The peripolar cell is a recently described glomerular epithelial cell, which may be an additional secretory component of the juxtaglomerular apparatus (JGA). I have described the human peripolar cell. Human peripolar cells were sparse and difficult to find. They were found in 12% of glomeruli on average. They were situated at the vascular pole of the glomerulus, between the visceral and parietal epithelial cells. Peripolar cells contained prominent intracytoplasmic granules, which showed similar staining reactions to the adjacent renin-containing cells of the JGA. However, immunohistochemical studies with an antiserum to human renin, showed that the human peripolar cell does not contain renin. By electron microscopy, the most striking feature was the intracytoplasmic secretory-type granules. Other organelles were sparse, although there were freguently complex membrane invaginations. Peripolar cells formed junctional complexes with adjacent parietal and visceral epithelial cells. Sheep peripolar cells were prominent and easily found. They were present in 64% of glomeruli on average, and were packed with cytoplasmic granules. Peripolar cells were sparse in rat kidneys, being present in only 6% of glomeruli on average. They were similar in appearance to human peripolar cells. Peripolar cells were most numerous in superficial cortical glomeruli, similar to renin-containing cells. In states of hyperplasia, renin-containing cells were also present in juxtamedullary JGA's, but this could not be confirmed for peripolar cells. Using immunohistochemical techniques, I have demonstrated plasma proteins in the granules of human and sheep peripolar cells. I have used a variety of antisera and monoclonal antibodies, but have been unable to demonstrate an immunophenotype specific for peripolar cells. I have examined the reactions of peripolar cells to stimuli, which are known to affect renin-secretion by the JGA. In rats, sodium-depletion or sodium-loading resulted in no alteration in numbers of peripolar cells. I have also examined 11 autopsy cases of Addison's disease, and found that peripolar cells were unaltered despite immunohistochemical evidence of hyperplasia of renin-containing cells. I investigated the response of the peripolar cell to a reduction in renal perfusion pressure by examining the 2-kidney 1-clip model of experimental hypertension in rats, and 10 human nephrectomy specimens with renal artery stenosis. In experimental renovascular hypertension, there was no alteration in numbers of peripolar cells, however in the unclipped kidney other glomerular epithelial cells acquired granules. There was hyperplasia of peripolar cells in a minority of cases of renal artery stenosis, but no significant alteration as a group. There was hyperplasia of renin-containing cells in both rats and humans. I examined 12 autopsy cases of malignant hypertension and found increased numbers of peripolar cells. In addition, other glomerular epithelial cells became granulated and their numbers correlated with peripolar cells. There was hyperplasia of renin-containing cells in some of the cases. Lastly, I investigated the reactions of peripolar cells in human renal disease. I examined 242 renal biopsies affected by 19 different disaeses. Peripolar cells were especially prominent in membranous glomerulonephritis, mesangioproliterative glomerulonephritis, and focal segmental glomerulosclerosis. Other granulated glomerular and tubular epithelial cells were most prominent in different diseases. This suggests that peripolar cells react specifically in certain immune-complex mediated renal diseases.
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