Browsing by Subject "Creatinine"

Sort by: Order: Results:

Now showing items 1-4 of 4
  • Bellomo, Rinaldo; Kellum, John A.; Ronco, Claudio; Wald, Ron; Martensson, Johan; Maiden, Matthew; Bagshaw, Sean M.; Glassford, Neil J.; Lankadeva, Yugeesh; Vaara, Suvi; Schneider, Antoine (2017)
    Acute kidney injury (AKI) and sepsis carry consensus definitions. The simultaneous presence of both identifies septic AKI. Septic AKI is the most common AKI syndrome in ICU and accounts for approximately half of all such AKI. Its pathophysiology remains poorly understood, but animal models and lack of histological changes suggest that, at least initially, septic AKI may be a functional phenomenon with combined microvascular shunting and tubular cell stress. The diagnosis remains based on clinical assessment and measurement of urinary output and serum creatinine. However, multiple biomarkers and especially cell cycle arrest biomarkers are gaining acceptance. Prevention of septic AKI remains based on the treatment of sepsis and on early resuscitation. Such resuscitation relies on the judicious use of both fluids and vasoactive drugs. In particular, there is strong evidence that starch-containing fluids are nephrotoxic and decrease renal function and suggestive evidence that chloride-rich fluid may also adversely affect renal function. Vasoactive drugs have variable effects on renal function in septic AKI. At this time, norepinephrine is the dominant agent, but vasopressin may also have a role. Despite supportive therapies, renal function may be temporarily or completely lost. In such patients, renal replacement therapy (RRT) becomes necessary. The optimal intensity of this therapy has been established, while the timing of when to commence RRT is now a focus of investigation. If sepsis resolves, the majority of patients recover renal function. Yet, even a single episode of septic AKI is associated with increased subsequent risk of chronic kidney disease.
  • Törmänen, Suvi; Pörsti, Ilkka; Lakkisto, Päivi; Tikkanen, Ilkka; Niemelä, Onni; Paavonen, Timo; Mustonen, Jukka; Eräranta, Arttu (2017)
    Background: We studied whether endothelin receptor antagonist and calcimimetic treatments influence renal damage and kidney renin-angiotensin (RA) components in adenine-induced chronic renal insufficiency (CRI). Methods: Male Wistar rats (n = 80) were divided into 5 groups for 12 weeks: control (n = 12), 0.3% adenine (Ade; n = 20), Ade + 50 mg/kg/day sitaxentan (n = 16), Ade + 20 mg/kg/day cinacalcet (n = 16), and Ade + sitaxentan + cinacalcet (n = 16). Blood pressure (BP) was measured using tail-cuff, kidney histology was examined, and RA components measured using RT-qPCR. Results: Adenine caused tubulointerstitial damage with severe CRI, anemia, hyperphosphatemia, 1.8-fold increase in urinary calcium excretion, and 3.5-fold and 18-fold increases in plasma creatinine and PTH, respectively. Sitaxentan alleviated tubular atrophy, while sitaxentan + cinacalcet combination reduced interstitial inflammation, tubular dilatation and atrophy in adenine-rats. Adenine diet did not influence kidney angiotensin converting enzyme (ACE) and AT(4) receptor mRNA, but reduced mRNA of renin, AT(1a), AT(2), (pro) renin receptor and Mas to 40-60%, and suppressed ACE2 to 6% of that in controls. Sitaxentan reduced BP by 8 mmHg, creatinine, urea, and phosphate concentrations by 16-24%, and PTH by 42%. Cinacalcet did not influence BP or creatinine, but reduced PTH by 84%, and increased hemoglobin by 28% in adenine-rats. The treatments further reduced renin mRNA by 40%, while combined treatment normalized plasma PTH, urinary calcium, and increased ACE2 mRNA 2.5-fold versus the Ade group (p <0.001). Conclusions: In adenine-induced interstitial nephritis, sitaxentan improved renal function and tubular atrophy. Sitaxentan and cinacalcet reduced kidney renin mRNA by 40%, while their combination alleviated tubulointerstitial damage and urinary calcium loss, and increased kidney tissue ACE2 mRNA.
  • Törmänen, Suvi; Pörsti, Ilkka; Lakkisto, Päivi; Tikkanen, Ilkka; Niemelä, Onni; Paavonen, Timo; Mustonen, Jukka; Eräranta, Arttu (BioMed Central, 2017)
    Abstract Background We studied whether endothelin receptor antagonist and calcimimetic treatments influence renal damage and kidney renin-angiotensin (RA) components in adenine-induced chronic renal insufficiency (CRI). Methods Male Wistar rats (n = 80) were divided into 5 groups for 12 weeks: control (n = 12), 0.3% adenine (Ade; n = 20), Ade + 50 mg/kg/day sitaxentan (n = 16), Ade + 20 mg/kg/day cinacalcet (n = 16), and Ade + sitaxentan + cinacalcet (n = 16). Blood pressure (BP) was measured using tail-cuff, kidney histology was examined, and RA components measured using RT-qPCR. Results Adenine caused tubulointerstitial damage with severe CRI, anemia, hyperphosphatemia, 1.8-fold increase in urinary calcium excretion, and 3.5-fold and 18-fold increases in plasma creatinine and PTH, respectively. Sitaxentan alleviated tubular atrophy, while sitaxentan + cinacalcet combination reduced interstitial inflammation, tubular dilatation and atrophy in adenine-rats. Adenine diet did not influence kidney angiotensin converting enzyme (ACE) and AT4 receptor mRNA, but reduced mRNA of renin, AT1a, AT2, (pro)renin receptor and Mas to 40–60%, and suppressed ACE2 to 6% of that in controls. Sitaxentan reduced BP by 8 mmHg, creatinine, urea, and phosphate concentrations by 16–24%, and PTH by 42%. Cinacalcet did not influence BP or creatinine, but reduced PTH by 84%, and increased hemoglobin by 28% in adenine-rats. The treatments further reduced renin mRNA by 40%, while combined treatment normalized plasma PTH, urinary calcium, and increased ACE2 mRNA 2.5-fold versus the Ade group (p < 0.001). Conclusions In adenine-induced interstitial nephritis, sitaxentan improved renal function and tubular atrophy. Sitaxentan and cinacalcet reduced kidney renin mRNA by 40%, while their combination alleviated tubulointerstitial damage and urinary calcium loss, and increased kidney tissue ACE2 mRNA.
  • Rakkolainen, Ilmari; Vuola, Jyrki (2016)
    Introduction: Neutrophil gelatinase-associated lipocalin (NGAL) is a novel biomarker used in acute kidney injury (AKI) diagnostics. Studies on burn patients have highlighted it as a promising biomarker for early detection of AKI. This study was designed to discover whether plasma NGAL is as a biomarker superior to serum creatinine and cystatin C in detecting AKI in severely burned patients. Methods: Nineteen subjects were enrolled from March 2013 to September 2014 in the Helsinki Burn Centre. Serum creatinine, cystatin C, and plasma NGAL were collected from the patients at admission and every 12 h during the first 48 h and thereafter daily until seven days following admission. AKI was defined by acute kidney injury network criteria. Results: Nine (47%) developed AKI during their intensive care unit stay and two (11%) underwent renal replacement therapy. All biomarkers were significantly higher in the AKI group but serum creatinine-and cystatin C values reacted more rapidly to changes in kidney function than did plasma NGAL. Plasma NGAL tended to rise on average 72 h perpendicular to 29 h (95% CI) later in patients with early AKI than did serum creatinine. Area-under-the-curve values calculated for each biomarker were 0.92 for serum creatinine, 0.87 for cystatin C, and 0.62 for plasma NGAL predicting AKI by the receiver-operating-characteristic method. Conclusion: This study demonstrated serum creatinine and cystatin C as faster and more reliable biomarkers than plasma NGAL in detecting early AKI within one week of injury in patients with severe burns. (C) 2015 Elsevier Ltd and ISBI. All rights reserved.