Decsa Medika Hertanto

PEMERIKSAAN KLINIS NEFROLOGI PRAKTIS Mengenal dengan mudah penderita Ginjal

1. Regulasi Cairan Ekstraseluler &

Tekanan Darah

2. Regulasi Osmolaritas

3. Regulasi Keseimbangan Elektrolit

4. Regulasi Keseimbangan Asam

Basa

5. Pembuangan sampah metabolit

6. Produksi Hormon

PAHAMI FUNGSI

GINJAL

• Arteri afferent > efferent

• Basal membran itu semipermeable

membran

• Terjadi proses difusi di basal

membran (untuk solut dengan ukuran

kecil)

• Protein dan molekul lain yang tidak

terfilter akan keluar ke efferent dan

menyebabkan peningkatan onkotik

untuk membantu proses reabsorbsi

pada peritubuler

• Jika volume cairan dari afferent besar

maka terjadi proses konveksi dimana

terjadi peningkatan tekanan pada

glomerulus sehingga membuat

beberapa solut besar ikut tersaring ke

basal membran

POLIURIA

Penyakit Ginjal

• Pada fase awal penyakit ginjal

justru yang pertama akan

menjumpai adalah dokter umum,

perawat, tenaga kesehatan lain

PENYAKIT GINJAL PGK

Adanya gangguan FUNGSI atau STRUKTUR > 3 Bulan

(National Kidney Foundation.K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification and Stratification. Am J Kidney Dis 39:S1-S266, 2002 (suppl 1))

NKF K/DOQI

(Sumber : IRR (Indonesian Renal Registry) 2015}

Klinis :

a. Sesuai penyakit yang mendasari (DM, ISK, HT,SLE)

b. Sindrom uremia

c. Gejala komplikasi (HT, Anemia, HF, Asidosis

metabolik, GGN elektrolit)

Laboratoris:

a.Sesuai penyakit yang mendasari

b.Penurunan fungsi ginjal : ureum ↑, kreatinin serum ↑ ,penurunan LFG.

c.Kelainan biokimiawi darah (Hb ↓, UA ↑, K↑, hiponatremia, hiper

/hipokloremia, fosfat ↑, kalsium ↓, asidosis metabolik hipokalsemia

d.Kelainan urinalisis (proteinuria, hematuria, leukosuria, sedimenuri)

Radiologis:

USG : ukuran ginjal yang mengecil,

korteks menipis, hidronefrosis atau batu

ginjal, kista, massa, kalsifikasi

DIAGNOSIS PGK

(KDIGO 2012 Clinical Practice Guideline for the Evaluation and management of Chronic Kidney Disease, vol.3, issue 1)

STADIUM PGK

Derajat LFG (ml/mnt/1,73m2) Rencana tatalaksana

1 ≥ 90 Terapi penyakit dasar , kondisi komorbid, evaluasi perburukan fungsi ginjal,

memperkecil resiko cardiovaskuler

2 60-89 Menghambat perburukan fungsi ginjal

3 30-59 Evaluasi dan terapi komplikasi

4 15-29 Persiapan terapi pengganti ginjal

5 < 15 Terapi pengganti ginjal

1. Pengobatan untuk penyakit dasar

2. Pengendalian keseimbangan air dan garam

3. Diet rendah protein dan tinggi kalori

4. Pengendalian gangguan keseimbangan elektrolit dan asam-basa

5. Pengelolaan hipertensi

6. Pengelolaan anemia

7. Deteksi dan pengobatan infeksi

8. Tatalaksana pengobatan dan keselamatan pasien

9. Persiapan dialisis dan transplantasi

10. Terapi pengganti ginjal

•Nutrisi : Asupan kalori 30 – 35 kkal/kgBB/hr

•Protein :

•Pasien non dialisis 0,6 – 0, 75 gr/kgBB/hr

•Pasien hemodialisis 1 – 1,2 gr/kgBB/hr

•Pasien Peritoneal dialisis 1,3 gr/kgBB/hr

•Pengaturan asupan lemak : 30 – 40 % dari kalori total.

•Pengaturan asupan karbohidrat : 50 – 60% dari kalori total

•Natrium : < 2 gr/hari

•Kalium : 40 – 70 mEq/hari.

•Restriksi Fosfat

•Asam Folat pasien HD : 5 mg

•Air : jumlah urin 24 jam + 500 ml (Insensible Water Loss)

PENYAKIT GINJAL AKI

• Increase in SCr by ≥ 0.3 mg/dl (≥ 26.5 µmol/l) within 48 hours; or

• Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have

occurred within the prior 7 days; or

• Urine volume <0.5 ml/kg/h for 6 hours.

KDIGO, 2012 ]

KDIGO, 2012

KDIGO, 2012

KDIGO, 2012

PRERENAL

POSTRENAL

INTRARENAL

Hypovolaemia

Haemorrhage

Volume depletion

Renal fluid loss (over-diuresis)

Third space (burns, peritonitis, muscle trauma)

Impaired cardiac function

Congestive heart failure

Acute myocardial infarction

Massive pulmonary embolism

Systemic vasodilatation

Anti-hypertensive medications

Gram negative bacteraemia

Cirrhosis

Anaphylaxis

Increased vascular resistance

Anaesthesia

Surgery

Hepatorenal syndrome

NSAID medications

Drugs that cause renal vasoconstriction (i.e. cyclosporine)

Ronco, 2016

Sigmund, 2016

Acute post-infectious

glomerulonephritis

Lupus nephritis

IgA glomerulonephritis

Infective endocarditis

Goodpasture syndrome

Wegener disease Renal ischaemia

(shock, complications of surgery, haemorrhage, trauma,

bacteraemia, pancreatitis, pregnancy)

Nephrotoxic drugs

(antibiotics, antineoplastic drugs, contrast media, organic

solvents, anaesthetic drugs, heavy metals)

Endogenous toxins

(myoglobin, uric acid)

Ronco, 2016

Interstitium

Infections

(bacterial, viral)

Medications

(antibiotics, diuretics, NSAIDs, and many more drugs)

Vascular

Large vessels

(bilateral renal artery stenosis, bilateral renal vein thrombosis)

Small vessels

(vasculitis, malignant hypertension, atherosclerotic or thrombotic emboli,

haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura)

Ronco, 2016

Extrarenal obstruction

Prostate hypertrophy

Improperly placed catheter

Bladder, prostate or cervical cancer

Retroperitoneal fibrosis

Intrarenal obstruction

Nephrolithiasis

Blood clots

Papillary necrosis

Ronco, 2016

• Volume restriction (eg, low fluid intake, gastroenteritis)

• Nephrotoxic drug ingestion (eg, nonsteroidal anti-inflammatory drugs [NSAIDs],

aminoglycosides)

• Exposure to iodinated contrast agents within the past week

• Infection/Sepsis

• Trauma

• Blood loss or transfusions

• Exposure to toxic substances

• Oliguric or anuric; history of kidney stones, BPH

Anamnesis of Etiologic Factors

Ronco, 2016

Anamnesis of Risk Factors

• Hypertension

• Chronic heart failure

• Diabetes

• Liver disease

• Obesity

• Multiple myeloma

• Chronic infection

• Myeloproliferative disorder

• Connective tissue disorders

• Autoimmune diseases

Ronco, 2016

Physical Examination

• Physical Examination : Circulatory, systemic, obstruction

• Urine Production & Urinalysis

• Serologies if indicated

• Other Examinations

Makris, 2016

• The urinalysis with sediment examination by urine microscopy is normal or near

normal in prerenal disease, unless superimposed on another cause.

• Granular, muddy brown casts in urine sediment are highly suggestive of tubular

necrosis. The presence of tubular cells or tubular cell casts also supports the

diagnosis of ATN. Often, oxalate crystals are observed in cases of ATN.

• WBC casts suggests pyelonephritis or acute interstitial nephritis.

• Eosinophils, as visualized with Wright Hansel stain, suggests interstitial nephritis

• Uric acid crystals may represent ATN associated with uric acid nephropathy. Calcium

oxalate crystals are usually present in cases of ethylene glycol poisoning.

Ronco, 2016

• Radiology : USG

• Evaluating renal disease and

obstruction

• Renal Biopsy : Intrarenal Cause and/or

Transplant

Ronco, 2016