Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analgesic nephropathy was first studied in Switzerland and Scandinavia, and most observers thought that papillary necrosis, a feature of the pathology, was the result of chronic interstitial nephritis, the other principal feature. From 1962, reports indicated a high incidence of analgesic nephropathy in Australia and suggested that papillary changes preceded cortical damage. Later, associated uroepithelial carcinoma was noted. Early papillary lesions consist of necrosis of elements around groups of collecting ducts. Necrosis extends upward through the medulla from the papilla and gradually intensifies to total papillary destruction. Fat and calcium accumulation and changes in matrix mucopolysaccharide are markers of papillary injury. Cortical atrophy is dependent upon collecting duct obstruction and is proportional to the degree of obstruction. Infection may complicate late pathologic changes. It is suggested that in the early stages the disease represents an injury to "concentrating columns" in the medulla.
 ...
PMID:Pathology of analgesic nephropathy: Australian experience. 71 65

Renal coccidiosis is reported for the first time in an auk (Alcidae). Infection was detected in seven of 50 nestling Atlantic puffins (Fratercula arctica) and a new species of coccidia, Eimeria fraterculae sp. n., is described. The structure and sporulation of oocysts are characterized. Meronts, gamonts, and developing oocysts were present in collecting duct epithelium of medullary cones. The predominant host response was hypertrophy of infected cells, tubule dilation, and a mild localized peritubular infiltration with mononuclear inflammatory cells.
 ...
PMID:Eimeria fraterculae sp. n. in the kidneys of Atlantic puffins (Fratercula arctica) from Newfoundland, Canada: species description and lesions. 350 38

The feasibility of water channel gene delivery to kidney tubules and microvessels was evaluated by delivery of an adenovirus encoding aquaporin 1 (AQP1-Ad5) to transgenic AQP1 null mice. In wild-type mice, AQP1 is expressed in kidney proximal tubule, thin descending limb of Henle, and descending vasa recta, where urine osmolality (Uosm) increases from 1000-1500 mOsm (before) to 2500-3500 mOsm after 36 hr of water deprivation. Uosm in AQP1 null mice remains nearly fixed at 650-750 mOsm. AQP1-Ad5 (with a CMV promoter) was generated and purified. Infection of CHO cells gave strong uniform AQP1 expression with plasma membrane localization and eightfold increased water permeability over noninfected cells. AQP1-Ad5 was delivered to 20 to 25-g AQP1 null mice by tail vein infusion (0-10(10) PFU). At 3-7 days, AQP1 protein expression was strongest in liver (approximately 20 microg of AQP1 protein per liver) and next strongest in kidney, with expression in proximal tubule apical and basolateral membranes, and renal microvessels. Functional analysis showed increased water permeability in apical membrane vesicles from proximal tubule. AQP1 expression was not detected in glomerulus, limb of Henle, or collecting duct. In water-deprived null mice receiving 5 x 10(9) PFU of AQP1-Ad5, Uosm increased by up to 510 mOsm (mean increase, 225 +/- 24 mOsm; n = 33 mice). Whereas the control null mice became lethargic and lost 34.2 +/- 0.6% body weight, the virus-treated mice remained relatively active and lost 32.3 +/- 0.7% body weight. Viral DNA and AQP1 transcript were detected in kidney and liver of null mice up to 17 weeks after virus infusion; partial correction of the urinary concentrating defect persisted for 3-5 weeks. These results demonstrate partial functional correction of a urinary concentrating defect by adenoviral delivery of the AQP1 gene.
 ...
PMID:Partial correction of the urinary concentrating defect in aquaporin-1 null mice by adenovirus-mediated gene delivery. 1072 35