scholarly journals SP265ACEI/ARB CAN DECREASE THE RISK OF CARDIORENAL SYNDROME TYPE I AND IN-HOSPITAL MORTALITY

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii467-iii467
Author(s):  
Xu Jiaqi ◽  
Cai Lu ◽  
Liang Xinling ◽  
Du Zhimin ◽  
Chen Yuanhan ◽  
...  
2021 ◽  
pp. 1-9
Author(s):  
Watanyu Parapiboon ◽  
Tanit Kingjun ◽  
Laddaporn Wongluechai ◽  
Waraporn Leawnoraset

<b><i>Introduction:</i></b> The aim of the study was to demonstrate the outcomes of peritoneal dialysis (PD) in critically ill cardiorenal syndrome type 1 (CRS1). <b><i>Methods:</i></b> A cohort of 147 patients with CRS1 who received PD from 2011 to 2019 in a referral hospital in Thailand was analyzed. The primary outcome was 30-day in-hospital mortality. Ultrafiltration and net fluid balance among survivors and nonsurvivors in the first 5 PD sessions were compared. <b><i>Results:</i></b> The 30-day mortality rate was 73.4%. Most patients were critically ill CRS1 (all patients had a respiratory failure of which 68% had cardiogenic shock). Blood urea nitrogen and creatinine at the commencement of PD were 60.1 and 4.05 mg/dL. In multivariable analysis, increasing age, unstable hemodynamics, and positive fluid balance in the first 5 PD sessions were associated with the risk of in-hospital mortality. The change of fluid balance per day during the first 5 dialysis days was significantly different among survivor and nonsurvivor groups (−353 vs. 175 mL per day, <i>p</i> = 0.01). <b><i>Conclusions:</i></b> PD is a viable dialysis option in CRS1, especially in a resource-limited setting. PD can save up to 27% of lives among patients with critically ill CRS1.


Cureus ◽  
2020 ◽  
Author(s):  
Venkata Sri Ramani Peesapati ◽  
Mohammad Sadik ◽  
Sadhika Verma ◽  
Marline A Attallah ◽  
Safeera Khan

2013 ◽  
Vol 3 (4) ◽  
pp. 239-245 ◽  
Author(s):  
Rohit Tandon ◽  
Bishav Mohan ◽  
Shibba Takkar Chhabra ◽  
Naved Aslam ◽  
Gurpreet Singh Wander

Author(s):  
Bilal Bin Abdullah

The burden of HF in India appears high and Acute kidney injury is a leading cause of morbidity and mortality. The mechanisms underlying this interaction are complex and multifactorial in nature.


2015 ◽  
Vol 24 (4) ◽  
pp. 523-526 ◽  
Author(s):  
Yoshihiro Maruo ◽  
Mahdiyeh Behnam ◽  
Shinichi Ikushiro ◽  
Sayuri Nakahara ◽  
Narges Nouri ◽  
...  

Background: Crigler–Najjar syndrome type I (CN-1) and type II (CN-2) are rare hereditary unconjugated hyperbilirubinemia disorders. However, there have been no reports regarding the co-existence of CN-1 and CN-2 in one family. We experienced a case of an Iranian family that included members with either CN-1 or CN-2. Genetic analysis revealed a mutation in the bilirubin UDP-glucuronosyltransferase (UGT1A1) gene that resulted in residual enzymatic activity.Case report: The female proband developed severe hyperbilirubinemia [total serum bilirubin concentration (TB) = 34.8 mg/dL] with bilirubin encephalopathy (kernicterus) and died after liver transplantation. Her family history included a cousin with kernicterus (TB = 30.0 mg/dL) diagnosed as CN-1. Her great grandfather (TB unknown) and uncle (TB = 23.0 mg/dL) developed jaundice, but without any treatment, they remained healthy as CN-2. Results: The affected cousin was homozygous for a novel frameshift mutation (c.381insGG, p.C127WfsX23). The affected uncle was compound heterozygous for p.C127WfsX23 and p.V225G linked with A(TA)7TAA. p.V225G-UGT1A1 reduced glucuronidation activity to 60% of wild-type. Thus, linkage of A(TA)7TAA and p.V225G might reduce UGT1A1 activity to 18%–36 % of the wild-type. Conclusion: Genetic and in vitro expression analyses are useful for accurate genetic counseling for a family with a history of both CN-1 and CN-2. Abbreviations: CN-1: Crigler–Najjar syndrome type I; CN-2: Crigler–Najjar syndrome type II; GS: Gilbert syndrome; UGT1A1: bilirubin UDP-glucuronosyltransferase; WT: Wild type; TB: total serum bilirubin.


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