scholarly journals Noradrenaline and Albumin for Type 1 Hepatorenal Syndrome: A Prospective Study from Eastern Nepal

2017 ◽  
Vol 6 (1) ◽  
pp. 20-28
Author(s):  
Rabin Sharma ◽  
Bickram Pradhan ◽  
Denis Peeyush ◽  
Manish Subedi ◽  
Sadhana Sah

Background : Hepatorenal Syndrome (HRS) is a serious complication of liver cirrhosis with critically poor prognosis with treatment currently based on vasopressors. We aimed to study the safety and effects of Intravenous Noradrenaline in patients with Type 1 HRS and also to define factors predictive of a response.Materials and Methods: It was a prospective observational study conducted in a tertiary care hospital in Eastern Nepal enrolling patients withType 1 HRSfrom 2014 to 2015. All patients received Noradrenaline (0.5-3 mg/hr, intravenously) and albumin (1 g/kg followed by 20–40 g/day). Primary outcome was improvement of renal function.Results : 60 Type 1 HRS patients were enrolled in the study -37 males (61.7%) and 23 females (38.3%), mean age 58.18±9.33 years. The therapy was well tolerated as only 6.7% of patients withdrew treatment. Reversal of HRS was observed in 38 patients (63.3%) with the mean duration of 6.39±1.33 days. Of the baseline variables, higher urine output, higher mean arterial pressure and lower serum creatininewere predictive of response. Multivariate analysis showed Mean arterial pressure to be an independent variable of response (adjusted odds ratio 0.588, 95% CI- 0.393-0.880, P>0.05). Finally mean arterial pressure had a negative correlation with serum creatinine and a positive correlation with Urine output.Conclusion : Noradrenaline and albumin are safe and effective in improving renal function in patients with Type 1 HRS.There is a need for studies with larger sample size to correlate improvement in renal function with overall survival.Journal of Nobel Medical CollegeVolume 6, Number 1, Issue 10 (January-June, 2017), page: 20-28

2008 ◽  
Vol 48 ◽  
pp. S83
Author(s):  
P. Casciato ◽  
A. Villamil ◽  
S. Marciano ◽  
J. Bandi ◽  
L. Rezzonico ◽  
...  

1999 ◽  
Vol 10 (8) ◽  
pp. 1778-1785
Author(s):  
JUDITH A. MILLER

Abstract. It has been demonstrated previously that moderate hyperglycemia without glucosuria can increase plasma renin activity and mean arterial pressure in young healthy males with early uncomplicated type 1 diabetes mellitus. This study was conducted to extend these observations by testing the hypothesis that mild to moderate hyperglycemia can affect renal function by increasing renin angiotensin system (RAS) activity in diabetic humans. The study included 10 men and women with early, uncomplicated type 1 diabetes (duration <5 yr), all ingesting a controlled sodium and protein diet. They were studied on four separate occasions, during a subdepressor dose of the angiotensin II (AngII) receptor blocker losartan, and during graded AngII infusion, 1.5 and 2.5 ng/kg per min, while euglycemic (blood glucose 4 to 6 mmol/L) and again while hyperglycemic without glucosuria (blood glucose 9 to 11 mmol/L), according to a randomized crossover design. Outcome measures included mean arterial pressure (MAP), GFR, effective renal plasma flow (ERPF), renal vascular resistance (RVR), filtration fraction (FF), and urine sodium excretion (UNaV) at baseline and in response to the above maneuvers. During hyperglycemic conditions, MAP was significantly higher compared with euglycemia, as were RVR and FF. After the administration of losartan, a significant renal and peripheral depressor effect was noted, with decreases in MAP, RVR, and FF, whereas during euglycemia the responses to losartan were minimal. AngII infusion resulted in elevations in MAP, RVR, and FF and a decline in UNaV during both glycemic phases, but the responses during hyperglycemia, most significantly at the 1.5 ng/kg per min infusion rate, were blunted. These data support the hypothesis that hyperglycemia affects renal function by activating the RAS. The mechanism remains obscure, but these contrasting responses may provide a link between the observations that maintenance of euglycemia and blockade of the RAS prevent or delay diabetic kidney disease, and furthermore, may clarify the mechanism whereby high glucose promotes renal disease progression in diabetes.


2007 ◽  
Vol 52 (3) ◽  
pp. 742-748 ◽  
Author(s):  
Eric Esrailian ◽  
Eugene R. Pantangco ◽  
Namgyal L. Kyulo ◽  
Ke-Qin Hu ◽  
Bruce A. Runyon

Sign in / Sign up

Export Citation Format

Share Document