Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The circadian rhythm of plasma aldosterone (PAC) and cortisol concentration (PCC), and renin activity (PRA) was measured in five steroid and five non-steroid treated kidney transplanted patients--all with denervated kidney grafts--and compared with four normal controls and two steroid-treated patients with non-renal disease and thus normal renal innervation. The non-steroid treated patients had a normal circadian thythm of PAC and PCC, but without variation of PRA, suggesting that denervation of the kidneys has no influence on the circadian rhythm of PAC. In both steroid treated groups the PAC showed an inverse diurnal variation--now correlating to the diurnal variation in PRA. The inverse circadian rhythm of PAC in patients with suppressed ACTH secretion remains unexplained, but is in accordance with the nocturnal peak of sodium and water excretion in steroid treated patients.
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PMID:Circadian rhythm of plasma aldosterone and plasma renin activity in steroid and non-steroid treated kidney transplanted patients. 33 62

1. The initial site of damage in analgesic abuse is the renal medulla and the characteristic lesion is renal papillary necrosis. The papillary necrosis appears to be an ischaemic infarct. The cortical lesion of chronic interstial nephritis is a non-specific change and secondary to obstruction to tubules in the necrotic medulla. 2. Medullary perfusion and the concentration mechanism appear to be important factors in the genesis of renal papillary necrosis. 3. Experimental and clinical studies suggest that abuse of compound analgesics containing aspirin, phenacetin and caffeine result in renal papillary necrosis and the clinical syndrome of analgesic nephropathy. In the APC mixture aspirin appears to be the major nephrotoxic agent while phenacetin plays a synergistic but secondary role in the renal nephrotoxicity.
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PMID:Pathology, aetiology and pathogenesis of analgesic nephropathy. 107 Sep 95

Analgesic nephropathy is part of a wider clinical syndrome associated with the abuse of APC compounds, that is, a minimum total intake of 2 kg of aspirin or phenacetin. Ischaemic heart disease and premature aging are newly recognized aspects of the analgesic syndrome. The diagnosis of analgesic nephropathy can be made precisely by the radiological demonstration of renal papillary necrosis. The most important aspect of management of established analgesic nephropathy and renal insufficency is total avoidance of all non-steroid antiinflammatory agents and this is commonly associated with stabilization or improvement in renal function. In the APC mixture, aspirin appears to be the major nephrotoxic agent while phenacetin and paracetamol play a secondary and synergistic role in the nephrotoxicity.
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PMID:Analgesic nephropathy. 108 2

A survey of 763 patients with rheumatoid arthritis and 145 with osteoarthritis in six clinics in New Zealand showed no association between aspirin intake and a score designed to detect analgesic nephropathy. Analgesic nephropathy was diagnosed clinically in three patients taking APC (aspirin, phenacetin, and caffeine or codeine or both) and in one who took aspirin and phenylbutazone and was suspected in one who took aspirin and paracetamol. Isolated aspirin was not implicated. The study showed that most people can take large quantities of salicylates without renal injury.The findings are, however, consistent with the view that there is a risk from APC compounds taken in large quantity, but the numbers at risk in this study were small. Aspirin may have an additive effect with other analgesics in causing renal damage. An increased frequency of urinary tract symptoms in those taking analgesics requires further investigation.
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PMID:Aspirin and the kidney. New Zealand Rheumatism Association Study. 482 Oct 7

Earlier chronic studies using both animal and human autopsy material have suggested that the initial lesion of analgesic nephropathy is papillary necrosis with secondary cortical interstitial nephritis. The present study was designed to define ultrastructural changes in renal tubules exposed to high levels of analgesics. Female New Zealand White rabbits were given 5-7 g APC and sacrificed after periods of 6 to 36 hours. As early as 6 hours after treatment, hydroxyapatite crystallite aggregates were seen impacted in Segment III (straight segment) of the proximal tubule at the cortico-medullary junction. Ultrastructural changes included selective calcification of the brush border, mitochondrial calcification, and peroxisomal changes. It was concluded, on the basis of ultrastructural changes, that calcification of altered tubular cells may be an initial event in analgesic nephropathy.
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PMID:Intratubular calcium phosphate deposition in acute analgesic nephropathy in rabbits. 706 18

A gene for the autosomal recessive kidney disorder juvenile nephronophthisis (NPH) is located on chromosome 2q between markers D2S1893 and D2S1888. Recently, the presence of large homozygous deletions was described in the majority of NPH patients. We constructed an integrated YAC/PAC contig of 54 markers and 30 PAC clones that encompasses this deletion and the flanking inverted duplication. Thirty-six novel sequence-tagged site markers were generated for this region of 2-3 Mb, 22 of which represent PAC ends. Ten of 18 multiplex NPH families show a homozygous deletion for 8 consecutive markers. BlastN database search and expressed sequence tag (EST) mapping led to the localization of 18 EST clones to the integrated contig, representing 11 putative transcribed sequences. Seven EST clones were localized to the NPHP1 region between D2S1893 and D2S1888. Two EST clones, zc07a11 from a human parathyroid tumor library and yy63e10 from a multiple sclerosis lesion library, are located in the deletion region. PCR amplification experiments indicate that zc07a11 represents a chimeric cDNA. Through FISH analysis the NPHP1 deletion region was localized to 2q12-q13. In summary, our study provides a high-resolution physical map of the NPHP1 region with 7 precisely localized expressed sequences, 2 of which have recently been shown to be part of a gene for NPH. These data will alleviate the identification of further genes of a homozygous gene deletion syndrome in patients with NPH and oculomotor apraxia and will be instrumental in the characterization of the molecular mechanism leading to the large homozygous deletion in this region. The data furthermore provide an important step toward the construction of a sequence-ready PAC contig of this region.
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PMID:Construction of a gene map of the nephronophthisis type 1 (NPHP1) region on human chromosome 2q12-q13. 947

The most common type of renal injury in multiple myeloma is chronic tubulointerstitial nephropathy associated with casts in tubule lumens, an entity referred to as "myeloma kidney" that often progresses to end-stage kidney diseases. Myeloma kidney is associated with a significant increase in all-cause mortality, yet no effective intervention, except a limited use of steroid, is available. Here, we report that pituitary adenylate cyclase-activating polypeptide with 38 residues (PACAP38) dramatically prevents injury of cultured renal proximal tubule cells caused by myeloma light chains through suppression of proinflammatory cytokines production, by inhibiting p38 MAPK and translocation of NFkappaB via both PAC(1) and VPAC(1) receptors. The suppressive effects of PACAP was as effective as dexamethasone in all of their cytokine assays and demonstrated both in vitro and in vivo. Furthermore, PACAP38 inhibits myeloma cell growth directly and may also indirectly by suppressing production of the growth factor, IL-6, from bone marrow stromal cells, that is stimulated by adhesion of myeloma cells. These findings render PACAP38 worth evaluation as a promising candidate for an effective and safe renoprotectant in myeloma kidney, and possibly other nephropathy, and also as a new antitumor agent in multiple myeloma.
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PMID:Potential protective action of pituitary adenylate cyclase-activating polypeptide (PACAP38) on in vitro and in vivo models of myeloma kidney injury. 1620 6

A 53-year-old female had a history of long-term hemodialysis. Periodic follow-up abdominal ultrasonography revealed a tumor measuring 4 cm in diameter in an area adjacent to the upper pole of the right kidney. Abdominal computed tomography and magnetic resonance imaging confirmed a right adrenal tumor. Furthermore, adrenal scintigraphy after dexamethasone inhibition showed accumulation in the right adrenal gland. An endocrinological test revealed that the plasma renin activity (PRA) was normal, and that the plasma aldosterone (PAC) level was increased to 1,021.8 ng/dl. The PAC-to-PRA ratio (ARR) was 5,109. Under a diagnosis of aldosterone-producing adrenal tumor, laparoscopic right adrenalectomy was performed. After surgery, the PAC level was normalized. Pathological findings showed adrenal cortical adenoma. Primary aldosteronism causes hypertension, hypopotassiumemia, hyporeninemia, and hyperaldosteronemia via excessive secretion of aldosterone in the adrenal glands. However, the patient showed a high serum level of potassium due to anuria, and hypertension was not noted. Thus, some dialysis patients with primary aldosteronism do not show any typical clinical symptoms. A previous study also indicated the presence of hyperaldosteronemia in patients with end-stage renal disease. A diagnosis should be carefully made.
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PMID:[A case of aldosterone-producing adenoma associated with end-stage renal disease]. 2010 5