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Nephrology and Hypertension
Agreement of Supervisor
Dr. Maimun Syukri SpPD, KGH, FINASIM
MANAGEMENT OF NEPHROTIC SYNDROME TYPE GLOMERULOSCLEROSIS
Alfi Syahrin, Abdullah, Maimun Syukri Division of Nephrology and Hipertension Department of Internal Medicine RSUDZA/ Medical Faculty of UNSYIAH Banda Aceh
Abstract Focal segmental glomerulosclerosis (GSFS) is part of the primary glomerulonephritis causing nephrotic syndrome characterized by edema anasarka, massive proteinuria> 3.5 g / day, hypoalbuminemia, hypercholesterolemia, and lipiduria. Diagnosis of GSFS confirmed by histopathological findings such as glomerular sclerosis and hialinosis. Reported one case of a man, 24 years old, with complaints swelling all over his body since 17 years ago, with a history of normal kidney function tests, and examinations +4 proteinuria, patients had received the drug methylprednisolone and cyclophosphamide. On examination vital signs within normal limits. In the laboratory: routine urine sediment and proteinuria albumin leukocytes 25: 300 (+4). Patients are encouraged by the results of renal biopsy expertise: diffuse global glomerulosclerosis with extensive tubulointerstitialis nephritis. Biopsy was performed in RSCM. Subsequently the patient received cyclosporine 2x75 mg, methylprednisolone 16 mg 10-0, methylprednisolone 8 mg 0-0-1, losartan 1x50 mg, simvastatin 10 mg 1x1, and vitamins. Patients currently undergoing refurbishment and control poly regularly. Key word: nephrotic syndrom, proteinuria, biopsy, glomerulosclerosis
losartan 1x50 mg. In the laboratory tests: Hb 15.010.5 g / dl. Subsequently the patient received cyclosporine 75 mg 2x1 . ct 5.6% GSFS. hypoalbuminemia. methylprednisolone 16 mg 1-0-0. and diabetes mellitus I. physical examination. GN membranoproliferatif (GNMP) due to systemic diseases such as lupus. hypercholesterolemia. Patients with renal biopsy results: diffuse global glomerulosclerosis with extensive tubulointerstitialis nephritis. nitrite (-). leukocytes 6000. II. difftel 5/0/1/58/26 / 10. Required to establish the diagnosis anamnesa tight. 24 years old.8 million. On examination vital signs BP: 130/80 mmHg. glucose (normal). with a history of normal kidney function tests.5% GNMN. Of 387 renal biopsies SN adult patients in Jakarta between 1990 to 1999 and representative to be reported.7. pH 7. Patients currently undergoing refurbishment and control poly regularly. platelets 216. GN mesangioproliferatif 14. urea 20. simvastatin 10 mg 1x1.5. albumin: 300 (+4).CASES Reported one case of a man.000. massive proteinuria> 3. and lipiduria 1. GNLM obtained 44. patients had received the drug methylprednisolone and cyclophosphamide. GNMP 8%. Biopsy was performed in RSCM. and examinations +4 proteinuria. Nephrotic syndrome can be caused by primary and secondary GN primary or idiopathic glomerulonephritis is the most common cause of SN. erythrocytes 5. with complaints swelling all over his body since 17 years ago. Routine urine examination macroscopic: yellow. and vitamins. Glomerulonefritis primer GN minimal lesions (GNLM) Glomerulonefritis secunder due to infections such as the GN post streptococcal infection or hepatitis B virus infection Glomerulosklerosis focal segmental (GSFS) caused by drugs such as nonsteroidal antiinflammatory drugs or preparations organic gold GN membranosa (GNMN). 25 leukocytes. 2 .INTRODUCTION Nephrotic syndrome (SN) is one of the clinical manifestations of glomerulonephritis (GN) is characterized by anasarka edema. and 6.2%. T: 36. HT 47%. creatinine 0. RR: 21 x / i. N: 80 x / I. methylprednisolone 8 mg 0-0-1. bj 1. bt 2.7%. laboratory and histopathological examination. LED 25 mm / hour.5 g / day. 11.
Common symptoms are prominent fatigue and malaise. Usually can not be revealed by immunofluorescence. which cause abnormalities in the glomerulus. Bowman space was not narrowed. After beberapan weeks or months. resulting in low precision diagnosis of glomerulonephritis. routine blood and kidney function within normal limits. Clinical picture is essential is that the course of the disease with acute onset. often with diarrhea. Tubule atrophy. Lesions often occur at the beginning of the nephron juxtamedular and disease associated with scarring periglomerullar. The patient also complained of back pain. piston. intersitium or vascular. and in severe cases quickly deteriorated into renal failure or known as Rapidly Progressive Glomerulonephritis (RPGN). legs felt heavy and cold. Kidney tissue obtained from renal biopsy actions that can not be done at all hospitals in Indonesia. Conclusion: diffuse global glomerulosclerosis with extensive tubulointerstitialis nephritis 3 .5 g% and lasts a long time is always accompanied by signs of malnutrition such as hair and nail changes. tubule atrophy and interstitial fibrosis in the affected glomeruli. it is not uncommon is the only complaint of the nephrotic syndrome. in some cases found that low back pain can be caused by capsular swelling of the kidney. Examination of vital signs. Diagnosis of GSFS confirmed by histopathological findings such as glomerular sclerosis and hialinosis. In patients with renal biopsy was performed in RSCM with the results: a.DISCUSSION Swollen is a major complaint. puffy settled. In the severe nephrotic syndrome with serum albumin less than 1. legs. Bersebukan fibrotic interstitial chronic inflammatory cells were mainly around the sclerotic glomeruli. and genitalia. Overview histopathology. tiroidisasi local experience. Bowman hoops not thickened. Immunofluorescence microscopy Renal biopsy was not representative. stomach. Blood vessel walls thicken b. Diagnosis of this disease requires histopathological examination of kidney tissue to see abnormalities in the glomerulus and interstium. In the nephrotic syndrome with severe hypoalbuminemia (serum albumin less than 2 grams%) swelled the whole body will be called anasarka. and the kidney may swell giving pain on palpation. clinical correlations in GN10 Glomerulonephritis is generally caused by inflammation in the glomerulus. Onset infiltrate mainly morning and gone during the day. Location is usually the puffy eyelids. In the routine examination of urine albumin proteinuria found: 300 (+4). Encountered in patients with a history of swollen since he was 7 years old and has reduced within 1 month prior to the visit to the poly. Light microscope Renal biopsy preparation consists of 2 pieces of tissue containing approximately 15 glomeruli which most (11 glomeruli) had sclerosing total / subtotal.III. Patients complain of shortness of breath. Muercke lines on nails. Glomerular others seem normoseluler. mesangium. parotid gland enlargement. most containing erythrocytes. Muscles atrophy of skeletal muscle primarily (muscle wasting) due to negative balance of nitrogen or a side effect of long-term corticosteroid administration. Electron microscopy can show the loss of immune deposits and mesangial sclerosis.
4 grams / day. The regimen used in those with potassium levels <5 mEq / liter and eGFR> 30 ml/menit/1.1 to 5. Maximum dose of MMF in GFR> 60 ml / min at 2000 mg and 1500 mg in the eGFR <60 ml / min. simvastatin 10 mg 1x1. when used orally dose 1.5-2 mg / kg / day and can be continued 6 to 12 months depending on the response.. Bianchi C. cyclosporine. in their study done by using intensive regimens in the treatment of primary glomerulonephritis. MMF dose ranging from 500 mg to 2000 mg / day in the absence of side effects and decrease intestinal tract hemoglobin / leukocytes. and diuretic therapy. When used intravenous dose of 0. 11. Proteinuria before treatment in all patients was 1.5 mEq / L and a decrease in eGFR> 30% compared to before treatment.THERAPY Aggressive therapy including reduction of hypertension and excess fluid and specific therapies against the disease-causing. cyclophosphamide. Of simvastatin given insurance if LDL cholesterol ≥ 160 mg / dl. During the use of cyclophosphamide should be evaluated leukocyte counts. treatment is stopped. 4 . The results of the lipid profile of patients total cholesterol 227 mg / dl. et al.5 In accordance with the mechanism of injury in the glomerulus in glomeruonefritis is immune mechanisms. Prednisolone reduced the dose during the second month of the administration within a day with a reduced dose of 10 mg per week until it is stopped at the end of the month to the fourth or fifth.IV. When any side effects appear. This regimen is the target blood pressure <130/80 mmHg and LDL cholesterol <100 mg / dl. The use of cyclophosphamide can reduce relapse and improve remission rates.5 mg / kg bw / day divided into 2 feedings every 12 hours. Dose adjusted to achieve levels in the blood (whole blood) of 125-225 mcgram / L. LDL cholesterol 134 mg / dl. HDL cholesterol 49 mg / dl. as well as high-dose statin plus spironolactone. mycophenolate mofetil. 73 m2 and tolerant of ACE / ARB. it is necessary to be considered an indication of treatment with this mechanism suppressing drugs. Patients were not given diuretics because they had found signs of puffiness and other fluid overload. and rituximab. Therapy given to patients is 2x75 mg cyclosporine. 4. losartan 1x50 mg. Side effects that must be considered in the use of this regimen is hyperkalemia (potassium> 5. How to use it can be administered orally or parenterally every day every month. methylprednisolone 8 mg 0-0-1. Inflammatory glomerular injury given corticosteroids and immunosuppressive agents. 12 hours after administration of cyclosporine. Equivalent glucocorticoid dose prednisone 1 mg / kg body weight. c) controlling the pressure blood (preferably using the drug group ACE or ARB-Inibitor 2. methylprednisolone 16 mg 1-0-0. turns toward meaningful in preventing progressive CKD stage V in 7 years is ACEI with ARB regimen. Can also be given glucokortikoid combination with cyclosporine . This treatment is not free of serious side effects. Cyclosporine starting dose of 3. so this time the patient is not given anymore simvastatin 10 mg. Reduced salt and water. Controlling the risk factors that aggravate the course of the disease to the decline in kidney function among others: a) reduce the degree of proteinuria or proteinuria that can eliminate the drug group ACE-Inhibitor or Angiotensin Receptor Blockers. b) controlling blood cholesterol levels with statin drugs group. Provide a mechanism of immune-suppressing drugs such as glucocorticoids.5 1g/m2. Nephrotic proteinuria. and vitamins. tacrolimus. which is resistant to glucocorticoids. given combination of glucocorticoids and MMF. it can be accepted that the treatment given is to suppress this mechanism.
Hypovolemia collapse 6. Delayed treatment after 6 months have a poor prognosis. but a collection of symptoms. Secondary infection Nephrotic syndrome patients are very sensitive to a variety of renal and urinary tract infections. decreased serum gamma globulin. Prognosis would be good if managed quickly and adequately. Coagulation disorders This situation is associated with a rise in coagulation factors: factor V and VII.Complications of nephrotic syndrome may include: 1.Malnutrition Severe hypoalbuminemia and prolonged malnutrition. Susceptibility to infection due to impaired humoral defense mechanisms. CONCLUSION Nephrotic syndrome is not a disease. Patient's prognosis is good. Complications or side effects of drugs 7. The earlier renal failure and hypertension. 2. V. Renal failure In patients not currently encountered complications. fibrinogen and platelets. Acceleration of atherosclerosis Hyperlipidemia prolonged and uncontrolled can accelerate the process of atherosclerosis blood vessels. This may lead to a hypercoagulable condition trombo-embolic phenomena in arteries and veins. Ig A persistent decline and rise in serum Ig M which is a dysfunction of T cells 3. 5. 4. and this time the patient has not experienced kidney failure. which can lead to worsening general condition. the prognosis depends on the underlying etiology. renal extra especially the respiratory tract (pneumonia). 5 . the prognosis is worse. because it has been treated since first discovered.
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