Grain is purchased at a discount when falling numbers are below 300 seconds (sec). This can result in serious financial losses for farmers. This article addresses many commonly asked questions about the Hagberg-Perten Falling Number test, and provides some suggestions for reducing losses due to low falling numbers

Andreas Kribben (117130)

Anja Bienholz (550853)

Benjamin Wilde (2591227)

Frank Petrat (452799)

Fuat Saner (3917225)

Hana Guberina (3917219)

Herbert de Groot (452800)

Joel Weinberg (3917222)

Jonas Reis (3917228)

Oliver Witzke (117125)

Pinar Sanli (3917216)

Thorsten Feldkamp (550856)

BMC Nephrology

PubMed

Abstract Background Ischemia and reperfusion (I/R) is one of the major causes of acute kidney injury (AKI). Citrate reduces hypoxia-induced mitochondrial energetic deficits in isolated proximal tubules. Moreover, citrate anticoagulation is now frequently used in renal replacement therapy. In the present study a rat model of I/R-induced AKI was utilized to examine renal protection by citrate in vivo. Methods AKI was induced by bilateral renal clamping (40 min) followed by reperfusion (3 h). Citrate was infused at three different concentrations (0.3 mmol/kg/h; 0.6 mmol/kg/h and 1.0 mmol/kg/h) continuously for 60 min before and 45 min after ischemia. Plasma calcium concentrations were kept stable by infusion of calcium gluconate. The effect of citrate was evaluated by biomonitoring, blood and plasma parameters, histopathology and tissue ATP content. Results In comparison to the normoxic control group bilateral renal ischemia led to an increase of creatinine and lactate dehydrogenase activity and a decrease in tissue ATP content and was accompanied by a drop in mean arterial blood pressure. Infusion of 1.0 mmol/kg/h citrate led to lower creatinine and reduced LDH activity compared to the I/R control group and a tendency for higher tissue ATP content. Pre-ischemic infusion of 1.0 mmol/kg/h citrate stabilized blood pressure during ischemia. Conclusions Citrate has a protective effect during I/R-induced AKI, possibly by limiting the mitochondrial deficit as well as by beneficial cardiovascular effects. This strengthens the rationale of using citrate in continuous renal replacement therapy and encourages consideration of citrate infusion as a therapeutic treatment for AKI in humans

Anja Bienholz

Jonas Reis

Pinar Sanli

Herbert de Groot

Frank Petrat

Hana Guberina

Benjamin Wilde

Oliver Witzke

Fuat H. Saner

Andreas Kribben

Joel M. Weinberg

Thorsten Feldkamp

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Citrate shows protective effects on cardiovascular and renal function in ischemia-induced acute kidney injury

Abstract
              
                Background
                Ischemia and reperfusion (I/R) is one of the major causes of acute kidney injury (AKI). Citrate reduces hypoxia-induced mitochondrial energetic deficits in isolated proximal tubules. Moreover, citrate anticoagulation is now frequently used in renal replacement therapy. In the present study a rat model of I/R-induced AKI was utilized to examine renal protection by citrate in vivo.
              
              
                Methods
                AKI was induced by bilateral renal clamping (40 min) followed by reperfusion (3 h). Citrate was infused at three different concentrations (0.3 mmol/kg/h; 0.6 mmol/kg/h and 1.0 mmol/kg/h) continuously for 60 min before and 45 min after ischemia. Plasma calcium concentrations were kept stable by infusion of calcium gluconate. The effect of citrate was evaluated by biomonitoring, blood and plasma parameters, histopathology and tissue ATP content.
              
              
                Results
                In comparison to the normoxic control group bilateral renal ischemia led to an increase of creatinine and lactate dehydrogenase activity and a decrease in tissue ATP content and was accompanied by a drop in mean arterial blood pressure. Infusion of 1.0 mmol/kg/h citrate led to lower creatinine and reduced LDH activity compared to the I/R control group and a tendency for higher tissue ATP content. Pre-ischemic infusion of 1.0 mmol/kg/h citrate stabilized blood pressure during ischemia.
              
              
                Conclusions
                Citrate has a protective effect during I/R-induced AKI, possibly by limiting the mitochondrial deficit as well as by beneficial cardiovascular effects. This strengthens the rationale of using citrate in continuous renal replacement therapy and encourages consideration of citrate infusion as a therapeutic treatment for AKI in humans.https://deepblue.lib.umich.edu/bitstream/2027.42/136552/1/12882_2017_Article_546.pd

Bienholz, Anja

Reis, Jonas

Sanli, Pinar

de Groot, Herbert

Petrat, Frank

Guberina, Hana

Wilde, Benjamin

Witzke, Oliver

Saner, Fuat H

Kribben, Andreas

Weinberg, Joel M

Feldkamp, Thorsten

Deep Blue Documents at the University of Michigan

Ionized plasma chloride levels. Box plots with whiskers indicating minimum and maximum, six rats per group. ** p < 0.01 vs. I/R control group. (PDF 30 kb

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Additional file 1: Figure S1. of Citrate shows protective effects on cardiovascular and renal function in ischemia-induced acute kidney injury

Steber, Camille M.

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