Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sensorineural hearing loss has been frequently reported in patients with renal failure but its etiology has not yet been established. Disturbance of Ca metabolism is present in renal failure and seems to cause hearing loss. The purpose of the present study was to determine whether the disturbance of Ca metabolism has any effect on cochlear function. The cochlear potentials were measured in 19 rats fed with a vitamin D deficient diet. The pathological findings showed prolongation of N1 latency with unchanged N1 amplitude and pseudothreshold, depression of CM amplitude and elevation of the CM pseudothreshold. The latencies of narrow-band APs were prolonged in the entire cochlear partition. Ca2+ concentration in perilymph was 3.2 X 10(-4) M (n = 4) in vitamin D deficient rats and 7.4 X 10(-4) M (n = 4) in the controls. These findings were milder than those obtained in surgically induced renal failure. It was concluded that although vitamin D deficiency is one cause of hearing loss in renal failure, other major factors must be involved. The authors postulate that hearing loss in vitamin D deficiency is mainly attributable to the depression of the Ca2+ concentration in perilymph.
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PMID:The effect of vitamin D deficiency on the cochlear potentials and the perilymphatic ionized calcium concentration of rats. 347 52

Morphofunctional studies of muscles, heart, liver and kidneys after different periods of compression and decompression, as well as literature data indicate that crush syndrome is one of the most severe forms of traumatic shock. A wide range of pathologic effects of catecholamines and other shock-causing agents in response to the emotional stress and pain occurs already at the compression period and results in hemodynamic disturbances in microcirculation of organs and tissues with the development of dystrophic and necrobiotic processes, depression of the monocytic phagocyte system and immune system. The consequences of shock are mostly manifest after decompression: hypercatecholaminemia, hypovolemia, intoxication with myolysis and pathogenic microflora products result in aggravation of monocytic phagocyte failure, as well as immune system, intravascular coagulation, membrane penetration insufficiency, cell necrosis. Monocytic macrophage depletion favours the progression of hepatic necrobiosis, formation of renal failure and detritus organization in the muscles of the extremities. Hypercatecholaminemia and hypoxia (leading to electrolyte-imbalance contractures of myofibrillar apparatus, metabolism disorder and intracellular conductivity disturbance) from the basis for cardiac insufficiency. Inadequate cardiac function, in its turn, maintains hemodynamic and hypoxic disturbances in tissues. Changes in renal blood flow, hemofiltration and tubular system are shown to reflect different aspects of pathogenesis of the acute renal failure in crush syndrome.
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PMID:[Morphology and pathogenetic problems of the crush syndrome]. 355 89

The first cases of fulminant hepatic failure due to paracetamol poisoning were reported in 1966, and in the United Kingdom this condition is now responsible for more cases of acute hepatic failure than any other cause. Adults account for the majority of serious and fatal cases of paracetamol poisoning and it is extremely rare for young children to ingest sufficient paracetamol to cause more than minimal liver damage. A single measurement of the plasma paracetamol concentration is an accurate predictor of liver damage provided that it is taken not earlier than 4 hours after ingestion of the overdose. Peak disturbance of liver function occurs 2 to 4 days after the overdose, often accompanied by mild jaundice, after which recovery is usually rapid and complete. In a few patients, fulminant hepatic failure, manifested by increasing jaundice and encephalopathy, may develop by the third to fifth day. Acute renal failure may complicate paracetamol poisoning, often in the context of severe liver damage. Renal failure, which is often non-oliguric, typically becomes apparent 24 to 72 hours after overdosage. The treatment of paracetamol intoxication should include gastric lavage, which has been shown to be of value for up to 6 hours after ingestion of a paracetamol overdose. Further general treatment may include parenteral fluid replacement and a prophylactic infusion of dextrose (5-10%) in patients at risk of hepatic failure. Specific protective agents in those patients at risk of paracetamol-induced liver damage include N-acetylcysteine and methionine which are most effective if given within 8 to 10 hours of ingestion of the overdose. Hepatic and renal failure should be managed conventionally. In recent years in the United Kingdom there has been a gradual decline in the number of hospital admissions and the number of deaths from aspirin poisoning. Salicylates in overdose directly stimulate the respiratory centre and so cause a respiratory alkalosis. Metabolic acidosis occurs in severe poisoning because of impairment of the oxidative metabolism of energy substrates. At very high salicylate concentrations respiratory depression may occur, possibly associated with neuroglycopenia, adding respiratory acidosis to the worsening metabolic acidosis. In addition to a mixed acid-base disturbance, hypokalaemia and hypoglycaemia may be present. Nausea and vomiting increase the fluid deficit. If dehydration is sufficiently severe, decreasing cardiac output may hasten development of lactic acidosis and acute renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-narcotic analgesics. Problems of overdosage. 355 83

Low cardiac output after cardiopulmonary bypass is not uncommon. This per- and postoperative cardiac depression is accompanied by an impairment of renal function, which recovers with the improvement of the low cardiac output. These two correlated failures may become resistant to cardiotonic and diuretic drugs. Indeed the fluid balance is strongly disturbed, although venous pressure is only moderately increased. The only possible treatment could be water withdrawal. Nine patients are reported, all suffering from cardiac and renal failure after cardiopulmonary bypass. They were successfully treated with the method of continuous ambulatory peritoneal dialysis. This method allowed us to stop all intravenous cardiac drugs within 36 h, whilst diuresis reappeared together with a better efficacy of diuretic drugs. This beneficial haemodynamic effect of water withdrawal is discussed. This phenomenon may be related to an influence of right ventricular filling on the left ventricle. Low cardiac output may occur as a result of septal displacement, especially if there is concomitant myocardial suffering. Withdrawing a small volume of water may have modified the septal displacement, and improved cardiac output. Continuous ambulatory peritoneal dialysis was simple and well tolerated; it seemed to have contributed to the haemodynamic recovery of all the nine patients.
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PMID:[Peritoneal dialysis in the treatment of the low cardiac output after extracorporeal circulation]. 363 59

Three horses less than or equal to 3 years old were evaluated because of stunted growth, weight loss, anorexia, depression, and lethargy of at least 1 month's duration. A neonatal foal was examined after its death. In each case, gross and microscopic renal lesions were compatible with bilateral renal hypoplasia (ie, cortical hypoplasia with severe medullary hypoplasia). In young horses with renal failure, bilateral renal hypoplasia should be considered in the differential diagnosis, and may represent a congenital lesion.
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PMID:Bilateral renal hypoplasia in four young horses. 374 81

Intravenous morphine infusions have been administered to 12 critically-ill patients during controlled ventilation. Acute oliguric renal failure was present in 4 patients, who were treated with a combination of haemofiltration and haemodialysis. Severity of physiological disturbance was assessed using a modified APACHE Score, level of sedation by a linear-analogue scale, and blood morphine levels by high-pressure liquid chromatography. Morphine clearance was impaired in renal failure, and was dependent on haemofiltration volumes; accumulation of morphine did not occur during this form of treatment. Conscious level was clearly more closely related to the degree of physiological disturbance than blood morphine levels; and for a given blood morphine level, depression of consciousness was more pronounced the greater the degree of physiological disturbance. Use of a physiological sickness score may help to clarify some of the factors influencing cerebral function during critical illness. Careful clinical monitoring of level of sedation is important in patients with oliguric renal failure receiving morphine, and haemofiltration appears to reduce the risk of morphine accumulation in these patients.
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PMID:Sedation in intensive care: morphine and renal function. 377 14

This paper illustrates several important points relating to the use of allopurinol in renal failure, or situations of purine overproduction: It is very easy to give too much allopurinol. Most of the side effects (bone marrow depression, exfoliative dermatitis, etc) are the result of overdosage due to the retention of oxipurinol, an effect exaggerated by thiazide diuretics. Monitoring of plasma oxipurinol levels (ideally less than 100 mumol/l) by high-pressure liquid chromatography is helpful for adjusting dosage in renal failure. Some estimate of the anticipated purine excess is equally vital in deciding dosage during tumour lysis if the risk of urate nephropathy is not to be substituted for the certainty of xanthine nephropathy. In this situation the use of allopurinol may even be questioned. Patients with HGPRT deficiency are exquisitely sensitive to allopurinol, and careful monitoring of the effect on urinary purine levels is essential if xanthine colic is to be avoided.
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PMID:Allopurinol in renal failure and the tumour lysis syndrome. 378 9

The purpose of this investigation was to compare the effects of ethanol and 4-methylpyrazole (4MP) on the toxicity and pharmacokinetics of ethylene glycol (EG) in the dog. All dogs received 173 mmol/kg EG, p.o. Dogs were randomly assigned to 3 groups: EG-treated only, EG + ethanol (19.3 mmol/kg, i.v. 3, 7, 14 and 24 h after EG) and EG + 4MP (0.24 mmol/kg, i.v. 3 h after EG, 0.18 mmol/kg at 24 h and 0.06 mmol/kg at 36 h). EG produced a rapid onset of metabolic acidosis (within 3 h) and acute oliguric renal failure (after 48 h), whereas administration of ethanol or 4MP greatly attenuated acidosis and prevented renal toxicity. The administration of ethanol, however, severely increased the central nervous system (CNS) depression that existed after ingestion of EG. The half-life of FG in serum was 10.8 +/- 0.7 h in the EG-only treatment group, 6.8 +/- 0.7 (P less than 0.05) in the EG + ethanol group and 9.8 +/- 0.9 h in the EG + 4MP group. Approx. 10% and 48% of the dose of EG was excreted unchanged in the urine at the 0-3 and 3-72 h periods, respectively. Treatment with 4MP increased the amount of EG excreted in the urine (71% from 3-72 h), whereas ethanol did not (51%). However, both ethanol and 4MP increased the rate constant of EG excretion into urine approx. 70%. These data demonstrate the utility of 4MP over ethanol for the treatment of EG-induced toxicity in dogs and indicate that ethanol and 4MP cause an increase in the rate constant of EG excretion in the urine and not a prolongation in EG half-life.
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PMID:Comparison of the effects of ethanol and 4-methylpyrazole on the pharmacokinetics and toxicity of ethylene glycol in the dog. 382 18

A pilot study is reported in which 18 children in end-stage renal failure, undergoing either haemodialysis or continuous ambulatory peritoneal dialysis were assessed with regard to adherence to their treatment regime. Measures were used to assess level of depression, locus of control and social desirability. Adherent behaviour was significantly related to high social desirability, and a shorter length of time on dialysis. There was no relationship between adherence and depression or locus of control.
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PMID:Adherence to medical regime and related factors in youngsters on dialysis. 382 99

Infection often complicates renal failure and frequently causes death, but the association between renal failure, impaired immunity and infection has not been proved. A recent study showed that patients on dialysis did not show an expected leucocytic response to infection, suggesting that the blunted response was evidence of the immunocompromised state of the uraemic patient. In this study, the relationship between leucocytic responses and infectious challenge was investigated in an animal model of chronic renal failure. Bacteraemia, peritonitis and a chronic lung infection were induced in normal and uraemic rats; the leucocytic response was then monitored. In all three infections, the total white blood cell response was significantly less in the uraemic animals. Neutrophil numbers actually increased, but this response was disguised by a pronounced depression in lymphocyte numbers. Our conclusion is that, although the leucocytic response of the uraemic host to infection may be depressed, the changes to individual leucocyte components in the peripheral blood are sufficiently characteristic to provide useful evidence of infection.
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PMID:Host immune status in uraemia. VI. Leucocytic response to bacterial infection in chronic renal failure. 388 87


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