June Mason

TL;DR: It is concluded that congestion of the outer medulla is a key event in ischemic renal failure, its occurrence is coincidental with the reduction in deep nephron perfusion and urinary concentrating power in the early and maintenance phase and its disappearance heralds the restoration of deep neephron perfusions and urinary concentrate ability in the recovery phase.

TL;DR: It is concluded that furosemide is only beneficial in models of acute renal failure with an obstructive or nephrotoxic pathogenesis, in which it acts by flushing out the noxious material and not by inhibiting the mechanism of tubuloglomerular feedback.

TL;DR: Differences in the intracellular concentrations of phosphorus, sodium, and chloride between proximal and distal tubular cells are demonstrated, demonstrating the presence of extracellular compartments in these regions.

TL;DR: Vascular obstruction, which appears to raise renal vascular resistance and lower blood flow and filtration rate, cannot be limited to the medulla but must also be present in the cortex and can be reversed or prevented by raising perfusion pressure or decreasing hematocrit.

TL;DR: The disturbance in electrolyte composition increases with the duration of ischemia, is less pronounced in the distal than proximal cells and, although initially completely reversible when blood flow is restored, reappeared in the proximal Cells 1 days after the initial injury.