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EN
Objectives. Post exercise proteinuria (PEP) is found in about 20–40% of sportsmen after intensive exercise. Urinary NGAL is a new marker of tubulointerstitial kidney damage. The relationship between PEP and uNGAL has not been defined yet. In presented study a resting uNGAL as a predictor of PEP was analyzed. The changes of albuminuria after exercise were monitored to estimate a frequency and range of PEP. Methods. 40 amateur healthy runners (mean age 36.65 ±10.61 years) participating in 10-km run took part in the study. Before and after the competition urine was collected. NGAL, albumin and creatinine were subsequently measured in urine. uNGAL to creatinine ratio (NCR) and albumin to creatinine ratio (ACR) were calculated. Results. 28 participants (mean age 37.9 ±11.46, 19 M, 9 F) with uNGAL below 15 ng/ml before competition were analyzed. The increase of ACR was observed in every case. Mean post-exercise ACR was 104.55 ±123.1 mg/g and was significantly higher than pre-exercise ACR 6.33 ±5.86 mg/g (p < 0.0005). The positive correlation was found between resting NCR and post-exercise ACR (r = 0.60, p < 0.05). Conclusions. Resting uNGAL positively correlated with PEP. The possible explanation of these findings is that persons with PEP had some early, occult tubulointersitial kidney damage. It is speculated that those runners have higher risk of chronic kidney disease.
EN
Background: The renoprotective effects of the direct renin inhibitor, aliskiren, in renal transplant recipients have been supposed, but not finally proven. We performed an exploratory double-blind, losartan controlled, cross-over study to evaluate the influence of aliskiren, direct renin inhibitor, on albuminuria and other surrogate markers of kidney injury in patients after renal transplantation. The safety of this therapy was also evaluated. Method: 16 of 18 patients (12 M, 4 F), 48.3 ± 9.0 years, 57.7 ± 9.1 months after kidney transplantation, with hypertension and stable serum creatinine 1.4 ± 0.08 mg/dl without proteinuria, completed the protocol. Each patient underwent two 8-week treatment periods (one with 150 mg of aliskiren, and one with 50 mg of losartan) in random order, allowing an 8-week placebo washout between them. Results: There were no differences in albuminuria, transforming growth factor β-1 and 15-F2t-isoprostanes urine excretion between aliskiren and losartan. Creatinine serum level, eGFR, 24 h systolic and 24 h diastolic blood pressure were stable through the study. There were no differences in haemoglobin and potassium serum concentration between studied drugs. Conclusion: Aliskiren decreases albuminuria in renal transplant recipients with clinically minimal side effects. The effect does not differ from that of losartan.
EN
Aliskiren is the first in a new class of antihypertensives – the direct renin inhibitors. It took a long time to discover it, mainly because of difficulties with creating an oral form with good bioavailability. It has been approved for the treatment of primary hypertension in United States and Europe in 2007. It provides good blood pressure efficacy, has good tolerability and small amount of undesirable side effects. Blocking renin, it prevents conversion of angiotensinogen to angiotensin I. First clinical trials concerning its use alone or in combination with ACEI or ARB give hope for greater reduction in blood pressure and more renal and cardiovascular protection that provided by ACEIs and ARBs. The ongoing clinical trial programme ASPIRE HIGHER will investigate the potential of aliskiren in improvement of renal and cardiovascular protection. Preliminary results are very promising. Aliskiren diminishes plasma renin activity from 50 to 80% in hypertensive patients after oral administration. It diminishes systolic and diastolic blood pressure. After single dose the effect of the drug lasts for 24 hours. Whole therapeutic effect is observed after two weeks.
PL
Aliskiren jest pierwszym przedstawicielem nowej grupy leków hipotensyjnych – bezpośrednich inhibitorów reniny. Badania nad jego powstaniem trwały długo, głównie z powodu trudności z uzyskaniem preparatu o dobrej biodostępności formy doustnej. W 2007 roku został dopuszczony do leczenia pierwotnego nadciśnienia tętniczego w Stanach Zjednoczonych i krajach Unii Europejskiej. Jest skutecznym lekiem hipotensyjnym, o małej liczbie działań ubocznych i dobrej tolerancji. Blokując reninę, zapobiega konwersji angiotensynogenu do angiotensyny I. Pierwsze badania kliniczne z jego wykorzystaniem dają nadzieję na addytywny efekt hipotensyjny i nefro- oraz kardioprotekcyjny, w przypadku połączenia go z inhibitorami konwertazy (ACEI) lub antagonistami receptora dla angiotensyny II (ARB). Podobnego efektu nie wykazano dla połączenia tycw dwóch grup leków. Największym, trwającym właśnie badaniem nad wykorzystaniem aliskirenu w udoskonaleniu nefro- i kardioprotekcji jest badanie ASPIRE HIGHER. Obejmuje ono ponad 35 tysięcy chorych, z planowanym okresem leczenia ponad 6 lat, i ma na celu sprawdzenie potencjalnej wyższości leku w zakresie działania nefroprotekcyjnego w porównaniu z ACEI i ARB. Wstępne wyniki wskazują na jego duży potencjał kardio- i nefroprotekcyjny. Po podaniu doustnym u chorych z nadciśnieniem zmniejsza on aktywność reninową osocza z 50 do 80%. Lek obniża wartość ciśnienia skurczowego i rozkurczowego, a działanie pojedynczej dawki utrzymuje się przez 24 godziny. Pełne działanie terapeutyczne osiąga po dwóch tygodniach.
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