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  • Title: [Clinical state of a patient with nephrotic proteinuria successfully treated with combined therapy with angiotensin II receptor antagonists and angiotensin II converting enzyme inhibitors and pentoxifylline].
    Author: Renke M, Rutkowski P, Tylicki L, Zietkiewicz M, Larczyński W, Rutkowski B.
    Journal: Przegl Lek; 2008; 65(6):312-4. PubMed ID: 18853664.
    Abstract:
    Pharmacological inhibition of the renin-angiotensin-aldosteron system (RAAS) constitutes a cornerstone strategy in the management of patients with chronic nephropaties and proteinuria. Angiotensin converting enzyme inhibitors (ACEI) as well as angiotensin II subtype 1 receptor antagonists (ARA) have been shown to decrease proteinuria, reduce the local renal inflammatory processes and slow the progression of renal insufficiency. Despite recent progress, there is still no optimal therapy which inhibits progression of renal disease. It is possible that pentoxifilline (PTX) an old medication which is still used to treat peripheral vascular disease will be the new adjunct to RAAS blockade. In addition, PTX has been shown to decrease the production of pro inflammatory cytokines and reactive oxygen species. 61-Year-old man with nephrotic proteinuria, diabetes type 2, hypertension, chronic viral hepatitis type C and slightly impaired renal function was desribed. Proteinuria as daily urine protein excretion (DPE), serum creatinine and eGFR (MDRD mode) were measured. Proteinuria was diagnosed in 2003 (DPE 3.5 g), creatinine 1.3-1.5 mg/dl. The patient had been examined in Department of Nephrology but exact reason of nephrotic syndrome was not recognized because he refused kidney biopsy. Therapy was started with ACEI and temporary effect as decrease of DPE to 0.2 g, eGFR was about 60 ml/min. and serum creatinine in normal range. In 2004 DPE increased to 8.98-9.42 g, serum creatinine 1.1-1.3 mg/dl. The dose of ACEI was increased and after then ARA was added. After one month of combined therapy DPE fell to 7.7 g, next the doses of both drugs were increased to maximum (losartan 100 mg and lisinopril 40 mg) and DPE fell to 6.8 g, serum creatinine was 1.4 mg/dl and potassium 5.4 mmol/l. Next PTF 800 mg/day was added and DPE fell to 0.55 g after 2 months' therapy. Similar DPE was after 6 months (0.53 g) since we started with combination of IKA, ARA and PTF.
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