Biomedical subjects
Publications and source records attributed to K Kayes.
We present a case of extrinsic compression of a ureter by spinal fixation hardware and adjacent fibrosis that resulted in progressive obstructive hydronephrosis, loss of renal function, and, ultimately, nephrectomy.
Magnetic resonance (MR) imaging is often used to assess the location and degree of ligamentous or cartilage damage in the knee following acute traumatic injury. Occasionally, these studies will also document abnormal signal within the adjacent subchondral bone. These "bone bruises" are considered incidental findings by some, while others suggest possible clinical significance. The purpose of this paper is to review the literature and consolidate current thinking on the radiographic characteristics, classification, histopathology and natural history of bone bruises.
We have previously reported that the Wistar/Furth (W/Fu) rat strain is resistant to mineralocorticoid hypertension. In the current study, we have examined renal mRNA levels for mineralocorticoid receptor (MR), glucocorticoid receptor (GR), renin and Na+, K(+)-ATPase in response to treatment with mineralocorticoids. Uninephrectomized male Wistar (WI) and W/Fu rats were treated with aldosterone or deoxycorticosterone acetate (DOCA) and were given 1% NaCl to drink. Rats were sacrificed after 1, 3 or 7 days of treatment. Renal MR and ATPase mRNA levels were significantly reduced in aldosterone and DOCA-treated WI rats (e.g. MR was 30% on day 3 and ATPase was 50% of control on day 7 of aldosterone treatment). Unexpectedly, GR mRNA levels paralleled the changes in MR. In W/Fu rats the level of message was either unchanged or only moderately altered by this treatment. In vivo administration of the MR antagonist RU28318 or the GR antagonist RU38486 to WI rats for 4 days reduced renal mRNA levels for both subunits of ATPase. In the W/Fu rat, this treatment resulted in no change in the alpha subunit and an increase in the beta subunit of ATPase. In preliminary studies, we have determined that the W/Fu rat is also resistant to dexamethasone-induced hypertension. These studies suggest that altered MR- and GR-mediated mechanisms may contribute to the resistance of the W/Fu rat strain to steroid-induced hypertension.
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