Effects of traumatic hypovolemic shock on renal function

Basal renal O2consumption and the efficiency of O2utilization for Na+reabsorption

“…Some studies of the effects of maneuvers that reduced T Na ϩ [e.g., reduced arterial pressure and/or renal blood flow (RBF) or the administration of diuretics] were excluded because of the unavailability of information on GFR and/or TNaϩ (10,11,18,20,26,32,36,37,59,75,78). Others were excluded because GFR was not reduced to zero and T Na ϩ was not measured or because there was no analysis of the relationship between GFR or T Na ϩ and V O 2 total from which basal percent renal V O2 could be derived (1,21,22,25,28,46,50,53,56,63,64,67,76,77) or because no significant correlation was observed between T Na ϩ and V O 2 total (47). We also excluded studies in which both renal V O 2 total and TNaϩ were measured, but the latter were not varied sufficiently to allow the ordinal intercept of the relationship(s) between V O 2 total and TNaϩ or GFR to be determined (7,38), or because the data were not presented in a form to allow this relationship to be extracted (29,42,54).…”

FFP:RBC Resuscitation Ratio and Post-Shock Fluid Uptake

“…A significant portion of the phase 2 UO occurred within the first 2 hours of operation when the kidneys, subjected to a HSI, have impaired concentrating ability probably related to an innermedullary washout due to a reduction in renal component 1 perfusion associated with severe hemorrhagic shock; the breakdown between this early phase 2 UO and later phase 2 UO was not stored in the database. 9,10 The average (SE) weight gain was 8.4 (0.4) kg. During phase 2, there was a uniform reduction in all serum proteins with the SA level falling to 2.6 (0.8) g/dL (to convert to grams per liter, multiply by 10) and the total serum protein level decreasing to 4.6 (0.9) g/dL (to convert to grams per liter, multiply by 10.0).…”

BRASH Syndrome Leading to Cardiac Arrest and Diffuse Anoxic Brain Injury: An Underdiagnosed Entity

“…It is a vicious cycle consisting of bradycardia that develops from a combination of hyperkalemia and AV nodal blocking medications along with renal failure that itself can lead to hyperkalemia and delayed clearance of AV nodal blocking medications. Patients ultimately develop shock (poor organ perfusion) with further kidney damage that worsens the hyperkalemia, and thus bradycardia and the vicious cycle continue until intervened [ 2 ]. These patients usually develop renal failure from either dehydration or nephrotoxic medications, e.g., angiotensin-converting enzyme inhibitors (ACEI)/angiotensin II receptor blockers (ARBs), but the etiology could be any.…”