Thread by @kidney_boy

Her original title was “Beyond the ouch hypothesis, a new paradigm to explain the harm in AKI.” #AspenKidney

Mortality in ICU:
No AKI, No HD 5%
ESRD HD 11%
AKI no HD 23%
AKI with HD 58%

Standardized for APACHE 2 scores

#AspenKidney

Injured kidneys may be lashing out, releasing substances that cause systemic effects contributing to mortality. These substances are unique from substances that accumulate with zero GFR.

#AspenKidney

She compared ischemic model of AKI (clamp and release) to bilateral nephrectomy.

Initial theory of mediator was cytokines. IL-6 quartile predict mortality. #AspenKidney

Faubel says IL 6 goes up with all stress. Happened with ischemic and nephrectomy model. #AspenKidney

Lung injury is mediated by IL-6 and kidney injury. All methods that inhibit IL-6 reduce lung injury #AspenKidney

Fluid removal does not correct pulmonary edema due to capillary leak. #AspenKidney

What dialysis can fix and what it cannot fix. #AspenKidney

Faubel says the answer to everything is metabolomics. Screen for small molecules (less than 2000 daltons). Only costs $60 per sample. There generate tons of data. #AspenKidney

AKI and the heart: mitochondria are not normal so function is not normal. #AspenKidney

The metabolomic study shows decreased amino acids in the heart in AKI. Aspartame and glutamate are decreased in bypass and cardioplegia solutions are supplemented with these to correct this. (May have gotten this wrong) #AspenKidney

She did mouse echocardiograms in mice with AKI. Mice have diastolic dysfunction and this persists for a year after recovery of AKI. Humans have similar increased risk of CHF after AKI #AspenKidney

Fall in ATP in the heart with mouse AKI #AspenKidney

Summary slide #AspenKidney

Hey @hswapnil @scoca1 note in her summary slide, still sticking with AKI associated with mortality, not causative.