Renal cystic disease induced by diphenylthiazole

Intranephron hydrostatic pressures were monitored while microperfusing proximal nephrons in diphenylthiazole (DPT)-exposed kidneys, a model in which increased compliance of tubular basement membrane is thought to predispose to cyst formation. Structural studies subsequently were done on these and additional kidneys. Results were compared to those obtained from the study of kidneys from normal rats. Intranephron hydrostatic pressures were shown to rise with microperfusion and did so at lower rates of perfusion among DPT exposed nephrons. For example, at four perfusion rates between 17 and 36 nl/min (60 to 130% of the SNGFR in DPT-fed rats), intranephron hydrostatic pressures were 6 to 14 cm H2O higher (P less than 0.05) in DPT-exposed kidneys. Subsequent light and electron microscopic examination of DPT-exposed kidneys showed micropolyps partially occluding inner medullary and intrapapillary collecting ducts. DPT-induced renal cystic disease resembles other forms of chemically induced renal cystic disease in its functional and structural parameters save that micropolyp formation appears to occur nearer the papillary tip. We conclude that conditions in the DPT-exposed rat kidney resemble more closely those predicted by the partial obstruction rather than by the increased compliance hypothesis of renal cyst formation.