Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The carboxyterminal propeptide of type I procollagen is a biochemical marker of type I collagen synthesis. We evaluated circulating carboxyterminal propetide of type I procollagen levels in patients with terminal renal failure before and after kidney transplantation. Serum carboxyterminal propeptide of type I procollagen, osteocalcin, total alkaline phosphatase, intact parathyrin, creatinine, calcium and phosphate levels were determined in 20 patients, before and 15, 30, 90 and 180 days after surgery. Serum creatinine and intact parathyrin concentrations showed a significant decrease after kidney transplantation. Immunosuppressive treatment consisted of low dose prednisone, cyclosporin and antilymphoblast globulin. In our group, only 5 patients (25%) showed serum carboxyterminal propeptide of type I procollagen levels higher than normal before kidney transplantation. At 15 and 30 days, carboxyterminal propeptide of type I procollagen concentrations showed a decrease, while at 90 and 180 days there was a significant increase above the normal range (p = 0.006; ANOVA). Serum osteocalcin and total alkaline phosphatase levels increased significantly at the same time. We found a significant correlation between carboxyterminal propetide of type I procollagen and osteocalcin at 15 and 30 days after kidney transplantation. We conclude that the significant increase in carboxyterminal propeptide of type I procollagen levels after kidney transplantation reflect an increase in bone turnover. The low doses of steroids employed do not seem to have a significant inhibitory effect on collagen synthesis.
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PMID:Evolution of circulating C-terminal propeptide of type I procollagen in patients with chronic renal failure pre and post renal transplantation. 896 Apr 63

The authors present a case of disseminated tuberculosis in a patient under dialysis with endstage renal disease. Fever, nocturnal sweating, anorexia, asthenia, ascites, lymph node involvement and granulomatous involvement of the bone marrow were observed. In the twenty nine months of renal failure which preceded the beginning of the tuberculosis, serum calcium levels were normal or low-normal and there was a secondary hyperparathyroidism. During that period the patient was treated with calcium carbonate and calcitriol. At the onset of tuberculosis, serum calcium levels rose above normal. Treatment with calcium and calcitriol was withdrawn but hypercalcemia remained unchanged. Serum concentration of parathormone fell significantly. Antituberculosis drugs were started. The resolution of active tuberculosis was accompanied by normalization of serum calcium levels and by elevation above normal of serum concentration of parathormone.
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PMID:[Tuberculosis and hypercalcemia]. 900 10

Macrophage dysfunction is considered an important contributory factor for increased propensity of infections in uremia. Because nitric oxide (NO) is believed to be an effector molecule of macrophage cytotoxicity, we propose that the dysfunction may be related to impaired NO synthesis. To verify this hypothesis, we evaluated macrophage NO synthesis in the presence of urea, a compound that accumulates in renal failure and is believed by some to be a uremic toxin. Macrophages (RAW 264.7 cells) were incubated with bacterial lipopolysaccharide to induce NO synthesis, whereas the test groups had various concentrations of urea in addition. NO synthesis was measured by assaying the supernatant for nitrites and nitrates by chemiluminescence. We observed that urea consistently produced a dose-dependent reversible inhibition of inducible NO production in macrophages, whereas parathormone, another toxin retained in uremia, had no such inhibitory effects. Further studies revealed that mRNA for inducible NO synthase was not inhibited by urea. We thus conclude that urea inhibits inducible NO synthesis in macrophages by a posttranscriptional mechanism and that this may be important in macrophage dysfunction of uremia.
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PMID:Urea inhibits inducible nitric oxide synthase in macrophage cell line. 943 93

To evaluate pancreatic exocrine function in uremia, 25 patients undergoing regular hemodialysis without clinical evidence of pancreatic disease and 25 healthy control subjects were studied by fecal elastase 1 and chymotrypsin. Abdominal ultrasonography and measurement of serum lipase, calcium, phosphate, and parathormone were also carried out. Fecal elastase was significantly lower (P < 0.001) in patients than in controls. Abnormally low values were found in 12/25 patients of whom six had values <100 microg/g. Fecal chymotrypsin was significantly lower (P < 0.05) in patients than in controls, with lower than normal values found in 10/25 patients. Fecal elastase was not related to the serum calcium, phosphate, or parathormone levels or to the period of dialysis. In patients serum lipase was normal or slightly elevated (<300 units/liter), and there was no evidence of pancreatic disease at ultrasound examination. The results lend further support to the existence of pancreatic function impairment in a significant number of patients with renal failure despite the absence of clinical and morphological evidence of pancreatic disease.
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PMID:Impaired fecal elastase excretion in uremic pancreopathy. 1121 50

Musculoskeletal problems remain among the main limitations of the quality of life of renal failure patients, in particular of those treated with long-term maintenance dialysis. Renal osteodystrophy continues to receive great attention. The mechanisms of uremic skeletal resistance to parathormone (PTH) are further investigated. The assay used for the dosage of "intact PTH" has been found to detect 7-84 fragments with an inhibitory effect on the action of the whole hormone. A decrease in the density of PTH receptor on osteoblasts is another recently evidenced factor. Investigations of the recently described RANK-RANKL system have demonstrated an increase in serum osteprotegerin levels, which, together with the two above-mentioned abnormalities, may explain bone resistance to PTH. These are important advances in the understanding of renal osteodystrophy as skeletal resistance to PTH appears to play an important part in the pathophysiology of secondary hyperparathyroidism and of adynamic bone disease. Because of this skeletal resistance, it has been recommended for several years that serum PTH level be monitored and kept twofold to threefold above the upper value of the normal level to maintain normal bone turnover in dialysis patients. Relative hypoparathyroidism has recently been found to be associated with increased spontaneous fracture rate and mortality, so this recommendation appears to hold adequate, despite the demonstration that serum PTH levels in this range are a poor predictor of bone turnover and that chronic parathyroid gland hyperplasia is likely to favor parathyroid gland autonomization. Recent publications have insisted on the role that hyperphosphatemia plays not only in the development of secondary hyperparathyroidism, but also of vascular, especially coronary, calcification and as a predictor of mortality. This "silent killer" of uremic patients is one of the main targets for therapeutic intervention. Extensive use of calcium-containing phosphate binders has been recently criticized as calcium overload appears to favor vascular calcification. Sevelaner (RenaGel) is a calcium- and aluminum-free phosphate binder that is an important advance in the management of renal osteodystrophy, especially in patients with extraskeletal calcification and hypercalcemia. The use of vitamin D derivatives has also raised concern because they enhance calcium and phosphorus absorption and reduce bone turnover. New metabolites with fewer hypercalcemic effects have been developed. Calcium-sensing receptor agonists are stimulating interest and are likely to take an important place in the future management of renal osteodystrophy. Uremic myopathy has received recent attention. Impaired muscle capillary oxygen transfer has been identified as a pathophysiologic factor, and progressive resistance training has been shown to improve the condition. Finally, a new entity, nephrogenic fibrosing dermopathy, has been described, which must be distinguished from calciphylaxis and scleromyxedema.
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PMID:Musculoskeletal manifestations of chronic renal failure. 1249 10

Twenty-four hour urinary excretion, fractional excretion and the filtered load of calcium and phosphorus were monitored as hyperparathyroidism evolved in a model of progressive canine renal failure. Thirteen beagles of both sexes aged four and a half months were used. Nine of them were subjected to a renal damaging schedule (neomycine, 60 mg/kg/48 h, IM, 32 weeks) in order to induce chronic renal failure leading to secondary hyperparathyroidism (2HPT group). The remaining four were kept as the control group. The experiment was conducted over 32 weeks. Blood and 24 h urine were collected every four weeks. Calcium, phosphorus and creatinine were analyzed. Plasma parathormone and calcitonin were determined at weeks 0, 12, 24 and 32. The level of renal function in the 2HPT animals was reduced to 25% of that of the controls (endogenous creatinine clearance was 0.45 +/- 0.22 mL/min/kg as opposed to 1.81 +/- 0.54 mL/min/kg). Hyperparathyroidism was confirmed by a progressive increase in the levels of the parathyroid hormone. Calcitonin levels were not modified. A tendency to hypocalcaemia was observed, reaching statistically significant levels from the twenty-eighth week of the study, when hyperphosphataemia also became significant. Daily urinary excretion of calcium and phosphorus remained at values considered normal throughout the experiment with no alteration imputable to the impaired renal function. This is explained by the decrease in the filtered load of these elements (in both cases statistically significant from the 24th week on) being associated with an increase in their fractional excretion. Thus, calcium and phosphorus urinary excretion values could be maintained in a normal range up to the end of the experiment, showing that renal calcium handling in dogs with experimentally induced renal failure seems to differ from that observed in human patients.
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PMID:Renal handling of calcium and phosphorus in experimental renal hyperparathyroidism in dogs. 1291 55

A 62-year-old man was hospitalized for recent renal colic and neurologic disorders. Routine biochemistry indicated the presence of hypercalcemia (serum total calcium = 15.3 mg/100 mL) and renal failure (serum creatinine = 3.72 mg/100 mL). The patient reported that he had been on treatment with a slow-release multivitamin preparation containing vitamin D and vitamin A, administered by i.m. injection. Plasma 25-OH vitamin D was > 150 ng/mL (normal range 16-74 ng/mL), plasma 1,25-(OH)2 vitamin D was 32.5 pg/mL (normal range 14-60 pg/mL), plasma parathyroid hormone 1.3 pg/mL (normal range 10-65 pg/mL). There were calcifications of left and right iliac artery at abdomen x-ray. Ultrasound and computed tomography of the glutei showed alterations of skeletal muscle and calcifications. Immediate treatment with infusion of isotonic saline, furosemide and prednisone induced rapid control of hypercalcemia and renal failure. Chronic treatment per os was discontinued after six months. The patient reported that the treatment with vitamin D had been prescribed by a physician also to his wife (55-year-old). For the woman, routine biochemistry indicated the presence of hypercalcemia (serum total calcium = 11.3 mg/100 mL) and renal failure (serum creatinine = 1.8 mg/ mL). Plasma 25-OH vitamin D was > 150 ng/mL, plasma 1,25-(OH)2 vitamin D 47.9 pg/mL, plasma parathyroid hormone was 2.5 pg/mL. Hypercalcemia was acutely treated by oral hydration, furosemide, and prednisone. Chronic treatment per os was discontinued after five months.
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PMID:Unusual cases of chronic intoxication by vitamin D. 1473 22

Amongst the principal metabolic situations that can require emergency attention in the oncology patient we find: hypercalcaemia, hyponatraemia, tumoural lysis syndrome, lactic acidosis, hyperuricaemia, renal failure, hyperammonaemia, hypermpotasaemia, etc. Hypercalcaemia is the most frequent metabolic complication in oncology, appearing in 10-30% of these patients. It has two main mechanisms, tumoural lysis and humoural hypercalcaemia mediated by PTHrP (a protein related to parathormone). The principal factor for its diagnosis is suspicion, since some symptoms are non-specific and can be attributed to other causes such as somnolence, constipation, etc. Treatment will be based on intensity and is started with calciuretic measures with an intense hydration with physiological serum and on some occasions with furosemide. Anti-reabsorptive measures include calcitonin, bisphosphonates, mithramycin, gallium nitrate and on occasions corticoids. Bisphosphonates such as pamidronate and zoledronate seem to be highly useful in these cases. Hyponatraemia is classified depending on plasmatic osmorality; when this is low we find ourselves facing an authentic hyponatraemia that can develop with an extra-cellular volume that is high (cardiac insufficiency, cirrhosis, nephrotic syndrome and renal insufficiency), low (renal and extra-renal sodium losses) and normal (principally SIADH, related to a high elimination of sodium in the urine with high urinary osmolarity in spite of this being low in blood). Several types of tumour and different chemotherapy drugs can produce this SIADH. Treatment will vary according to the type and intensity, but in general this is based on hydric restriction and the replacement of the sodium deficit, either through physiological serum or through hypertonic saline serums depending on the case, and on occasions furosemide for the elimination of excess water.
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PMID:[Metabolic emergencies in the oncology patient]. 1572 5

A prospective study was carried out to assay the level of serum intact parathormone and its correlation with biochemical parameters in patients with chronic renal failure (CRF). The study included 64 children (44 with CRF, and 20 age and sex matched controls). Serum intact parathormone (iPTH), serum creatinine, urea, calcium, inorganic phosphate and alkaline phosphatase were estimated. Creatinine clearance (Ccr) was estimated by Schwartz formula. Patients with CRF were divided into four groups based on their Ccr (mild CRF with mean Ccr 59.17 +/- 1:18.53 mL/min/1.73 m2 (n = 6) moderate CRF with mean Ccr 34.98 +/- 7.75 mL/min/1.73 m2 (n = 7); severe CRF with mean Ccr 17.71 +/- 5.40 mL/min/1.73 m2 (n = 15); and end-stage renal disease with mean Ccr 6.46 +/- 1.71 mL/min/1.73 m2 (n = 16). Mean serum iPTH levels were 93.00 +/- 46.62 pg/mL in CRF and 16.52 +/- 9.35 pg/mL in controls. Groupwise mean serum (iPTH) levels were 48.50 +/- 4.76, 67.29 +/- 7.91, 82.42 +/- 9.67 and 130.66 +/- 58.74 pg/mL in mild, moderate, severe CRF and endstage renal failure respectively. Mean serum iPTH level of CRF (93.00 +/- 46.42 pg/mL) negatively correlated with mean Ccr (22.02 +/- 18.53 mL/min/l.73 m2) (P < 0.001) and mean serum calcium (7.30 +/- 1.02 mg/dL) (P < 0.001) and positively correlated with mean inorganic phosphate (5.76 +/- 1.1 mg/dL) (P < 0.05) and mean alkaline phosphatase (355.14 +/- 185.53 UL) (P < 0.001). We conclude that increased iPTH level occur even early in the course of CRF and progressive hypocalcemia and hyperphosphatemia are the initiating factors for the development of hyperparathyroidism.
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PMID:Correlation of serum parathormone level with biochemical parameters in chronic renal failure. 1581 73

Skeletal involvement in chronic kidney disease manifests long before the initiation of dialysis. This study aimed at identifying the extent of renal bone disease among predialysis and on maintenance dialysis patients. Thirty-two patients (Group 1) on maintenance hemodialysis (MHD) for a variable period of time were compared with 20 newly detected irregularly treated advanced renal failure (immediately predialysis), patients (Group 2) for their clinical, biochemical and imaging features. The mean age of Group 1 and Group 2 patients was 45+/-14 vs. 34+/-15 years (p<0.05). Comparison of blood biochemistries between Groups 1 and 2 showed serum creatinine 9.9+/-2.9 vs. 13.4+/-4.4 mg/dL (p<0.01); calcium 10.1+/-1.8 vs. 7.8+/-1.2 mg/dL (p<0.001); phosphate 4.4+/-1.2 vs. 7.9+/-2.1 mg/dL (p<0.001); alkaline phosphatase 116.4+/-31.7 vs. 85.7+/-30.6 IU/L (p<0.05); and parathormone 71.7+/-48.2 vs. 146.9+/-92.1 pg/mL (p<0.05). Radiological changes present in the 2 groups were as follows: osteopenia 63% vs. 65% (ns); trabecular resorption 53% vs. 20% (p<0.05); soft tissue calcification 31% vs. 10% (p<0.05); bone cysts 16% vs. 26% (ns); and subperiosteal bone resorption 16% vs. 20% (ns). Technetium 99 methylene diphosphonate (Tc-99 MDP) bone scans in both groups of patients showed similar increased uptake in wrist joint, tibia-fibula, costochondral junction, vertebral column, sternum, radius-ulna and mandible. X-ray findings were positive for bone involvement in 59% of cases, and Tc-99 scan was positive in 80% (p<0.05). It is concluded that newly detected, irregularly treated patients with advanced renal failure who are predialysis may present with deranged calcium homeostasis and a high prevalence of bone involvement similar to MHD patients.
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PMID:Biochemical and imaging alterations of renal bone disease in newly detected predialysis and on maintenance dialysis patients. 1622 39


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