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)

An anti-kidney antibody was demonstrated by the indirect immunofluorescence method in the serum of patients with primary tumours of the liver or kidney. The distribution of fluorescence in rabbit kidney was consistent with that of antibody to collecting ducts. The anti-collecting duct antibody (anti-CDA) could be absorbed from serum by normal adult rabbit or human kidney tissue and by one of three specimens of renal-cell carcinoma tissue. Anti-CDA differed from anti-mitochondrial antibodies and from anti-liver/kidney microsomal antibody in the pattern of fluorescent staining obtained with rabbit kidney. Two-hundred sera from patients with cancer and other diseases and forty-three from healthy hospital personnel were tested for anti-CDA. Eleven of the twenty-five positive sera were from patients with primary cancer of the liver or urinary tract, and all but six of the remainder were from patients with tumours involving the liver or with liver disorders that may be associated with nodular hyperplasia or tumour.
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PMID:Circulating antibody to renal collecting ducts in patients with hepatoma or renal-cell carcinoma. 17 72

The systemic and renal adaptations for the maintenance and correction of metabolic alkalosis generated by chloride depletion (CDA) are the focus of this review. The hypothesis that extracellular fluid (ECF) volume expansion is essential for the correction of CDA is refuted, while the concept that Cl- repletion is necessary and sufficient for correction is developed. Contraction of ECF volume probably can occur as a consequence of CDA. The principal mechanisms by which the kidney corrects CDA appear to reside primarily in the collecting duct, which is endowed with the anion exchange mechanisms and the capacity to effect the necessary changes in body anion composition. Although the remainder of the collecting duct is undoubtedly important in this response, the cortical segment appears to have the paramount role since it can either absorb or secrete HCO3-. Alterations in the delivery of Cl- or HCO3- to the collecting duct may also be important but changes in glomerular filtration rate appear to have a minor role. Major unanswered questions in the pathophysiology of CDA are the manner in which exogenous Cl- repletion is detected and the kidney is signaled to excrete HCO3- and the cellular mechanisms by which this is accomplished in the various nephron segments.
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PMID:Adaptations to chloride-depletion alkalosis. 192 24