Review II Blok Uropoetika

7/28/2019 Review II Blok Uropoetika

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REVIEW BLOKSYSTEMA UROPOETIKA

dr. Zainuri SN

GINJAL Struktur dan Fungsi

Beberapa fungsi ginjal :1. Eliminasi produk sisa2. Kontrol keseimbangan cairan dan elektrolit3. Kontribusi keseimbangan asam basa.

Ginjal memproduksi beberapa hormon:1. Renin mempengaruhi tonus vaskuler dan tekanan darah2. Erythropoetin meningkatkan produksi eritrosit3. 1,25 dihydroxy vitamin D meningkatkan absorbsi calsium di usus dan menjaga mineralisasi

tulang

GlomerulusGlomerulus tersusun dari invaginasi anyamankapiler, derivat dari arteriola afferen, ke dalamcapsula bowman merupakan awal dari tubulusproximal. Glomerulus merupakan filter yang

sangat efisien dengan permukaan luas dikontrololeh struktur yang terdapat pada kapilerglomerulus itu sendiri.

Ada 2 tipe sel mesangial :1. Contractile smooth muscle

cells mengatur alirandarah.

2. Sel fagosit (macrophage) ingesti protein dankompleks immun.

Ketiga lapisan di atas mengatur permiabilitas glomurular. Pori-pori endotelium yang lebar memungkinkansemua komponen mencapai membrana basal (basement membran).

Membrana basal memilikikekuatan anion (negatif)sangat kuat yang menolakprotein plasma melewatinya(juga anion). Lapisan ini jugamemiliki lamina densa.

Sel-sel epitel menempelpada membrana basal olehkaki-kaki processus,dipisahkan oleh gapdiametrer 30-60 nm.


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Filtrat glomerular adalah cairan bebas proteinplasma.Pengaruh beberapa faktor mempengaruhi urineoutput. Penurunnan jumlah urine dapatdisebabkan oleh penurunan aliran darah ke ginjalmisalnya pada keadaan syok dandehidrasi.Sedangkan peningkatan urine output dapat

disebabkan oleh hemokonsentrasi, atau akibatobstruksi aliran keluar urine.

Tubulus r enalis

Tubulus renalis mengubah filtrat glomerulus. Diawali dengan filtrat yang isotonik dan netral, menjadi

hipertonik dan sangat asam. Dalam 24 jam, 180 liter filtrat dirubah menjadi 1,5 liter urine melalui tigamekanisme yaitu:

1. Absorbsi akti fterhadap substansi dari filtrat oleh epitel tubular2. Difusi pasifantara filtrat dan jaringan intertisial untuk memelihara keseimbangan osmotik3. Sekresi oleh epitel tubuler

Penting:Reabsorbsi aktif membutuhkan energi; dan memiliki proses dengan kapasitas terbatas dikenal

sebagai kapasitas tubuler maksimal (Tm). Bila kapasitas max. terlampui, partikel tertentu (glukosa,dll)akan ditemukan di urine.Pengasaman urine ion H, diekresi lewat tubulus distal, menyebabkan 3 reaksi penting:

1. H + HCO3 = H2CO32. H + NH3Cl = NH4Cl3. H + HPO4 + Na = NaH2PO4

Proses reaksi di urine diatas menghasilkan urine yang bersifat asam.

I. AcidProducingDieta. Body buffers minimize pH due to H+; kidneys recycle HCO3 & excrete H+b. Tubular Acidification

i. 90% of HCO3 (4300mEq/day) absorbed in PCT => slight pHii. lowest pH occurs in collecting ducts, where H+ is actively secreted

iii. min pH = 4.5-5.0iv. excess H+ secreted as weak acids (titrated) and ammonium

c. Bicarbonate Reabsorptioni. Early Proximal Tubulehigh capacity, reabsorbs most filtered HCO3

1. HCO3 from lumen moves into cells; IC carbonic anhydrase converts CO2 H+ + HCO3

a. H+ secreted to tubule lumenb. HCO3 reabsorbed w/ Na+ w/o changing luminal pH

ii. Late Proximal Tubulehigh capacity, generates new bicarbonate1. CO2 from bloodmoves into cells, where carbonic anhydrase breaks it down

=> NEW HCO3!!

a. H+ secreted to tubule lumen, where it combines w/ weak acids(AW-) => HAW

b. HCO3 reabsorbed w/ Na+


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2. small drop in luminal pH: 7.4 6.8iii. Collecting Ductlow capacity, but can generate large pH gradients

1. proton pumps secrete H+ into lumen2. large drop in luminal pH: 6.8 4.53. CO2 from bloodcontinues to move into cells, where carbonic anhydrase

breaks it down => NEW HCO3!! to blood stream

d. Ammonia (NH4+)

i. Strong acids are broken down and excreted as ammonia (NH4+) and A-NH3 + H+ NH4+

1. NH3 readily diffuses thru cell membranes, NH4+ is less permeable2. Ammonia generated from glutamine breakdown in mitochondria;

also generates a-ketogluterate => new HCO3 production!Glutamine 2NH4+ + a-ketoglutarate 2HCO3-

e. H+ Secretion & Excretioni. Net H+ excretion = titratable acidity + NH4+

1. only refers to amount of H+ ion eliminated from body in urine2. only net H+ excretion generates new HCO3

ii. Total H+ secretion = HCO3 reabsorption + titratable acidity + NH4+f. Summary:

i. HCO3 reabsorption in PCT (over 90%)ii. Creation of new HCO3 in PCT via 1) CO2 & H2O during addition of H+ to conjugate

bases of weak acids, 2) production of ammonia

iii. In CCD, H+ secretion & HCO3 production continue, NH4+ becomes trapped in lumenby low pH

II. BaseProducingDieta. Urine is alkaline b/c excess base is secreted

b. Differences from Acid-producing dieti. Reduced reabsorption of HCO3 by PCT

ii. No titration of weak acidsiii. Decreased production of NH4+

iv. Secretion of HCO3 by collecting ducts

Acidosis will stimulate kidneys to generate lots of NH3 to buffer H+ in the lumen. Once it becomes NH4+ it

cannot diffuse back into cells and is stuck in the lumen and will be excreted.

NH3 is the main acid buffer in the urine.

Metabolic alkalosis is the generation or excess reabsorption of HCO3. Like acidosis, this doesnt actually

imply a change in pH. So in metabolic alkalosis or acidosis,pH may be normal. Changes in actual pH arecalled alkalemia and acidemia.

In metabolic alkalosis, HCO3 rises, and then CO2 rises (respiratory compensation). HCO3, CO2, and pH

all increase.

In respiratory alkalosis, CO2 and HCO3 both decrease. So HCO3 and pH move oppositely

Metabolic Acidosisexcess production of keto-acids => IC, EC, & urine pH => compensation for acid

by lungs & kidneys

Metabolic Alkalosisloss of H+ => IC & urine pH => compensation by ventilation rate

Manifestasi klinis Kerusakan tubuler.Kerusakan tubulus menyebabkan perubahan biokimia darah dan urine.

1. Hilangnya mekanisme kontrol terhadap keseimbangan elektrolit, air, dan urea2. Perubahan keseimbangan asam-basa

3. Hilangnya substansi ysng seharusnya diabsorbsi total: glukosa, kalium, dan asam amino.

PENYAKIT GLOMERULAR

Kerusakan glomerulus umumnya menimbulkan gejala:1. Penurunan urine output2. Proteinuria3. Hematuria

Patomekanisme:

Endotelium bengkak aliran darah urin output.

Inflamasi permeabilitas membran proteinuria


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Kerusakan/kehilangan epitelium dan endotelium proteinuria dan hematuria.

Penyakit glomerular umumnya muncul dalam bentuk 3 syndrom klinik, yaitu:1. Syndroma nefritik khas bila dijumpai proteinuria moderat, hematuria, oedema, oliguria, dan

sering timbul gangguan renal. Hipertensi sering menyertai gangguan jenis ini.2. Syndroma nefrotik khas menunjukkan gejala proteinuria berat hipoalbuminemia

oedema.

3. Renal Failure biasanya tipe GGK.

Clinical feature Nephrotic Nephritic

Renal Function normal renal function impaired renal function

Proteinuria >3.5 grams per day whites, 1 and 2 forms, hematuria and HTN assoc, nonselective proteinuria,recurs in allografts, variable progression to ESRD

Pathology: name says it all + IgM & C3 on IF + morphological variants as follows

- Early/recurrent: podocyte effacement, possible adhesion of GBM to capsule- Classic: segmental sclerosis with perihilar hyalinosis

- Collapsing glomerulopathy: plus podocyte hyperplasia

- HIV nephropathy: tubuloreticular inclusions, cystic tubular dilation- Tip lesion: sclerosis opposite hilum, foam cells; may be more benign

Pathogenesis: epithelial cell injury, as well as circulating factor, glomerular HTN, glomerular

hypertrophy, hyperlipidemia, viral infection

Rx: plasmapheresis (early treatment key), steroids often ineffective

Membranous glomerulopathy

Clinical: more common in adults, idiopathic and 2 forms, no consensus on therapyPathology:

Thickened capillaries, perhaps with basement membrane spikes

IF: granular IgG and C3EM: subepithelial deposits, podocyte effacement

Pathogenesis: immune complex deposition; Ag is unknown (idiopathic), or microbial, drugs,tumor, or autoimmune

Diabetic nephropathy

Clinical: multistage progression beginning with GFR, microalbuminuria indicates incipientdisease, poor prognosisPathology

Mesangial thickening, possibly Kimmelstiel-Wilson nodules

Hyalinosis: arteriolar and/or capsular droplet

EM: thick basement membranePathogenesis: glomerular HTN, hypertrophy, glycosylation of matrix/GBM proteins with

decreased degradation, genetic predisposition


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Glomerular Pathophysiology

The glomerular filtration barrier is made up of:1. Endothelial cells of the glomerular capillaries, which prevent passage of cells but not

macromolecules.

2. BM (made of collagen) prevents passage of large proteins. It is negatively charged!

3. Epithelial podocytes form filtration slits that are the finest barrier and prevent even

small proteins.

GFR

The rate of GFR is determined by Starling forces.

GFR = LpS(Pgc Pbs gc) = Kf(Pgc Pbs gc) = Kf(Puf)

where Lp is capillary wall permeability, S is surface area, and Kf is the filtration coefficient.(Pgc Pbs gc) is the net filtration pressure and is simplified to Puf.

The largest drop in renal circulation pressure occurs across the afferent/efferent arterioles.

The Kf of the glomerulus is 100x that of normal capillaries, to allow high filtration.

The Kf is dramatically decreased with inflammation of the glomerulus.

GFR is controlled most by altering the glomerular capillary pressure and thus P uf.

Constriction of afferent arterioles or dilation of efferent arterioles reduces Pgc.

Dilation of afferent arterioles or constriction of efferent arterioles increases Pgc.

The renal plasma flow (RPF) will be reduced with any increase in vascular tone, whether it be

afferent or efferent. Constriction of afferents reduces both RPF and GFR, whereas

constriction of efferents reduces RPF but increases GFR.

resistancevascularrenal

pressurevenousrenal-pressureaorticRPF =

Factors that affect arteriolar tone:

--Angiotensin II

--Intrinsic myogenic control--tubuloglomerular feedback (TGF)

--NE, which constricts both afferents and efferents, thus decreasing GFR.

--prostaglandins, which dilate afferents and efferents, and which are inhibited by NSAIDS.

Autoregulation

1. Renin-AGT-Aldosterone system activates when blood pressure or volume drops. JGA in the macula

densa release renin in response to low volume. Renin cleaves angiotensinogen to AGT-1, which is

converted by ACE to AGT-II. AGT-II and aldosterone both increase tubular sodium reabsorption to boostvolume. AGT-II is a systemic vascoconstrictor, but it constricts efferents more than afferents. This is to

maintain normal GFR at a lower volume.ACE inhibitors decreases AGT-II, thus decreasing BP and Pgc.

ADH is not a first-line effectorfor correcting blood volume. With small fluctuations in

pressure it doesnt change much. With a 10-15% BP drop, ADH suddenly shoots up

exponentially. This will help maintain volume butsacrifices normal osmolality because itreabsorbs water without sodium.

2. Intrinsic myogenic control. Normal vascular smooth muscle contracts when it is stretched, so

increased BP should increase both RBF and GFR. But myogenic control causes afferentarteriole to respond more strongly to stretch, which normalizes RBF and GFR.

3. Tubuloglomerular feedback. The JGA is part of the TAL of the nephron and is in contact with

efferents/afferents. The macula densa is a patch of the TAL that causes granular cells of these arterioles


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to secrete renin. Tubuloglomerular feedback is the JGA control over GFR and RBF. Increased GFRcauses increased Na+ at the macula densa. Macula densa releases adenosine, causing constriction of the

afferent arteriole and decreasing GFR.

If GFR always increased proportionally with BP, too much sodium would enter kidney, and

sodium and water would be wasted. So tubuloglomerular feedback helps conserve sodium and keep

GFR and Pgc at reasonable levels despite BP.

Estimating GFR

Inulin is freely filtered, and is never reabsorbed, secreted, or metabolized in the tubules.

So filtered inulin equals excreted inulin.

Creatinine is often used instead of inulin to estimate GFR. Creatine is a normal product of skeletal

muscle breakdown. It issecreted into tubules, so rate of creatinine excretion is about 10% higher than

actual filtration rate.

*Clearance rate = ( )RateFlowUrine]creatinine[Plasma

]creatinine[UrineGFR=

*The plasma creatinine concentration varies non-linearly with GFR, so at normal blood levels large

changes in GFR create little change in the plasma creatinine concentration.

Glomerular Permselectivity

1. Architecture.

2. Negative charge. Sialic acid moieties give the barrier a negative charge which repels proteins such as

albumin. Reduction of this charge results in proteinuria.

ProteinuriaUsually suggestsglomerulardisease, but may be due to tubular damage or protein overproduction.

Glomerular proteinuria1. Selective proteinuria means that albumin is selectively increased, usually due to loss of

negative charge. Often happens in Minimal Change Disease. Albuminuria is a sign of

glomerular disease.

2. Nonselective proteinuria means that all plasma proteins increase in their normal proportion.

Tubular proteinuria

Small MW proteins such as 2, but not albumin or Igs, are increased. Small MW proteinuria is a sign

of proximal tubule disease.

Overproduction proteinuria

Multiple myeloma produces excess Ig light chains. This is not detected by normal dipsticks which

only detect albumin. An SSA test is needed to detect these Ig chains.

1. Glomerulonefritis proliferatif difus akut:

Penyakit ini muncul 2-3 minggu setelah infeksi biasanya didahului pharingitis oleh strptococcus grup A.biasanya menyerang anak dan remaja dan berkembang menjadi SYNDROM NEFRITIK : oliguria,proteinuria, hematuria, hipertensi sedang dan oedema periorbita/facial.


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3. Fokal glomerulonefritis

merupakan bentuk glomerulonefritis yang TIDAK merusak seluruh glomerulus. Meskipun hanya beberapasaja yang mengalami kerusakan, namun biasanya meluputi 1-2 lobulus ginjal.

Fokal GN secara umum membentuk IgA nephropaty (bergers disease) umumnya menyerang laki-lakimuda. Kelainan ini ditandai oleh proteinuria dan episode berulang hematuria ringan serta tenggorokankering. Peningkatan IgA dalam darah dan kerusakan glomerulus terjadi akibat IgA immun kompleks yangmendendap di glomerulus.

Patomekanisme:

Prognosis : baik pada anak meskipun proteinuria, hematuria dan hypertensi menetap. Pada dewasa,sering secara lambat berlanjut ke gagal ginjal dalam 10-20 tahun (kadang 3-5 tahun).

4. Glomerulonefritis Membranosa

Jenis ini ditemukan 30% dari kasus syndroma nefrotik usia dewasa. Beberapa pasien mengalamiproteinuria asimtomatik.

Etiologi:1. 70% idiopatik2. Obat-obatan : penicilamin dan emas untuk treatmen reumatoid arthritis3. Tumor : ca. paru dan lympoma4. Infeksi : malaria.

Patologi: secara merata terjadi penebalan kapiler membrana basalis.


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Perubahan tubuler: tahap awal, droplet protein dan lipid globuler menempel di epitel tubuler. Lipid jugaditemukan di jaringan intertisial. Timbul granuloma antara makrofag dan giant cell pada deposit kolesterol penyempitan kapiler glomerulus atropi iskemik tubulus dan fibrosis intertisial.Prognosis: 25% kasus remisi spontan, 25% lagi berlanjut ke proteinuria, dan 50% nya disertai gagal ginjal.

5. Glomerulonefritis Membranoproliferative (Mesangiocapillary)

GN yang ditandai khas adanya peningkatan jumlah sel dan matrix di dalam glomerulus.

Etiologi: karena aktivasi komplemen (tipe1 C3 dan IgG; tipe 2 C3 tanpa Imunoglobulin).Gambaran Klinis: umumnya pada anak dan dewasa muda, dengan gejala nephrotic syndrome atauproteinuria ringan atau dengan nephritic syndrome.

Prognosis: gagal ginjal disertai hipertensi.

6. Glomerulonefritis Kronik (GNK)

Jenis ini merupakan stadium akhir dari semua bentuk glomerulonefritis.

Resume:

Patomekanisme secara umum

Komplex imun dapat terdeposit dan merusak endotelium fenestrata dan menyebabkan tekananintraluminar meningkat. Berikut ini ilustrasi dari deposit imun komplex:


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Patologi: kedua ginjal mengecil (granular contracted kidney)

Pada GNK sering berlaku siklus berikut:Pasien bisa saja Gagal ginjal kronis sebagai problem awal,atau gagal ginjal muncul setelah beberapa tahun menderitaGlomerulonefritis.

Hipertensi Renal

Ada dua aspek mengenai kaitan ginjal dengan peningkatan tekanan darah.a. Beberapa penyakit renal yang menyebabkan hipertensib. Hipertensi sendiri menyebabkan kerusakan ginjal

Lingkaran setan yang terjadi:

Patomekanismenya meliputi aktifasi dari Renin-angiotensin.

Perubahan vaskuler terjadi dan dapat dibedakan antara hipertensi renal benigna dan maligna.

Hipertensi Benigna:

adanya emboli kecil dari ateroma menyebabkan iskemik dan jaringan parut (scarring) pada kasishipertensi benigna.


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Hipertensi Maligna:

Pada hipertensi ini, tekanan darah meningkat dengan cepat dan merusak a. renalis, arteriola, danglomerulus. Gagal ginjalsering terjadi kecuali hipertensinya diterapi.

PENYAKIT TUBULER

Nekrosis tubuler akut (ATN)

Kerusakan terjadi karena 2 masalah:1. Selama terjadi shock, misal: perdarahan,

luka bakar luas, obstruksi intestinal akut,inkompatible transfusi dan operasiabdonmen.

2. Lanjutan dari proses zat nefrotoxik:

karbontetrachloride, ethylen glycol, mercury,uranium, chromic acid, dan obet-obattertentu seperti antibiotika.

Shock

Perfusi jaringan iskemia parenkim kerusakan tubulus.


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Toxic (nephrotoxic)

Efek toxic akan melebar dan biasanya mengenaiseluruh nefron. Toxin berpengaruh maximal ditubulus proximal, dan secara intensifkonsentrasinya meningkat di tubulus. Contohberikut toxisitas oleh karbon tetraklorida.

Manifestasi klini s terdapat 2 fase klinis:

1. Oliguria

2. DiuresisRusaknya epitelium tubuler akan diganti oleh selbaru yang bekerja tidak selektif lagi. Sehinggavolume besar dilut urine dapat lolos.Patomekanismenya dapat dilihat disamping.

Tubulo-intertisial disease

Merupakan penyakit dengan kerusakan tubulus dan jaringan intertisial ginjal.Bentuk-bentuk kelainannya meliputi:

1. Nekrosis tubuler akut2. Infeksi pyelonephritis3. Intertisial nephritis4. Gangguan metabolik misal: gout, nephrocalsinosis, hypokalemia.5. Myeloma ginjal6. Abnormalitas tubuler.

Lesi tubuler metabolik:


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Urat nephropaty:

Sering terjadi pada gout. Peningkatansekresi asam urat menyebabkanterbentuknya kristalasam urat di tubulusdistalis.

Gagal Ginjal AKUT (GGA)

Acute Renal Failure (ARF)

Acute renal failure is the loss of GFR and buildup of nitrogenous wastes in the blood.It doesnt correlate perfectly with creatinine creatinine rises a few days afterrenal failure begins.

Azotremia is the accumulation of nitrogenous wastes.

Uremia issymptomatic renal failure.

Manifestations of ARF include:

--hyperkalemia, which can be lethalif acute

--metabolic acidosis--volume overload--rapid rise in creatinine

Postrenal acute failure may occur with upper or lower urinary tract obstruction (stones, tumor, enlarged

prostate). This will often produce flank pain and hematuria. Pressure in Bowmans Space goes up, and

GFR decreases. Treated with catheters, stents.

Most common etiologies of ARF areprerenal ARFand acute renal tubular necrosis.Predisposing factors include age, proteinuria, myeloma, diabetes, NSAIDS, and diuretics.

Prerenal acute renal failure (renal hypoperfusion):

Liver failure, CHF, and nephrotic syndrome all raise AGT-II, vasopressin, and sympathetics, leading to

renal vasoconstriction and decreased GFR. Patients will be edematous with bulging neck veins and

orthostatic BP changes, yet feel dry mucous membranes. The kidneys are experiencing hypoperfusion.

BUN:Creatinine ratio > 20Low urine sodium, but elevated urine osmolality (because lots of water is reabsorbed).

*Urine concentration will be very high but not with sodium.

Fractional excretion of sodium (FENA) is decreased.

)/()(

)/()(

))((

))((FENa

CrCr

NaNa

Na

Na

PU

PU

GFRP

VU==

Intrinsic Acute Renal Failure

The problem may be in the glomerulus, tubules, or interstitium.RBC casts are pathgnomonic for glomerulonephritis!

Acute interstitial nephritis (AIN):

Usually due to an allergic reaction with lymphocyte infiltration and eosinophilia in the renal

interstitium. Often caused by infections, drugs (penicillin, rifampin, NSAIDs), orsystemic diseases (SLE, sarcoidosis, Sjogrens).

Will see fever, rash, and eosinophils in the urine. May see WBC casts or hematuria as well.

Acute tubular necrosis (ATN):Ischemia, azotemia, hypotension, nephrotoxic drugs (mostly aminoglycosides or contrast dyes),

or hemoglobin can all cause acute tubular necrosis. Mortality is 50%.

Tubules become obstructed with debris, and filtrate leaks directly back through destroyed tubular

basement membrane.*High urine sodium, but normal overall urine osmolality.

Muddy granular casts are seen in the urine.

Treatment includes dialysis for hyperkalemia and volume overload.


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Acute Glomerulonephritis:Nephritic/nephrotic syndrome with high proteinuria, hematuria, andRBC casts.

Caused by Streptococcus infections, other infections, orthrombotic microangiopathies (HUS,thrombotic thrombocytopenic purpura).

Gagal Ginjal K ronik (GGK)

Kerusakan progresif ginjal pada beberapa penyakit ginjal sering berlanjut menjadi gagal ginjal kronik.Penyebab utamanya meliputi:

1. Glomerulonefritis kronik (GNC)2. Pielonefritis kronik dan nefritis intertisial3. Nephropathy deabetic4. Obstructive uropathy5. Polycystic kidneys

Berat-ringannya gagal ginjal dapat dimonitor melalui pemeriksaan serum urea, kreatinin dan GFR (GFR

normal 100 ml/menit)

Chronic Renal Failure

If you remove lots of kidney, the remaining nephrons drastically increase their GFR (net GFR is stilldecreased, though). Most symptoms of renal failure dont appear until 90% of renal function has been

lost.

When corrected for GFR, the reabsorption of glucose, bicarb, phosphate, ions, etc are the same in the

diseases and intact kidney. ESRD is when total GFR cant go any higher.

Both sodium and potassium have increasedfractionalexcretion but decreasedtotalexcretion.Chronic renal failure presents with edema, HTN, hyperkalemia, acidosis, and uremia .

Sodium

A greaterfraction of filtered sodium is excreted as GFR drops. Totalsodium levels are actuallyincreasing, soANP is high. But pretty much all sodium going to the kidney is excreted.

When GFR gets extremely low, this increased fractional excretion of sodium cant keep up with sodium

intake, and sodium retention and edema occur unless patient starts low-sodium diet. Hypertension

follows.

Potassium

Increased potassium excretion, mediated by aldosterone. There is also increasedfecal loss of

potassium. These patients can actually maintain K

+

homeostasis, but because theyre alreadyat maximum excretion, they cant handle potassium loads.

Despite the potassium excretion, these patients are usually hyperkalemic.

Other solutes

Serum PO42- increased

Serum Ca2+ decreased

PTH increased1,25 Vitamin D decreased

Magnesium increased

Uric acid increased

Acid/Base balance

As GFR decreases,NH4+

excretion decreases, so less acid is buffered. This leads to acidosis.Acid is normally buffered by three mechanisms: HPO4-, HCO3-, and NH3.

Water balance

Nephrons lose ability to concentrate or dilute urine. This is isosthenuria because urine osmolality equals

plasma osmolality.CCD also responds less to ADH, so more water is lost.

Urine output becomes dependent on solute intake.

Uremic Syndrome

Accumulation ofuremic toxins.

Deficiency ofVitamin D and Epo.


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PTH increased because of low serum calcium.HTN and edema due to salt retention.

Toxic compounds that often accumulate include uric acid, B2 microglobulin, guanidino compounds.

Symptoms of uremic syndrome include anorexia, mental problems, pruritus, restless legs,

weight gain, orthopnea, numbness.

Bone problems Renal Osteodystrophy1. Bone (CaCO3) buffers H+ as acidosis increases, resulting in progressive bone loss.

2. In chronic renal failure, PO42- isnt excreted, so it accumulates and complexes with serum Ca2+.

3. PTH levels increase because oflow serum Ca2+, which leads to more bone loss (osteitis fibrosa).

4. 1,25 Vitamin D requires synthesis in the kidney, so its levels are decreased. Loss of Vitamin D causesrickets (osteomalacia).

5. Patients may actually calcify soft tissues (metastatic calcification) due to altered hormones.

Blood problems Anemia and Thrombocytopenia

1. Kidneys normally make Epo. Epo is reduced in renal failure, so there is low RBC production.

2. Also, the concentration of blood toxins can kill RBC and platelets, causing GI blood loss.

Toxins will impair platelet functioning and cause bleeding diathesis.

There may also be hyperlipidemia.

Neurologic problems1. Uremic encephalopathy (insomnia, fatigue, lethargy, coma, restless legs, tremors).

2. Peripheral neuropathy (restless legs,pruritis/burning/tingling).

Insulin problems

As GFR decreases, insulin levels decline.

Diabetes + CRF = severe hypoglycemia.

In renal failure:

Both sodium and potassium have increasedfractionalexcretion but decreasedtotalexcretion.

Chronic renal failure presents with edema, HTN, hyperkalemia, acidosis, and uremia.

Sodium

A greaterfraction of filtered sodium is excreted as GFR drops. Totalsodium levels are actually

increasing, soANP is high. But pretty much all sodium going to the kidney is excreted.

When GFR gets extremely low, this increased fractional excretion of sodium cant keep up with sodium

intake, and sodium retention and edema occur unless patient starts low-sodium diet. Hypertensionfollows.

PotassiumIncreased potassium excretion, mediated by aldosterone. There is also increasedfecal loss of

potassium. These patients can actually maintain K+ homeostasis, but because theyre alreadyat maximum excretion, they cant handle potassium loads. Despite the potassium excretion, these

patients are usually hyperkalemic.

Acid/Base balance

As GFR decreases,NH4+ excretion decreases, so less acid is buffered. This leads to acidosis.Acid is normally buffered by three mechanisms: HPO4-, HCO3-, and NH3.

Water balance

Nephrons lose ability to concentrate or dilute urine. This is isosthenuria because urine osmolalityequals plasma osmolality.

CCD also responds less to ADH, so more water is lost.

Urine output becomes dependent on solute intake.

Uremic Syndrome

Accumulation ofuremic toxins.Deficiency ofVitamin D and Epo.

PTH increased because of low serum calcium.HTN and edema due to salt retention.

Toxic compounds that often accumulate include uric acid, B2 microglobulin, guanidino compounds.

Symptoms of uremic syndrome include anorexia, mental problems, pruritus, restless legs,weight gain, orthopnea, numbness.


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Mekanisme kompensasi:

Efek Gagal ginjal kronik:

1. Gangguan keseimbangan air dan elektrolit .

2. Gangguan keseimbangan asam basa

3. UremiaGinjal gagal mengekresikan produk nitrogen sisa terakumulasi dalam darah.Gejala uremia meliputi: letargi, anoreksia, nausea dan vomitus dengan bingung, kejang sampai meninggal

4. Abnormalitas Hormon

ada tiga hormon mengalami produksi yaitu: eritropoetin, parathormon dan vitamin D.

5. Hipertensi


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6.Eksudat fibrinoid misal: pericarditis fibrinosa, colitis uremia7. Ulkus hemorragik pada saluran gastrointestinal8. depresi immunologi infeksi mudah timbul pada penderita GGK.

Penanganan Gagal Ginjal Terminal:

Meliputi 1) dyalisis, dan 2) transplantasi ginjal.Komplikasi dari masing-masing tindakan terapi tersebut adalah:

Dialysis1. Haemodialysis

Lokal infeksi dan trombosis vasa tempat punususkan.Systemic toxisitas alumunium dimensia hebat atau osteomalasia.

2. Continuous Ambulatory Peritoneal Dialysis (CAPD) peritonitis: terutama oleh bakteri stapilococcus,bakteri garam (-) dan jamur.

Transplantasi ginjal.Penolakan (rejection) menjadi komplikasi utama. Berdasarkan lama penolakan, dibedakan menjadi 3 yaitu:1) hiperakut dalam jangka menit/jam, 2) akut dalam beberapa minggu, dan 3) kronik setelahbeberapa bulan sampai tahun.

Review II Blok Uropoetika

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