Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to elucidate the blood serum calcium, inorganic phosphorus, parathyroid hormone (PTH) and calcitonin (CT) content in the course of the development of chronic renal failure (CRF), 80 patients with chronile glomerulonephritis were examined. Of these, in 24 glomerular filtration (GF) was normal, whereas 56 had CRF of varying degree. Thirty-three out of the 80 patients had the nephrotic syndrome (NS). The parameters enumerated were also determined in 45 patients with CRF treated by hemodialysis. In patients without the NS, hypocalcemia was discovered only at the final predialysis stage of CRF, while in the presence of the NS, it was detectable in normal GF and was aggravated as CRF progressed. The PTH level ascended if GF was lower than 40 ml/min, not correlating with calcium concentration in the serum. A direct correlation was disclosed between the PTH level and that of inorganic phosphorus. The role of the latter in stimulation of PTH and CT secretion in CRF is discussed. In patients treated by hemodialysis, the PTH level significantly rose with treatment time increase. There was also a tendency toward elevation of CT concentration. The activity of the osseous fraction of blood serum alkaline phosphatase in patients treated by hemodialysis was increased in 61-84% of cases depending on the treatment period.
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PMID:[Phosphorus and calcium metabolism and its hormonal regulation in chronic kidney failure]. 398 31

Bone mineral content (BMC) was measured in the nondominant arm of 18 children (aged 3 7/12 to 17 1/2 years) for a total 783 months after renal transplantation. Using photon absorptiometry, 89 measurements were made; 17 of the 18 patients had a functioning graft and one patient died. Significant demineralization, a BMC greater than -2 SD below appropriate control volumes, was found in 11 of 18 patients (62%) and 55 of 89 measurements (61%). Bone loss was progressive; among the 16 patients followed for more than 6 months, ten showed a decline of more than 0.5 SD in BMC, five had no change, and only one showed improvement. No relationship was found between BMC and the use of furosemide, type of transplant (15 living, seven cadaver), prior renal disease (six with glomerulonephritis, 11 tubulointerstitial), need for a second graft (five patients), chronic anticonvulsant therapy, or serum calcium and phosphate values. BMC was slightly correlated (P less than .05) with alkaline phosphatase values. BMC was more strongly correlated with serum creatinine (y = -0.48x + 1.25, r = -.042, P less than .001) and prednisone dose (mg/kg/d) (y = -0.65x + 0.481, r = -.543, P less than .001) in an inverse relationship. Patients whose serum creatinine value was less than 1 mg/dL had a BMC of -0.71 +/- 0.34 SD; those with serum creatinine value greater than 2 mg/dL had BMC of -3.32 +/- 0.31 SD, different at P less than .001. Patients receiving daily prednisone therapy had a significantly lower BMC than those receiving alternate-day therapy (-3.11 +/- 1.23 SD v -1.72 +/- 1.29 SD, P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistence of diminished bone mineral content following renal transplantation in childhood. 636 39

The experiment was undertaken to make a discrimination between glomerulonephritis (GN, Masugi-type) and tubular damage (TD, cephaloridine-induced) in rats by means of urinary alkaline phosphatase (AlP). Urinary AlP concentrations were increased 13 times in GN rats amd 8 times in TD rats, in comparison with the corresponding controls. Cellulose acetate plate electrophoresis before and after neuraminidase digestion revealed that urinary AlP from GN rats migrated similarly to serum and intestinal AlP, while the mobility of urinary AlP from TD rats resembled that of the kidney. The sensitivity of urinary AlP from GN to the inhibitors, L-phenylalanine and urea, was almost equivalent to that of intestinal AlP, and the sensitivity of urinary AlP from TD rats was similar to that from kidney AlP. Histochemically, AlP activity in the kidney appeared normal in GN rats, but it was markedly decreased in TD rats. Those results suggest that the urinary AlP from GN rats is identical to serum AlP originating from intestines, i.e., a selective increase in glomerular permeability in disturbed glomerular filtration occurs. On the other hand, urinary AlP from TD rats originated mainly from the kidney due to the disquamation in the proximal convoluted tubular epithelia. Thus the properties of urinary AlP are important for estimating the site of renal damage.
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PMID:[Studies on experimental renal damage in rats. I. Analysis of urinary alkaline phosphatase (author's transl)]. 708 15

Anti-rat glomerular basement membrane (GBM) rabbit serum was produced by immunizing rabbits with the supernatant substance of trypsin-digested rat GBM. Nephritis was induced in rats by a single intravenous administration of 0.25 ml of anti-serum and changes in pathohistological and biochemical parameters during the process of the disease were investigated in comparison with those of Masugi nephritis and the modified type of Masugi nephritis previously reported. In light microscopic studies, histological changes seen in the kidneys closely resembled those of typical human glomerulonephritis. Changes such as hypercellularity, adhesion between capillary wall and Bowman's capsule, crescent formation and hyalinization in glomeruli and interstitial infiltration were the most pronounced on the 30th day after the anti-serum injection. In immunofluorescent studies, a linear fixation of rabbit IgG was observed along the GBM from the 1st day and the staining of a certain intensity was preserved throughout the experimental periods. A linear staining with anti-rat IgG serum was recognized from the 10th day. The fixation of fibrinogen was also seen in not only the glomerular capillary walls, but also in Bowman's space after the 10th day. Proteinuria significantly increased from the 1st day, reached a peak of 12 times the control level, and thereafter gradually decreased. The patterns of progress of urinary alkaline phosphatase and N-acetyl-beta-glucosaminidase activities were much the same as those seen in cases of proteinuria and the levels at their peak times were about 10 and 3 times control levels, respectively. Plasma urea nitrogen level transiently increased on the 5th day and then reverted to the control level by the 30th day. Plasma cholesterol levels were significantly high from the 5th to the 20th days. It is concluded that glomerular damages in this model are more severe, so-called, "nephritic type" and continue for longer periods than in cases of Masugi nephritis, however, do not differ in degree and duration from findings in the modified type of Masugi nephritis.
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PMID:[Pharmacological studies on experimental nephritic rats (11). Changes in pathohistological and biochemical parameters in anti-rat GBM rabbit serum-induced nephritis (author's transl)]. 728 45

Glomerular extracapillary cellular proliferation with crescent formation initially presenting as rapidly progressive glomerulonephritis is a rare clinical manifestation of multiple myeloma. We report here a case of a 58 year old female who initially presented with haematuria, loss of weight and appetite and history of febrile episodes and was diagnosed following renal biopsy as rapidly progressive glomerulonephritis. Haemodialysis was carried out a month later because of uremic symptoms and maintained with monitoring of serum, calcium, phosphate, alkaline phosphatase, albumin and iPTH levels. After 6 months, she complained of bone pains over anterior chest wall which persisted even with low calcium haemodialysis. Serum protein electrophoresis and bone marrow aspiration revealed multiple myeloma. On starting chemotherapy, bone pain subsided but the patient expired within 15 days of therapy.
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PMID:Multiple myeloma presenting as proliferative (crescentic) glomerulonephritis. 873 63

Infiltration of leukocytes into glomerular and interstitial regions of the kidney is a key event in the pathogenesis of human glomerulonephritis. This process is mediated by specific adhesion molecules, some of which are expressed in a coordinated fashion following endothelial cell activation. We have assessed the pattern of expression of the selectins (E, P and L), and the counter-receptors (LFA-1 and ICAM-1, and VLA-4 and VCAM-1 in 119 renal biopsies using sequential sections, and have correlated this with the degree of histological damage (tubular atrophy and interstitial fibrosis) and the intensity of the macrophage infiltrate. Sections were stained with the monoclonal antibodies using a standard alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. There were strong correlations between the following: (1) expression of LFA-1, VLA-4, and L-selectin in the periglomerular region, interstitium and in focal interstitial infiltrates and the presence of macrophages in these regions; (2) de novo tubular expression of ICAM-1 and VCAM-1; (3) staining for ICAM-1 and VCAM-1 on focal cellular infiltrates within the interstitium; and (4) staining for E- and P-selectin on extraglomerular endothelium. These are also strongly correlated with the degree of chronic histological damage. There was, however, no correlation between glomerular expression of adhesion molecules or glomerular macrophage infiltration and chronic histological damage. Although expression of VCAM-1 by the glomerular mesangium was strongly correlated with the presence of cells staining for VLA-4 within the glomerulus, glomerular expression of adhesion molecules correlated poorly with their expression in other sites. These results show that coordinated up-regulation of adhesion molecule expression in the tubulointerstitium is associated with interstitial fibrosis and tubular atrophy and may contribute, therefore, to the progression of renal disease.
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PMID:Adhesion molecule interactions in human glomerulonephritis: importance of the tubulointerstitium. 877 Sep 58

Secondary hyperparathyroidism (2'HPT) improves after renal transplantation (RTx) along with recovered function of the renal allograft. However, normal renal function does not last long due to rejection, drug-induced nephrotoxic nepthropathy, or recurrence of post-transplant glomerulonephritis. Therefore, improved calcium and phosphate metabolism, and parathyroid function after RTx fluctuate in accordance with the function of the renal allograft. In cases with severe 2'HPT, parathyroidectomy should be performed before RTx because hypercalcemia due to secondary or tertiary hyperparathyroidism aggravates the renal allograft function. In the follow-up of mild 2'HPT after RTx, hypercalcemia and vascular calcification should be monitored carefully by serum parathyroid hormone, calcium and phosphate concentrations, alkaline phosphatase activity, and bone X-ray film. If serum calcium level exceeds 12 mg/dl, parathyroidectomy (PTx) should be performed to prevent the acceleration of vascular calcification. Total PTx with forearm allograft is a preferred surgical procedure for 2'HPT even after RTx.
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PMID:Renal transplantation and secondary hyperparathyroidism. 908 65

Connexin43 (Cx43) is a major component of gap junctions. These are widely distributed in the human kidney and are thought to be involved in the inflammatory response and in the regulation of cell growth. Cellular adhesion molecules (CAMs) are also thought to be important in these processes, where they possibly facilitate gap junction formation. The aims of the current study were to define for the first time the expression of Cx43 in inflammatory glomerulonephritis and to compare the localization of this connexin with that of the intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Human renal biopsies and control sections of normal human kidney were stained using the alkaline phosphatase/anti-alkaline phosphatase immunohistochemical technique, demonstrating that Cx43 was strongly expressed on inflammatory cells, on damaged tubular cells, and on interstitial cells. This pattern of expression was paralleled closely by that of ICAM-1 and, to a lesser extent, by that of VCAM-1. Cx43 is therefore primarily implicated in tubulointerstitial inflammation.
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PMID:Upregulation and co-localization of connexin43 and cellular adhesion molecules in inflammatory renal disease. 930 56

Signalment, clinical signs, and physical examination and clinicopathologic findings in dogs diagnosed with Hepatozoon canis parasitemia (n = 100) were compared with those in Hepatozoon-negative dogs (n = 180). A subset (n = 15) of Hepatozoon-positive dogs with unusually high (> 800 H canis gametocytes/microL of whole blood) parasitemia was compared with dogs that had low parasitemia (n = 85) and with Hepatozoon-negative dogs (n = 180). Hepatozoon-positive dogs significantly differed from Hepatozoon-negative dogs in body temperature, total red blood cell count, hemoglobin concentration, hematocrit, and platelet count. Dogs with high H canis parasitemia significantly differed from those with low parasitemia in hemoglobin concentration, hematocrit, and total neutrophil count. Clinical findings from dogs with high H canis parasitemia included emaciation, lethargy, hyperglobulinemia, hypoalbuminemia, and increased serum alkaline phosphatase and creatine kinase activities. Findings at necropsy included hepatitis, pneumonia, and glomerulonephritis associated with H canis schizonts and extensive parasitism of bone marrow, spleen, and lymph nodes. Low hemoglobin concentration, low platelet count, and concurrent parvovirus infection together represented the best predictor variables for Hepatozoon positivity in dogs presenting to the hospital.
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PMID:Retrospective case-control study of hepatozoonosis in dogs in Israel. 947 Jan 63

IgA nephropathy (IgAN) is one of the most frequent forms of glomerulonephritis (GN). However, its association with polycythemia vera (PV) has rarely been described. We report a case of IgAN combined with PV. The patient was a 46-year-old male with chronic renal failure, heavy proteinuria and erythrocytosis. He also presented hypertension and hematuria as well as splenomegaly, high arterial oxygen saturation and elevated leukocyte alkaline phosphatase activity. Possible causes of secondary erythrocytosis were ruled out. The renal biopsy revealed mesangial proliferative GN with predominant IgA deposition in mesangium. He was diagnosed as having IgAN and PV concomitantly. After administration of hydroxyurea, enalapril and felodipine, blood cell count and blood pressure normalized, while azotemia persisted. There was also a partial remission of the heavy proteinuria. We describe a case of IgAN associated with PV, and possible pathophysiologic relationships between two diseases are discussed with review of the literature.
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PMID:IgA nephropathy in a patient with polycythemia vera. Clinical manifestation of chronic renal failure and heavy proteinuria. 1216 77


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