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Biomedical subjects

E Bourke

Publications and source records attributed to E Bourke.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of nonsteroidal antiinflammatory drugs on renal function in sickle cell anemia.

Renal hemodynamics and solute and water handling were evaluated in 19 sickle cell patients and 8 matched normal subjects during water diuresis, before and after acute oral administration of a nonsteroidal antiinflammatory drug (NSAID). Baseline GFR and RPF were higher in the patients compared to the normals. In contrast to normals, indomethacin and sulindac induced a 16% and 14% decrease in GFR, respectively. Indomethacin resulted in a slight increase in UOsm in normals, but a substantially greater rise in the patients. Following indomethacin a greater fall in FENa, fractional solute delivery to the diluting segment of the nephron [(CH2O + CNa + K)/GFR], fractional solute reabsorption in the diluting segment [CH2O/GFR] and the fraction of distally delivered solute reabsorbed [CH2O/(CH2O + CNa + K)] was observed in the sickle cell patients than in the normal subjects. A similar trend, but of significantly lesser magnitude than that induced by indomethacin, was observed following sulindac in the sickle cell patient. The data imply that the supranormal GFR observed in the sickle cell patients was prostaglandin-mediated. The effects of NSAID's on renal solute and water handling in the sickle cell patients are compatible with a prostaglandin-dependent decreased salt reabsorption in the medullary thick ascending limb of Henle, together with a hyperfunctioning proximal tubule. The data also imply an additional indomethacin-sensitive antinatriuretic effect in the diluting segment in these patients. Moreover, the results suggest that in sickle cell anemia sulindac may not have a "renal sparing" advantage over other NSAID's.

Adolescent↗
PubMed1987

Acidotic alterations in oxidative metabolism influencing rat renal slice ammoniagenesis.

We believe that two findings are interconnected and help to comprehend a major mechanism behind the regulation of renal ammonia production during acidosis. First, slices from acidotic compared to control and alkalotic rats produce more ammonia from glutamine. Second, inhibition of renal oxidative metabolism at various points by metabolic inhibitors augments slice ammoniagenesis. Based on this, our purpose was to determine whether enhanced renal ammoniagenesis during acidosis could occur through the same mechanism as the metabolic inhibitors. However, metabolic inhibitors (malonate; arsenite; 2,4-dinitrophenol) usually decrease while acidosis increases slice gluconeogenesis. There is one known exception. Fluorocitrate, which blocks citrate metabolism, simulates the acidotic condition by enhancing both ammonia and glucose production. Accordingly, a block of oxidative metabolism if located prior to citrate oxidation in the tricarboxylic acid cycle could theoretically augment ammoniagenesis during acidosis. Lactate, is a major renal fuel whose oxidative metabolism would be blocked by fluorocitrate. There, we concentrated on the effects of acidosis on lactate as well as glutamine metabolism. Lactate decarboxylation decreases in the face of increased glucose production during acidosis, and lactate inhibition of glutamine decarboxylation decreases in slices from acidotic rats. Also, we found lesser oxygen consumption in the presence of lactate by kidney slices from acidotic rats compared to control and alkalotic rats. We postulate that relatively less incorporation of lactate into the TCA cycle, causing decreased citrate formation and citrate oxidation during acidosis, contributes, at least in part, to acidotic adaptation of ammoniagenesis.

Acidosis↗
PubMed1987

Light chain cast nephropathy and acute renal failure associated with rifampin therapy. Renal disease akin to myeloma kidney.

Acute renal failure developed in a patient with a normal serum creatinine level, after treatment with rifampin was begun for tuberculosis. Renal biopsy revealed an obstructive nephropathy due to tubular casts. Immunoperoxidase and immunofluorescence studies demonstrated the presence of heterogeneous light chains within these casts. This unique drug-induced renal disease is discussed with reference to the literature and to possible analogies with myeloma kidney.

Acute Kidney Injury↗
PubMed1987

Indomethacin in streptozocin-induced nephrogenic diabetes insipidus.

A 14-year-old female patient with metastatic carcinoid developed streptozocin-induced glomerular, proximal, and distal tubular dysfunction. The latter was in the form of nephrogenic diabetes insipidus, with urine volumes in excess of 11 L/24 h. The prostaglandin synthetase inhibitor, indomethacin, rapidly corrected the polyuria both initially and on rechallenge, independent of change in glomerular filtration rate.

Administration, Oral↗
PubMed1987

Metabolic aspects of the regulation of systemic pH.

Catabolism of protein produces CO2, NH4+, and HCO3-. Mammals readily lose CO2 through the lungs, but the bicarbonate produced in metabolism of a typical diet (in humans, approximately 1 mol/day from approximately 100 g of protein) would cause alkalosis if not disposed of. Air-breathing animals solve this problem by incorporating NH4+ into organic compounds in which N is not protonated; thus each NH4+ ion loses a proton in the course of the synthesis. These protons serve to titrate HCO3-. In mammals, ureagenesis is the pathway by which protons are liberated from NH4+. The rate of ureagenesis therefore determines the rate of disposal of bicarbonate, and must be an important factor in the maintenance of pH homeostasis. Ammonium ion that is not needed for urea synthesis is packaged into glutamine by the liver. Hepatic glutamine synthetase is localized in the last rank of cells around the pericentral venule; thus glutamine synthetase cannot compete for NH4+ or interfere with the control of pH by urea synthesis. Ammonium excretion in the urine does not represent excretion of acid, and is not stoichiometrically related to renal generation of bicarbonate. The quantitatively major processes by which the HCO3-/CO2 ratio, and hence the pH, is regulated in blood and interstitial fluid are excretion of CO2 through the lungs and disposal of HCO3- as a consequence of ureagenesis in the liver.

Acid-Base Equilibrium↗
PubMed1987

Effect of acute hypercapnia on PTH-stimulated phosphaturia in dietary Pi-deprived rat.

The effects of respiratory acidosis on renal inorganic phosphate (Pi) handling are controversial. Clearance experiments, therefore, were performed in fasted, chronically parathyroidectomized (PTX), dietary Pi-deprived rats. The objectives were twofold: to study the effects of compensated and uncompensated hypercapnia per se on renal Pi excretion and to examine the interaction between acute hypercapnia, dietary Pi, and parathyroid hormone (PTH) on the renal handling of Pi. Acute hypercapnia increased the plasma Pi (delta 2.82 +/- 0.65 mg/dl, P less than 0.05) without altering the glomerular filtration rate (GFR). The FEPi increased (delta 7.26 +/- 0.48%, P less than 0.001) but the TRPi/GFR also increased. PTH (3 U X kg-1 X h-1) superimposed on hypercapnia resulted in a plasma Pi comparable to hypercapnia alone. The FEPi (7.56 +/- 0.78 vs. 24.43 +/- 2.20%; P less than 0.001) was higher and the TRPi/GFR (117 +/- 4 vs. 80 +/- 2 micrograms/min, P less than 0.01) lower, in the former group. PTH infusion during normocapnia resulted in a lower FEPi (0.20 +/- 0.10 vs. 24.43 +/- 2.20%, P less than 0.001) and a higher TRPi/GFR (106 +/- 2 vs. 80 +/- 2 micrograms/min, P less than 0.01) compared with PTH infusion during hypercapnia. Urinary adenosine 3',5'-cyclic monophosphate (cAMP) excretion was similar between the groups. During hypercapnia, when the extracellular acidemia was neutralized, the phosphaturic action of PTH persisted. These studies offer direct evidence that in chronically PTX, dietary Pi-deprived rats, the phosphaturic action of PTH is restored by hypercapnia per se. This effect appears to be independent of extracellular acidemia, changes in the plasma Pi and calcium, urinary pH and Na and cAMP excretion.

Acidosis, Respiratory↗
PubMed1987

Effects of inhibition and modulation of gamma-glutamyltransferase on glutamine and glutamate metabolism in control and acidotic rat proximal tubules.

The possible role of gamma-glutamyltransferase (gamma-GT) in renal ammonia production from glutamine remains controversial, prompting the current investigation. In rat proximal tubules, compounds known to activate the enzyme including the endogenously produced organic anion, hippurate, induced a significant increase in glutamine-ammoniagenesis both in nonacidosis and chronic metabolic acidosis although in absolute terms the increase was not more marked under the latter conditions. AT-125, which irreversibly inactivates gamma-GT, but not phosphate-dependent glutaminase, reduced the production of ammonia from glutamine in both acid-base states. In absolute terms, again, this reduction was similar under both acid-base conditions, implying an unimportant role for gamma-GT in vitro in the augmentation in renal ammoniagenesis induced by chronic metabolic acidosis. Maleate-stimulated glutamine-ammoniagenesis recently attributed to its intramitochondrial inhibitory effect in the dog is substantially due to the activation of gamma-GT in rat proximal tubules.

Acidosis↗
PubMed1986

Mesangial glomerulonephropathy with decreased circulating C4 and predominant mesangial C4 deposition in association with one null gene at the C4B locus.

We report a case of mesangial glomerulonephropathy associated with decreased circulating C4 in a young man with recurrent microscopic hematuria and one null gene at the C4B locus. Mesangial deposits moderately reactive with anti-C4 and weakly reactive with anti-C3 and anti-IgA were found on renal biopsy. No evidence was found to support a diagnosis of IgA nephropathy or any other of the recently described mesangial glomerulonephropathies with immunoglobulin and complement deposition. This case apparently represents a unique, heretofore undescribed variant of mesangial glomerulonephropathy associated with mesangial C4 deposition and C4 hypocomplementemia.

Adolescent↗
PubMed1986

Bartter's syndrome and the atrial natriuretic factor gene.

We investigated whether the gene for atrial natriuretic factor, a recently discovered peptide hormone with potent natriuretic, diuretic, and vasorelaxant properties, was pathogenetically linked to an uncommon but well-defined fluid and electrolyte disorder, Bartter's syndrome. Restriction fragment length polymorphisms in the atrial natriuretic factor gene were sought in a large kindred with six of 23 family members being affected. A Bgl II polymorphism, identified in two of 40 (5%) apparently normal subjects, was found in one of two first-generation family members. This polymorphism was also present in five of seven unaffected second-generation siblings but in only three of six affected siblings. The failure of the absence or the presence of the polymorphism to cosegregate with the disease clearly indicates that in this kindred, the gene for atrial natriuretic factor is not linked to Bartter's syndrome.

Atrial Natriuretic Factor↗
PubMed1986

MR imaging of renal transplants.

Fifty-six MR studies were obtained in 32 renal transplant patients, by using T1-weighted, spin-echo, and inversion-recovery pulse sequences. The findings, particularly the loss of corticomedullary differentiation, and the extent of vascular penetration into the renal parenchyma, were compared with the clinical and histologic diagnosis of transplant rejection. Thirteen MR studies on 11 patients with clinically normal renal transplants demonstrated normal corticomedullary differentiation. Renal vessels extended into the parenchyma in all 11 patients and to the cortex in 38%. In 37 MR studies on 22 patients with a clinical or histologic diagnosis of acute and/or chronic transplant rejection, the corticomedullary differentiation was normal in 8%, faint in 24%, and absent in 68%. Renal parenchymal vessels were visualized in 32%, but extended to the level of the cortex in only 8%. In 68% of the studies with transplant rejection, no parenchymal vessels were seen. When the corticomedullary differentiation was either faint or absent, the vascular pattern was normal in 6%; in 68% of cases no parenchymal vessels could be identified. We conclude the corticomedullary differentiation and the renal vascular pattern are useful parameters in the evaluation of renal transplant rejection.

Female↗
PubMed1985

Effect of insulin on renal phosphorus handling in the rat: interaction with PTH and nicotinamide.

Previous studies suggested an antiphosphaturic action of insulin. However, effects of parathyroid hormone (PTH), anti-natriuresis, or other variables were not vigorously controlled. Recently it has been suggested that nicotinamide restores phosphaturia in several antiphosphaturic states. Clearance studies were therefore performed in acutely parathyroidectomized rats to test the hypothesis that insulin abolishes the phosphaturic action of PTH and that this effect is prevented by nicotinamide. Superimposition of euglycemic hyperinsulinemia on PTH infusion (plasma insulin 19.1 +/- 2.7 vs. 9.8 +/- 1.1 microU/ml, P less than 0.05) during steady-state Pi excretion decreased fractional excretion (FE) of Pi compared with PTH-infused controls (3.16 +/- 0.61 vs. 18.02 +/- 0.81%, P less than 0.001). Renal cortical NAD+ was lower in the former than the latter group (455 +/- 22 vs. 689 +/- 30 pmol/mg, P less than 0.01). Nicotinamide pretreatment prevented the antiphosphaturic action of insulin and the decrease in cortical NAD+ in both the presence and absence of exogenous PTH. These studies offer direct evidence that in acutely parathyroidectomized rats insulin can abolish the phosphaturic action of PTH, independent of glomerular filtration rate, the filtered loads of Pi and glucose, FENa+, and cAMP excretion, an effect that is prevented by nicotinamide pretreatment. In the absence of nicotinamide pretreatment, superimposition of insulin on PTH infusion was associated with a decrease in renal cortical NAD+. A role for intracellular NAD+, probably indirect, in the antiphosphaturic action of insulin is suggested.

Animals↗
PubMed1984

HLA typing in bartter syndrome.

The mode of inheritance of Bartter syndrome is unclear; however, autosomal recessive inheritance seems likely. A consistent genetic marker of the carrier state likewise remains elusive. HLA typing was done in a family in whom six of 12 sibs have the syndrome. No significant HLA-syndrome linkage was found. This is in contrast to another familial hypokalemic syndrome in which a significant HLA association was found.

Bartter Syndrome↗
PubMed1983

T and B lymphocyte subsets in fenoprofen nephropathy.

Renal failure due to combined acute interstitial nephritis and minimal-change glomerulopathy is reported in two patients after fenoprofen therapy. In the interstitial infiltrates, T lymphocytes predominated over B lymphocytes in a ratio of four to one. The majority of B lymphocytes present were IgE-bearing cells. Among the T cells, the ratio of cytotoxic/suppressor cells to helper-inducer cells was three to one. Repeated renal biopsy in one patient after steroid-induced clinical remission demonstrated resolution of the inflammatory infiltrate and restoration of normal glomerular foot processes. The theoretic and practical implications of these findings are discussed.

Acute Kidney Injury↗