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Biomedical subjects

R G Luke

Publications and source records attributed to R G Luke.

At least 109 records · Page 6Linked to original sources
PubMed1981

Surgical therapy for persistent hypertension after renal transplantation.

The presence of the original diseased native kidneys in renal allograft recipients is associated with an increased prevalence of persisting post-transplant hypertension. In 9 of 10 such transplant patients bilateral nephrectomy of these native kidneys, performed at least 1 year after successful transplantation of a renal allograft, resulted in improved blood pressure control. Although these 10 patients had higher peripheral plasma renin activity (PRA) than normotensive patients (5.9 +/- 1.3 ng/ml/hr versus 1.5 +/- 0.3 mg/ml/hr), selective renal vein renin measurements did not consistently demonstrate higher renin concentrations from the native kidneys. Removal of the original kidneys was beneficial even in some patients who had stenosis of the allograft artery demonstrated by arteriography.

Follow-Up Studies↗
PubMed1981

Acute renal failure due to seminoma metastatic to the kidneys.

A patient with seminoma presenting with bilateral symmetrical enlargement of the kidneys, massive proteinuria and acute renal failure is described. No factor other than infiltration due to seminoma was found to explain the renal failure. Renal function improved markedly along with renal size and architecture in response to radiotherapy. Renal dialysis is justified in metastatic seminoma to determine the effect of tumor therapy.

Acute Kidney Injury↗
PubMed1980

Focal and segmental glomerular sclerosis in reflux nephropathy.

Reflux nephropathy was diagnosed in 23 patients (14 per cent of all the patients who received transplants) between 1973 and 1977, and nephrectomy was performed in all. Histology and immunofluorescence revealed a glomerular sclerosis associated with the idiopathic nephrotic syndrome. No focal and segmental glomerular sclerosis was seen in kidneys removed from patients with nonglomerular renal disease. Twenty-four hour urinary protein excretion in grams was 3.1 +/- 0.3 (mean +/- SEM) and was greater than that in our patients with end-stage nonglomerular renal disease. Thirty-one renal transplants were performed in these 23 patients; thereafter, maximum protein excretion was 1.4 g. Focal and segmental glomerular sclerosis was seen in only one (chronic rejection, protein excretion less than 0.5) of the 20 kidneys available for histologic study. Thus, focal and segmental glomerular sclerosis is extremely common in reflux nephropathy, accounts for "glomerular" proteinuria and may contribute importantly to progressive renal failure but, unlike that associated with the idiopathic nephrotic syndrome, rarely recurs after renal transplantation.

Adolescent↗
PubMed1980

Inhibition of renin secretion by HCl is related to chloride in both dog and rat.

To determine if inhibition of renin release by HCl is related to acidosis or to Cl-, the effects of peripheral venous infusions of HCl and H2SO4 on plasma renin activity (PRA) were compared in the dog and the rat. In NaCl-deprived, pentobarbital-anesthetized dogs, either 0.15 M HCl (n = 10) or 0.075 M H2SO4 (n = 7) was infused for 60 min. In 5 of the 10 HCl-infused dogs (group A), urine Cl- excretion increased (P less than 0.01) during HCl infusion. In the remaining five dogs (group B), Cl- excretion did not increase. Cl- excretion also did not increase during H2SO4 infusion. Comparable acidosis was produced in all three groups. PRA decreased (P less than 0.01) in response to HCl in group A but did not change (P greater than 0.8) in group B HCl-infused dogs or in H2SO4-infused dogs. In NaCl-deprived, anesthetized rats, PRA was suppressed (P less than 0.05) by HCl (from 40.6 +/- 9.4 to 27.4 +/- 5.3 ng . ml-1 . h-1 (SE)) but not H2SO4 (from 37.1 +/- 4.2 to 37.0 +/- 6.3 ng . ml-1 . h-1), despite comparable acidosis. Cl- excretion increased only in HCl-infused rats. In conclusion, inhibition of PRA by acute infusion of HCl is specifically related to Cl-.

Animals↗
PubMed1980

Factors influencing chloride reabsorption in the collecting duct segment of the rat.

To study factors influencing Cl reabsorption in the collecting duct segment of the rat, excretion of Cl and of 36Cl injected into late distal tubule segments of superficial nephrons were examined by microinjection and free-flow micropuncture techniques. Selective dietary Cl restriction for 7-10 days decreased urinary 36Cl recovery for microinjection [74 +/- 5% (SE)] compared with normal rats (90 +/- 3%, P < 0.01). Infusion of 0.15 M NaHCO3 (10% body wt) in the Cl-restricted rat led to marked increases in urinary flow rates and sodium excretion but did not increase 36Cl recovery. In these NaHCO3-infused rats, recovery of 36Cl was unaffected by increasing Cl concentration in the injectate from 40 to 140 peq/nl, but increased to levels not different from control (89 +/- 3%) when amphotericin B was included in the injectate. Equivalent infusion of 0.15 M NaCl in the Cl-restricted rats also increased 36Cl recovery to control levels (89 +/- 3%). This response was not altered by administration of DOCA. Absolute chloride delivery to late distal tubule sites was not different in NaCl- and NaHCO3-expanded groups, and (TF/UF)Cl was less in the NaHCO3 group (0.27 +/- 0.03 vs. 0.37 +/- 0.02, P < 0.05); therefore, the chemical gradient for Cl did not favor Cl efflux. There was a significant correlation between urinary recovery of 36Cl and urinary Cl excretion in the NaCl- and NaHCO3-expanded animals. It is suggested that Cl restriction alters, by an as yet unknown mechanism that is independent of changes in Na balance, the intrinsic Cl-absorbing capacity of the collecting duct.

Animals↗
PubMed1980

Effect of prednisone dose spacing on plasma lipids.

We have previously reported a low prevalence of hyperlipidemia in renal transplant recipients who were treated with alternate-day corticosteroid. To determine whether alternate-day prednisone per se is associated with lower plasma lipids than is daily prednisone, we studied 14 renal transplant recipients with good allograft function (serum creatinine less than 2.5 mg/dl) who were normolipidemic on alternate-day prednisone. All patients were treated with 6 months of daily prednisone (10.9 +/- 0.4 mg, mean +/- S.E.) and then returned to 6 months of alternate-day prednisone (21.6 +/- 1.0 mg). Mean plasma triglyceride, cholesterol, and cholesterol fractions on either regimen were normal and not different. There were no differences in fasting or 2 hr postprandial glucose and insulin levels. Twelve patients gained weight on daily prednisone, and 11 patients lost weight on reversion to alternate-day prednisone. The changes in ideal body weight in both periods correlated (p less than 0.05) with changes in plasma triglycerides. These data suggest that a daily prednisone regimen per se as compared to an alternate-day regimen does not dispose normolipidemic patients to hyperlipidemia. The factors contributing to the low prevalence of hyperlipidemia in our renal transplant recipients remain obscure.

Adult↗
PubMed1980

Does vesicoureteric reflux result in renal allograft failure?

Vesicoureteric reflux (VUR) into transplanted kidneys has been cited as an often disregarded but frequent complication of transplantation which is associated with a glomerular lesion that resembles membranoproliferative glomerulonephritis, marked proteinuria, and graft failure. To determine the prevalence of this complication in our transplant population, all of our 23 patients with marked proteinuria and 27 controls without proteinuria had voiding cystourethrograms performed approximately two years after transplantation. In our population, VUR was infrequent (8%). Moreover, in the three of the four cases detected renal function has not deteriorated and three of the four do not have marked proteinuria. We cannot confirm the suggestion that VUR is a frequent cause of late renal allograft failure.

Adolescent↗
PubMed1980

Renal vein thrombosis in IgA nephropathy.

We report the first known case of renal vein thrombosis (RVT) in a patient with IgA nephropathy. We discuss the possible significance of this finding in support of the concept that RVT is a complication of glomerular disease.

Adult↗
PubMed1979

Renal transplantation for patients with type I and type II membranoproliferative glomerulonephritis: serial complement and nephritic factor measurements and the problem of recurrence of disease.

Fourteen patients with membranoproliferative glomerulonephritis as their original kidney disease received 16 renal allografts. All 14 patients are alive, 11 currently have functioning allografts, and one graft was lost to recurrence of membranoproliferative glomerulonephritis. Originally depressed serum complement (C3) concentrations returned to normal soon after transplantation in those patients with no clinical evidence of recurrence. Two patients with type II membranoproliferative glomerulonephritis had recurrence of disease. Nephritic factor (C3NeF) was high in both these patients before they received their transplants and was absent soon thereafter. However, abnormally high levels were again detected in their course. The one recurrence of type I membranoproliferative glomerulonephritis was associated with depressed C3, Clq, C4 and factor B but without C3NeF activity. Despite warnings of "high risks/ and "high mortality" associated with renal transplants in patients with membranoproliferative glomerulonephritis, we, because of these results and a review of the literature, continue to recommend renal transplants from both living related (LRD) and cadaver (CAD) donors in otherwise suitable patients who have renal failure due to membranoproliferative glomerulonephritis.

Adolescent↗
PubMed1979

Controversy in renal transplantation: antireflux versus non-antireflux ureteroneocystostomy.

A comparison of 118 consecutive nephroureteral allografts suggests that ureteroneocystostomy provides excellent results with (60 cases) or without (52 cases) an antireflex procedure. Reflux was noted in less than 10% of each group after transplantation and no morbidity could be attributed to reflux when it was found. There was no obstruction or anastomotic leakage in either group. The advantages of each procedure are discussed.

Adolescent↗
PubMed1979

Hemodialysis and kidney transplantation in a patient with glucose phosphate isomerase deficiency.

End stage failure in a patient with congenital hemolytic anemia attributable to glucose phosphate isomerase deficiency was treated successfully with maintenance hemodialysis and renal transplantation. Increased transfusion requirements, intolerance to immunosuppressive agents, and frequent infections were not encountered. Induction of the deficient erythrocyte enzyme by renal transplantation was not expected or realized.

Adult↗
PubMed1979

Volume expansion-induced alterations in proximal tubule chloride gradient in the rat.

To elucidate the mechanisms by which acute volume expansion (AVE) induces a decrease in proximal tubule transepithelial chloride gradient, male Sprague-Dawley rats were studied before and after AVE with Ringer lactate. In group 1, after AVE equivalent to 10% body wt, there were decreases in both tubule fluid to plasma inulin ratio ((TF/P)In) (from 2.28 +/- 0.10 to 1.57 +/- 0.05) and tubule fluid to ultrafiltrate chloride ratio ((TF/UF)Cl) (from 1.25 +/- 0.02 to 1.18 +/- 0.02). Group 2 was studied during carbonic anhydrase inhibition (CAI) produced by benzolamide before and during superimposed AVE (20% body wr). Both (TF/P)In (from 1.91 +/- 0.10 to 1.41 +/- 0.08) and (TF/UF)Cl (from 1.07 +/- 0.02 to 1.01 +/- 0.01) decreased. Group 3 was studied during maintained AVE (15% body wt) as a control for group 4, in which CAI was superimposed on maintained AVE. In group 3, (TF/P)In and (TF/UF)Cl did not change, but in group 4 CAI was associated with a decrease in (TF/P)In (from 1.55 +/- 0.05 to 1.21 +/- 0.05) and in (TF/UF)Cl (from 1.16 +/- 0.01 to 1.04 +/- 0.07). These data suggest that in the superficial proximal convoluted tubule of the rat, AVE-induced alterations in transepithelial chloride gradient are dependent on a mechanism(s) other than changes in carbonic anhydrase-mediated bicarbonate reabsorption.

Animals↗
PubMed1979

Stimulation of renin by acute selective chloride depletion in the rat.

To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 M NaHCO3 or 0.15 M NaNO3. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRA1) and 105 minutes after (PRA2) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [131I]albumin. In experiment 1, rats were prepared on a normal diet. PRA2 (7.0 +/- 1.0 ng/ml per hr, mean +/- SEM) was increased (P less than 0.05) over PRA1 (4.7 +/- 0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRA1 = 5.3 +/- 0.7, PRA2 = 6.1 +/- 0.7, P = NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 weeks on a low salt diet. PRA2 (47 +/- 5 ng/ml per hr) was increased as compared to PRA1 (24 +/- 2 ng/ml per hr, P less than 0.005) in the Cl-depleted group but not in the control group (PRA1 = 24 +/- 3, PRA2 = 27 +/- 6 ng/ml per hr, P = NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2a we infused chloride-depleted rats with three times as much albumin as controls and with KHCO3, 100 mEq/liter. Despite volume expansion and potassium loading, PRA2 (41 +/- 6 ng/ml per hr) was significantly elevated as compared to PRA1 (25 +/- 4 ng/ml per hr, P less than 0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-stimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO3; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRA2 levels again were higher (36 +/- 6 ng/ml per hr, P less than 0.05) as compared to PRA1 (23 +/- 4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cl-depleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release.

Alkalosis↗
PubMed1978

Effects of potassium depletion on renal tubular chloride transport in the rat.

Potassium depletion (KD) causes renal chloride-wasting. To investigate the effects of KD on renal tubular reabsorption of chloride, balance, clearance, micropuncture, and microinjection studies were performed on potassium-depleted rats. KD was produced by omitting potassium from the diet and by administration of DOCA on days 2 and 3; rats were studied on days 9 to 12. Diets were chloride-free in both control and KD groups. In the KD group, balance experiments confirmed greater chloride depletion and continued chloride-wasting, and clearance studies showed an increased FECl. Muscle potassium was reduced by 27% as compared to control. Whole kidney and single nephron GFR were reduced in KD rats to 72 and 74% of control. Fractional (6 +/- 6% vs. 22 +/- 4%, P less than 0.05) and absolute chloride reabsorption in the proximal tubule was not different. Fractional reabsorption of delivered chloride was reduced in the loop of Henle (92 +/- 0.8% in KD vs. 95 +/- 0.7% in control, P less than 0.02). Transtubular chloride ratio (0.28 +/- 0.02 vs. 0.21 +/- 0.02, P less than 0.02) was increased at the early distal tubule. Fractional delivery of chloride (8 +/- 0.9 vs. 5 +/- 0.5%, P less than 0.02), and fluid (26 +/- 1 vs. 22 +/- 1%, P less than 0.05) were also increased in KD at the early distal tubule. Recovery of chloride 36 injected into late distal tubules was 88 +/- 1% on a normal chloride intake, 62 +/- 2% in chloride depletion, and 88 +/- 2% in potassium and chloride depletion. Thus, KD depresses chloride reabsorption in the proximal tubule and in the loop of Henle, and it decreases chloride 36 efflux from the collecting duct.

Animals↗