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Biomedical subjects

J Waisman

Publications and source records attributed to J Waisman.

At least 109 records · Page 6Linked to original sources
PubMed1975

Chronic experimental hyperuricemic nephropathy.

Sustained, moderately severe hyperuricemia and severe uricosuria were produced in male Wistar rats by feeding dietary supplements of oxonic acid (0.4 gm. per day) and uric acid (0.6 gm per day). After 1 month, the kidneys showed the previously described histologic features of urate-blockade nephropathy characterized by intratubular deposits, tubular injury, and an exudative response consisting of neutrophilic granulocytes with early tophus formation. After 36 and 52 weeks of hyperuricemia, and with no gross evidence of renal failure, the kidneys showed a predominantly interstitial mononuclear cell infiltrate around regenerated tubules, an increase in interstitial fibrous tissue, infrequent renal tophi, and renal stones. The glomeruli and blood vessels appeared completely normal. There was no evidence of arthritis and no other target organ damage was detected. The chronic renal changes present in this animal model of induced hyperuricemia resemble those seen in human gouty nephropathy. The evolution of the experimental urate nephropathy observed during 1 year suggests that a primary acute inflammatory tubular injury is followed by a diffuse chronic interstitial nephritis and that the glomeruli and blood vessels are not primarily involved in the renal disease. This animal model may provide the opportunity to study factors influencing the renal sequelae of sustained hyperuricemia.

Animals↗
PubMed1975

Acute hyperuricemic nephropathy in rats. An electron microscopic study.

Hyperuricemia and uricosuria were induced in rats fed uric acid and oxonic acid. Kidneys then were studied by light and electron microscopy. After 1 day of hyperuricemia, animals had deposits of uric acid and urate crystals within collecting tubules of the renal papillae, and tubular cells were altered. By 10 days, there was an exudative response with further injury to epithelium. Clear spaces within lumens, epithelium, and neutrophils suggested the presence of crystals; however, there was no direct ultrastructural evidence that neutrophils or epithelial cells ingested crystals and suffered injury. Presumably, crystals readily seen in frozen, unfixed tissue were lost during preparation for electron microscopy. Nonetheless, the ultrastructural findings indicated that hyperuricemic nephropathy was initiated in a fashion analogous to urate arthropathy. Urate crystals formed within collecting tubules, epithelial cells were altered, and most likely there was chemotaxis of neutrophils which underwent degranulation and vacuolation followed by lysis freeing any ingested urate. Release of ingested crystals plus precipitation of new crystals both might serve to sustain the nephritis.

Animals↗
PubMed1975

Spironolactone bodies in an adrenal adenoma.

Spironolactone bodies were observed in an adrenal cortical adenoma that was removed from a patient with primary hyperaldosteronism (Conn syndrome) treated preoperatively with spironolactone. The electron microscopical evaluation of this adrenal cortical adenoma shows origin of spironolactone bodies from whorls of endoplasmic reticulum in cells with the cytoplasmic features of those from the zona glomerulosa of the adrenal gland. There was no evidence that the bodies were derived from mitochondria, which confirms recent ultrastructural findings in patients treated with spironolactone. These bodies have been described in the adrenal cortex only in patients who have received spironolactone, and the pharmacologic specificity of the bodies strongly suggests a direct mode of action by spironolactone on aldosterone production by cells of the adrenal zona glomerulosa.

Adenoma↗