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)

NH4Cl was infused into the left renal artery of anesthetized dogs at 50-125 mum/kg/min for up to 110 min. Renal blood flow declined early then increased to supra-control levels during infusion. Kidneys perfused at 125 mum/kg/min for 90 min showed patchy to confluent mixtures of cortical necrosis and tubular necrosis. Experimental kidneys invariably showed lower urine osmolality than contralateral controls 48 h after perfusion. Kidneys with necrosis showed depressed creatinine clearance as well. Renal artery infusion of NH4 acetate or intravenous infusion of NaHCO3 during arterial infusion of NH4Cl prevented significant acidosis and caused minimal histological changes, but depression of urine osmolality was not prevented. It is concluded that renal ammonium concentrations up to 40 mum/liter for 90 min does not cause tubular necrosis but does impair urine concentration. Severe tissue damage followed renal exposure to high ammonium concentrations in the presence of metabolic or renal acidosis.
Nephron 1976
PMID:Some effects of ammonium salts on renal histology and function in the dog. 0 Jun 32

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.
Nephron 1978
PMID:Deficiency of T and B lymphocytes in uremic subjects and partial improvement with maintenance hemodialysis. 30 46

The rate coefficients and fluxes of sodium across the outside and inside barriers of an in vitro, short-circuited frog skin preparation were determined in the presence of a uremic serum fraction to localize the site of action of an inhibitor of sodium transport. In unpaired studies, the mean depression of short-circuit current (SCC) resulting from the addition of the uremic serum fraction (21.9+/-2.2%) was significantly greater than the decrease in SCC resulting from either frog Ringer's wash or normal serum fractions. Paired studies comparing active and inactive uremic serum fractions indicated that the reduction in net sodium transport, whether calculated from changes in SCC(-0.55+/-0.12muEq/h) or changes in unidirectional Na fluxes (-0.56+/-0.15 muEq/h) was significantly greater in hemi-skins treated with the active fraction. The depression in sodium transport was associated with a significant decrease of sodium movement from the skin to the inside compartment, phi22 (-0.62+/-0.2 muEq/h). The results of these studies suggest that the inhibition of sodium transport ascribed to the uremic serum fraction is due to an inhibition of the active transport mechanism located at the serosal barrier.
Nephron 1978
PMID:Site of action of a uremic serum fraction inhibiting sodium transport in frog skin. 31 42

Using a 2-hour 47Ca absorption test, significant depression of active calcium absorption was demonstrated in 48 vitamin D untreated haemodialysis patients. This malabsorption of calcium could be corrected by the daily oral administration of 1--2 microgram of 1alphaOHD3 and 1--1.5 microgram of 1,25(OH)2D3. 5 microgram daily for 2 weeks of 3-deoxy-1alphaOHD3 AND 16 and 64 microgram daily for 1 week of 24R,25(OH)2D3 proved ineffective. In 32 successfully transplanted patients, restoration of normal or near normal renal function (serum creatinine less than 1.9 mg/100 ml) was not always followed by an immediate improvement in active calcium absorption. Calcium absorption, especially in female patients, was adversely affected by the required immunosuppressive prednisone therapy and improvement was slow.
Nephron 1978
PMID:Effect of 1alpha-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, 3 deoxy-1alpha-hydroxycholecalciferol, 24R, 25-dihydroxycholecalciferol and successful renal transplantation on calcium absorption in haemodialysis patients. 34 40

Clearance and micropuncture techniques were used to evaluate the effects of MK-196 on uric acid and electrolyte excretion by the rat kidney. The urinary excretion of sodium, uric acid, calcium and magnesium increased significantly following MK-196 administration. The major site of action with respect to sodium reabsorption was in the ascending limb of Henle's loop as revealed by depression of both free-water clearance and reabsorption. By contrast, microinjection studies with [2-14C]-urate revealed the major site of altered urate absorption to be in the proximal convoluted tubule, a site where sodium and water reabsorption was unchanged.
Nephron 1979
PMID:Effects of MK-196 on urate and electrolyte excretion in the rat. 47 Nov 48

The effects of p-aminohippurate (PAH) on electrolyte clearances were measured in 8 human volunteers. At plasma PAH levels used to measure renal plasm flow, the only significant increase was in sodium clearance, while with PAH levels used to measure maximum tubular secretion, the clearances of sodium, potassium and phosphorus were all significantly increased. The antriuresis combined with a depression of free water clearance and the absence of a chloruresis led to the conclusion that PAH- changed the anion composition of the filtrate delivered to the ascending limb, thus interfering with coupled Na+ reabsorption. This finding must be taken into account when electrolyte excretion is being measured during PAH infusion. A similar mechanism may operate in patients with chronic uremia whose endogenous hippurate level is increased.
Nephron 1976
PMID:The natriuretic effect of p-aminohippurate in man. 124 77

From a total of 81 patients on maintenance hemodialysis who underwent coronary angiography, 8 patients fulfilled the criteria: significant coronary artery disease, hematocrit less than 27%, reproducible (ECG) positive treadmill test, no disturbance of repolarization in ECG at rest. Exercise stress testing was performed at a hematocrit of 25 +/- 2% and following erythropoietin therapy at a hematocrit of 34 +/- 0.5%. Symptom-limited exercise performance increased in all patients (1.10 +/- 0.3 W/kg b.w. vs. 1.44 +/- 0.31 W/kg b.w., p less than 0.01) as well as exercise duration (489 vs. 362 s, p +/- 0.01). ST segment depression during maximal exercise was reduced from a mean of 2.1 to 0.4 mm (p less than 0.01). It is concluded that amelioration of renal anemia by erythropoietin in dialysis patients with significant coronary artery disease reduces exercise-induced myocardial ischemia.
Nephron 1992
PMID:Effect of erythropoietin on ischemia tolerance in anemic hemodialysis patients with confirmed coronary artery disease. 143 8

A disease-specific questionnaire was developed for patients receiving chronic hemodialysis by interviewing patients to determine which aspects of their quality of life were adversely affected by their disease. The final questionnaire contained 26 questions in five dimensions (physical symptoms, fatigue, depression, relationships with others, frustration). The questionnaire demonstrated construct validity when compared with the Sickness Impact Profile, time trade-off technique and an exercise stress test. It was reproducible in stable, placebo-treated patients (correlation coefficient 0.85-0.98 for the 5 dimensions). It was more responsive than other measures in detecting an improvement with erythropoietin therapy in a randomized, placebo-controlled trial. This questionnaire should be useful for the assessment of the effect of various interventions upon the quality of life of hemodialysis patients.
Nephron 1992
PMID:A disease-specific questionnaire for assessing quality of life in patients on hemodialysis. 156 82

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.
Nephron 1991
PMID:Hyperlactataemia and metabolic acidosis during haemofiltration using lactate-buffered fluids. 175 38

Continuous, non-invasive measurement of arterial oxygen saturation (SaO2) during haemodialysis was performed in 18 patients with chronic renal failure. They were dialyzed three times for 2 1/2-3 1/2 h weekly using a capillary polysulfone (F60) or a cuprophane (D2) filter. The total number of O2 saturation curves analyzed was 48. The whole group showed a significant mean decline in SaO2 by 1.9% as compared with predialysis values. In 7 patients with three or more recordings, the significant mean decline in SaO2 was 1.5-4.2% and occurred within 15-60 min after onset of haemodialysis. Evaluation of SaO2 during episodes of severe depression of blood pressure was not possible due to loss of the signal as a consequence of peripheral vasoconstriction. Changes in SaO2 which occurred without any clinical signs or symptoms included very short episodes of depression of SaO2 by 3-22%; a decrease in SaO2 by 3-6% occurring towards the end of the treatment and followed by depressed values for a period of 20-60 min; episodes of marked instability of SaO2 values with differences of up to 10%, lasting 20-60 min and occurring towards the end of the treatment. Application of cuprophane instead of polysulfone filter membranes, first use and reuse of dialyzers, and microemboli blood filters were not found to influence the changes in SaO2. There was a significant difference in the initial decrease in SaO2 during acetate as compared with bicarbonate dialysis.
Nephron 1990
PMID:Continuous pulse-oxymetry during haemodialysis. 239 88


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