HEPATIC RETINOPATHY - MORPHOLOGICAL FEATURES OF RETINAL GLIAL (MULLER) CELLS ACCOMPANYING HEPATIC-FAILURE

More than 80 years ago, Alzheimer described changes in the brains of p atients who had suffered hepatic failure. Astrocytes are primarily aff ected; their nuclei become swollen, their intermediate filament protei n composition is altered and their cytoplasm becomes vacuolated. Cells with these features are called Alzheimer type II astrocytes and these changes have been attributed to the toxic effects of elevated ammonia levels. The present study investigates whether the dominant glia of a nother part of the central nervous system, the Muller cells of the ret ina, undergo similar changes. Retinae of patients who had died with sy mptoms of hepatic failure were processed for histology, histochemistry , and immunocytochemistry. Cell nuclei were measured from brain astroc ytes (insula cortex), Muller cells, and retinal bipolar neurons. Hepat ic failure resulted in the enlargement of nuclei in astrocytes and Mul ler cells, and the enhanced expression in Muller cells of glial fibril lary acidic protein, cathepsin D, and the beta-subunit of prolyl 4-hyd roxylase (glial-p55). In some retinae, signs of gliosis were also obse rved. We conclude that increased levels of serum ammonia resulting fro m hepatic insufficiency cause changes in Muller cells that are similar to those seen in brain astrocytes. We term this condition hepatic ret inopathy.