Plasma Citrate Levels Research Articles

Anterior horn cell disease seen in South India

Thirty-two patients with clinical evidence of anterior horn cell dysfunction are described. This group of patients could be divided into those with bulbar dysfunction, and those without. Eighth cranial nerve involvement was seen in 10%. The commonest peripheral distribution seen was symmetrical involvement of all four extremities. During the period of follow-up (1 to 5 years) none of the patients without bulbar dysfunction initially developed such symptoms. In all these patients electromyographic evidence of anterior horn cell disease was confirmed. The motor nerve conduction velocities in all of these patients were normal. None of them showed signs of pyramidal tract involvement. Muscle biopsy showed evidence of group fibre atrophy in 10 cases, was normal in 3, and showed a myopathic pattern in 1. Sural nerve biopsy obtained in a single patient was considered histologically normal. Plasma citrate and plasma pyruvate levels obtained in 5 patients of this group, showed elevated values for plasma citrate with normal plasma pyruvate levels. Conspicuous absence of pyramidal signs, elevated plasma citrate, normal plasma pyruvate values and the extremely slow progression suggest that this group of patients are different from other varieties of anterior horn cell dysfunction previously described.

Parathyroid hormone secretion during exchange transfusion.

Plasma concentrations of calcium, phosphate, citrate, albumin, and parathyroid hormone (PTH) were measured during and after exchange transfusion of infants suffering from haemolytic disease using blood anticoagulated with acid-citrate and dextrose (ACD) or heparin. Pretransfusion plasma PTH and phosphate both correlated positively with postnatal age but not with each other. Transfusion with ACD blood caused a twelvefold rise in plasma citrate levels but no significant change in plasma calcium, phosphate, or PTH of the infant, despite the concentration of these substances being lower in the donor blood. The concentration of calcium, phosphate, and albumin was higher in heparinized than in ACD donor blood, and infants transfused with heparinized blood showed no change in the plasma concentration of any substance measured during transfusion. The addition of 50 mug glucagon to ACD donor blood had no effect on PTH secretion. 3 hours after transfusion there was a rise in the plasma PTH infants who had received ACD blood but not in those given heparinized blood. Transfusion with ACD blood caused a net loss of calcium, phosphate and albumin from the infant, whereas transfusion with heparin blood did not. Both types of transfusion caused a net loss of PTH but this was significantly greater in those given ACD blood. These results show that transfusion with ACD blood results in increased secretion of PTH, probably due to the fall in ionized calcium concentration caused by the citrate load.

Calcitonin effects on plasma and urinary citrate levels in rats.

Calcitonin effects on plasma and urinary citrate levels in rats.

Biochemical aspects of motor neurone disease--Madras pattern

A detailed study of four cases of MND-Madras has shown a significantly low plasma citrate level in these subjects. Comparison with other related groups of neurological disorders indicates the citrate/pyruvate ratio to be of diagnostic value in MND-Madras. This seems to suggest that the pathophysiology of MND-Madras may centre round altered citrate metabolism.

Plasma citrate levels during exchange transfusion.

Plasma citrate levels during exchange transfusion.

Parathyroid hormone effects on soft-tissue citrate levels.

The intravenous administration of parathyroid hormone (PTH) to rats resulted in an immediate and transient increase in kidney citrate levels. The kidney response to PTH was apparent in six minutes and returned to normal in 15 minutes. In addition, liver citrate levels were increased within 15 minutes after PTH administration and the effect was sustained for approximately two hours. Plasma citrate levels were not increased by PTH before one to two hours. Kidney citrate levels exhibited a second increase between two and six hours after PTH injection. These results suggest that the rapid response of the kidney and liver might be due to a "direct" effect of PTH. The delayed response of the kidney conceivably results from secondary effects of PTH injections such as the associated increased plasma calcium. PTH did not result in an increased plasma citrate prior to plasma calcium changes. The results suggest that PTH activities might be associated with effects on citrate metabolism of soft tissues.

Citrate metabolism in diabetes: I. Plasma citrate in alloxan-diabetic rats and in clinical diabetes

A “bimodal” increase in plasma citrate levels was observed in alloxan-diabetic rats. Three days following alloxan injection, the plasma citrate levels in cardiac puncture blood was 9.40 mg. 100 ml. as compared to 4.95 for the control. At 14 days the value approximated that in the normal rats, whereas at 28 days (and subsequent time periods), the citrate levels were markedly elevated. In a second series of experiments in which the animals were killed by decapitation, a similar “bimodal” change in plasma citrate values was noted; however, the plasma citrate levels in both diabetic and control rats were generally higher than was the case when blood was drawn by cardiac puncture. No relationship could be established between the blood sugar level and plasma citrate values. In treated human diabetics, plasma citrate values were not significantly different from the normal, i.e., 2.70 as compared to 2.41 mg. 100 ml. However, in 2 cases of untreated human diabetes exhibiting severe ketoacidosis, the plasma citrate values were markedly elevated. In one, the initial value was 44.4 mg. 100 ml. serum; the level rapidly returned toward normal; at 4 weeks it was 1.56 mg. 100 ml. The increased serum citrate levels were not the result of citrate mobilization from bone, since there was no concomitant increase in the serum calcium levels. These results suggest the possibility that there may be an alteration in the tricarboxylic acid cycle in diabetes (both experimental and clinical), and that this alteration results in the accumulation of plasma citrate.

The renal clearance of citrate in man

Because of the paucity of data in man concerning the renal clearance of citrate, citrate and creatinine chromogen clearances were simultaneously determined in 10 normal subjects and in 8 patients with proved hyperparathyroidism prior to and after surgical correction. The hyperparathyroid patients were hypercalciuric and had recurrent renal stones but were free of infection at the time of this study. Similar determinations were performed repeatedly in 9 patients with idiopathic renal stones without urinary tract infection and in 10 hypoparathyroid patients before specific therapy, to further evaluate the relationship between renal stones, parathyroid hormone and the clearance of citrate in man. No differences in plasma citrate levels were found between these 4 groups of patients. Citrate clearances expressed per 100 ml. of GFR were similar in the normal and idiopathic stone forming group. The mean citrate clearance was slightly lower in the hyperparathyroid patient group preoperatively. Citrate clearances were low in the hypoparathyroid patients and fell to similar significantly low levels postoperatively in the cured hyperparathyroid group. In 5 normal patients parathyroid extract administration did not alter plasma levels or citrate clearances, despite exhibition of its other typical biochemical effects. These data indicate that citrate clearance can vary independently of the plasma levels of citrate in man and suggest that endogenous parathyroid hormone exerts an effect on citrate excretion at the renal level. In addition the data suggest that stone fromation in the hypercalciuric state of hyperparathyroidism and in the idiopathic stone forming group is not due to any absolute decrease in citrate excretion.

Citrate Excretion in Renal Tubular Acidosis

Case Studies1 January 1963Citrate Excretion in Renal Tubular AcidosisJAMES F. MORRISSEY, M.D., MANUEL OCHOA JR., M.D., WILLIAM D. LOTSPEICH, M.D., CHRISTINE WATERHOUSE, M.D., F.A.C.P.JAMES F. MORRISSEY, M.D.Search for more papers by this author, MANUEL OCHOA JR., M.D.Search for more papers by this author, WILLIAM D. LOTSPEICH, M.D.Search for more papers by this author, CHRISTINE WATERHOUSE, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-1-159 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMetabolic and respiratory acidosis has been shown to decrease the urinary citrate excretion in man (1). Conversely, metabolic or respiratory alkalosis will increase this parameter, without associated increase in the plasma citrate level (2). In these situations, usually the urine pH varies directly with the pH of the blood which does not allow one to differentiate the significance of either factor in the renal excretion of citrate. Recently, Evans, Maclntyre, Macpherson, and Milne (2) have shown that potassium repletion in a patient with primary aldosteronism was associated with an increased urinary citrate excretion. In their case, this occurred in the...

Effect on the plasma citrate of treatment of primary hypothyroidism with triiodothyronine.

DURING the course of metabolic studies on myxœdematous subjects it was noted that the plasma citrate-level was in some cases raised. In the hope that useful information might be obtained on the mode of action of thyroid hormones on tissue metabolism, the plasma citrate-level was followed during the treatment of four female patients suffering from primary myxœdema, using ordinary replacement doses of triiodothyronine. Triiodothyronine was also administered to four normal medical students, two male and two female, and their plasma citrate-levels were followed.

Effect of vitamin D on plasma citrate and calcium response to nephrectomy.

Young rats fed a diet deficient in vitamin D and optimal in calcium and phosphate respond to prophylactic administration of the vitamin with elevated plasma citrate and calcium levels. Feeding vitamin D to D-deficient young rats markedly increased the plasma citrate response to nephrectomy. The D-deficient animal requires between 24 and 48 hr to develop the maximal response to vitamin D as judged by the plasma citrate response to nephrectomy. The plasma citrate response to nephrectomy after administration of the vitamin is virtually linear over a narrow range of vitamin D dosage. These data are discussed in terms of the possible role of citrate in relation to parathyroid function and the maintenance of plasma concentration of calcium.

EFFECT OF INFUSIONS OF CITRATED PLASMA ON THE PLASMA CITRATE LEVEL OF INFANTS

The effect of infusions of citrated plasma given at varying rates on the plasma citrate level of infants has been studied. The plasma citrate as a rule rose from 0.17 to 2.0 mM/1. after single infusions to fall rapidly at first and more slowly later. In two instances levels of 2.6 and 2.8 mM/1. were observed. Considerable decreases in the calcium ion concentration, assuming unchanged total calcium values, were calculated. ECGs indicated some lengthening of the duration of the Q-T interval, compatible with a decrease in the calcium ion concentration, but to a degree less than expected. One infant suffered a nearly fatal reaction, considered to be tetanic in nature. The examination of the citrate in the plasma of an infant dead after infusion of plasma showed a high citrate level of 2.8 mM/1. It is assumed that normally physiologic forces are operative to counteract the calcium-ion-lowering effect of citrate.