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Biomedical subjects

D S Fraley

Publications and source records attributed to D S Fraley.

At least 37 records · Page 2Linked to original sources
PubMed1982

Fenoprofen nephropathy: lipoid nephrosis and interstitial nephritis. A possible T-lymphocyte disorder.

Five patients are presented, each of whom had an acute idiosyncratic reaction to fenoprofen calcium (Nalfon) characterized by acute renal failure and marked proteinuria. Renal pathology was similar in all patients. Light microscopy revealed marked lymphocytic inflammatory infiltrates and normal glomeruli. Immunofluorescent staining was minimal or absent. Electron microscopy showed fusion of podocytes in otherwise normal glomeruli. Two patients were studied using T-cell and B-cell specific fluorescent staining, which revealed that the interstitial infiltrates were composed exclusively of T-lymphocytes. This finding is considered in relation to prior experimental and theoretic work. It is suggested that the various clinical and pathologic findings in fenoprofen nephropathy are all manifestations of a disordered cell-mediated immunity.

Acute Kidney Injury↗
PubMed1981

Mechanism of volume expansion on citrate, ammonia, and acid excretion in the rat.

Potassium-depleted rats receiving sodium chloride or i.v. mannitol decrease their blood bicarbonate concentration isohydrically, reduce urinary citrate, and increase urinary ammonia excretion per milligram of urinary creatinine. To determine the mechanisms of these renal changes, we volume expanded normal rats with mannitol, normal saline, or saline bicarbonate solutions. Blood pH in each group remained constant, but blood bicarbonate fell significantly in the mannitol and saline-infused rats. In these two groups, urinary citrate per unit GFR decreased 27% and 25% (P less than 0.01) but urinary ammonia excretion per unit GFR increased 120% and 90% (P less than 0.01). By contrast, in saline bicarbonate rats, citrate excretion increased 27% and urinary ammonia excretion rose 29% (P greater than 0.2). Rats with metabolic acidosis given saline did not alter blood pH or bicarbonate. Citrate excretion per unit GFR increased 150% (P less than 0.02) but urinary ammonia excretion rose insignificantly by 11%. Calculated net tubular reabsorption of citrate increased in the mannitol and saline-infused rats. The rise in urinary pH in these two groups during expansion suggest that renal ammonia production was also increased. We conclude that volume expansion changes renal citrate and ammonia metabolism by isohydrically reducing blood bicarbonate concentration, thereby demonstrating another effect of bicarbonate, independent of pH, on renal metabolism.

Acid-Base Equilibrium↗
PubMed1981

Rapid progressive glomerulonephritis: relapse after prolonged remission.

Three patients with epithelial cell crescents and rapid progressive glomerulonephritis (RPGN) had prolonged remission, presumably induced by treatment with maintenance oral prednisone and cyclophosphamide plus plasmapheresis. Patient 1 had anti-glomerular basement membrane-mediated RPGN, patient 2 had an immune complex disease, and patient 3 did not show any immune deposits. After a two-year remission in two patients and a greater than one-year remission in the third patient, renal function deteriorated. Epithelial cell crescents were again demonstratable on repeated renal biopsy specimens in each patient. One patient again received triple therapy, while the other two patients received megadoses of intravenous prednisolone sodium succinate in place of plasmapheresis. Each patient again entered a stable remission. These three cases demonstrate that RPGN may recur after prolonged remission in all three varieties of this syndrome. If the exacerbation is treated promptly, a second remission may be induced.

Aged↗
PubMed1980

Infectious complications with plasmapheresis in rapidly progressive glomerulonephritis.

We recently used plasmapheresis to treat eight patients with rapidly progressive glomerulonephritis. Life-threatening infections developed in five patients, three of which were caused by opportunistic pathogens. In contrast, only two infections occurred in 21 patients with similar renal disease treated with immunosuppressive drugs but not with plasmapheresis. Although infectious complications of plasmapheresis therapy have not been amphasized previously, our experience, coupled with that of previous reports, suggests that serious infections will develop in one third of patients undergoing plasmapheresis for renal disease. Plasmapheresis should be used with caution in patients with rapidly progressive glomerulonephritis.

Adolescent↗
PubMed1980

Propranolol-related bronchospasm in patients without history of asthma.

Three patients with no history of asthma or allergy developed bronchospasm while taking propranolol for hypertension. The bronchospasm was severe in all three and in one patient resulted in respiratory arrest. Since the bronchospasm was relieved with discontinuation of propranolol and supportive bronchodilator therapy, the bronchospasm was believed to be caused by propranolol. Furthermore, each patient was subsequently treated with other antihypertensive medications which, like propranolol, contain the stabilizer additive tartrazine. Bronchospasm did not recur, making it unlikely that tartrazine hypersensitivity caused this problem. Regardless of a negative history of asthma, therefore, life-threatening bronchospasm must be considered a possible complication of propranolol therapy.

Bronchial Spasm↗
PubMed1979

Respiratory failure secondary to Mycoplasma pneumoniae infection.

Three previously healthy patients presented with bilateral pulmonary infiltrates, hypoxemia, and respiratory failure associated with Mycoplasma pneumoniae infection. None had underlying pulmonary or immune deficiency diseases. One died with dense fibrotic reorganization of the lungs, and another survived after prolonged mechanical ventilatory assistance. Two developed pulmonary superinfections with Pseudomonas aeruginosa. All had extrapulmonary complications: one had Coombs'-positive hemolytic anemia, another myocarditis, and all three had abnormal results of liver function tests, consistent with hepatocellular dysfunction.

Adult↗
PubMed1979

Life-threatening metabolic alkalosis in a comatose patient.

A 63-year-old man with obstructive pulmonary disease developed severe metablic alkalosis and coma while receiving steroid therapy and nasogastric suction. Treatment, which included the acute induction of hypercarbia and the simultaneous administration of acetazolamide and saline, restored acid-base balance within 24 hours. This combined approach eliminated the need to infuse hydrochloric acid.

Acetazolamide↗
PubMed1979

An extrarenal role for parathyroid hormone in the disposal of acute acid loads in rats and dogs.

Acid infusion studies were performed in nephrectomized rats and dogs with either intact parathyroid glands (intact) or after thyroparathyroidectomy (thyroparathyroidectomized [TPTX]) to determine the role of parathyroid hormone (PTH) in extrarenal disposal and buffering of acutely administered acid. 29 intact rats given 5 mM/kg HCl and 6 intact dogs given 7 mM/kg HCl developed severe metabolic acidosis but all survived. However, each of 12 TPTX rats and 4 TPTX dogs given the same acid loads died. Intact rats and dogs buffered 39 and 50% of administered acid extracellularly, respectively, whereas extracellular buffering of administered acid was 97 and 78% in TPTX rats and dogs, respectively. 17 TPTX rats and 6 TPTX dogs given synthetic PTH 2 h before acid infusion survived. The blood bicarbonate and extracellular buffering in these animals, measured 2 h after acid infusion, was similar to intact animals. Changes in liver, heart, and skeletal muscle pH determined from [(14)C]5,5-dimethyl-2,4 oxazolidinedione distribution seemed insufficient to account for the increased cell buffering of PTH-replaced animals. Indeed, muscle pH in TPTX dogs given PTH and acid was only 0.06 pH units lower than in control dogs given no acid, suggesting that another tissue, presumably bone, was the target for PTH-mediated increased cell buffering. This conclusion was supported by the observation that PTH did not alter the pH of intact rat diaphragms in vitro. These results indicate that PTH is necessary for the optimal buffering of large, acute acid loads presumably by increasing bone buffering.

Acidosis↗
PubMed1978

Metabolic acidosis after hyperalimentation with casein hydrolysate. Occurrence in a starved patient.

A 29-year-old woman with short bowel syndrome and prolonged starvation developed hyperchloremic metabolic acidosis after initiation of hyoeralimentation with a casein hydrolysate solution. The acidosis was not due to bicarbonate loss but was associated with diminished ability of the kidney to increase urinary acid excretion, particularly titratable acidity. Supplemental parenteral bicarbonate administration was necessary for two weeks until urinary acid excretion rose to normal.

Acidosis↗
PubMed1977

Correction of hyperkalemia by bicarbonate despite constant blood pH.

Patients having hyperkalemia often are given bicarbonate to raise blood pH and shift extracellular potassium into cells. Blood pH in many hyperkalemic patients, however, is compensated. To determine whether bicarbonate, independent of its pH action, affects plasma potassium, 14 hyperkalemic patients were treated with bicarbonate in 5% dextrose. In five patients (changed pH group), blood pH rose at least 0.08, while in nine (constant pH group), it changed less than 0.04. In the first group, pH rose 0.12, bicarbonate rose 5.9 mEq/liter, and plasma potassium fell 1.6 mEq/liter, and plasma potassium fell 1.4 mEq/liter. The correlation between changes in plasma potassium and bicarbonate was identical in the two groups and independent of urinary potassium excretion. Four additional patients, who were treated with 5% dextrose alone, did not significantly lower their plasma potassium, although subsequent treatment with bicarbonate in 5% dextrose lowered their plasma potassium. Thus, bicarbonate lowers plasma potassium, independent of its effect on blood pH, and despite a risk of volume overload, should be used to treat hyperkalemia in compensated acid-base disorders, even in the presence of renal failure, provided the plasma bicarbonate concentration is decreased.

Adult↗
PubMed1977

Potassium and intracellular pH.

Recent work has clarified some of the complex interrelationships between cell pH and potassium. These studies have been limited by the techniques available for accurately measuring cell pH. At present it is obvious that intracellular pH is a major regulator of the cellular potassium concentration, but the precise relationship between these two is still uncertain. It has become increasingly clear, however, that no simple relationship exists between the intracellular to extracellular hydrogen ion and potassium ion ratios. Many experiments do demonstrate that the extracellular metabolic alkalosis of potassium depletion is accompanied by a decrease in skeletal muscle pH in rat, rabbit, and probably dog. The response of cardiac and renal tubular cell pH to potassium depletion is less clear, although most evidence indicates that there is also a reduction in the pH of these tissues. This effect on cell pH appears to be independent of chloride. By contrast, hyperkalemia seems to raise muscle cell pH at the same time it induces an extracellular metabolic acidosis. The metabolic and physiologic consequences of potassium-induced alterations in cell pH have yet to be fully elucidated.

Acid-Base Equilibrium↗
PubMed1976

Isohydric regulation of plasma potassium by bicarbonate in the rat.

pH and bicarbonate affect many metabolic reactions but each may change independently. To study bicarbonate's effect onplasma potassium, blood bicarbonate in normal, hypokalemic or hyperkalemic rats was either maintained constant, lowered by hydrochloric acid or raised by sodium bicarbonate administraion. Blood pH was maintained constant by changing PCO2. In normokalemia lowering bicarbonate increased plasma potassium 2.0mEq above values obtained in the other groups. To eliminate urinary potassium losses, experiments were also performed in rats with bilateral ureteral ligation. Again, plasma potassium concentration rose significantly more in the lowered bicarbonate group. Similarly, in hypokalemia, plasma potassium rose 1.2 and 0.4mEq in the lowered and unchanged groups, but fell 0.2mEq/liter in the elevated group. Differences could not be ascribed to renal potassium losses as potassium excretion was essentially zero in each group. In hyperkalemia, plasma potassium concentration remained elevated for 150 min in the lowered bicarbonate group but fell 1.3 and 2.0mEq in the unchanged and elevated groups, respectively. Urinary potassium losses in the three groups were statistically identical. In all experiments blood pH was maintained unchanged during the experiment. The data show that bicarbonate, independent of blood pH, alters transcellular potassium distribution suggesting the usefulness of bicarbonate therapy in hyperkalemia even at a compensated blood pH.

Acid-Base Equilibrium↗
PubMed1975

Effect of volume expansion on renal citrate and ammonia metabolism in KCl-deficient rats.

When rats with desoxycorticosterone acetate (DOCA)-induced potassium chloride deficiency are given sodium chloride there is simultaneously a partial correction of metabolic alkalosis and a marked reduction in urinary citrate excretion and renal citrate content. To examine DOCA's role in this phenomenon and to determine how sodium chloride alters renal metabolism, rats were made KC1 deficient using furosemide and a KC1-deficient diet. Renal citrate and ammonia metabolism were then studied after chronic oral sodium chloride administration or acute volume expansion with isotonic mannitol. Although both maneuvers partially corrected metabolic alkalosis, sodium chloride raised serum chloride concentration while mannitol significantly decreased it. Urinary citrate excretion decreased to 10% of control in rats given NaCl and to 50% of control in rats infused with mannitol. The filtered load of citrate was constant or increased indicating increased tubular citrate reabsorption. Renal cortical citrate content also decreased approximately 50%. Renal cortical slices from KCl-deficient rats incubated in low or normal chloride media produced equal amounts of 14CO2 from (1, 5-14C) citrate. In addition, urinary ammonia excretion increased by over 300% in both groups. This occurred in the mannitol group despite increased urinary pH and flow rate indicating a rise in renal ammonia production. It seems that neither DOCA nor an increase in serum chloride concentration explains the experimental results. Rather, it appears that volume expansion is responsible for increased renal tubular citrate reabsorption and renal ammonia production. As these renal metabolic responses ordinarily occur in response to acidosis, the data are consistent with the hypothesis that volume expansion reduces renal cell pH in 3KCl-deficient rats.

Ammonia↗