Long-term recovery of superficial and deep glomeruli after acute renal failure evoked by warm ischemia.

A study was made on the number of glomeruli in the outer cortex, midcortex, and inner cortex 4 weeks after 45 min of warm ischemia, using alcian blue to stain functioning glomeruli. During this time the stainable glomeruli in the kidney as a whole had decreased in number from 32,000 to 16,800. The superficial glomeruli were reduced by only about 30%, whereas in the juxtamedullary zones the number of functioning nephrons were reduced by 80%. This shows that the juxtamedullary nephrons are the most susceptible to degeneration in the recovery phase of acute renal failure caused by ischemia. The decrease in the number of glomeruli was accompanied by a reduction in total glomerular filtration rate to about the same extent. In contrast, the kidney weight was reduced by only about 20%, suggesting compensatory hypertrophy of the remaining tubules. Fluid reabsorption, urine osmolality, and potassium-secreting ability also remained decreased. The contralateral kidney responded with a compensatory hypertrophy and an increase in glomerular filtration rate, whereas the number of glomeruli in the cortex as a whole and in the individual cortical zones in this kidney remained the same as in control kidneys. It is suggested that the trapping of red cells in the juxtamedullary circulation seen soon after restoration of circulation to kidneys subjected to warm ischemia will also cause a further degeneration of the juxtamedullary nephrons.