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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of patients with chronic renal failure managed conservatively, the rise in the plasma-myo-inositol (myoinositol) concentration has been found to be related to depression of sural-nerve conduction velocity. There was no correlation with motor-nerve conduction velocity in the peroneal nerve, or with either of these variables in a series of patients receiving chronic haemodialysis. Despite the negative correlation with sural-nerve conduction velocity, there was no correlation between the plasma-myoinositol concentration and the presence of peripheral neuropathy as assessed clinically. It is concluded that hypermyoinositolaemia may depress nerve conduction velocity, but there is no evidence that it is responsible for the development of uraemic polyneuropathy.
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PMID:Plasma-myoinositol concentrations in uraemic neuropathy. 6 75

Seventeen patients with well compensated chronic renal failure undergoing periodic hemodialysis were studied with regard to absolute number of T and B lymphocytes, spontaneous and PHA induced lymphocyte blastogenesis both with autologous and homologous compatible plasma. A normal lymphocyte count as well as a normal relative and absolute number of T and B lymphocytes was found in most cases. Spontaneous blastogenesis was normal. Lymphocyte response to PHA was reduced both with autologous and homologous plasma, but the depression was more relevant when autologous plasma was used in culture. The authors discuss these findings with respect to available data, particularly concerning inhibitory factors in uraemic plasma.
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PMID:T mediated immunity in patients undergoing periodic hemodialysis. 31 13

A patient in chronic renal failure, who was receiving large doses of the combined alpha- and beta-blocking agent, labetalol, was selected for renal transplantation. A low concentration of halothane was used for induction and maintenance of anaesthesia, but severe myocardial depression occurred which proved unresponsive to atropine or isoprenaline, although it responded to a dopamine infusion. Synergism has already been reported between labetalol and high concentrations of halothane, but this case suggests that, in patients with previous myocardial damage, much lower concentrations of this inhalational agent may prove fatal.
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PMID:Synergism between halothane and labetalol. 37 19

The phagocytic and metabolic functions of the reticuloendothelial system (RES) were determined, by measuring the plasma clearance rate of 125I-labelled microaggregated human serum albumin and the increase in plasma metabolites of this test substance, in patients with chronic renal failure and in renal transplant recipients at different times after transplantation. All transplant recipients received triple immunosuppressive therapy consisting of azathioprine, corticosteroids, and antilymphocyte globulin. The intravascular clearance of microaggregated albumin was significantly depressed in patients when tested at 1 to 12 days (P less than 0.001), 1 to 4 months (P less than 0.02), and 6 to 9 months (P less than 0.001) after transplantation compared to pretransplantation. The 1- to 3-year transplant survivors had a normal RES phagocytosis. Furthermore, the metabolic RES function in all groups of transplant recipients except the group of patients tested at 1 to 4 months after transplantation was significantly impaired compared to pretransplantation. Administration of antilymphocyte globulin and extremely high daily doses of steroids were probably responsible for the significant depression in the RES functions recorded immediately post-transplantation. The further development of the phagocytic ability of the RES was shown to be correlated to the cumulative dose of steroids given over the last 12 months. The azathioprine regime seemed to have no influence on the RES functions.
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PMID:Reticuloendothelial function in human renal allograft recipients. 38 18

Initial observations in adults revealed that peripheral neuropathy, as documented by reduced conduction velocity is common in chronic renal failure. Critical analysis of this problem in children on long-term dialysis is scarce, consisting of a simgle report which demonstrated that the motor nerve conduction velocities were decreased early and frequently with more severe depression in peroneal nerve velocities. This is in distinct contrast to data from adults, in whom uniform rates of deterioration are encountered. In addition, a direct correlation of the degree of nerve conduction defect with the severity of the renal failure is found in adult patients. The present study showed a relative lack of nerve conduction defects in 11 children on long-term hemodialysis. With rare exceptions, the conduction velocities were normal. To date, no clinical symptoms of neuropathy were evident in our patients. It would seem that, with the short-dialysis schedule of 12--14 h/wk over a period of up to 5 yr, there is no progressive neuropathy as quantitated by nerve conduction measurements.
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PMID:Long-term hemodialysis and nerve conduction in children. 47 89

In early chronic renal failure, the state of the bones resembles that of type II primary hyperparathyroidism. Cortical bone becomes thinner and more porous, and there is increased extent of surface remodeling. These changes are followed in turn by osteomalacia and osteitis fibrosa, although sometimes these may be alternate rather than successive stages. Bone turnover is less than would be expected for the elevation of PTH level, probably because of 1,25 (OH)2D3 deficiency. The resorption velocity and lamellar bone appositional rates are depressed, but woven bone appositional rate may be increased, possibly because of hyperphosphatemia. Bone mass reflects the summation of three independent processes: loss of lamellar bone due to hyperparathyroidism (depending on the extent of insulation by osteoid); accumulation of partly mineralized osteoid because of osteomalacia; accumulation of woven bone because of osteitis fibrosa. Osteosclerosis may be growth-related metaphyseal, subchondral or diffuse axial, and periosteal neostosis may also occur. Some patients on hemodialysis lose bone because of planing rather than lacunar or dissecting resorption, combined with depression of both lamellar and woven bone formation. Hyperparathyroid bone disease tends to improve slowly after renal transplantation. Persistent hypocalcemia reflects a defect in the calcium homeostatic system and cannot be explained solely by the known stimuli to secondary hyperparathyroidism. The increment in plasma calcium in response to PTH infusion is subnormal, both in early chronic and in acute renal failure, probably because of 1,25(OH)2D3 deficiency. This is also the most likely explanation for the depressed level of blood-bone equilibrium. The activity of all three of the PTH responsive cell systems in bone is depressed in renal failure, probably because all three require 1,25(OH)2D3 in order to function normally. In pseudohypoparathyroidism, as in chronic renal failure, hypocalcemia results from a defect in the regulation of the blood-bone equilibrium. The bone-remodeling system shows all gradations of response, from slight depression of bone turnover to overt osteitis fibrosa, but bone turnover is never as low as in PTH deficiency. These differences may reflect the presence or absence of resistance to PTH of the osteoprogenitor cell as well as of the calcium homeostatic system, or may be due to varying degrees of 1,25(OH)2D3 deficiency, as in chronic renal failure. An increase in plasma calcium in response to PTH can occur either in the untreated state or after treatment with vitamin D because either the error-correcting or remodeling system remains responsive to PTH. Pseudohypoparathyroidism may be subdivided into three types, depending on whether the urinary cyclic-AMP response to PTH remains defective despite treatment with vitamin D, improves with treatment, or is normal before treatment. Only the former is associated with the genetic syndrome of Albright's hereditary osteodystrophy...
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PMID:The actions of parathyroid hormone on bone: relation to bone remodeling and turnover, calcium homeostasis, and metabolic bone disease. Part IV of IV parts: The state of the bones in uremic hyperaparathyroidism--the mechanisms of skeletal resistance to PTH in renal failure and pseudohypoparathyroidism and the role of PTH in osteoporosis, osteopetrosis, and osteofluorosis. 78 23

Clinical and experimental studies were carried out in order to evaluate the role of myocardial dysfunction in the genesis of circulatory congestion associated with renal failure. Among the patients with chronic renal failure, those with circulatory congestion had greater blood volume and higher venous pressure while lower cardiac index and stroke work index than those without circulatory congestion. After peritoneal dialysis, although blood volume and venous pressure decreased in both groups, cardiac index increased in the former while it decreased in the latter group. In 15 dogs, acute renal failure was produced by ligating both ureters. As uremia developed, blood volume and left ventricular end-diastolic pressure increased with or without an increase in cardiac index. The depression of ventricular function curve was evident in all the dogs. The peritoneal dialysis performed at this stage resulted in a prompt recovery of left ventricular end-diastolic pressure with minimum change in cardiac index. The measurement of dp/dt/IIT also indicated a depression of myocardial contractility at uremic stage and its recovery after dialysis. We conclude that impairment of myocardial function is implicated in the development of circulatory congestion in renal failure.
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PMID:Changes of cardiac performance in renal failure. 116 Jan 87

Lymphocyte blastogenic transformation in response to plant lectins and allogenic cells was studied in patients with nonuremic, far-advanced, chronic renal failure and in healthy controls. Cell cultures were studied in the presence of normal sera, patient's sera, and with media of different buffering capacities. Minimal blastogenic depression was observed when patient's lymphocytes were cultured in indifferent plasma with effective bicarbonate buffering compared with the use of pooled patient's plasma or HEPES buffer. Fresh plasma in culture depressed concanavalin A (Con A) blastogenesis. The data suggest that, under optimal conditions, lymphocytes from patients with chronic severe renal insufficiency are more responsive to stimuli than previously reported and as a group are near normal control values. Further, the defect observed may be a result of intracellular acidosis.
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PMID:Lymphocyte blastogenesis in patients receiving hemodialysis. 127 24

Twenty anephric and 20 healthy patients received a bolus dose of mivacurium 150 micrograms kg-1. When the first EMG response (T1) of the train-of-four had recovered to 5% of control (T0), an infusion of mivacurium 10 micrograms kg-1 min-1 was started and adjusted to keep T1 at 5%. Ten patients in each group were given neostigmine 35 micrograms kg-1 when the infusion was stopped when T1/T0 had recovered to 20%; in the others recovery was spontaneous. After the bolus dose of mivacurium, mean (SD) depression of T1 was greater in the anephric group than in the normal group (98.4 (3.5) vs 96.8 (4.4)%; P less than 0.01) and recovery of T1/T0 to 5% was slower (15.3 (6.9) vs 9.8 (3.5) min; P less than 0.01). Anephric patients required a slower infusion rate (6.3 (1.9) vs 10.4 (2.8) micrograms kg-1 min-1; P less than 0.001). Neostigmine hastened recovery of both T1/T0 and T4/T1 in both groups. Spontaneous recovery of T1/T0 (from 25% to 75%) after the infusion was also slower in anephric patients (12.2 (8.2) vs 7.7 (1.2) min; P less than 0.05). Plasma cholinesterase activity was less in the anephric group (785 (207) vs 943 (217) iu litre-1; P less than 0.05) and there was a (negative) correlation overall between cholinesterase activity and time to 5% recovery of T1/T0 after the bolus dose (r = -0.42; P less than 0.02). We conclude that patients with chronic renal failure may require a reduced dose of mivacurium.
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PMID:Use of mivacurium chloride by constant infusion in the anephric patient. 164 38

We have investigated the effect of an exogenous lactate load given during machine haemofiltration treatment in 22 patients with acute renal failure and 12 patients with chronic renal failure, without any overt evidence of liver disease. Hyperlactataemia occurred in all patients, but the expected changes in acid base status, an increase in bicarbonate and a reduction in arterial hydrogen ions were observed in less than 40% of the treatments in the acute renal failure group. Ultrafiltrate losses of lactate and bicarbonate could not alone explain the changes in acid-base status. There was a positive correlation between the increase in arterial lactate and hydrogen ion concentrations, r = 0.52, p less than 0.01. Lactate accumulation in patients at, or close to, their threshold for lactate utilisation may result in further depression of cardiac function and peripheral lactate utilisation. Hyperlactataemia due to use of lactate-based dialysis/haemofiltration solutions in critically ill patients may result in a worsening of the acid-base status, and arterial pH should be monitored so that bicarbonate solutions can be substituted if the changes are progressive.
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PMID:Hyperlactataemia and metabolic acidosis during haemofiltration using lactate-buffered fluids. 175 38


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