Gene/Protein Disease Symptom Drug Enzyme Compound
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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.
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PMID:Pathology of analgesic nephropathy: Australian experience. 71 65

Medullary tubules in renal biopsies from twelve patients suffering from ischemic acute tubular necrosis (ATN) and nine patients with allergic, drug-induced acute interstitial nephritis (AIN) were investigated by electron microscopy using quantitative and semiquantitative methods. For comparison, 12 biopsies from patients without renal disease or with minimal change nephropathy were studied. The mean scores for reduction of brush border and basolateral infoldings of the cell surface were significantly increased in the straight part of the proximal tubule and the thick ascending loop of Henle (straight part of the distal tubule) compared with medullary controls, and these changes were significantly greater than the scores for the corresponding convoluted tubules in the cortex. The numbers of missing tubular epithelial cells (indicating sites of cellular desquamation) were significantly increased in the thick ascending loop of Henle in ATN as well as in AIN and in the straight proximal tubule in ATN. This single cell lesion also occurred in the collecting duct. These findings are discussed in the light of recent experimental data indicating the importance of medullary tubules for the pathogenesis of ATN.
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PMID:Ultrastructure of medullary tubules in ischemic acute tubular necrosis and acute interstitial nephritis in man. 228 9

Recent studies have suggested that crescents are primarily of monocytic origin and that epithelial cells are a minor factor in their composition. Frozen sections of renal biopsies from 11 cases of crescentic glomerulonephritis (CGN) and 5 controls (2 acute interstitial nephritis, 1 focal glomerulosclerosis, 1 benign recurrent hematuria, 1 normal kidney) were stained for intracellular cytokeratin (CK) with a mouse monoclonal anti-CK antiserum (PKK1) and nonspecific esterase (NSE) activity. Indirect immunofluorescence with PKK1 antiserum showed that in all biopsies there was positive staining of collecting duct and proximal and distal tubular epithelium but no reactions in blood vessels or interstitium. In control case glomeruli there was no staining of the tuft, including the visceral epithelium. In all cases some parietal epithelium was CK-positive. In 4 CGN biopsies the majority of the crescents showed cytoplasmic staining for CK in more than 50% of the crescent cells. In 2 cases most crescents contained between 10-50% CK-positive cells, whereas in 5 biopsies little or no CK was present in the majority of crescents. In all but one CGN case the majority of crescents contained fewer than 30% NSE-positive cells (monocytes). Electron microscopy demonstrated intermediate filaments in many crescent cells and scattered desmosomes within crescents. The results indicate that epithelial cells, probably of parietal epithelial origin, contribute significantly to crescent formation.
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PMID:Histogenesis of glomerular crescents. Immunohistochemical demonstration of cytokeratin in crescent cells. 241 Nov 41

Nucleated nonsquamous cells in urine of patients with crescentic glomerulonephritis (CN), noncrescentic glomerulonephritis (NCN), acute tubular necrosis (ATN) and drug related acute interstitial nephritis (AIN) were identified using monoclonal antibodies and immunoperoxidase stain. Cell viability was determined by trypan blue permeability. CN was distinguishable from NCN by total cell numbers exceeding 30,000/ml (p less than 0.001) and counts of granulocytes exceeding 10,000/ml (p less than 0.05), monocytes exceeding 3,000/ml (p less than 0.001), T4 lymphocytes exceeding 1,500/ml (p less than 0.001), T8 lymphocytes exceeding 1,500/ml (p less than 0.001), glomerular epithelial cells exceeding 4,000/ml (p less than 0.001), proximal tubular cells exceeding 8,000/ml (p less than 0.001), loop of Henle cells exceeding 1,500/ml (p less than 0.01) and urothelial cells exceeding 1,500/ml (p less than 0.05). AIN was distinguishable from ATN by total cell numbers exceeding 75,000/ml (p less than 0.001) and counts of granulocytes exceeding 150,000/ml (p less than 0.001), monocytes exceeding 5000/ml (p less than 0.001), T4 lymphocytes exceeding 3,000/ml (p less than 0.01), T8 lymphocytes exceeding 2,500/ml (p less than 0.01) and cell viability exceeding 60% (p less than 0.05). Proximal tubular, loop of Henle, distal tubular/collecting duct and urothelial cells were present in high numbers in CN, ATN and AIN. CN can be distinguished from NCN, and ATN can be distinguished from AIN by identifying and quantifying the nucleated cells present in the urine.
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PMID:Immunoperoxidase identification of nucleated cells in urine in glomerular and acute tubular disorders. 266 90

Nine patients with the unusual combination of renal failure, nephrotic-range proteinuria, and biopsy-proved interstitial nephritis are described. Six of these patients had received nonsteroidal anti-inflammatory agents (three fenoprofen, one ibuprofen, one zomepirac, and one tolmetin). The remaining three patients had no history of exposure to drugs known to cause interstitial nephritis. Immunologic characterization of the infiltrating cells with monoclonal antibodies showed that the majority of cells in most cases were cytotoxic T cells, although some B cells were present in all cases. Giant collecting duct cells were seen in half the patients with drug exposure but in none of the others. Otherwise, there were no conspicuous morphologic differences between patients with and without drug exposure. Many of the patients had associated glomerular abnormalities. Only the zomepirac and tolmetin recipients showed pure interstitial disease. The three fenoprofen recipients and the zomepirac and tolmetin recipients regained normal renal function after the drug was discontinued. The combination of renal failure, nephrotic range proteinuria, and interstitial nephritis is one form of nephrotoxicity observed in patients treated with nonsteroidal anti-inflammatory agents. However, this lesion, which may be mediated by cytotoxic T cells, may also be seen rarely in patients with no apparent drug exposure.
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PMID:Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs. Immunologic characterization of the inflammatory infiltrate. 637 63

Many renal diseases involving the tubular epithelium appear to preferentially affect certain nephron segments. While major portions of the nephron, such as proximal and distal convoluted tubules and collecting ducts, can be identified in the normal kidney, the distinction of diseased nephron segments can be difficult in tissue sections. Thus, to identify which nephron segments are involved in pathologic changes is usually impossible by routine histologic examination alone. Recently antibody and lectin probes that react with specific nephron segment-specific epitopes and carbohydrates, respectively, have become available. Some of these antibodies and lectins can be used on formalin-fixed, paraffin-embedded, archival tissues. Because renal tubules appear to retain their nephron segment-specific epitopes and glycoprotein moieties under most pathologic conditions, these nephron segment-specific tubular epithelial markers provide a method to study renal diseases involving the tubular system also in archival material. Such nephron segment-specific tubular epithelial markers are: the lectins, Tetragonolobus purpuras and Phaseolus vulgaris erythroagglutinin (proximal tubular markers); antibodies to low-molecular-weight cytokeratin (AE1/AE3); epithelial membrane antigen and the lectin Arachis hypogaea (distal nephron [distal convoluted tubule and collecting duct] markers); and antibodies to Tamm-Horsfall protein (labeling the thick ascending limb of Henle). We review the application of these and other renal tubular epithelial markers in the normal kidney and in various renal diseases including cystic disease of the kidney, interstitial nephritis, tubular atrophy, acute tubular necrosis, myeloma cast nephropathy, and renal tumors.
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PMID:Immunohistochemical and lectin dissection of the human nephron in health and disease. 825 Jun 94

Renal and metabolic adverse effects of lithium therapy are illustrated by the case report of a manic depressive woman aged 78 years, so treated for about 25 years. Long term lithium therapy with plasma lithium level in the therapeutic range impairs renal concentrating ability in 25-50% of the patients (when the total ingested amount reaches 100-200 mol, 700-1400 g). About 10-15% of the patients have overt nephrogenic diabetes insipidus (NDI) with elevated antidiuretic hormone plasma level and unresponsiveness to desmopressin. In rats, lithium treatment down regulates expression of the main water channel, aquaporin 2, in the renal collecting duct. NDI may be complicated by hypernatremic dehydration if the access to water is restricted, whatever the cause. Treatment of NID is best started with nonsteroidal antiinflammatory drugs, being then substituted for amiloride. Prolonged lithium therapy may induce chronic interstitial nephritis. In some patients this may result in mild or moderate non progressive chronic renal insufficiency. Acute lithium intoxication (with supratherapeutic doses) may be complicated by acute renal failure (ARF); even in the absence of ARF hemodialysis is indicated when plasma lithium level reaches 4 mmol/l or more. Other metabolic adverse effects of lithium therapy include: hypercalcemia due to hyperparathyroidism (in 5-10% of the patients); hypothyroidism (often latent); hyperthyroidism. In conclusion, these renal and metabolic adverse effects are generally mild or moderate, allowing the continuation of lithium therapy in most affected patients.
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PMID:[Renal and metabolic complications of lithium]. 1079 6

To distinguish biological molecular processes of osmotic stress occurring in inner medulla, we utilized microarrays to monitor expression profiles. RNAs from three segments (cortex, outer medulla, and inner medulla) of mouse kidney were isolated and applied to microarrays. We found 35 genes expressed highly in inner medulla. Next, microarrays for the RNAs from mouse medullary collecting duct cell line (mIMCD) cells and osmotically adapted mIMCD cells (HT cells) were performed (designed as resistant to 1270mOsm/H(2)O). Of 35 genes highly expressed in inner medulla, 6 genes such as; B-cell translocation gene protein (BTG), myc-basic motif homologue, gelsolin, cell surface glycoprotein, laminin beta2, and tubulo-interstitial nephritis antigen, were also expressed highly in HT cells. Using real-time PCR, we confirmed the expression of six genes. Additionally acute osmotic stress induced the BTG. By comparing the inner medulla to a mIMCD3, we identified genes which respond to acute and chronic hyperosmotic stress.
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PMID:Osmoadaptation-related genes in inner medulla of mouse kidney using microarray. 1531 98

Transmembrane protein 174 (TMEM174) mRNA is easily detectable in human kidney tissues and activates AP-1 and promotes 293T cell proliferation. In the present study, RNA in situ hybridization was used to detect TMEM174 gene expression in various malignant renal cancer and normal renal tissues. The results showed that TMEM174 exhibits differential expression in renal tissues, with a high positive rate of expression in squamous cell carcinoma with necrosis, papillary renal cell carcinoma and transitional cell carcinoma, and a low positive rate of expression in clear cell carcinoma, interstitial nephritis, undifferentiated carcinoma, retroperitoneal metastatic clear cell carcinoma, adrenal gland metastatic clear cell carcinoma, pelvic cavity metastatic chromophobe carcinoma, severe atypical hyperplasia of transitional epithelium and hyperplasia. Extremely weak expression was exhibited in collecting duct carcinoma, Wilms' tumor, chronic pyelonephritis, acute pyelonephritis, cancer adjacent normal renal tissue and normal renal tissue. In conclusion, the TMEM174 gene exhibited high expression levels in certain renal carcinomas, which may indicate that TMEM174 may have a significant role in the development and progression of these renal carcinomas.
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PMID:Analysis of TMEM174 gene expression in various renal cancer types by RNA in situ hybridization. 2520 93

A Bourke's parrot (Neopsephotus bourkii) originating from an aviary in Australia, containing two species of parrots, five species of finch and a species of dove, was presented for necropsy. The Bourke's parrot died from gastritis caused by Macrorhabdus ornithogaster, but also had an interstitial nephritis and ureteritis with adenovirus-like inclusion bodies within collecting duct epithelial cells. The adenovirus causing the lesions was shown to be Psittacine adenovirus-2 (PsAdV-2) using a PCR assay specific for adenoviruses and sequencing of amplicons. A survey of droppings from other birds in the aviary using the same PCR assay with amplicon sequencing found a high prevalence of infection of PsAdV-2 in Bourke's and scarlet-chested parrots (Neophema splendida). PsAdV-2 was also present in droppings from a Namaqua dove (Oena capensis). Gouldian finches (Erythrura gouldiae), red-billed firefinches (Lagonosticta senegala), and red-throated parrot finches (Erythrura psittacea) were shedding Gouldian finch adenovirus-1 (GFAdV-1). Two novel adenoviruses, an atadenovirus and a siadenovirus, were detected in the droppings from long-tailed finches (Poephila acuticauda). Kidney tissue from three of four scarlet-chested parrots submitted for necropsy from a second aviary were also positive for PsAdv-2. These findings and previously reported findings of widespread PsAdv-2 infection in captive orange-bellied parrots (Neophemia chrysogaster) raise the possibility that PsAdV-2 is enzootic in Australian aviculture. This represents the first report of GFAdV-1 in Australia and first identification of infection in finch species other than the Gouldian finch. Identification of two novel adenoviruses in long-tailed finches suggests that other novel adenoviruses are circulating in other finch species. RESEARCH HIGHLIGHTS Psittacine adenovirus-2 was present in high prevalence in two Australian aviaries. Gouldian finch adenovirus-1 (GFAdV-1) was detected in Australia for the first time. The host range of GFAdV-1 host range was expanded to other finch species. Novel atadenovirus and siadenovirus were detected in Estrildid finches.
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PMID:A survey of a mixed species aviary provides new insights into the pathogenicity, diversity, evolution, host range, and distribution of psittacine and passerine adenoviruses. 3108 48


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