?:abstract
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Rationale & Objectives: Previously we reported a cohort of COVID19-associated acute kidney injury (AKI) patients with striking biochemical evidence of tissue breakdown in the absence of apparent rhabdomyolysis. Herein we sought to quantify the extent of tissue catabolism in similar patients. Study design: During acute peritoneal dialysis (PD) in COVID-AKI patients we measured urea Kt/V adequacy and calculated daily urea nitrogen generation rate while quantifying their daily protein intake. Setting and population: We did calculations in 8 COVID-AKI patients undergoing acute PD at the Mount Sinai Hospital in NYC. As a comparator we obtained urea kinetic parameters from our database of ambulatory patients on maintenance PD. Exposure or predictors: 8 COVID-AKI patients undergoing acute PD. Outcomes: Urea nitrogen generation rate in relation to daily protein intake. Analytical Approach: Urea nitrogen generation rate from urea kinetics was related to measured daily dietary protein intake in these patients and compared it to this relationship in ambulatory maintenance PD patients where both parameters were calculated from urea kinetics. Results: Urea nitrogen generation rate in AKI patients was 10.2 + 5g/day, which is >2 fold higher than stable outpatients on maintenance PD (4.7 + 3g/day), despite similar dietary protein intake (74.8 + 11g/day vs 67.2 + 29g/day, respectively). This strongly suggests endogenous protein breakdown, probably from muscle. Urea nitrogen generation rate in these AKI patients corresponds to 315g/day of ongoing muscle breakdown and cumulative 2.5kg muscle breakdown during the early course of AKI. Limitations: Small number of participants as well as assumptions in comparing Urea nitrogen generation rate with protein intake. Conclusions: In highly catabolic patients, an endogenous source of urea generation, such as muscle protein breakdown, seems to be the most likely explainable cause for our findings. This is the first study that we are aware of to quantify the degree of endogenous protein breakdown induced by COVID cytokine storm.
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Rationale & Objectives: Previously we reported a cohort of patients with coronavirus disease 2019 (COVID-19)-associated acute kidney injury (AKI) with striking biochemical evidence of tissue breakdown in the absence of apparent rhabdomyolysis We sought to quantify the extent of tissue catabolism in similar patients Study Design: During acute peritoneal dialysis (PD) in patients with COVID-19-associated AKI, we measured urea Kt/V adequacy and calculated the daily urea nitrogen generation rate while quantifying daily protein intake Setting & Population: We did calculations in 8 patients with COVID-9-associated AKI undergoing acute PD at Mount Sinai Hospital in New York City As a comparator, we obtained urea kinetic parameters from our database of ambulatory patients receiving maintenance PD Exposure or Predictors: 8 patients with COVID-19-associated AKI undergoing acute PD Outcomes: Urea nitrogen generation rate in relation to daily protein intake Analytical Approach: Urea nitrogen generation rate from urea kinetics was related to measured daily dietary protein intake in these patients and we compared it with this relationship in ambulatory maintenance PD patients for whom both parameters were calculated from urea kinetics Results: Urea nitrogen generation rate in patients with AKI was 10 2 +/- 5 g/d, which is more than 2-fold higher than for stable outpatients receiving maintenance PD (4 7 +/- 3 g/d) despite similar dietary protein intake (74 8 +/- 11 vs 67 2 +/- 29 g/d, respectively) This strongly suggests endogenous protein breakdown, probably from muscle Urea nitrogen generation rate in these patients with AKI corresponds to 315 g/d of ongoing muscle breakdown and cumulative 2 5 kg of muscle breakdown during the early course of AKI Limitations: Small number of participants and assumptions in comparing urea nitrogen generation rate with protein intake Conclusions: In highly catabolic patients, an endogenous source of urea generation such as muscle protein breakdown seems to be the most likely explainable cause for our findings This is the first study that we are aware of to quantify the degree of endogenous protein breakdown induced by COVID-19-related cytokine storm
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