NEPHROLOGI PWM Olly Indrajani 12-6-2012.

Presentasi berjudul: "NEPHROLOGI PWM Olly Indrajani 12-6-2012."— Transcript presentasi:

1 NEPHROLOGI PWM Olly Indrajani

2 Nephrologi Batasan: ilmu yg mempelajari fungsi dan patofisiologi ginjal dan saluran2 penunjangnya serta penyakit2nya. Dasar2 yg perlu: 1. Anatomi & histologi 2. Fisiologi & biokimia 3. Patologi & laborat.

3 Introduction: 150gm: each kidney
1700 liters of blood filtered  180 L of G. filtrate  1.5 L of urine / day. Kidney is a retro-peritoneal organ Blood supply: Renal Artery & Vein One half of kidney is sufficient – reserve kidney function: Filtration, Excretion, Secretion, Hormone synthesis.

4 STRUCTURE OF THE KIDNEYS

5 Kidney Anatomy:

6 STRUCTURE OF THE KIDNEYS

7 Kidney Anatomy:

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9 Introduction Functions of the kidney: Diseases of the kidney
excretion of waste products regulation of water/salt maintenance of acid/base balance secretion of hormones Diseases of the kidney glomeruli tubules interstitium vessels

10 Renal Pathology Outline
Glomerular diseases: Glomerulonephritis Tubular diseases: Acute tubular necrosis Interstitial diseases: Pyelonephritis Diseases involving blood vessels: Nephrosclerosis Cystic diseases Tumors

11 Pendekatan klinis: Anamnesis Pemeriksaan fisik Laboratorium
Pem. Penunjang: a. radiologis: - BOF - IVP - CT Scan - MRI b. biopsi ginjal.

12 Anamnesis: 1. Keluhan utama:
a. dysuria,polyuri,polakisuri, b. edema c. nyeri d. penurunan fungsi ginjal e. hematuria 2. Penyakit terdahulu 3. Anamnesa keluarga.

13 Pemeriksaan fisik: inspeksi auskultasi perkusi palpasi

14 Pem.laboratorium: 1.Urinalisis: - pH, BJ, warna - albumin - reduksi - bilirubin/urobilin - sedimen: eri,leko, kristal,silinder epitel. 2. Kimia darah: kreatinin plasma klirens kreatinin konsentrasi ureum plasma.

15 Abnormal findings Azotemia:  BUN, creatinine
Uremia: azotemia + more problems Acute renal failure: oliguria Chronic renal failure: prolonged uremia

16 Clinical Syndromes: Nephritic syndrome. Nephrotic syndrome.
Oliguria, Haematuria, Proteinuria, Oedema. Nephrotic syndrome. Gross proteinuria, hyperlipidemia, Acute renal failure Oliguria, loss of Kidney function - within weeks Chronic renal failure. Over months and years - Uremia

17 Nephrotic syndrome Nephritic syndrome Massive proteinuria
Hypoalbuminemia Edema Hyperlipidemia/-uria Nephrotic syndrome Hematuria Oliguria Azotemia Hypertension Nephritic syndrome

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22 What are the possible causes of this appearance of the kidneys?

23 Glomerulopathy Proses inflamasi glomerulus
Terjadi akibat berbagai sebab yg berbeda etiologi, patofisiologi ataupun patogenesanya Dulu dikenal dg istilah glomerulonephritis Peyebab utama Gagal Ginjal Manifestasi klinis bisa tanpa gejala sampai gejala yang berat Terpenting:menghambat progresifitas kerusakan

24 Klasifikasi glomerulopathy
Klasifikasi klinis Klasifikasi lesi histopatologi Klasifikasi berdasar etiologi&patogenesis Klasifikasi berdasar proses imunologi

25 Klasifikasi klinis: Kelainan urine tanpa keluhan Sindroma nefrotik
Sindroma nefritik akut Sindroma nefritik kronik Sindroma RPGN (Rapid Progressive Glomerulonephritis)

26 Klasifikasi lesi histopatologis
Lesi minimal Lesi glomerulosklerosis fokal segmental Lesi mesangioproliferatif (IgM) Lesi mesangioproliferatif (IgA) (penyakit Berger) Lesi proliferatif akut Lesi membranoproliferatif Lesi membranosa Lesi bulan sabit (crescentic) Lesi glomerulosklerosis.

27 Klasif. Etiologi& patogenesa
Kelainan imunologi Kelainan metabolik: - nefropati diabettik - nefropati as. Urat - amiloidosis primer/sekunder Kelainan vaskuler Disseminated Intravascular Coagulopathy (DIC) Kel. Herediter: sindr.Alport, peny.Fabry Patogenesis tak diketahui: lipoid nefrosis

28 Klasifikasi. imunologi
Peny. Kompleks immun: 1. Circulating immune complex: Nephropathy Berger Henoch-Schonlein Purpura Nefritis Lohlein (endokar.bakteri) 2. Pembentukan komplek imun insitu: Glom. Post Streptococcus infection Glom. Membranosa b. Peny.AGBM: sindroma Goodpasteur.

29 Minimal change disease

30 Normal glumerular structure
Minimal change disease Normal glumerular structure

31 Normal glomerulus Minimal change disease

32 Focal Segmental Glomerulosclerosis
Primary or secondary Some (focal) glomeruli show partial (segmental) hyalinization Unknown pathogenesis Poor prognosis

33 Focal segmental glomerulosclerosis

34 Membranous Glomerulonephritis
Autoimmune reaction against unknown renal antigen Immune complexes Thickened GBM Subepithelial deposits

35 Membranous glomerulonephritis

36 Post-infectious glomerulonephritis

37 IgA Nephropathy Common!
Child with hematuria after (URI) Upper Respiratory Infection IgA in mesangium Variable prognosis

38 IgA nephropathy

39 Sindroma nefrotik Batasan: sindroma klinik ok.berbagai penyakit yg ditandai dg meningkatnya perm.membran basal glomerulus thd protein dg.G/ utama proteinuri > 3,5 gram/24 jam. Patofisiologi: meningkatnya perm.GBM  proteinuri Bila loss albumin> produksihipoalbuminemi Hipoalbumin  edema anasarka Hiperlipidemia : patogenesanya belum jelas Ggn. Metab.lemaklipiduria: oval Fat Bodies

40 Etiologi: Glomerulopati primer Glomerulopati sekunder:
a. infeksi: sifilis, malaria, TBC, tifus,virus b. nefrotoksin: diuretik merkuri, bismuth, preparat emas c. allergen: sengatan lebah, gigitan ular, tepung sari. d. peny.kolagen: SLE, PAN,dermatomiositis, peny.Goodpastur, giant cell arteritis. e. peny.lain: Hodgkin, mieloma, leukemi, DM, feokromositoma, miksedema, gagal jantung kongestif, SBE, perikarditis konstriktif, amiloidosis, trombosis vena renalis, obstruksi vena cava inferior.

41 Nephrotic Syndrome Massive proteinuria Hypoalbuminemia Edema
Hyperlipidemia Lipiduria

42 Gejala klinis: kencing berbuih
Sembab tungkai yg progresif s/d anasarka Sesak nafas (bila ada cairan pleura) Sebah dan perut buncit (bila ada asites)

43 Pemeriksaan & diagnosis
1.urinalisis: - proteinuri +3  +4, lipiduria - torak eritrosit: khas utk SN prim - glukosuri: bila ok DM. 2.ekskresi protein 24 jam (Esbach) 3.kadar albumin serum 4. Elektroforesa protein serum & protein urin 5.kadar lipid plasma 6.tes imunologi 7.pem.radiologi: BOF, IVP, foto thorax 8. Biopsi ginjal.

44 Diagnosis banding: Penyakit dg edema dan hipoalbuminemi lain:
Penyakit hati kronis Malnutrisi Gagal jantung

45 Penatalaksanaan Diet TKTP rendah garam. Obat: a. diuretik
b. antiagregasi platelet: dipiridamol c. infus albumin d. kortikosteroid:prednison 2mg/kg/hr 4 minggu lalu tapering off e. imunosupresif: siklofosfamid 2 mg/ kg/hr atau klorambusil 0,2 mg/kg/hr selama 8 minggu. 3. Koreksi penyakit primernya

46 Komplikasi: Kelainan kardiovaskuler (atherosclerosis) Shock hipovolemi
Mudah terserang infeksi Gagal ginjal kronik.

47 UTI

48 Identify the pathophysiology and clinical manifestations of urinary tract infections.
UTI (Cystitis): Evaluation: History and physical examination includes queries about risk factors; s/s such as pain, odor, hematuria, vital signs, temperature, U/A, culture. Treatment: Antimicrobial therapy, pain medication.

49 Identify the pathophysiology and clinical manifestations of urinary tract infections.
Pyelonephritis: An infection of the renal pelvis and interstitium. Causes include: kidney stones, reflux, pregnancy, neurogenic bladder, instrumentation, female sexual trauma. Pathophysiology: Can be spread by ascending microorganisms along the ureters or blood borne pathogens. Inflammation affecting the pelvis, calyces, medulla. Signs/Symptoms: Fever, chills, flank or groin pain, frequency, dysuria. Evaluation: Urine culture, U/A, clinical s/s, radiologic evaluation. Treatment: Antibiotic therapy, pain management

50 Describe glomerulonephritis including etiology, pathophysiology, and clinical manifestations.
Inflammation of the glomerulus Glomerular disease is the most common cause of chronic and end-stage renal failure. Etiology (Varied): Immunological causes (most common), drugs, toxins, vascular disorders, and systemic diseases Types: Acute, rapidly progressive, chronic.

51 Describe glomerulonephritis including etiology, pathophysiology, and clinical manifestations.
Urine Hematuria w/red blood cell casts Proteinuria exceeding 3-5 g/day (associated w/nephrotic syndrome) Decrease in UOP/decrease in GFR Evaluation Defined by progressive development of clinical manifestations and laboratory findings. Abnormal U/A w/ proteinuria, RBC's, WBC’s, and casts. Microscopic evaluation from renal biopsy shows specific determination of renal injury and type of pathologic condition. Treatment: Treating the primary disease, preventing or minimizing immune responses, symptomatic treatment for edema, hypertension, infections (antibiotics), corticosteroids (decrease inflammatory response).

52 Describe nephrotic syndrome including etiology, pathophysiology, and clinical manifestations.
Excretion of 3.5 g or more of protein/day, hypoproteinemia, edema. Characteristic of glomerular injury Etiology: Any condition causing increase in glomerular membrane permeability: glomerulonephritis, diabetes, infectious process, toxins, drugs, malignancies. Pathophysiology: Plasma proteins (albumin, immunoglobulins) cross the injured glomerular filtration membrane. Basement membrane of the glomerulus looses negative charge. Hypoalbuminemia ensues. Loss of albumin stimulates lipoprotein synthesis by the liver and hyperlipidemia.

53 Describe nephrotic syndrome including etiology, pathophysiology, and clinical manifestations.
Signs/Symptoms Proteinuria, edema, hyperlipidemia, lipiduria, loss of vitamin D leading to hypocalcemia. Evaluation: Protein level in urine is > 3.5 g. Serum albumin decreases, and cholesterol, phospholipids, and triglycerides increase. Pathologic condition is identified by biopsy. Treatment: Diet (normal protein, low fat, salt restriction), treat cause if known, diuretics, steroids, albumin IV. Monitor closely for hypovolemia, hypokalemia or hyperkalemia secondary to renal insufficiency.

54 Terimakasih