvi ( karbamid i kreatinin,
Na i voda)
Zadravanje duikovih spojeva u krvi= AZOTEMIJA
Zbog smanjene GF i djelovanja hormona nastaje FUNKCIJSKA OLIGURIJA
U kojoj je sastav mokrae tipino promijenjen
Zbog bubrene ishemije otputa se renin, angiotenzin i aldosteron
Zbog poviene osmolarnosti plazme otputa se ADH
Raste osmolarnost mokrae zbog malog protoka filtrata kroz H.petlju te se time
puno vode stigne reapsorbirati (>500 mmol/kg)....zatim nastaje koncentracijski
gradijent koji pogoduje reapsorpciji ureje (ali uz ADH u sab. i dist.kanaliima)
Ureja se pojaano reapsorbira u sabirnim kanaliima te
nastaje smanjen omjer koncentracije urin/plazma ( U/P)
Omjer kreatinina urin/plazma je velik ( >40 mmol/l) iz razloga to se voda
reapsorbira u sabirnim kanaliima te ostane koncentriran kreatinin u urinu, a za
razliku od ureje kreatinin se ne moe reapsorbirati
Zato je omjer plazmatske koncentracije ureje/ kreatinina u plazmi 40:1, a
normalno je 20:1
VANO!!!:::
Daljnje smanjivanje GF e povisiti kreatinin i u plazmi,....to dovodi
Do lano normalnog omjera ureja/kreatinin u plazmi
Koncentracija Na+ je smanjena u mokrai (zbog aldosterona i promjena u
hemodinamici=mali protok zbog smanjene GF uvjetuje potpuniju, odnosno
koliinski veu reapsorpciju Na+) = ekskrecijska frakcija Na+ je oko 1%
Sediment urina je uglavnom normalan jer nema znatnijeg oteenja
bubrega (jedino moda vei broj hijalinih cilindara zbog koncentriranije
mokrae.)
esto su prekriveni debelim slojem amorfnih soli urata ili fosfata koje se dodatkom kapi octene
kiseline otapaju, ili su prekriveni masnim kapljicama.
Njihov manjak u mokrai je povezan sa poveanom uestalou stvaranja kamenaca
RENALNI POREMEAJI BUBRENE FUNKCIJE
Kompleksi antigen-antitijelo nastali negdje drugdje u organizmu
Poremeaji
Antigeni glomerularne funkcije
mogu biti egzogeni (oteenja koja nastaju pokretanjem
i endogeni
upalne reakcije)
Egzogeni: tue bjelanevine kao u serumskoj bolesti i
poststreptokoknom
Najei uzrok suGNimunosni mehanizmi:
(reakcija preosjetljivosti tip III), antigeni
od bakterijskih, virusnih ili parazitnih infekcija kao i nakon nekih
lijekova
1. Nefritisi uzrokovani imunokompleksima: 70%
Endogeni: ulomci DNA, autologni imunoglobulini, tumorski
2.antigeni
Nefritisi uzrokovani cirkulirajuim protutijelima na antigene
i tireoglobulin.
glomerularne membrane 5%
Mali imunokompleksi su skloniji taloenju od velikih koji lake
aktiviraju komplement!!
RENALNI POREMEAJI BUBRENE FUNKCIJE
Poremeaji
Posljedicaglomerularne funkcije
vezivanja protutijela (oteenja
protiv koja nastaju
fiksnih antigena pokretanjem
u samom
upalnemembrane
glomerulu, pogotovo antigena bazalne reakcije)(Goodpastureov sindrom--
reakcija preosjetljivosti tip II--fiksni Ag+ cirkulirajua AT)-to su zapravo
AUTOANTITIJELA
Najei uzrok su imunosni mehanizmi:
1. Nefritisi
Nefritisi uzrokovani
uzrokovanivezanjem protutijela na antigene
imunokompleksima: 70% in situ
ine ih imunosne reakcije na antigene koji nisu sastavni dio glomerula,
2. Nefritisi uzrokovani cirkulirajuim protutijelima na antigene
nego se zadre u mezangiju ili u subepitelnom prostoru
glomerularne membrane: 5%
Egzogeni (virusi hepatitisa B , neki lijekovi) i endogeni (cirkulirajui
DNK antigeni)
Imunokompleksi se mogu smjestiti subepitelno, subendotelno, intramembranski
ili u mezangijskom matriksu.
(PODOCITI)
Filtracijska pora (pukotina, rascjep)
0 Scheme of filtration barrier (blood-urine) in the kidney.
A. The endothelial cells of the glomerulus; 1. pore (fenestra)
B. Glomerular basement membrane: 1. lamina rara interna 2. lamina densa 3.
lamina rara externa
Nephritic syndrome: As with nephrotic syndrome, antigen/antibody complexes are deposited within the slit
pores or within the mesangial artery, but in nephritic syndrome, these complexes evoke a complement based
response.
Nephritic syndrome
It is postulated that MCD is a disorder of T cells, which release a cytokine that injures the glomerular epithelial foot processes. This, in turn, leads to a decreased synthesis of
polyanions. The polyanions constitute the normal charge barrier to the filtration of macromolecules, such as albumin. When the polyanions are damaged, leakage of albumin
follows. The identity of this circulating permeability factor is uncertain, although it is postulated that it may be hemopexin. Hemopexin induces nephrin-dependent
reorganization of the actin cytoskeleton in podocytes.
Membranous glomerulonephritis
Membranous glomerulonephritis may cause either nephrotic or a nephritic picture. About two-thirds are associated with auto-antibodies to phospholipase A2 receptor, but other
associations include cancers of the lung and bowel, infections such as hepatitis B and malaria, drugs including penicillamine, and connective tissue diseases such as systemic
lupus erythematosus. Individuals with cerebral shunts are at risk of developing shunt nephritis, which frequently produces MGN.
Microscopically, MGN is characterized by a thickened glomerular basement membrane without a hyperproliferation of the glomerular cells. Immunofluorescence demonstrates
diffuse granular uptake of IgG. The basement membrane may completely surround the granular deposits, forming a "spike and dome" pattern. Tubules also display the
symptoms of a typical Type III hypersensitivity reaction, which causes the endothelial cells to proliferate, which can be seen under a light microscope with a PAS stain
Prognosis follows the rule of thirds: one-third remain with MGN indefinitely, one-third remit, and one-third progress to end-stage kidney failure. As the glomerulonephritis
progresses, the tubules of the kidney become infected, leading to atrophy and hyalinisation. The kidney appears to shrink. Treatment with corticosteroids is attempted if the
disease progresses.
In extremely rare cases, the disease has been known to run in families, usually passed down through the females. This condition, similarly, is called Familial Membranous
Glomerulonephritis. There have only been about nine documented cases in the world.
IgA nephropathy
IgA nephropathy, also known as Berger's disease, is the most common type of glomerulonephritis, and generally presents with isolated visible or occult hematuria, occasionally
combined with low grade proteinuria, and rarely causes a nephritic syndrome characterised by protein in the urine, and visible blood in the urine. IgA nephropathy is classically
described as a self-resolving form in young adults several days after a respiratory infection. The classic presentation (in 40-50% of the cases) is episodic hematuria which
usually starts within a day or two of a non-specific upper respiratory tract infection (hence synpharyngitic) as opposed to post-streptococcal glomerulonephritis which occurs
some time (weeks) after initial infection. Less commonly gastrointestinal or urinary infection can be the inciting agent. All of these infections have in common the activation of
mucosal defenses and hence IgA antibody production. A smaller proportion (20-30%), usually the older population, have microscopic hematuria and proteinuria (less than 2
gram/day). These patients may not have any symptoms and are only clinically found if a doctor decides to take a urine sample.
Very rarely (5% each), the presenting history is:
Nephrotic syndrome (3-3.5 grams of protein loss in the urine, associated with a poorer prognosis)
Acute kidney failure (either as a complication of the frank hematuria, when it usually recovers, or due to rapidly progressive glomerulonephritis which often leads to chronic
kidney failure)
Chronic kidney failure (no previous symptoms, presents with anemia, hypertension and other symptoms of kidney failure, in people who probably had longstanding undetected
microscopic hematuria and/or proteinuria)
IgA nephropathy is the most common glomerulonephritis worldwide. Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. There are
other diseases associated with glomerular IgA deposits, the most common being Henoch-Schnlein purpura (HSP), which is considered by many to be a systemic form of IgA
nephropathy
Henoch-Schonlein purpura refers to a form of IgA nephropathy, typically affecting children, characterised by a rash of small bruises affecting the buttocks and lower legs, with
abdominal pain.
Post-infectious
Post-infectious glomerulonephritis can occur after essentially any infection, but classically occurs after infection with the bacteria Streptococcus pyogenes. It typically occurs 14
weeks after a pharyngeal infection with this bacterium, and is likely to present with malaise, a slight fever, nausea and a mild nephritic syndrome of moderately increased blood
pressure, gross haematuria, and smoky-brown urine. Circulating immune complexes that deposit in the glomerules may lead to an inflammatory reaction.
Diagnosis may be made on clinical findings or through antistreptolysin O antibodies found in the blood. A biopsy is seldom done, and the disease is likely to self-resolve in
children in 14 weeks, with a poorer prognosis if adults are affected.
Membranoproliferative
Membranoproliferative GN (MPGN), also known as mesangiocapillary glomerulonephritis, is characterised by an increase in the number of cells in the glomerulus, and
alterations in the glomerular basement membrane. These forms present with the nephritic syndrome, hypocomplementemia, and have a poor prognosis. Two primary subtypes
exist:
Type 1 MPGN is caused by circulating immune complexes, typically secondary to systemic lupus erythematosus, hepatitis B and C, or other chronic or recurring infections.
Circulating immune complexes may activate the complement system, leading to inflammation and an influx of inflammatory cells.
Type 2 MPGN, also known as Dense Deposit Disease, is characterised by an excessive activation of the complement system. The C3 Nephritic Factor autoantibody stabilizes
C3-convertase, which may lead to an excessive activation of complement.
PRIMJER: Akutni poststreptokokni GN-
Vrlo esto oboljenje u djece, nastaje 1 -3 tjedna nakon infekcije gornjih
dinih puteva nefritogenim sojevima beta hemolitikog streptokoka grupe
A
Dokaz streptokokne infekcije: M Antitijela, antitijela na enzime bakterije:
streptolizin O, streptokinazu..
Radi se o taloenju imunokompleksa (tip III reakcije preosjetljivosti), kao
u serumskoj bolesti
Umnaaju se endotelne i mezangijske stanice, infiltracija upalnim
stanicama, odlaganje izmeu epitelnih stanica i bazalne membrane
Klinika slika: od vrlo blagih simptoma do slike opasne po ivot
U svom klasinom obliku se manifestira kao akutni nefritiki sindrom
NALAZ URINA KARAKTERISTIAN: hematurija, proteinurija, cilindrurija
(eritrocitni cilindri)
NALAZ KRVI: poviena SE, povieni leukociti i anemija, poviena razina
kreatina i ureje
RTG: moe se nai i pleuralni izljev, EKG je poremeen zbog hiperkalijemije(
smanjena GF)
Imunoloki testovi: najznaajniji je nalaz cirkulirajua At na streptokokne
antigene i snien ukupni komplement i C3 komponenta komplementa
Type 1 is Goodpasture syndrome, an autoimmune disease also affecting the lung. In Goodpasture syndrome, IgG antibodies directed against the glomerular
basement membrane trigger an inflammatory reaction, causing a nephritic syndrome and the coughing up of blood. High dose immunosuppression is required
(intravenous methylprednisolone) and cyclophosphamide, plus plasmapheresis. Immunohistochemistry staining of tissue specimens shows linear IgG deposits.
Type 2 is characterised by immune-complex-mediated damage, and may be associated with systemic lupus erythematosus, post-infective
glomerulonephritis, IgA nephropathy, and Henoch-Scholein purpura.
Type 3 rapidly progressive glomerulonephritis, also called pauciimmune type, is associated with causes of vascular inflammation including Wegener
granulomatosis and microscopic polyangitis. No immune deposits can be seen on staining, however blood tests may be positive for the ANCA antibody.
Histopathology: The majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of
increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of endothelial cells of Bowman capsule, and an influx of
monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and decreases the Bowman space, which leads to kidney failure within
weeks or months.
SEKUNDARNI GLOMERULONEFRITISI
.
Secondary causes of nephrotic syndrome have the same histologic patterns as the primary
causes, though they may exhibit some difference suggesting a secondary cause, such as
inclusion bodies. They are usually described by the underlying cause. Nephritic syndrome is caused by inflammation of glomerulus and
has urine waste, furthermore the cause can be infectious,
Diabetic nephropathy: is a complication that occurs in some diabetics. Excess blood sugar autoimmune or thrombotic. The causes can be divided between
accumulates in the kidney causing them to become inflamed and unable to carry out their normal age groups as follows:
function. This leads to the leakage of proteins into the urine.
Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among Children/Adolescents
them the kidney, due to the deposit of immunocomplexes that are typical to this disease. The
disease can also cause lupus nephritis. IgA nephropathy
Post-streptococcal glomerulonephritis
Sarcoidosis: This disease does not usually affect the kidney but, on occasions, the accumulation Hemolytic uremic syndrome
of inflammatory granulomas (collection of immune cells) in the glomeruli can lead to nephrotic Henoch-Schoenlein purpura
syndrome.
Adults
Syphilis: kidney damage can occur during the secondary stage of this disease (between 2 and 8
weeks from onset).
Goodpasture syndrome
Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage SLE
them. Rapidly progressing glomerulonephritis (RPGNs)
Infective endocarditis
Sjgren's syndrome: this autoimmune disease causes the deposit of immunocomplexes in the
glomeruli, causing them to become inflamed, this is the same mechanism as occurs in systemic
lupus erythematosus.
HIV: the virus antigens provoke an obstruction in the glomerular capillarys lumen that alters
normal kidney function.
Amyloidosis: the deposit of amyloid substances (proteins with anomalous structures) in the
glomeruli modifying their shape and function.
Multiple myeloma: the cancerous cells arrive at the kidney causing glomerulonephritis as a
complication.
Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow
and damages the kidney.
Cancer: as happens in myeloma, the invasion of the glomeruli by cancerous cells disturbs their
normal functioning.
Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein
nephrin, a component of the glomerular filtration barrier, is altered.
Drugs ( e.g. gold salts, penicillin, captopril):gold salts can cause a more or less important loss of
proteins in urine as a consequence of metal accumulation. Penicillin is nephrotoxic in patients with
kidney failure and captopril can aggravate proteinuria.
Nepfrotiki sindrom:
1. Masivna proteinurija
2. Hipoalbuminemija
3. Edem
4. Hiperlipidemija/hiperlipidurija
Nefritiki sindrom:
1. Hematurija
2. Oligurija
3. Azotemija
4. Hipertenzija
5. Oligurija
6. Proteinurija
NEFROTIKI SINDROM
Sastoji se od masivne proteinurije,
hipoalbuminemije, edema,
hiperlipidemije i
hiperkoagulabilnosti.
Membranozna
Proliferacija endotelnih
nefropatija- stanica
zahvaa samo BM
Minimalna
bolest(lipoidna Membranoproliferacijska
Proliferacija epitelnih stanica
nefroza) (ini bolest-obuhvaa BM i
80%nefrotskog mezangij (7%) Proliferacija mezangijskih
sindroma)
stanica
Stvaranje fibrinoida
Edema
KRONINI NEFRITIKI SINDROM
Hipertenzije ILI GLOMERULONEFRITIS
Smanjene GF Definiran kao perzistencija ili progresija izvornog
patolokog procesa
Prisutna je lagano progredijentna bubrena
insuficijencija praena proteinurijom, hematurijom i
hipertenzijom. veinom ima neprimjetan tok s
akutnim pogoranjima i s vremenom prelazi u
ireverzibilno bubreno zatajenje
POREMEAJI GLOMERULARNE FUNKCIJE U
GLOMERULONEFRITISU
Ovisi o stupnju propusnosti glomerularne membrane, nestanku negativno
nabijenih
Mijenja sijaloproteina
se integritet
Zbog smanjene i broju arinih
glomerularnih
povrine napuklina
kapilara
glom.membrane, kapilarneprotoka
zbog smanjenog stijenkekroz
glom.kapilare
Zato
Mijenja (zbogmokrae
umnaanja
u glomerulopatijama
se sastav glomerularnih
moemo stanica,proteinurije,
nai hematurije, intrakapilarnog
lipidurije i
odlaganja
piurije. fibrina..)
Mijenja se veliina GF-e
Gubitkom
Prisutnost proteina
cilindaraurinom
uvijek smanjuje se koliina oteenju
govori o bubrenom plazme u !!osim
cirkulacijskom
hijalinih.
Nastaju
sustavu, a edemi
time i iGF
hipertenzija
I. Faza:
Veliina GF je od 30-50 ml/min
Nema subjektivnih tegoba
Ekskrecijske, biosintetike i regulacijske bubrene
funkcije su odrane
II. Faza:
GF od 15-30 ml/min
Azotemija
Smanjenje koncentriranja urina pa postoji poliurija s izostenurijom
Poetni znakovi zatajenja: anemija i HA
Netolerancija UH (smanjeni metabolizam inzulina), hiperuricemija,
hipertrigliceridemija (smanjena aktivnost lipoproteinske lipaze)
Jo nema subjektivnih tegoba
III. Faza:
Uremija
Kardiovaskularni ,GI , ivani poremeaji
GF oko 10 ml/min
Tea anemija i HA
Povien K+ u krvi, ali bez klinikih oitovanja
Uremija
Opis: Nalaz azotemije i drugih zadranih metabolita u krvi sa
pridruenim odredenim klinickim znakovima, simptomima, te
laboratorijskim abnormalnostima. Uremija je karakterizirana
poremecajem ekskretorne funkcije bubrega, ali i metabolikim i
endokrinim promjenama. Uz to se nalaze i sekundarne
gastrointestinalne (npr. uremicni gastroenteritis), kardiovaskularne
(npr. uremicni fibrozni perikarditis) i neuromuskularne (npr. periferna
neuropatija) promjene koje zajedno cine uremini sindrom.
IV. Faza:
Terminalna uremija
GF manja od 5 ml/min
Uremiki sindrom (odstranjuje se samo hemodijalizom)
WBC + granular
VOTANI
WBC + RBC
Najei uzroci bubrene hematurije: glomerulonefritis, tubulointersticijska
oteenja i vaskulitisi
Izvanbubrena krvarenja: ureter, mokrani mjehur, prostata, uretra
Pri ozljedama uretre: krv u poetnom mlazu
Pri anomalijama kod trigonuma: krv u zavrnom mlazu
Stalna prisutnost krvi: krvarenje iz bubrega, mokraovoda ili mokranog
mjehura
Hematurija + leukociturija (piurija) ili ista piurija= infekcija (sa potvrdom
od >105 bakterija/ml)
Ako u obinoj urinokulturi nema bakterija: moe se raditi o TBC
Umjerena leukociturija u kombinaciji sa hematurijom, proteinurijom i
cilindrurijom: bubrene bolesti kao akutni glomerulonefritis i nefrotiki
sindrom
Sediment urina u piuriji (neutrofili), ponekad eozinofili-alergijski intersticijski
nefritis ili limfociti- u fazi odbacivanja presatka
Epitelne stanice: iz tubula, pelvisa, uretera, mjehura, uretre i vagine, a jedino su
bubrene stanice dijagnostiki vane.
Siguran dokaz bubrenog oteenja: epitelne stanice u obliku cilindara (akutna
tubularna nekroza, glomerulonefritis, pijelonefritis, nefrotiki sy)
Cilindri- odljevi tubula pa su uvijek bubrenog podrijetla
Svi uglavnom imaju Tamm-Horsfalov mukoprotein podrijetlom stanica iz
uzlaznog dijela H.p. i distalnih tubula
Kristali u sedimentu: stvaranje ovisi o zasienosti mokrae sastojcima koji ine
kristale, prisutnosti ili odsutnosti inhibitora kristalizacije, o mokranom pH koji
utjee na topivost kristala i ionski sastav kristala.
KALCIJ-OKSALATNI KRISTALI BILIRUBINSKI URINI KRISTALI
KRISTALI
Cilindrurija
Bakteriurija: >10 5/ ml bakterija u urinu se smatra znaajnim
1. ODREIVANJE BUBRENIH KLIRENSA
Klirens neke tvari je volumen plazme koji se prolaskom kroz bubrege u
jedinici vremena oisti od te tvari
FORMULA:
klirens plazme (ml/min) = volumen mokrae (ml/min) x konc. tvari u
mokrai/ konc. tvari u plazmi
U svrhu procjene bubrenog klirensa obino se rabi klirens kreatinina
Kreatinin se filtrira i malo secernira u proksimalnim tubulima ali to ne
utjee na konaan rezultat (viak za 10-20%) , ali se pogreka ponitava
zbog greke mjerenja kreatinina u plazmi.
Rez Jedin
Analiza Referentni raspon
ultat ice
Bilirubin neg konv.
Urobilinogen norm konv.
Ketoni neg konv.
Askorbinska
konv.
kiselina
Glukoza neg konv.
Proteini neg konv.
Eritrociti 0-5 konv.
pH 5-7 konv.
Nitriti neg konv.
Leukociti 0-5 konv.
Specifina teina 1.015 1.025 konv.
Cardiac
Inhibits maladaptive cardiac hypertrophy
Mice lacking cardiac NPRA develop increased cardiac mass and severe fibrosis and die suddenly
[7]
Re-expression of NPRA rescues the phenotype.
It may be associated with isolated atrial amyloidosis.[8]
Adipose tissue
Increases the release of free fatty acids from adipose tissue. Plasma concentrations of glycerol and
nonesterified fatty acids are increased by i.v. infusion of ANP in humans.
Activates adipocyte plasma membrane type A guanylyl cyclase receptors NPR-A
Increases intracellular cGMP levels that induce the phosphorylation of a hormone-sensitive lipase
and perilipin A via the activation of a cGMP-dependent protein kinase-I (cGK-I)
Does not modulate cAMP production or PKA activity
Correlation of Urine Color
Color or Appearance Possible Cause
OBAVEZNO
RAZLIKOVATI:
"protustrujni
umnoiva" (dogaaji u
sustavu tubula)
"protustrujni
izmjenjiva" (vasa
recta)