Acute renal failure:

Renal insufficiency

Numerous causes, divide to prerenal, intrarenal and post renal. Pre is before kidneys, intra
within kidnesy – tubular or glomerular, post renal- after kidneys
Syonymous with azotemia, which is an elevation of the BUN an creatinine levels: if sytpoms
of renal failure are present ( not just lab no) the diagnsosi shifts to uremia and hemodialysis
will be necessary.
What does uremia cause directly?
Pericardiitis uria ifnlammes tissue of heart, pericardium sensitive to those toxins
Bleeding platelet done’t function in around this, bleeding and azotemia = dialysis
Suceptibilty to infection- wbc can’t degranulate, cause bleeding, cells can’t function if bathe
in urea, wbc can’t do their job even if you have them

When do we dialyze the patient (AEIOU)

Acidemia ( metabolic acidosis)- can’t get rid of hydrogen ions, can’t get rid of protons in
distal tubules, not get rid of protons, maintain H and ph drops in blood
Electrolyte abnormalities w EKG changes ( hyperkalemia) tall T, kidneys repsosnible for
getting rid of potassium, if can’t build up in blood, affects heart, peaked T waves
Intoxication ( salicylic acid, lithium isopropanol, Mg containing laxaitves, ethylene glycol),
and Infection related to uremia. Wbc can function to help fight infection
Overload of fluid not responsibe to diuretics
Uremia complications (pericarditis, encephalitis ,GI bleed)

Treatment depends on cause

First have to know hwere to look  your CMP and urine test will help.

Urine sodium (U Na) : the concen of sodium in the urine.

Fraction excretion of sodium Fe Na) Perce
ntat of sodium excreted in kidney that si filtered in the urine (normal is 1%)
Urine osmolality : U osm: the cocn of solute in in the urine. How much water in urine. More
water in urine, low urine osmolality, when urine conc, low water in urine, high urine
osmolality. Concentrated menas pull water out pull back into blood stream absorbed.
If low urine osmolality, urine dilute, let more water to be filtered out of urine,
Proportional to the reabosrptin of water. Excrete more urine not reabsorb, low urine
osmolality.
BUN: Cr the ratio f BUN in serum to Cr in serum normal is 10:1 and 20:1.
Generally Bun : Cr is higher whne theres more reabsorption and lower when theres less
reabsorption
More reabosrtion : higher, bc BUN absorbed in kidneys, if more reabsorbed, more UBN
reapbrospe into blood stream so ratio goes up. If less abrobtion Bun : cr ration goes down.
Presence of blood cells, casts, sediments: point otwards intrarenal failure

Fraction exretio nfo Soiudm (Fe Na)

Urine sodium – if low, means that not areaborbtion sodium. If top no is lower this fraction
is lower, if urine sodium is higher bottom no is higher so
So urine sodium is low, fraction exretio will be low <1%, if urine soiudm is high, fractional
excreti nof soiudm will be high. Fracitonal sodium if >1% is high if less thn<1% it’s low.

Pre rean land psot renal labs are very similar

Low urine soiud , low fractional excretion Fe Na,
Urine osmolality is high bc pull water out of urine andback to blood stream. Reabsorb water.
More reabosrbtion, both sodium and water reabsorb more BUN so in pre and post have
high BUN: Cr ration, more pronounced np re than post but still high.
Intrareanl causes: labs are more obvious is actue tubular and itnertiial and
glomerulonephritis ATN and AIN- happens in more distal part.
Glomerulus filtered afferent arterior tand that part is disordered, get proteins blood cells all
gho trough here. Look for red cell casts hematuran and proteinuria in glomerular .

Chronic kidney failure disease

Irreversible loss of nephrons – the functional unit of kidneys
Toxic state uremia
Kidneys connects ureter to bladder, descending aorta
Acute kidney failure
Hypertension
Diabetes
Other kidney disease
All this can cause irreversible oss of nephron

ACUTE RENAL FAILURE

 reversible
Pre renal
Intrarenal and post renal causes
Pre renal  renal artery stenois, heart failure nad hemorrhage
Intra renal  FN, tubular necrosis and intersitital nephritis
Post renal cause BPH, renal stones and tumors
Pre rena ldn post renal often casue to itnra renal cause
All cause acute renal failure.

Hypertension:
Renal artery nad renal vein,functional unit of kidney are nephrons, head of nephron is
bowman’s capsule has capilalries entering an exiting, blood filtered through to
nephron.when normal blood pressure eerythign is filtered.
Bowman’s capsule area, blood vessels from renal artery, when someone has hypertension
thickening of bood vessels causes narrowing of lumen = less blood flow to neprhons,
afferent arteriole brings blood towards head of nephron, with less blood, less decrease in
filtration nand thus decreased glomerular filtration rate, cells in this area that detect this
and produces renin, starts RAAS system.
RAAS system leads to increase in heart rate nad further hypertension, unfortunate bc less
blood is flowing to kidneys, kidney thinks by increase bp it will receive more blood. Can
work sometime but viscious scycle, more narrowing and more thickening, all lead to
glomerulosclerosis thickening and hardening of vessels in bowman’s capsule glomerulus,
glmerosclerosis causes ischemic inru yand thus nephron loss itself.
Diabetic nepphorpathy
4 main changes:
Mesangial expansion
And proliferation
Podocytopathy hypertrophy and later atrophy
GBM thickening and
Sclerosisi.

HT can casue DM, high blood glucose casues overproduction of ROS, these ROS leads to a
cascade of events, leads to activation and production of growth factors, proinflammatory
cytlkines and oxidative stress causes all 4 diabetic neprhotpathy changes.

Loss of nephrons in area, blod flow will shift to neprhones still alvie and working, causes
glomerular hyperfiltration. Blood flow will shift to functional nephron, causeisng glomerular
hyperfiltration, in early stage glomerular hypertfiltratio nis tolerated, get big increae in GFR
in functional nephron. After a while this hyperfiltration nresults in sclerososi bc so much
pressure and evnetualy glomerulnperhons is will cause irreversible looss of nerphon too and
cycle continues.
Irreversible loss of nerphone, glomerula hyprtilgratin, increased GFR early, then glomerular
sclerosis and more loss
In the late stage, loss so much of kidneys function that the GFR decerease, urine output
decrease and start retaining waste = uremia.

Clinical manifestations:
1. Na+ balance and H20
 decerase in GFR leads to increased and sodum and water rentiaton, causing
increase in BP and thus peripheral edema. Important ot restrict fluid intake and
when vomiting and diarrhea occurs in CKD this is very dangerous bc already
restricted for intake, fuhter loss from voimit and diarrhea can be very dangerous
2. K balance- decrase in GFR leads to increased K retentation, causing hyperkalemia,
resulting in ECG changes, fibrillations, improntat ot note that loss of nephron leads
to decrease renin and thus decrease adsterone.decerase aldosterone the distable
na/K pump doesn’t work causing K retention. Thus using K+ psaring diuretics and ace
inhibitors can further accelerate aggravate problem bc promoting more potatssium.
NA K atp ase is in furthest distal parto f nephron and resposnbile for exchange of
soiudm and potassium. If aldosterone nto produced, this pump doesn’t work and so
we retain potassium.
3.
4. Metabolic acidosis-dimished capaicyt to excrete H+ and to generate bicarbonate,
which leads to acidosis. Acodisos leads to bone decalcification amongst many.other
things xdation, and holds . normalyy neprhn maintains BP produce bicaronate isf
necessary or to secrete h+ ions of necessary

5. Mineral blanacen osteodystrophy-loss of neprhons  kidney can’t produce calcitriol,

with no calcitriol have decreased ca reabsrbtipn of calcium from GIT and kidneys,
leads to hypocalcemia, hypocalciem and decerased calcitriol will stimulate the
 parathyroid glands always continuously leading to secondary hyperpartathroidism,
casuing osteodystrophy due to parathyroid hormone, stimulates bone breakdown.
Loss f neprhons also eads to decreaded GFR, hyperphosphatemia, body can’t secrete
phsopahate.

Other manifestations of uremia:

Lots of urea in blood, usually excreted by kidneys in urine.
Vasa recta secretions of substances into nephron and reabsrobi of substances from eprhon.
In the last part of nephron the urea is actually reabsorbed into vasa recta, helps drag water
into these vessels. The urea is then secreted back into nephron and water remains in vessels
bc sodium is laso reabsorbed pulling water to stay there
Retain urea = uremia, uremia is bad bc results in neurological sytpoms like hiccups cramps,
gastro problems anorxeai vomiting, production decreased oesterone and testosterone,
amenorpha impotence. Ureami also causes skin changes.

In late CKD, when lots are lost, dcreased renin, decreased in BP,
Dcreased in EPO results in anemia
Decreased in calcitrial which casues renal osteodystrophy.

CKD suble decrease function greater than 3 months

Acute kidney injury decrease in function in less than 3 months
Rregualtes whats in blood remove waste, steady and ad regulate water
Make hromones.
Blood from renal artery, goes to clumps of arterioeles called glomeruli where it’s filtered.
Filtrate moves to renal tubule.
Rate at which filtration occurs is GFR, in normal around 100-120ml /min/1.73m2
Slightly less in women than man and decreases less with age.
Common caue is hypertension. The walls of arteryestart o thicken to witstand pressure,
causing narrow lumen, less blood and O2 delivered to goes to kidney casues ischemic injury
to neprones glomerulus. Immune cells like macrophages nad foam cells slip into damaged
glomeruls and starts secereting growth factors like TGF B1, these growth factors cause
mesangial cells to regress back to mesangioblasts, then they secrete extracellular matrix,
this extra ECM leads to glomerulsclerosis which leads to hardening and scarring, diminishing
nephrons ability to filter blood leads to CKD
Common cause is Diabetes, excess glucose in blood stick to proteins called no neyzmatic
glycation, no enyzmes involved, affects efferent arterior casuign it to become stiff and
narrow = hyaline arteriosclerosis, creates obstruction which makes it hard for blood to leave
glomerulus,increases pressure within glomerulus leads to hyperfiltration, push more fluid
through. In response to high pressure state the mesangial cells secrete more and more
structural matrix which expands size of glomerulus, over many years this sproess of
glomerulosclerosis, dimisihses nephrons bility to filter blood leads to CKD.

Other causes as well, systemic diz like lupus and RA, also causes glomerulosclerosis
Other causes like infectiosn like HIV
Long terms use of meds like NSAIDs nad ntoxins like tobacoo
Usually urea in blood excreted in urine ,when decreased GFR, less urea gets filtered out and
builds up in blood called azotemia.
Azotemia causes general symtpoms like nausea nad loss of appetite, as urea levels increases
more affects nervous system causing encephalopathy resulting in asterixis-tremor of hand
like bird flapping its wings, seen with hand extension
Can lead to ocm and death
Also cause pericarditis
Increased tendency for bleeding becaue excess urea in blood makes paltelets less likey to
stick to each other less clot formation
Uremic frost- where urea crystals deposi in skin and looks like powsdery snowflakes.
Electrolyte balace -K levels important, usually kidneys help with excretion, in CKD, less K is
excretd so more builds up in blood, hyperkalesmia causes cardiac arrythmais
Calcium level balance  Normally kidnsy help activate Vit D and activated Vit D helps ca2+
absorbtio nfrom diet, with CKD less activativated Vit D less ca albsorbed into the blood
leaing to hypocalcemia, low calcium leves,
As ca in blood falls, parathyroid hormone released, casuing bones to lose ca2+
Resorbtion of ca from bones leads to weak nad brittle bones, renal osteodystrophy

Kidneys also releases key hromones, usually if theres low fluid, they secrete renin to
increase bp.
In CKD, falling GFR leads to more nad more renin secretion and thus hypertension. HT
casues CKD, so theres viscious cycle.

Kideys also usually secretes Erythropoeitin EPO, which stimulates production of RBC from
bone marrow, in CKD EPO falls, leads to slowered production of RBC and ultimately anemia.

Diagnosis:
Changes in GFR over time
CKD suspected of GFR if <90 ml/min
Irreversible kidney damage if less than 60ml
Confirm using biopsy look for gloemrulosclerosis.
Treatment:
Managing underlying cause
In severe dialysis and transplant.
CKD – Paul Bolin
Characterized yb a long term, permanent decline in renal fucntin as measured by the
glomerular filtration rate
End stage renal diz – the final stage of CKD in which the patient is depend on dialysis for
survivial. The no 1 causeso ESRD diabetes mellitus combined with hypertension.
Most patients have both of them.

Based on GFR not based on symtpoms:

Stage I – GFR 90-120
Stage 2 GFR 60-89
Stage 3 30-59
Stage 4 15-29 – must prepratred for RRT
Stage 5 <15- ESRD requires transplant or dialys

Stae 3 is very important, one patient progresses to stage 3, at a fork I nthe road, can get
better and stay in stage 1,2  wont’ need long term dialysis
But if down hits stage 4, will be on dialysis, stage 4 will progress to 5 won’t be reversible.

Whether or not you choose to dialyze is based on syptoms not GFR

Acidemia – metabolic acidosis  kidneys can’t excrete the acid
Electrolyte abnormalities – usually hyper K w/ EKG changes  peaked T waves,
Intoxication (salicylates, lithium , Isopropanol, Methanol, Ethylnee glycol)don’t see with
CKD
Overload of fluid unrepsonsibe to diruetics
Uremic sx (pericarditis, encephalopathy, other neuro sx, severe bleeding diathesis. Esp. GI)
 too much nitrogenous waste in blood stream. Altered mental status, myoclonus, severe
bleeding esp in GI system. Low GFR with melena or hematoschezia = dialysis indication!

1. Hypoclacemia nad hyperphophatemia.

Kidney responsible for production of 1,25 OH2 VIt D. Repsosnbiel for increasing GI
abosrbton of Ca, increasing bone reaborbtion of Ca
Hypocalcemia
Liver gives hydroxylation at one part and kidney at another part, Vit D hydroixylated
at 2 diff points need to to be active.
If kidney not work then decreased activated 1,24 Vit D
Resposnbiel for increasing GI abosrbtion of ca and bone reaborti, increase activity of
osteoclast that breakdw down bone, if not enough of this active get HYPOCALCEMIA.
If hypocalcemia we will trigger parathyrodis.
Low ca  increased PTH
Increased PTH  can’t absorb Ca, but still can absorb PO4 
hyperphosphatemia.absorbt more phophsat,e can’t absorb calcium bc don’t have
the right vit D, absorb extra phosphate bc extra PTH.
May result in osteodystrophy. Keep that PTH from being so high, need to inhibit this,
 Tx using cinacalcet blocks production of PTH, and bind phosphate using sevalemer
and lanthamum  get rid of hyper phosphatemia

2. Anemia
Reduced producito nof erythropoein EPo hwic tirgers production of RBC.
Def  normocytic anemia. Def of RBC, like in chornic dz, bc don’t’ have lack of iron,
or dz, just not producitng enough.
Unviersial in pts with ESRD.
Sx : fatigue , pallor
Labs decreased Hct, Hgb: normal MCV, normal TIBC. If have anemia of chornic dz,
have low TIBC, TIBC how to differentiate anemia of chronic dz with normocytic
anemia due to decreased EPO w
Tx: EPO replacement.

3. Electrlyte abnormalities
Most cirtical electrolyte excretion nproducts of kine yare potassium, acid, and
mangeisu. Loss of renal function leads to high levels of all
Hyperkalemia – any hyperK with renal dizseas warrants prompt EKG. Tx dialysis if
EKGchanges peaked T waves. Can casue asystole.
Acidosis- metabolic acidosis: Tx Dialysis, not getting rid of protons,
Hypermagnesmia – Tx : low magnesium diet. >5mm is peaked T waves, for limb
leads bigger than half a big box. Peaked T waves!! If look at precordial leads,
anything with T wave greater than 1 big box, 1 cm or greater.

4. Uremia:
Build up of nitrogenous waste in blood
Azotemia may cause pericarditis, encephalitis, bleeding inc risk of infection. Uremia
is when we start having systoms due to azotemia.
Tx: dialysis if symptomatic, DDAVP if minor bleeding
Infection is the #2 cause of deatih in ts with ESRD.
Ureamia causes pericarditis- pericardium is irriated from nitrogenous waste products
Encephalitis- nerve aso affected
Infection bc wbc can’t degranulate
And bleeding bc platelets can’t stick together
Gums bleeding or increased bleeding time – admnsiter DDAVP – increase VWB
factors
If GI bleed , emelena, hematoschezia- dialyzeee
No 1 is hypertension and DM

Fluid overload
Inability to filter lfuid thru the glomerulus due toreduce GFR.decreae GFR can’t get extra
water out thru idneys so eceess ewater extravascate into third spaces get edema.
Can try diuretics with stage 1-3, some renal function so diuretics can help pee off that water
but pat who fail diruetics or in stage 4 or 5 dialysis will be necessary.

Long term maangemetn for all CKD pts.

Diet restriction : low potassium ,low sodium, and low phosphate.
Fluid intake restrictions 500ml to 1 L or that which does not cause volume overload.food like
fruits with lots of water also
ACE inhibitor Lisinopril, enalapril, captopril ace inhibitors are reno-protective, always
good esp in ptx with stage 1-3
Avoidance of NSAIDS (aceotminophien OK), definetley avoid aminoglycosides. Renally toxic.
If ptx has gram – infection use newer tygocyclines, great gram – activity, not excreted thru
kidneys.

Most improtnat is AEIOU, based on symtpsm nto GFR

Renla trnapslant : survival is better with trnaplant ahan twith longer dialsis.
PO will need long term tx w cyclosporine, tacroliumus and mycophenolate VERY effective
Anti rejection regiment.
Reduce T cell activity and very effective

RPD:
Pasien menyangkal adanya riwayat batu ginjal.
Pasien tidak ada riwayat sakit lambung.
Pasien menyangkal adanya riwayat trauma.
Pasien menyangkal adanya riwayat keganasan, penyakit hati, penyakit jantung, penyakit
paru, dan stroke.

Riwayat pengobatan:
Pasien konsumsi Amlodipine 1x10mg dan Bisoprolol 1x5g setiap hari, PO, untuk pengobatan
hipertensinya sejak 4 tahun terakhir ini.
Pasien mendapatkan suntikan Epotrex 2 kali sebulan di rumah sakit sejak 3 bulan yang lalu.
Sodium bicarbonate
Folic acid 1x1mg
Simvastatin 1x 20mg

Riwayat penyakit keluarga:

-Di keluarga, ibu dari pasien dulu juga menderita penyakit ginjal kronis dan ada riwayat cuci
darah sebelum meninggal. Ibu dari pasien juga ada riwayat hipertensi.
-Di keluarga pasien ada riwayat keganasan. 1 kakak perempuan dan 1 adik perempuan dari
pasien kena Ca mammae.
-Tidak ada anggota keluarga yang menderita penyakit jantung, asma, diabetes mellitus,
stroke.

Riwayat kebiasaan:
Pasien tidak memiliki riwayat merokok.
Kebiasaan minum alkohol dan minum obat obat terlarang disangkal.
Kebiasaan tidak menggunakan jarum suntik dan tidak ada riwayat transfusi darah.
Sebelum sakit 6 bulan yang lalu, pasien masih bisa olahraga jalan pagi setiap hari selama
30menit-1 jam, namun tambah lama merasa tambah lemas dan hanya bisa jalan dirumah. 1
minggu terakhir pasien drop lagi dan sejak itu jalan ke toilet dari ranjang tidur pun sudah
merasa capek.
Pasien tidak memiliki alergi apapun.

Riwayat social ekonomi:

Pasien tinggal bersama anaknya. Sehari-hari pasien hanya beraktivitas dirumah.
Keluarga pasien merupakan keluarga menegah keatas.
Lingkungan tinggal pasien bersih, ventilasi bagus.

Riwayat Diet:
Sejak didiagnosis penyakit ginjal 6 bulan yang lalu, pasien masih makan 3x sehari namun
makanan protein dikurangkan dan sayuran harus direndem dulu sebelum dikonsumsi. Jika
tungkai lagi bengkak, minuman juga harus ditaker.

Berdasarkan derajat penyakit yang ditentukan dari nilai laju filtrasi glomerulus, CKD stage V
ditegakkan bila nilai LFG <15ml/menit/1.73m2.
Gejala klinis yang ditunjukkan oleh penderita CKD terdiri dari: (1) penyakit yang mendasari
seperti diabetes melitus, infeksi traktus urinarius, batu traktus urinarius, hipertensi,
hyperureseia dll. (2) gejala-gejala Sindrom uremia yang tidiri dari lemah, letargi, anroksia,
mula muntah, kelebihan volume cairan (volume overload), neuropati perifer, pruritus,
urimic frost, pericarditis dan kejang-kejang smapai koma. (3) Gejal komplikasinya antar lain
hipertensi, nameia, osteodistrofi renal, payah jantung, asidosis metabolic, gnagguan
keseimbangang elektrolit (sodium, kalium dan klorida).
Berdasarkan teori disebuatkan bahwa, ini Pada pasien ini dipikirkan CKD karena dari
anamnesis kita dapatkan keluhan mual, muntah, penurunan nafsu makan, bengkak pada
kaki, disertai pusing, buang air besar warna hitam,
Pada pasien dipikirkan CKD overload dan serangan akut on CKD Stage V karena dari
anamnesis kita dapatkan keluhan sindroma uremikum seperti mual dan muntah yang hebat,
lemah seluruh badan(general weakness), anoreksia (penurunan berat badan samapi 7 kg
dalam 6 bulan). Pasien juga memiliki riwayat penyakit hipertensi dan diabetes mellitus tipe
2; hipertensi baru diobati sejak 4 tahun yang lalu dan untuk riwayat diabetes mellitus tidak
minum obat secara teratur.

Penunjang:
Didapatkan pada pemerikssan darah hari pertama datang ke RS terdaat penngkata kadar
ureum sebesar dan kadar kreatinin, dan juga permeksaan darah
Dari hasil tersebut juga didpatakn eGFR

Neurologic symptoms: weakness and fatigue, restlessness of legs, CAD: sob, tachypnea,
kussmaul type respi, GI- vomiting diarrhea, hematologic-anemia, MSK-loss of muscle
strengths,

Anemia
Anaemia ditegakkan atas dasar pasien yang mengeluhkan adanya lemas di seluruh
badannya,
PF pasien tampak pucat, konjunctiva anemis
Penunjang pemeriksaan kadar Hb darah yang menunjukan kadar Hb sangakat rendah
dibawah naili normal dengan rincian
Acidosis metabolic:
Ph <7.35
Ada riwayat diaetes mellitus, gagal ginjal akut dan kornik, kelainan bentuk
ginjal???hhilangnya basah bikarbonat melalui saluran pencernaan karena diare,

Intereprestasia: anemia berat normokromi normsitik

Interpretasi: Azotemia
AGD: Interpretasi: aisdosi metabolic terkompensasi parsial

Klasifikasi penyakit ginjal kronik didasarkan atau dua hal, yaitu atas dasar derajat
(stage) penyakit dan atas dasar diagnosis etiologi. Klasifikasi penyakit ginjal kronik atas dasar
derajat penyakit sebagai berikut:

Manifestasi klinis penyakit ginjal kronik tidak spesifik dan biasanya ditemukan pada
tahap akhir penyakit. Pada stadium awal, stadium 1-3, pasien biasanya masih belum mengalami
gejala apapun seperti gangguan keseimbangan cairan ,elektrolit, endokrin dan metabolik yang
tampak, walaupun kadar urea dan kreatinin serum sudah meningkat. Namun jika pasien sudah
masuk stadium 4 dan 5, mulai tampak gejala klinis seperti badan lemah, mual, nafsu makan
berkurang, kaki bengkak, kehilangan nafsu makan, atau kebingungan. Komplikasi dari CKD
bisa terjadi ketidakseimbangan elektrolit, anemia, penyakit tulang dan uremia.
Penyebab ginjal kronik disebabkan oleh bermacam-macam hal, antara lain diabetes
mellitus, tekanan darah tinggi, glomerulonephritis akibat infeksi, dan penyakit ginjal polikistik.
Beberapa faktor risiko untuk terjadinya CKD adalah umur diatas 60 tahun, riwayat keluarga
dengan kondisi tersebut. Diabetes mellitus, hipertensi atau penyakit karidovaskular, infeksi
saluran kemih yang berulang, penggunaan obat nefrotoksik berulang dan kontak dengan bahan
kimia yang berulang. Diagnosis umumnya dengan tes darah untuk mengukur laju filtrasi
glomerulus dan tes urin untuk mengukur albumin. Tes lebih lanjut seperti USG atau biopsi
ginjal dapat dilakukan untuk menentukan penyebab yang mendasarinya.
Penurunan fungsi ginjal dikarenakan adanya gangguan atau kerusakan pada ginjal,
terutama pada komponen filtrasi ginjal, seperti membran basal glomerulus, sel endotel, dan sel
podosit. Kerusakan komponen tersebut disebabkan secara langsung oleh kompleks imun,
mediator inflamasi, atau toksin. Sitokin dan growth factor juga bermain peran dalam kerusakan
ginjal melalui peningkatan aktivitas aksis renin-angiotensin-aldosteron intrarenal yang
berkontribusi terhadap hiperfiltrasi dan hipertrofi kompensatori yang terjadi karena
pengurangan massa ginjal.
Tatalaksan CKD dilakukang untuk menghambat penuruan LFG, mencegah
progresivitas dan komplikasi. Edukasi penting untuk pasien dan untuk modifikasi gaya hidup
mereka. Perawatan awal mungkin termasuk obat-obatan untuk mengelola tekanan darah, gula
darah, dan menurunkan kolesterol. ACE inhibitors, ARB atau CCB bisa digunakan untuk
mengontrol tekanan darah; dan melakukan pemeriksaan HbA1C dengan target <6.5% untuk
mengontrol kadar gula darah. NSAID harus dihindari karena toksik terhadap ginjal. Langkah-
langkah lain yang direkomendasikan termasuk beraktivitas fisik rutin dan perubahan pola
makan tertentu seperti restriksi asupan protein dengan diet rendah protein, dan membatasi
asupan cairan dan garam . Pada CKD tahap lanjut mungkin memerlukan hemodialisis, dialisis
peritoneum, atau transplantasi ginjal. Perawatan untuk komplikasi CKD seperti anemia dan
asidosis metabolic juga mungkin diperlukan. Untuk mengatasi anemia dapat diberika EPO jika
kadar Hb <=10g/dL dan Ht <=30%, atau diberikan transfusi darah apabila Hb <7g/dL. Asidosi
metabolic dapat dikoreksi dengan pemberian bikarbonat.