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Biomedical subjects

R A Sutton

Publications and source records attributed to R A Sutton.

At least 73 records · Page 4Linked to original sources
PubMed1984

Diffuse proliferative lupus glomerulonephritis. Determination of prognostic significance of clinical, laboratory and pathologic factors.

Clinical, laboratory and pathological factors in 35 females with diffuse proliferative lupus glomerulonephritis were analyzed to determine the prognostic significance of the individual variables. The clinical and laboratory variables were age, serum creatinine (Cr), serum C3, serum C4 and proteinuria at the time of biopsy while the biopsy ones included intraglomerular monocytic infiltration (NSE index), total glomerular deposits, extent of subendothelial deposits, extent of extraglomerular deposits, tubulo-interstitial inflammation, relative tubulo-interstitial volume and total pathologic score. Standard morphometric and counting procedures were used to determine the levels of all pathologic variables but pathologic score and extra glomerular deposits where grading estimates were done. Survival curves were determined by the life table method. Logrank and chi-square tests were used to establish levels of statistical significance. Seven patients developed established renal failure (Cr greater than or equal to 2.0 on two or more occasions at least 3 months apart) and nine showed significant deterioration of renal function (decrease in CrCl of 25% or more in between biopsy and last follow-up visit or an increase in serum Cr of 0.4 mg/dl or more over the follow-up period). The 5-year renal survival rate (absence of established renal failure) for the whole group was 77%. Serum Cr (p less than .005) and extent of extraglomerular deposits (p less than .025) were shown to be significant prognostic factors for renal survival. Of the seven patients who developed renal failure none had an NSE index greater than 3.0 and one had a C3 greater than or equal to 45 mg/dl. Statistically these factors were weak prognostic indicators (0.5 less than p less than .1). Multivariate analysis demonstrated that the extraglomerular deposit factor contributed significant additional prognostic information to that provided by Cr. Although not important as a prognostic factor on its own, the NSE index significantly improved the prognostic performance of serum Cr. The product of the NSE index and serum C3 proved to be a strong prognostic factor (p less than .005).

Adolescent↗
PubMed1983

Effects of acute metabolic acid-base changes and furosemide on magnesium excretion in rats.

The effect of acute metabolic acid-base changes on renal magnesium transport is not well defined. We have examined renal magnesium handling in three groups of ten acutely thyroparathyroidectomized rats infused with isotonic NaCl (controls), NH4Cl (acidosis), and NaHCO3 (alkalosis). To define the interactions of furosemide with acid-base changes and in an attempt to localize the site of action of acidosis and alkalosis on tubular magnesium transport, the rats were studied in a second phase after administration of a maximal dose of furosemide. Before furosemide, the blood pH was 7.40 in the controls, 7.27 (P less than 0.001) in the acidotic rats, and 7.56 (P less than 0.001) in the alkalotic rats. The filtered magnesium load was not significantly different in the three groups, but fractional excretion of magnesium (FEMg) was 33.7%, 37.4%, and 13.3% in the controls, the acidosis group, and the alkalosis group, respectively. Following furosemide, the blood pH was unchanged in each group, but FEMg increased significantly to 55.4%, 71.1% (P less than 0.01 compared with controls), and 41.4% (P less than 0.01 compared with controls) in the controls, the acidotic rats, and the alkalotic rats, respectively. These data indicate that metabolic alkalosis per se enhances renal magnesium transport, and this effect is also evident after blockade of loop magnesium reabsorption by a maximal dose of furosemide. Acidosis per se does not significantly alter magnesium transport, but an inhibitory effect of acidosis on magnesium reabsorption becomes evident when distal magnesium delivery is greatly increased by furosemide. These interactions suggest that metabolic acid-base changes and furosemide may influence magnesium reabsorption at different tubule sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗
PubMed1983

Renal calcium handling in familial hypocalciuric hypercalcemia.

We have determined calcium and sodium excretion rates in three members of a kinship with familial hypocalciuric hypercalcemia (FHH) and in four patients with primary hyperparathyroidism (PHP) under control conditions and following the intravenous administration of chlorothiazide or furosemide. The characteristic hypocalciuria of FHH, evidenced by a significantly reduced urinary calcium/creatinine ratio compared with that of PHP, is present under control conditions (0.08 vs. 0.26 mg calcium/mg creatinine, respectively, P less than 0.05), and after chlorothiazide (0.14 vs. 0.53, respectively, P less than 0.01). However, after furosemide infusion the calcium/creatinine ratio is no longer lower in FHH than in PHP (1.12 vs. 1.14, respectively, P greater than 0.05). These data suggest that, in FHH, tubular calcium reabsorption is enhanced in the thick ascending limb of Henle's loop, the site of action of furosemide. However, the data do not exclude the presence of an abnormality at a more distal site in the nephron.

Adult↗
PubMed1983

Renal tubular calcium transport: effects of changes in filtered calcium load.

Micropuncture experiments were performed in thyroparathyroidectomized dogs to examine the influence of changes in filtered calcium load on segmental tubular calcium reabsorption. Filtered calcium load was changed either by reducing glomerular filtration rate (GFR) by aortic clamping (group I) or by progressive calcium infusion (group II) to increase plasma ultrafilterable calcium concentration (UFCa). The results suggest that fractional proximal calcium reabsorption responds similarly to altered filtered load, whether produced by changes in GFR or UFCa. In contrast, fractional reabsorption by the loop segment is progressively reduced as UFCa is increased but is relatively unchanged by alterations in filtered load secondary to altered GFR. These data indicate a specific parathyroid hormone-independent reciprocal effect of UFCa on calcium reabsorption in the loop segment, which may be an important determinant of urinary calcium excretion.

Absorption↗
PubMed1983

Effects of metabolic alkalosis on calcium excretion in the conscious dog.

The tubular reabsorption of calcium has been studied in chronic metabolic alkalosis and acidosis. Clearance studies were performed in five conscious mongrel dogs during control periods and during alkalosis and acidosis both before and after thyroparathyroidectomy. After thyroparathyroidectomy, normocalcemia was maintained with oral dihydrotachysterol, and thyroxine was replaced. An initial control study was followed by the induction of chronic metabolic alkalosis by repeated gastric drainage for 4 days through a previously implanted gastric fistula. A second control study 1 week after alkalosis was followed by the induction of acidosis by feeding ammonium chloride, 10 gm daily for 3 days. A final control study was performed 1 week later. Serum proteins, GFR, and filtered calcium load were not significantly different in control, alkalosis, or acidosis. Alkalosis, in both intact and TPTX dogs, was associated with no change in TRNa in comparison with controls (94.6% vs. 95.4 in intact, p greater than 0.05; 95.0% vs. 96.3% in TPTX, p greater than 0.05). By contrast, TRCa increased significantly (97.2% vs. 95.5, p less than 0.05 in intact; 98.0% vs. 95.0, p less than 0.05 in TPTX). In acidosis, TRNa in both intact and TPTX dogs was unchanged in comparison with control (96.4%, p greater than 0.05 and 96.6%, p greater than 0.05, respectively), and TRCa was significantly decreased (to 91.9%, p less than 0.01 and 83.3%, p less than 0.001, respectively). These data indicate that chronic metabolic alkalosis increases the TRCa independently of changes in TRNa, filtered calcium load, or parathyroid activity.

Acidosis↗
PubMed1982

Review of the social situation of paraplegic and tetraplegic patients rehabilitated in the Hexham Regional Spinal Injury Unit in the north of England over the past four years.

The various aspects of the social circumstances of patients rehabilitated in the North of England Regional Spinal Injury Unit between 1975 and 1979 have been investigated. The study was carried out by making use of computerised analysis of a specially developed questionnaire. A Research Medical Social Worker was appointed to visit each patient at their home in order to record all relevant information into the questionnaire. A summary of the resulting information is presented. The study has been of particular value in two respects. Firstly, it has revealed the comprehensive social circumstances of these patients. Secondly, it has enabled us to evaluate the quality of service provided by the Hexham Regional Spinal Injury Unit, and it has enabled us to recommend an expansion of some of the aspects of the service provided by a Spinal Injury Unit.

Adolescent↗
PubMed1981

Acute gastric dilatation as a relatively late complication of tetraplegia due to very high cervical cord injury.

Patients sustaining an injury to the cervical spine at C3/4 level, with extensive cord damage, are difficult to manage. The injury is associated with a high mortality. The respiratory complications, including those associated with tracheostomy and intermittent-positive-pressure ventilation, are well recognised. The initial ileus and its management is also well documented. This report describes the development of acute gastric dilatation occurring 4 weeks after injury. The condition is particularly serious as many complications may have been overcome by this time resulting in a false sense of security. Two case histories are described. It is suggested that to a variable degree this complication probably occurs frequently in these patients. The aetiology of the acute gastric dilatation is discussed and recommendations are made (based on experience with one of the cases described), which may reasonably be expected to minimise the development and progress of the condition.

Acute Disease↗
PubMed1981

Acidosis and renal calcium excretion in experimental chronic renal failure.

In renal failure, absolute calcium excretion is low, but fractional excretion (FE) of filtered load is increased. In order to determine the role of metabolic acidosis in contributing to increased FECa, we have studied thyroparathyroidectomized dogs in a control phase and following the induction of chronic renal failure, both during spontaneous metabolic acidosis and after correction with NaHCO3. FECa was 3.7% in controls and increased to 13.7% in azotemic acidotic dogs (p less than 0.01). After correction of acidosis FENa was not significantly changed, but FECa fell significantly, to 8.1% (p less than 0.01), while glomerular filtration rate, plasma calcium and filtered calcium load were unchanged. Thus although FECa is increased in nonacidotic azotemic dogs, acidosis further enhances calcium excretion by inhibiting renal tubular calcium reabsorption. These effects of metabolic acidosis may contribute to hypocalcemia and bone disease in azotemia.

Acidosis↗
PubMed1980

Responses to hydrochlorothiazide and acetazolamide in patients with calcium stones. Evidence suggesting a defect in renal tubular function.

Urinary excretion of sodium, calcium, and magnesium has been measured after single oral doses of hydrochlorothiazide (100 mg) and acetazolamide (500 mg) in unselected patients with calcareous renal stone formation and in normal control subjects. With hydrochlorothiazide, 36 stone formers had significantly greater increments in sodium (P less than 0.01), calcium (P less than 0.05), and magnesium (P less than 0.05) excretion than 20 normal subjects. With acetazolamide, 13 stone formers had a smaller increment in sodium excretion (P less than 0.05) than 10 normal subjects. The abnormal responses to both diuretics were most marked in the patients with hypercalciuria during fasting. These data suggest that the tubular handling of sodium, magnesium, and calcium may be abnormal in patients with calcareous renal stones and are consistent with the presence of a defect in proximal-tubular reabsorption of fluid and electrolytes that may be partly offset by increased reabsorption in the distal nephron.

Acetazolamide↗
PubMed1980

Renal tubular transport in phosphate depletion: a micropuncture study.

The acute effects of intravenous infusions of phosphate and parathyroid hormone (PTH) upon the renal tubular handling of sodium, potassium, calcium, magnesium, and phosphate were examined in phosphate-depleted dogs using recollection micropuncture techniques. Hypercalciuria in phosphate depletion results from an impairment of calcium reabsorption between proximal and distal sampling sites, which can be partially corrected by the acute administration of PTH or by phosphate infusion. Magnesium reabsorption was normal in phosphate-depleted dogs but increased in parallel with calcium in the distal tubule following PTH and phosphate infusion. Phosphate was avidly reabsorbed in the phosphate-depleted dog so that excretion was very low even during the infusion of PTH or of neutral phosphate. Only with the infusion of both PTH and phosphate was a normal phosphaturic response observed.

Animals↗
PubMed1979

Effects of metabolic acidosis and alkalosis on sodium and calcium transport in the dog kidney.

Clearance and micropuncture studies have been performed in dogs to examine the effects of acute and chronic metabolic acidosis and acute alkalosis on tubular sodium and calcium transport. Acute metabolic acidosis, induced by the infusion of hydrochloric acid, decreased proximal fluid reabsorption and increased the fractional delivery of sodium and calcium to the distal tubule, but not to the final urine. In comparison with normal dogs, dogs with chronic metabolic acidosis (induced by feeding ammonium chloride) showed an increase in proximal fluid reabsorption and a dissociation of calcium from sodium reabsorption more distally, leading to an increased delivery of calcium relative to sodium at the distal tubule and in the final urine. The infusion of sodium bicarbonate to correct chronic metabolic acidosis, both in intact and thyroparathyroidectomized (TPTX) dogs, reduced proximal fluid reabsorption and caused a selective enhancement of calcium reabsorption relative to sodium in the more distal nephron, resulting in a reversal of the dissociation observed in acidosis, both at the distal tubule and in the final urine. By contrastin fusion of sodium chloride in parathyroid-intact acidotic dogs did not reduce proximal fluid reabsorption or enhance tubular calcium reabsorption. In nonacidotic dogs, both intact and TPTX, infusion of sodium bicarconate to induce acute alkalosis resulted in selhese data demonstrate the presence of a component of tubular calcium reabsorption situated beyond the proximal tubule, which is inhibited by chronic (but not acute) metabolic acidosis and enhanced by metabolic alkalosis (or bicarbonate infusion) independently of parathyroid hormone.

Acidosis↗
PubMed1979

A portable electronic 'calling device' as an aid to 'weaning' ventilator-dependent tetraplegic patients from intermittent positive pressure ventilation.

An electronic calling device has been developed. It is easily portable and can be operated by the severely paralysed tetraplegic patient in order to attract attention. The patient can operate the sensor either during artificial ventilation or when breathing spontaneously via the tracheostomy tube at a stage prior to the insertion of a speaking tube.

Adolescent↗