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

Treatment of chronic uremia by hemodiafiltration requires replacement of the filtrate. Using Ringer's solution alone, there is a depression of pH because of bicarbonate loss. To bring the acid base status back to normal, sodium lactate in increasing concentrations (283 mg% = 32 mM/1, 361 mg% = 40 mM/1; 462 mg% = 51 mM/1; 508 mg% = 57 mM/1) was added to the replacement fluid. The optimal concentration is 450 mg% (=50 mM/1) sodium lactate, provided the following conditions are fulfilled: (a) substitution after the filter; (b) mixing ratio of blood and substitution fluid 1:2. Using 12-15 liters of substitution fluid during a 5 hr treatment, the added lactate amounts to 60 g (=0.54 M). With continuous addition of lactate, the serum concentration of lactate is 3.5 times normal and the concentration of serum pyruvate 4 times normal. An excess lactate concentration, according to Huckabee [1,2], was thus not observed. The sieving coefficients were the following: sodium, potassium, urea, lactate, pyruvate, and phosphate 1; chloride greater then 1; calcium and protein less than 1. Serum osmolality fell, on the average, 9 mOsmol/1 during diafiltration.
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PMID:Acid base status during treatment of chronic uremia with diafiltration. 2 47

Subcellular fractions in hearts from rats with severe acute uremia (24 hours after total nephrectomy) and moderate chronic uremia (2 weeks after five sixths nephrectomy) were studied and compared with preparations from acute and chronic sham-operated rats, respectively. Calcium- and magnesium-sensitive actomyosin adenosine triphosphatase (ATPase) activities were normal in both groups. Acute uremia was associated with a significant depression of sarcolemmal Na+,K+ ATPase activity. Calcium transport by fragmented sarcoplasmic reticulum was also depressed in the presence and absence of oxalate in acute uremia. Mitochondrial calcium transport and adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were normal in these animals. Chronic uremic animals showed no abnormal subcellular mechanisms. These data suggest a direct effect of acute uremia on some membrane functions in myocardial cells. The discrepancies observed between acute and chronic uremic groups may be due to a different degree of uremic state. The observation of depressed calcium transport by fragmented sarcoplasmic reticulum (FSR) in acute uremic hearts which were previously shown to have increased contractile reserve suggests that studies of calcium transport in FSR may not always truly reflect the contractile capacity of the heart.
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PMID:Studies of subcellular control factors in hearts of uremic rats. 13 36

In a retrospective analysis to determine whether secondary hyperparathyroidism in uremia has a role in uremic peripheral neuropathy, we simultaneously measured motor-nerve conduction velocity and serum parathormone level in 42 uremic patients. We compared age-matched groups of nondiabetic uremic patients, divided into three groups according to serum parathyroid hormone, for degree of impairment of motor-nerve conduction velocity, and 12 diabetic patients with uremia. The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second). Mean serum calcium and creatinine were not significantly different between groups. Nerve conduction velocity was similarly depressed in 17 patients on additional dialysis studied prospectively and divided into groups according to parathyroid hormone levels. These results suggest a relation between high parathormone levels and uremic neuropathy and implicate parathyroid hormone as a uremic toxin.
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PMID:Search for the uremic toxin. Decreased motor-nerve conduction velocity and elevated parathyroid hormone in uremia. 20 86

Lymphopenia of a group of uremic patients was associated with normal percentages of T cells but reduced percentages of B cells. Lymphocyte counts improved after a period of maintenance hemodialysis, although not to control levels, and B cell percentages returned towards normal. Uremia is therefore associated with depression of total T and B cell numbers, with a relatively more pronounced effect on B cells. A period of maintenance hemodialysis produces increase in numbers of both cell types and depression becomes nonselective.
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PMID:Deficiency of T and B lymphocytes in uremic subjects and partial improvement with maintenance hemodialysis. 30 46

As the prolonged metabolic clearance rate of insulin in chronic uremia cannot be entirely explained by impaired removal and degradation of insulin by the kidney, we set out to determine whether prolonged uremia depresses other major sites of insulin degradation. The study was conducted with livers and skeletal muscle obtained from normal control rats and uremic rats 4 weeks after 80% nephrectomy. Despite a significant difference between renal function in the control and uremic rats (BUN, 18 vs. 46 mg/dl), there was no significant difference in the clearance of insulin by isolated uremic or control livers perfused with a bloodless medium. Similarly, the 125I-insulin degrading activity of liver homogenates was not depressed by uremia. In contrast, binding and degradation by uremic liver cell membranes was significantly reduced to 58% and 85% of the controls, respectively. Degradation by homogenates of skeletal muscle and by intact epitrochlaris muscle was significantly less in uremics than in controls. These results indicate that chronic uremia depresses skeletal muscle insulin degradation but not hepatic insulin removal or degradation despite a decrease in insulin binding and degradation by liver plasma membranes. It thus appears that depression of insulin degradation by muscle may contribute to the prolonged insulin metabolic clearance rate seen in chronic uremia. Furthermore, it is possible that the impaired binding of insulin to liver membranes may play a role in the insulin resistance of uremia.
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PMID:Effect of prolonged uremia on insulin metabolism by isolated liver and muscle. 39 15

Nutritional treatment of children with renal insufficiency presents special problems related to undernutrition, i.e., insufficient caloric intake to permit normal growth, vitamin D intake, and protein needs, as well as depressed appetite. With regard to energy, it is suggested that uremia may lead to increased caloric requirements, thus exacerbating growth depression. Protein requirements, which actually may not be as important as caloric needs, have not been determined for uremic children. Another factor in growth failure in such children involves vitamin D metabolism and its role in renal osteodystrophy. Successful dietary management of these various interrelated aspects of childhood renal disease requires sensitive, knowledgeable personnel.
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PMID:Nutritional implications of renal disease. IV. Nutritional aspects of chronic renal insufficiency in childhood. 40 47

Aspects of immune potential in uraemic subjects, categorized by glomerular filtration rate, were intercompared and compared with results obtained from a group of normal volunteers. Evidence is presented to show that depression of both cellular and humoral immune potential occurs with progressive reduction of glomerular filtration rate. Lymphocyte transformation testing to the non-specific mitogen PHA revealed a significant elevation of blastogenic response in uraemia after 96 hours of incubation.
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PMID:Immune potential in human uraemia. 1. Relationship of glomerular filtration rate to depression of immune potential. 78 7

Despite experimental evidence that myocardial depression resulting from rapid transfusion of ACD blood (citrate binds ionic calcium) is avoidable by simultaneous calcium administration, most hypovolemic patients receive calcium either after transfusion or not at all. Similar iatrogenic hypocalcemic myocardial depression occurs in normovolemic patients with known myocardial damage who are dialyzed for acute uremia when ACD blood prime is used at high initial flow rates (350 c.c. per minute) and when dialysis is performed against low calcium dialysate (2.5 mEq. per liter or less). This study tests the hypotheses that (1) rapid transfusion of as little as one unit of CPD blood causes a significant reduction in ionized calcium, (2) the depressive effect of CPD blood is significant and similar to that of ACD blood, (3) rapid blood transfusion (ACD or CPD) is safe if calcium is given simultaneously, (4) addition of calcium to the extracorporeal heparinized blood prime used in dialysis prevents initial depression, and (5) hemodynamic instability during dialysis is prevented when the dialysate is normocalcemic. From the results of our study, we made the following conclusions: (1) Ionized calcium is reduced significantly by rapid transfusion of CPD blood; (2) acute myocardial depression noted with CPD blood is similar to that previously observed with ACD blood and is prevented during transfusion of either type of blood by simultaneous calcium administration; and (3) hemodialysis in patients who have had cardiac surgery is safe if calcium is added to blood prime and dialysate is made normocalcemic.
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PMID:Acute clinical hypocalcemic myocardial depression during rapid blood transfusion and postoperative hemodialysis: a preventable complication. 96 82

Parathormone (PTH) excess limits renal bicarbonate reabsorption. This may aggravate the acidosis in patients with renal insufficiency and secondary hyperparathyroidism. Why parathormone, the primary action of which is thought to be stabilization of the inonized fraction of calcium, affects acid-base balance remains uncertain. Parathormone not only promotes the release of calcium from bone but also mobilizes salts, including bicarbonate and phosphate. Accumulation of these anions in the extracellular fluid would limit the ionization of calcium. Teleologically it is not unexpected to find that, coincident with evolution of a mechanism which permits rapid mobilization of calcium from bone, a system had to develop which removed the byproducts of bone dissolution. If this concept is valid, parathormone-induced depression of renal bicarbonate reabsorption in uremia represents an undesired side effect of an adaptive mechanism. This would extend Bricker's "trade-off" hypothesis which ascribes metabolic bone disease due to PTH-induced phosphate loss to include metabolic acidosis resulting from diminished renal bicarbonate regeneration. Parathyroidectomy or phosphate restriction have been proposed for correction of the side effects of secondary hyperparathyroidism. These therapeutic manipulations cannot be recommended for general use. A more rational apprach for prevention of secondary hyperparathyroidism is the combined use of phosphate restriction with a short-acting vitamin D derivative.
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PMID:Parathyroid hormone and the regulation of acid-base balance. 110 50

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


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