laporan

BAB 1

PENDAHULUAN

Gagal ginjal kronik (GGK) adalah suatu sindrom klinis yang disebabkan penurunan

fungsi ginjal yang bersifat menahun, berlangsung progresif, dan cukup lanjut. Hal ini terjadi

apabila laju filtrasi glomerular (LFG) kurang dari 50 mL/mnt. Gagal ginjal kronik sesuai

dengan tahapannya, dapat ringan, sedang atau berat. Gagal ginjal tahap akhir (end stage)

adalah tingkat gagal ginjal yang dapat mengakibatkan kematian kecuali jika dilakukan terapi

pengganti. Insufisiensi ginjal kronik adalah penurunan faal ginjal yang menahun tetapi lebih

ringan dari GGK.

Perbedaan ini tidak selalu sama diseluruh dunia, tetapi ada baiknya dibedakan satu

sama lain untuk mencegah kesimpangsiuran. Istilah azotemia menunjukkan peningkatan

kadar ureum dan kreatinin darah, akan tetapi belum ada gejala gagal ginjal yang nyata.

Sedangkan uremia adalah fese simtomatik gagal ginjal dimana gejala gagal ginjal dapat

dideteksi dengan jelas.

1.1 DEFINISI

Gagal ginjal ditandai oleh ketidakmampuan ginjal mempertahankan fungsi normalnya

untuk mempertahankan volum dan komposisi cairan tubuh dalam keadaan asupan makanan

normal. Gagal ginjal kronik terjadi setelah berbagai macam penyakit yang merusak massa

nefron.

Gagal ginjal kronik merupakan keadaan klinis kerusakan ginjal yang progresif dan

irreversibel yang berasal dari berbagai penyebab. Gagal ginjal kronik terjadi setelah berbagai

macam penyakit yang merusak massa nefron ginjal. Bila proses penyakit tidak dihambat,

maka pada semua kasus seluruh nefron akhirnya hancur dan diganti dengan jaringan parut.

Meskipun penyebabnya banyak, gambaran klinis gagal ginjal kronik sangat mirip satu dengan

yang lain.

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Kriteria penyakit ginjal kronik adalah :

1. Kerusakan ginjal yang terjadi selama 3 bulan atau lebih, berupa kelainan struktur atau

fungsi ginjal, dengan atau tanpa penurunan laju filrasi glomerulus (LFG), berdasarkan :

Kelainan patologik atau

Petanda kerusakan ginjal, termasuk kelainan pada komposisi darah atau urin, atau

kelainan pada pemeriksaan pencitraan.

2. LFG <60 ml/mnt 1,73 m² yang terjadi selama 3 bulan atau lebih, dengan atau tanpa

kerusakan ginjal.

1.2 ASPEK EPIDEMIOLOGI

Kita tidak dapat mengetahui dengan tepat prevalensi GGK sebetulnya oleh karena

banyak pasien yang tidak bergejala atau dirujuk. Angka yang lebih tepat adalah banyaknya

pasien GGK yang masuk fase terminal oleh karena memerlukan atau sedang menjalani

dialisis. Dari data yang didasarkan atas kreatinin serum abnormal, saat ini diperkirakan pasien

GGK adalah sekitar 2000 per juta penduduk (PJP). Kebanyakan diantara pasien ini tidak

memerlukan pengobatan pengganti, karena sudah terlebih dahulu meninggal oleh sebab lain.

Dibandingkan dengan penyakit jantung koroner, strok, DM, dan kanker, angka ini jauh lebih

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kecil, akan tetapi menimbulkan masalah besar oleh karena biaya pengobatannya amat mahal.

Dari data Negara maju (Australia, Amerika serikat,Inggris, Jepang) didapatkan variasi yang

cukup besar pada insidensi dan prevalensi GGK terminal. Insidensi berkisar antara 77-283

per juta penduduk (PJP), sedangkan Prevalensi yang menjalani dialisis antara 476-1150 PJP.

Perbedaan ini disebabkan antara lain perbedaan kriteria, geografis, etnik, dan fasilitas

kesehatan yang disediakan.

Data dan studi epidemiologis tentang GGK di Indonesia dapat dikatakan tidak ada.

Yang ada tetapi juga langka, adalah setudi atau data epidemiologis klinis. Pada saat ini tidak

dapat dikemukakan pola prevalensi diIndonesia, demikian pula pola morbiditas dan

mortalitas. Data klinis yang ada, berasal dari RS rujukan Nasional, RS rujukan Propinsi, dan

RS Swasta Spesialistik. Dengan demikian dapat dimengerti bahwa data tersebut berasal dari

kelompok khusus.

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BAB II

PATOGENESIS

2.1 ETIOLOGI

Umumnya penyakit ginjal kronis disebabkan penyakit ginjal instrinsik difus dan

menahun. Tetapi hampir semua nefropati bilateral dan progresif akan berakhir dengan gagal

ginjal kronik. Umumnya penyakit diluar ginjal, misal nefropati obstruktif dapat menyebabkan

kelainan ginjal intrinsik dan berakhir dengan gagal ginjal kronik. Glomerulonefritis,

hipertensi esensial dan pielonefritis merupakan penyebab paling sering dari gagal ginjal

kronik, kira-kira 60%. Penyakit ginjal kronik yang berhubungan dengan penyakit ginjal

polikistik dan nefropati obstruktif hanya 15-20%.

Glomerulonefritis kronik merupakan penyakit parenkim gagal progresif dan difus,

sering kali berakhir dengan penyakit ginjal kronik. Glomerulonefritis mungkin berhubungan

dengan penyakit penyakit sistemi (glomerulonefritis sekunder) seperti SLE, poliartritis

nodosa, granulomatosus Wagener. Glomerulonefritis yang berhubungan dengan diabetes

mellitus (glomerulosklerosis) tidak jarang dijumpai dan dapat berakhir dengan penyakit ginjal

kronik. Glomerulonefritis yang berhubungan dengan amiloidosis sering dijumpai pada pasien

dengan penyakit menahun seperti tuberculosis, lepra, osteomielitis, arthritis rheumatoid dan

mieloma. Penyakit ginjal hipertensif (arteriolar nephrosclerosis) merupakan salah satu

penyebab penyakit ginjal kronik. Insiden hipertensi esensial berat yang berakhir dengan gagal

ginjal kronik <10 %.

PATHOPHYSIOLOGY OF CHRONIC RENAL FAILURE:

I. Disturbance of water excretion:

Total body water is a major determinant of its solute concentrations. Keeping

the total body water within the normal range is mandatory for keeping the body

internal milieu. The kidney is the major determinant for adjusting total body

water. This is achieved through it's capacity to dilute and to concentrate urine.

With chronic renal failure, this capacity is deranged as the following:

a. Loss of the renal ability to concentrate urine: this occurs early in renal failure

leading to nocturia and polyuria. This is due to the fact that with kidney

damage the number of functioning nephrons is decreasing while the amount

of osmotically active molecules produced by the body is stable (about 600

mosmol/day). This will create an osmotic load on the functioning nephrons

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with subsequent polyuria. If water intake is decreased or if there is fluid loss

(e.g. vomiting or diarrhea), the urine volume will not decrease in parallel, but

rather a little decrease will occur (due to decreased renal blood flow). As the

kidney is unable to concentrate urine to excrete more toxins, retention of

wastes will occur. Furthermore, dehydration will result in renal ischaemia

which will aggravate the renal damage. When urine osmolarity is as plasma

(300 mosmol/L), at least 2000 c.c. of urine is needed for excretion of the daily

produced wastes which is the situation in uraemic patients, while in normal

kidney only 500 c.c. of maximally concentrated urine (1200 mosmol/L) are

sufficient.

b. Loss of the renal ability to dilute urine: This occurs late in renal failure. If the

uraemic patient receives excess fluid he may pass into fluid overload, even

pulmonary oedema. In normal persons, urine osmolarity can drop down to 50

mosmol/L (specific gravity 1.001) i.e. urine which is hypotonic to plasma,

while with advanced uraemia, dilution will drop down to only 300 mosmol

(S.G. 1.010) i.e. equal to plasma. In addition, the diseased kidney will dilute

urine very slowly in comparison to the intact one.

II. Disturbance of sodium excretion: As renal failure progresses, the ability of the

nephron to adjust sodium balance decreases. The following disorders may occur:

a. Hyponatraemia, this is usually dilutional hyponatraemia that is due to

retention of excess water taken associated with salt loss such as by sweating,

vomiting and diarrhoea.

b. Salt and water retention which may cause hypertension

c. Salt losing nephropathy which occurs in diseases such as analgesic

nephropathy, cystic kidney diseases and tubulointerstitial nephritis. This will

manifest with hypovolaemia, dehydration and hypotension which if not treated

(by excess salt intake) may lead to acute on chronic renal failure.

III. Disturbed potassium excretion:

The kidney has a high capacity to excrete potassium. Accordingly serious

hyperkalaemia rarely occurs unless GFR is less than 10ml/min. Other reasons for

hyperkalaemia should be looked for if GFR is more than 10 ml/min, these are:

• Excess potassium load

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• Hyporeninaemic hypoaldosteronism

• Severe acidosis with volume contraction

• Drugs as ACEI, B-blockers, and aldosterone antagonists

IV. Disturbance of Acid-base balance:

Chronic renal failure may result in metabolic acidosis which will manifest in

advanced stages by Kussmaul's breathing (air hunger). In cases with tubulo

interstitial diseases, acidosis may manifest earlier (discrepant with serum

creatinine). This condition will be aggravated by increased acid load and sodium

depletion.

With chronic acidosis, bone will be used as a buffer with consequent skeletal

calcium loss and bone disease.

Metabolic acidosis in uraemic patient is due to the following

a. decrease in titratable acid (phosphates, sulfates...) excretion due to decreased

GFR,

b. decrease in ammonia production by the proximal convoluted tubules; and c-

bicarbonate wastage.

V. Disturbance of calcium-phosphate metabolism: This disorder could be

summarized as the following:

a. Retention hyperphosphataemia: As the kidney is the main route of phosphate

elimination, decrease of GFR below 30 ml/min will be accompanied by

hyperphosphataemia. At first, this may occur transiently but later it may be

persistent. In earlier phases of uraemia, hyperphosphataemia may occur post

prandially especially with meals heavy in protein and dairy products.

b. Hypocalcaemia: due to the dynamic equilibrium between serum calcium and

phosphate, hypocalcaemia will occur with any increase in serum phosphate.

Other causes of hypocalcaemia in uraemic patient are defective activation of

vitamin D in PCT and decreased dietetic intake.

c. Hyperparathyroidism: will occur in response to hypocalcaemia. Secondary

hyperparathyroidism will result in bone demineralization through osteoclast

activation. This occurs in attempts to correct hypocalcaemia. With correction

of hypocalcemia, parathyroid activity is arrested, yet as phosphate is high,

deposition of phosphate and calcium in soft tissues will occur to keep the

dynamic equilibrium (serum Ca X serum Po4=50). Again, calcium level gets

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low and parathyroid gland becomes active with consequent bone

demineralization. So far uraemia is persistent, this viscious cricle will keep

active. Long term stimulation of parathyroid gland will result in development

of adenoma which is autonomus i.e despite calcium is getting high parathyroid

gland will keep secreting parathromone (tertiary hyperparathyroidism). This

will lead to more aggressive bone disease and soft tissue calcification. In

addition, it will lead to bone fibrosis and aggravation of anaemia.

d. Bone disease, sometimes called renal osteodystrophy, it is due to multiple

factors including negative calcium and protein balance, lack of active vit. D,

hyperparathyroidism as well as aluminium intoxication. Aluminum

intoxication is due to long term use of aluminum containing antacids as

phosphate binder and the use of aluminium contaminated water in preperation

of dialysate for patients under hemodiamysis treatment.

e. Soft tissue calcification: is due to hyperphosphataemia, secondary

hyperparathyroidism, mobilization of bone calcium to blood with the

consequent increase of the constant value (serum calcium X serum phosphate).

Deposition of calcium occurs in all soft tissues including skin, conjunctiva,

vessels wall and even the heart. Calcified papillae shown in plain film of the

renal tract in a patient with uraemia. Extensive periarticular calcification in a

haemodialysis patient. Vascular and soft tissue calcifications in secondary

hyperparathyroidism of chronic renal disease.

f. Retention of uraemic toxins: These retained toxins are responsible for most of

the uraemic symptoms, including lethargy, malaise, nausea, vomiting,

pericarditis, pleurisy, uremic colitis, platelet dysfunctions...etc. Removing

these toxins by dialysis will be followed by improvement in the manifestations

of uraemic syndrome. The nature of uraemic toxins is yet uncertain.

However, they may be:

a. Urea, creatinine, uric acid, guanidines, phenols, products of nucleic acid

breakdown... etc.

b. Middle molecules which are substances of molecular weight 300 to 2000

Dalton.

g. 7. Failure of the renal hormonal functions including: Erythropoietin,

activation of vitamin D and disturbed Renin excretion

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BAB III

GEJALA DAN TANDA

3.1 MANIFESTASI KLINIS

Tinjauan mengenai perjalanan umum gagal ginjal kronik dapat diperoleh dengan

melihat hubungan antara bersihan kreatinin dengan laju filtrasi glomerulus sebagai persentase

dari keadaan normal, terhadap kreatinin serum dan kadar nitrogen urea darah (BUN) karena

massa nefron dirusak secara progresif oleh penyakit gagal ginjal kronik.

Perjalanan klinis umum gagal ginjal progresif dapat dibagi menjadi 3 stadium :

Stadium pertama

Disebut penurunan cadangan ginjal. Selama stadium ini kreatinin serum dan kadar

BUN normal, dan pasien asimtomatik. Gangguan fungsi ginjal hanya dapat terdeteksi dengan

memberi beban kerja yang berat pada ginjal tersebut, seperti tes pemekatan urine yang lama

atau dengan mengadakan tes GFR yang teliti.

Stadium kedua

Perkembangan tersebut disebut insufisiensi ginjal, bila lebih dari 75% jaringan yang

berfungsidtelah rusak (GFR besarnya 25% dari normal) . Pada tahap ini kadar BUN baru

mulai meningkat diatas batas normal. Peningkatan konsentrasi BUN ini berbeda-beda,

bergantung pada kadar protein dalam makanan. Pada stadium ini, kadar kreatinin serum

mulai meningkat melebihi kadar normal. Azotemia biasanya ringan ( kecuali bila pasien

mengalami stress akibat infeksi, gagal jantung, atau dehidrasi). Pada stadium insufisiensi

ginjal ini mulai timbul gejala-gejala nokturia dan poliuria ( akibat gangguan kemampuan

pemekatan). Gejala – gejala ini timbul sebagai respon terhadap stress dan perubahan

makanan atau minuman yang tiba-tiba. Pasien biasanya tidak terlalu memperhatikan gejala-

gejala ini, sehingga gejala tersebut hanya akan terungkap dengan mengajukan pertanyaan-

pertanyaan yang teliti. Nokturia (berkemih dimalam hari) didefinisikan sebagai gejala

pengeluaran urin waktu malam hari yang menetap sampai sebanyak 700 ml atau pasien

terbangun untuk berkemih beberapa kali waktu malam hari. Nokturia disebabkan oleh

hilangnya pola pemekatan urine diurnal normal sampai tingkat tertentu dimalam hari. Dalam

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keadaan normal perbandingan jumlah urine siang hari dan malam hari adalah 3:1 atau 4:1.

Sudah tentu, nokturia kadang – kadang dapat terjadi juga sebagai respon kegelisahan atau

minum cairan yang berlebihan, terutama teh, kopi atau bir yang diminum sebelum tidur.

Stadium ketiga

Disebut stadium akhir atau uremia. ESRD (gagal ginjal stadium akhir) terjadi apabila

sekitar 90% dari massa nefron telah hancur. Nilai GFR hanya 10% dari normal. Pada keadaan

ini kreatinin dan kadar BUN akan meningkat dengan sangat mencolok. Pasien mulai

mersakan gejala-gejala yang cukup parah. Pasien menjadi oligourik karena kegagalan

glomerulus.

Pada stadium akhir (sindrom uremik) terjadi kompleks gejala yang berkaitan dengan retensi

metabolit nitrogen.Dua kelompok gejala klinis dapat terjadi pada sindrom uremik. Pertama,

gangguan fungsi pengaturan dan ekskresi , kelainan volum cairan dan elektrolit, ketidak

seimbagan asam basa, retensi metabolit nitrogen dan metabolit lainnya, serta anemia yang

disebabkan oleh defisiensi sekresi ginjal. Kedua, timbul gejala yang merupakan gabungan

kelainan kardiovaskular, neuromuskular, saluran cerna dan kelainan lainnya.

CLINICAL FEATURES OF CHRONIC RENAL FAILURE

The details of this features include:

I. Gastrointestinal Manifestations:

a. Mouth: The high concentration of urea in saliva causes unpleasant taste (taste

of ammonia) and uraemic odour of the mouth (ammoniacal smell). The

tongue appears dry, dirty, brown or white coated and may be ulcerated. Later,

stomatitis, ulceration of the mouth and pharynx may occur. The mouth is

always dry due to dehydration and mouth breathing. Dental caries is also

common.

b. Stomach: Gastritis and sometimes gastric erosions may occur. This occurs

due to the high concentration of urea in saliva and gastric juice causing

chronic irritation of the gastric mucosa. The patient may suffer from anorexia,

nausea and vomiting. Upper G.I.T. bleeding (haematemesis) and melena may

even occur. Hiccough occurs in terminal stages of uraemia and is aggravated

by food. The cause of hiccough in uraemic patient is most probably due to

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irritation of the phrenic nerve or may be due to a central effect induced by

uraemic toxins.

c. Intestine: Usually, there is constipation due to dehydration, but diarrhea or

even bloody dysentery (uraemic dysentery) may occur in terminal uraemia.

This is due to urea deposition in the mucosa of the colon which leads to

mucosal ulceration which is liable to superadded infection which may cause

diarrhea. In severe cases of mucosal ulceration, there may be bleeding per

rectum.

II. Neurological manifestations: These include the following:

a. Cerebral: Headache, lassitude, drowsiness, insomnia, sometimes inverted

sleep rhythm, and vertigo are common manifestations of uraemia. These

manifestations are caused by the retained uraemic toxins. Uraemic coma

occurs in advanced cases.

b. Neuromuscular: The following are the common neuromuscular manifestations

of uraemia:

o Flabbing tremors (asterixis) and proximal myopathy with paradoxically

brisk tendon reflexes.

o Peripheral neuropathy is usually mixed (motor and sensory) and mainly

affecting legs. Patients present mainly with paraesthesia.

o Muscle twitches and convulsions are mainly due to hypokalaemia and

hypocalcaemia.

o Muscle weakness is due to hyperkalaemia, hyponatraemia and

hypovitaminosis D.

III. Hematologic and cardiovascular Manifestations:

a. Anaemia: Anaemia is a common feature of uraemia and usually normocytic

normochromic. It is partly responsible for many of the debilitating symptoms

of uraemia such as lethargy, tiredness and exertional dyspnea. The main

causes of anaemia in uraemic patient are the followings:

a) Bone marrow depression by the uraemic toxins and due to erythropoietin

deficiency.

b) Short life span of R.B.Cs due to the uraemic toxins.

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c) Nutritional deficiency due to dietatic restrictions and dyspepsia (protein,

Vit. B12, and folic acid)

d) Iatrogenic causes as frequent blood sampling in hospitalized patients and

the blood loss in the dialyzer at the end of each haemodialysisb session.

e) Bleeding tendency as GIT bleeding and metrorrhagia.

f) Aluminium toxicity

g) Bone marrow fibrosis due to hyperparathyroidism

h) Hypersplenism especially in multiple transfused patient. Sometimes

anaemia is microcytic hypochromic due to iron deficiency. White cell

count and platelet count are normal but with decreased functions.

b. Bleeding tendency: May result from: • Qualitative platelet defects: Platelet

aggregation is reduced and ADP release is inhibited leading to increased

capillary fragility and prolongation of bleeding time. • Increased fibrinolytic

activity of the blood because fibrinolysin is normally eliminated by the kidney.

• Anaemia: This bleeding tendency is corrected by dialysis, correction of

anaemia or administration of DDAVP or oestrogen.

c. Hypertension: Hypertension in uraemic patients is either due to high renin

secretion or salt and water retention. It occurs in about 80% of cases. In

uraemics, hypertension is characterised by resistance to drug treatment and by

tendency to develop malignant hypertension more than in other forms of

hypertension. Hypertension aggravates the renal disease which further

increases the blood pressure and a vicious circle is produced.

d. Uraemic pericarditis: This occurs due to deposition of urea on the smooth

inner surface of the pericardial sac changing it into rough surface. Continuous

friction between the visceral and parietal pericardium during cardiac systole

and diastole results in dry pericarditis which manifests by pericardial pain and

pericardial rub on auscultation. Later, haemopericardium develops which

progresses to cause cardiac compression (tamponade). This manifests

clinically by a triad of:

a) progressive systemic venous congestion with congested neck veins,

congested liver, and anasarca.

b) Progressive hypotension due to reduction of stroke volume as venous

return is progressively decreasing.

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c) Progressive increase in cardiac size on clinical examination and by plain

X-ray. Echo cardiography shows that the increase is mainly due to fluid

collection in the pericardium. It also shows the defective cardiac filling

and reduced stroke volume. Cardiac tamponade, if not treated urgently,

will be fatal. Treatment is by pericardiocentesis. If recurrent, treatment is

by making pericardial window (between pericardial sac and pleural sac) or

by partial pericardiectomy. Pericarditis is one of the signs of terminal

uraemia which indicates urgent dialysis.

e. Heart failure: This is usually a left sided heart failure which is due to: 1-

hypertension 2- anaemia 3- fluid overload 4- uraemic cardiomyopathy.

f. Cutaneous manifestations: • Muddy face (sallow skin), due to retention of

some toxins (urochromogens). • Puffy face, due to salt and water retention. •

Pallor, due to anaemia. • Dry skin with urea frost (white spots due to

deposition of urea present in high concentration in the sweat). Also the skin is

fragile, thin and bruises easily. • Pruritis results from skin dryness or from

irritation of the cutaneous sensory nerves by calcium deposits or by

parathormone. • Purpura and skin infection. • Nails may be white with tips

discoloured brown.

g. Respiratory manifestations: These include the following: • Kaussmaul's

(acidotic or hissing) breathing • Exertional dyspnea, paroxysmal nocturnal

dyspnea with heart failure. • Increased incidence of pulmonary infection. •

Rarely, dry uraemic pleurisy.

h. Ocular manifestations: These include the following: • Retinopathy. • Uraemic

amaurosis (rare): which is sudden transient loss of vision. • Red eye due to

conjunctival congestion and calcium deposition. • Calcium may be deposited

as plaques in the conjunctiva.

i. Musculo-Skeletal and soft tissue manifestations: These include the following:

a) Muscular : fatigue, and wasting (myopathy) which is mainly proximal in

lower limbs (Waddling gait). It is due to retained uraemic toxins,

electrolyte disturbances, vitamin D deficiency, hyperparathyroidism and

nutritional deficiency

b) Skeletal : include bone aches, fractures, and deformity in childhood cases.

Gout (uric acid deposition) and pseudogout (calcium deposition) cause

joint pains.

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c) Soft tissue calcification which manifests according to the tissue involved

e.g. pruritus when skin and sensory nerves are involved, red eye when

conjunctiva is affected, arthritis when calcium deposition involves

periarticular tissues, and finger tips gangrene when small arterioles are

involved (Calcifelaxis)

j. Gonadal disturbances: The following gonadal disorders are commonly seen

in uraemic patients: • In males : decreased libido, impotence, gynecomastia,

reduced spermatogenesis. • In females : decreased libido, infertility and

menstrual dysfunctions.

k. Endocrinal disturbances: The following are the endocrine disorders which are

common in uraemic patients: • Hyperparathyroidism • Lack in activation of

vit. D. • Increased renin activity • Lack of erythropoietin • Decreased

testosterone level resulting in a decreased libido, potency and

spermatogenesis. • Increased prolactin and L.H. causing menstrual disorders,

gynecomastia and infertility. • Insulin: there are two opposing effects of

uraemia on insulin. The first effect is tissue resistance to insulin due to the

uraemic milieu. The second is decreased renal tubular degradation of insulin

with a consequent increase in the insulin half life. The upper hand is usually

for the second effect with consequent fall in insulin requirement (insulin daily

dose) in diabetic patients when they become uraemic. Features of the

underlying disease may be present: As manifestations of D.M., SLE or renal

stone disease.

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3.2 KLASIFIKASI

Pada individu dengan GGK, klasifikasi stadium ditentukan oleh nilai laju filtrasi

glomerulus (LFG), yaitu stadium yang lebih tinggi menunjukkan nilai LFG yang lebih rendah

berdasarkan ada atau tidak adanya penyakit ginjal.

Klasifikasi penyakit ginjal kronik didasarkan atas dua hal yaitu :

Derajat (stage) yaitu berdasarkan LFG dengan rumus Kockroft – Gault.

(Pada wanita x 0,85)

Klasifikasi atas dasar diagnosis.

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BAB IV

DIAGNOSIS

4.1 DIAGNOSIS GGK

Bila GGK telah bergejala, umumnya diagnosis tidak sukar ditegakkan. Gejala dan

tanda GGK akan dibicarakan sesuai dengan gangguan sistem yang timbul.

4.2 PEMERIKSAAN PENUNJANG PADA GGK

Pemeriksaan Laboratorium

Laboratorium darah

BUN, Kreatinin, Elektrolit (Na,K,Ca,Phospat), Hematologi

(Hb,Trombosit,Ht,Leukosit), Protein, Antibody (kehilangan protein dan

immunoglobulin).

Pemeriksaan Urine

Warna, PH, BJ, Kekeruhan, Volume, Glukosa, Protein, Sedimen, SDM, Keton, SDP,

TKK/CCT.

Pemeriksaan EKG

Untuk melihat adanya hipertropi ventrikel kiri, tanda perikarditis, aritmia, dan

gangguan elektrolit (hiperkalemia, hipokalsemia).

Pemeriksaan Radiologi

Renogram, Intravenous Pyelography, Retrograde, Renal Aretriografi dan Venogrfi,

CT Scan, MRI, Renal biopsi, Pemeriksaan Rontgen dada, pemeriksaan rontgen

tulang, foto polos abdomen.

Pemeriksaan Ultrasonografi (USG)

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Menilai besar dan bentuk ginjal, tebal korteks ginjal, kepadatan parenkim ginjal,

anatomi sistem pelviokalises, ureter proksimal kandung kemih serta prostat.

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BAB V

PENATALAKSANAAN

5.1 PENATALAKSANAAN UMUM

Penatalaksanaan terhadap gagal ginjal meliputi :

1. Restriksi konsumsi cairan, proten dan fosfat

2. Obat-obatan : diuretik untuk meningkatkan urinasi; alumunium hidroksida untuk terapi

hiperfosfatemia; anti hipertensi untuk terapi hipertensi serta diberi obat yang dapat

menstimulasi produksi RBC seperti epoetin alfa bila terjadi anemia.

3. Dialisis

4. Transplantasi Ginjal.

Perubahan Fungsi Ginjal.

Ginjal mengendalikan tekanan darah melalui beberapa cara :

Jika tekanan darah meningkat, ginjal akan menambah pengeluaran garam dan air,

yang akan menyebabkan berkurangnya volume darah dan mengembalikan tekanan

darah ke normal.

Jika tekanan darah menurun, ginjal akan mengurangi pembuangan garam dan air,

sehingga volume darah bertambah dan tekanan darah kembali ke normal.

Ginjal juga bisa meningkatkan tekanan darah dengan menghasilkan enzim yang

disebut renin, yang memicu pembentukan hormon angiotensi, yang selanjutnya akan

memicu pelepasan hormon aldosteron.

Ginjal merupakan organ penting dalam mengendalikan tekanan darah, karena itu

berbagai penyakit dan kelainan pada giinjal bisa menyebabkan terjadinya tekanan darah

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tinggi. Misalnya penyempitan arteri yang menuju kesalah satu ginjal (stenosis arteri renalis)

bisa menyebabkan hipertensi. Peradangan dan cedera pada salah satu atau kedua ginjal juga

bisa menyebabkan naiknya tekanan darah.

Beberapa komplikasi hipertensi yang terjadi antara lain :

a. Retinopati hipertensif

b. Penyakit kardiovaskular

c. Penyakit serebrovaskular

d. Penyakit ginjal seperti nefrosklerosis.

5.2 DIET PENYAKIT GINJAL KRONIK

Tujuan diet penyakit ginjal kronik

a. Mencapai dan mempertahankan status gizi optimal dengan memperhitungkan

sisa fungsi ginjal, agar tidak memberatkan kerja ginjal.

b. Mencegah dan menurunkan kadar ureum darah yang tinggi (uremia)

c. Mengatur keseimbangan cairan dan elektrolit

d. Mencegah atau mengurangi progresivitas gagal ginjal, dengan memperlambat

turunnya laju filtrasi glomerulus.

Syarat Diet

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a. Energi cukup, yaitu 35 kkal/kg BB

b. Protein rendah, yaitu 0,6-0,75 g/kg BB. Sebagian harus bernilai biologik

tinggi.

c. Lemak cukup, yaitu 20-30% dari kebutuhan energi total. Diutamakan lemak

tidak jenuh ganda.

d. Karbohidrat cukup, yaitu kebutuhan energi total dikurangi energi yang berasal

dari protein dan lemak.

e. Natrium dibatasi apabila ada hepertensi, edema, asites, oliguria, atau anuria.

Banyaknya natrium yang diberikan antara 1-3 g.

f. Kalium dibatasi (40-70 mEq) apabila ada hiperkalemia (kalium darah > 5,5

mEq), oliguria atau anuria.

g. Cairan dibatasi, yaitu sebanyak jumlah urine sehari ditambah pengeluaran

cairan melalui keringat dan pernapasan (± 500 ml)

h. Vitamin cukup, bila perlu diberikan suplemen piridoksin, asam folar, vitamin

C, dan vitamin D.

Jenis Diet dan indikasi pembelian

Ada tiga jenis diet yang diberikan menurut berat badan pasien, yaitu;

a. Diet protein rendah I ; 30 g protein. Diberikan kepada pasien dengan berat badan 50

kg.

b. Diet protein rendah II : 35 g protein. Diberikan kepada pasien dengan berat badan 60

kg.

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c. Diet protein rendah III : 40 g protein. Diberikan kepada pasien dengan berat badan 65

kg.

Karena kebutuhan gisi pasien penyakit ginjal kronik sangat bergantung pada keadaan

dan berat badan perorangan , maka jumlah protein yang diberikan dapat lebih tinggi atau

lebih rendah dari pada standar. Mutu protein dapat ditingkatkan dengan memberikan asam

amino esensial murni.

Cardiovascular disease (CVD)is the leading cause of death in patients with CKD.

o Reducing risk factors for development of CVD is beneficial.

E.g. treatment of hyperlipidemia, lifestyle and dietary changes

Tight blood pressure control:

o Reducing damage due to the end organ effects of hypertension on the kidney

as well as the heart.

o Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II

receptor blockers(ARBs) block the effects of angiotensin II on (i) sodium and fluid

retention, (ii) vasoconstriction, (iii) stimulating ADH release, (iv) stimulating

aldosterone release, and (v) inducing a sympathetic response.

ACEIs and ARBs also slow down progression of proteinuria in patients

with diabetic CKD.

Diabetes management:

o Tight glucose management slows the progression of vascular and heart

disease.

Avoidance of IV contrast, NSAIDs, and nephrotoxic drugs:

o These agents can potentially induce an acute kidney injury (AKI) on the

underlying kidney disease and therefore exacerbate the baseline CKD.

Diet:

o Mixed evidence exists whether dietary protein restriction is beneficial in

slowing disease progression.

o Proteins affect the renal hemodynamics, raising the GFR, in hypothesized 2

ways.

Hormonal effects – proteins cause secretion of glucagon, IGF-1 and

kinins, all of which have been shown to raise the GFR.

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Tubuloglomerular effects – high amino acid (AA) filtration leads to

increased AA and hence the sodium uptake in the proximal convoluted tubule. A

decreased sodium delivery to the distal convoluted tubule leads to the rennin-

angiotensin system activation via the macula densa and these work to raise the

GFR (mechanisms above)

o Controlling hyperphosphatemia: Protein restriction also limits phosphorus

consumption. Hyperphosphatemia plays a major role in the progression of renal

osteodystrophy. Phosphate binders are used to reduce phosphate absorption through

the GI tract. 

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