Glucose interferes with inulin determination by the resorcinol method: overestimation of glomerular filtration rate in diabetic patients.
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Biomedical subjects
Publications and source records attributed to G Boner.
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We studied urinary acidification daily during the hospital course of 16 infants with acute gastroenteritis and metabolic acidosis. Urine pH value on admission was higher than 5.5 in 14 (87%) patients. We hypothesized that inappropriate urinary acidification was due to sodium deficiency and inadequate sodium delivery to the distal nephron. Forty-one urinary samples were collected during metabolic acidosis. The mean pH of 24 urine samples with sodium concentration less than 10 mmol/L was significantly higher than the pH of 17 samples with sodium concentration greater than 10 mmol/L (6.04 +/- 0.06 vs 5.19 +/- 0.1; p less than 0.001). The urine ratios of titratable acid to creatinine and of total acidity to creatinine were significantly higher in urine samples containing more sodium (p less than 0.02), whereas the ammonium/creatinine ratio was not. After administration of furosemide or correction of the sodium deficit, appropriate acidification was observed. We conclude that impaired urinary acidification is frequently found during metabolic acidosis in infants with acute gastroenteritis and results from a sodium deficit rather than from transient distal renal tubular acidosis.
Psychosocial adjustment and psychological distress was compared in 31 male nondiabetic successful renal transplant and 31 hospital hemodialysis patients, matched for duration of treatment, age, education, and family status. The only significant difference between the two groups was that the transplant patients were more satisfied with the medical staff. Vocational rehabilitation was similar in both groups. Sexual interrelationships, as reported by the patients, were slightly, but insignificantly, better in the transplanted group. Thus, the psychological adjustment of transplant and hemodialysis patients is similar when demographic differences are accounted for.
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In the present study reference values for the albumin excretion rate (AER) and the albumin/creatinine ratio (A/C) in overnight 8-h urine collections (n = 73, group 1) and in 24-h urine collections (n = 25, group 2) were obtained from healthy, nondiabetic, normotensive volunteers. Furthermore, we examined the relationship of these values to age, sex and ethnic group. Albumin was determined by RIA. The mean (+/- SD) values obtained for AER and A/C in overnight urine collections were 6.5 +/- 3.8 mg/24 h and 6.7 +/- 3.6 micrograms/mg creatinine, respectively. These values were significantly lower (P less than 0.001) than the values obtained in 24-h urine collections (AER 11.6 +/- 4.7 mg/24 h and A/C 10.9 +/- 5.0 micrograms/mg creatinine). No difference in AER was observed when the subjects were divided into 10-year age-groups. AER in males was similar to that in females, and AER in European subjects was not different from values obtained for subjects of Oriental (Middle Eastern or North African) origin. Freezing urine specimens resulted in a 25% decrease in AER values. We recommend using freshly obtained 8-h or 24-h urine collections, and considering the excretion of 14 mg/24 h (10 micrograms/min) or 21 mg/24 h (15 micrograms/min), respectively, as the upper limit of normoalbuminuria.
Specific binding of bacteria to phagocytic cells mediated by antibody and complement (opsonins) or by lectin-carbohydrate interactions is required for their efficient uptake and killing by opsonophagocytosis or lectinophagocytosis, respectively (Ofek and Sharon, Infect. Immun. 56, 539, 1988). An early step in these processes is activation of the phagocytes by the bound bacteria, as evidenced by appearance of an oxidative burst. Previous work has shown that protein kinase C (PKC) is involved in activation of human granulocytes by opsonized Escherichia coli. In the present study, we used three inhibitors of PKC to examine the possible involvement of the enzyme in activation of human granulocytes and peritoneal macrophages by type 1 fimbriated (mannose-specific) Escherichia coli in the absence of opsonins. Activation, as measured by chemiluminescence, was completely inhibited by sphingosine (50 microM) and only partially (50%) by 100 microM H-7 [1-(5-isoquinolinesulfonyl)-2-methylpiperazine]; in both cases it was fully reversible. The third inhibitor, K252a, also inhibited almost completely the activation at 1 microM. The inhibitors acted similarly on activation of the phagocytic cells by opsonized bacteria or by phorbol-12-myristate-13-acetate (0.1 microM). Down regulation of the kinase, by pretreatment of the human granulocytes or macrophages with a high concentration (1.6 microM) of phorbol myristate acetate, abolished their ability to respond to stimulation by the bacteria. Our findings provide evidence for the involvement of PKC in the activation of phagocytic cells by type 1 fimbriated bacteria.
Human peritoneal macrophages isolated from uremic patients undergoing peritoneal dialysis bind type 1 fimbriated Escherichia coli in the absence of opsonins. The number of bacteria bound per macrophage was 6.9, as determined by microscopic examination. Methyl alpha-mannoside (0.1 mM) and p-nitrophenyl alpha-mannoside (0.01 mM) inhibited this binding by about 66%. The ability of peritoneal macrophages to bind E. coli in a mannose-specific manner was confirmed in further experiments using an enzyme-linked immunosorbent assay (ELISA) with an antibacterial antibody, radiolabelled E. coli, and counts of colony-forming units (CFU). The number of bacteria bound per macrophage was 7 to 12 in the ELISA and 5.5-8.5 in the CFU assay. Methyl alpha-mannoside caused 70% inhibition of binding in the ELISA and 84% in the CFU assay, whereas p-nitrophenyl alpha-mannoside showed inhibition of 79% and 90%, respectively. Most bound bacteria (76-80%) were subsequently killed. Nonfimbriated E. coli 827 bound poorly to the macrophages (approximately 22%) as compared to that of the fimbriated bacteria. Although this binding was not inhibited by methyl alpha-D-mannoside or p-nitrophenyl alpha-mannoside, the percentage of bacteria killed was similar to that of the fimbriated phenotype. The peritoneal macrophage is thus able to phagocytose E. coli in the absence of opsonins. This may explain the relative rarity of E. coli as an etiologic agent of peritoneal infections in the dialysed patient.
Cyclosporin is poorly tolerated in patients with amyloidosis due to familial mediterranean fever who are receiving colchicine. There is a high incidence of gastrointestinal side-effects and muscle weakness, both of which are reversible on stopping cyclosporin. Thus in patients with amyloidosis secondary to familial mediterranean fever treated with colchicine, the use of cyclosporin as an immunosuppressive agent may be restricted.
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In the present study the possible role of endogenous prostaglandins in modulating the renal effects of angiotensin II was investigated in the isolated perfused rat kidney. Angiotensin II (5 ng/ml) caused both an increase in prostaglandin E2 synthesis and an increase in renal vascular resistance, as well as an increase in perfusate flow rate and glomerular filtration rate. Filtration fraction did not change. Inhibition of prostaglandin synthesis did not influence these effects of angiotensin II. In addition, angiotensin II caused natriuresis and to a lesser degree kaliuresis. These effects were independent of intrarenal hemodynamic effects. Inhibition of renal prostaglandin synthesis did not have any effect on the angiotensin-induced natriuresis. We conclude that the natriuretic effect of angiotensin II is independent of renal prostaglandin synthesis.
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Cimetidine inhibits the renal tubular secretion of creatinine and digoxin is partly excreted by the same pathway. In order to investigate a possible interaction between the two drugs, a randomized cross-over acute study has been conducted. Six patients with duodenal ulcers were given a single dose of digoxin (Dig) 0.75 mg i.v. with and without oral cimetidine 1200 mg/day. Cimetidine significantly reduced creatinine clearance from 157 to 132 ml/min. There was no significant difference in inulin clearance, 99.2 vs 97.5 ml/min, Dig elimination half life 53.9 vs 56.9 h, apparent volume of distribution 11.3 vs 11.6 l/kg, systemic clearance 2.42 vs 2.35 ml/min/kg, renal clearance 1.48 vs 1.62 ml/min/kg or urinary excretion of digoxin 49.5 vs 51.6% of dose without or with cimetidine. These results suggest that cimetidine does not influence the disposition of digoxin.
Forty-four consecutive patients referred for treatment because of hypertension (greater than 150/90 mmHg) occurring during pregnancy were randomly allocated to one of two treatment groups, hydralazine alone (n = 21) or hydralazine combined with pindolol (n = 23). Satisfactory blood pressure control (diastolic pressure less than 90 mmHg) was achieved in 86% of patients receiving hydralazine alone and 91% of those on combined therapy. Although the treatment did not lower the overall incidence of hypertensive complications it appeared to delay the onset of such complications until successful surgical intervention was possible. Fetal outcome was similar in both groups and there was no perinatal mortality in this high-risk population. Although blood pressure control was similar in both groups of patients, combined therapy with hydralazine and pindolol can be considered to be superior to hydralazine monotherapy, since in patients treated with the combination the incidence and intensity of troublesome side-effects was markedly lower.
Benign nephrosclerosis seldom is associated with significant proteinuria or reduced renal function. This study demonstrated that, despite the finding of benign nephrosclerosis on a renal biopsy specimen, concomitant proteinuria is predictive of a poor prognosis. Twelve patients, ranging in age from 24 to 59 years, with hypertension, proteinuria (greater than 1 g/d), and findings of benign nephrosclerosis on renal biopsy specimens were studied retrospectively. In three of these patients, the hypertension and proteinuria were diagnosed during pregnancy. Follow-up was possible in 11 patients. Nine patients became nephrotic in the course of their disease. Two patients had endstage renal disease and required maintenance dialysis treatment. Seven patients had decreased renal function as shown by the increase in serum creatinine levels. Thus, the combination of hypertension, proteinuria (greater than 1 g/d), and benign nephrosclerosis may be indicative of a progressive condition with a high percentage of patients having renal failure.
Minoxidil was given to 16 men with hypertension of various degrees of severity, in conjunction with a diuretic and atenolol. Mean supine and standing blood pressures (BP) on diuretic + atenolol were 172/106 and 162/104 mm Hg, respectively. Minoxidil was added and the dose titrated to lower the diastolic pressure to less than 90 mm Hg. All drugs were taken together once daily. At the end of a maintenance period of 6 months on an average dose of minoxidil of 12 mg (range 2.5 to 20.0 mg), supine BP was 147/87 and standing BP 139/88 mm Hg. Similar BP had been measured throughout the maintenance period, and monitoring of the BP showed that the once daily regimen provided good control for 24 h. A strong correlation was found between the dose of minoxidil necessary to normalize the BP and the mean arterial pressure prior to minoxidil (r = 0.73, P less than 0.005). Serious adverse effects of the drug were observed only in patients receiving doses greater than 10 mg or those with widespread atherosclerosis, or both. We conclude that, when added to a diuretic and a beta-blocker in a once-a-day regimen, minoxidil in a daily dose of less than or equal to 10 mg is effective and well tolerated in mild to moderate hypertension, especially in patients who are free of atherosclerotic complications.
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