Effect of oral glucose tolerance test on urine sodium excretion in obese and non-obese pre-menopausal females

We have investigated the changes in urinary sodium excretion during an oral glucose tolerance test [OGTT] through the associated changes in plasma atrial naturetic peptide [ANP], endogenous insulin and renal kallikrein excretion, in 10 normatensive obese and 10 healthy non-obese pre-menopausal females. Baseline blood glucose did not differ between obese and non-obese females. Blood glucose levels during the OGTT were significantly higher in obese than in non -obese females [P<0.01]. Obese females had significantly higher values of serum insulin at baseline and 2 hours after oral glucose load in comparison to non-obese females [P<0.01, <0.0001 respectively]. A similar finding was also obtained regarding fasting insulin resistance index [FIRI][P<0.0001] Prior to OGTT, urine sodium and kallikrein excretion did not differ between obese and non-obese subjects. After oral glucose load there were significant reduction of urine sodium [P<0.0001] and kallikrein excretion [P<0.0001] only in non-obese females. Obese females had insignificant decrease in urine sodium excretion and insignificant increase in urine kallikrein excretion. The decrease in urine sodium excretion was similar in obese and non-obese females. The plasma ANP level was significantly higher both in obese [P<0.0001] and non-obese [P<0.0001] females after glucose load. However, the percent increase was less in obese than in non-obese females [P<0.05]. In conclusion, changes in endogenous insulin induced by oral glucose were associated with a similar decrease in urine sodium excretion in obese and non-obese normatensive pre-menopausal females but the decrease was only significant in non-obese females. Insignificant reduction in urine sodium excretion in obese females could be due to the counteracting natriuretic effects of renal kallikrein and ANP

Apoptosis and endotoxins-induced secretion of interleukin-1B and tumor necrosis factor O by mononuclear cells in patients with acute versus chronic renal failure

Previous reports suggested a protective effect of chronic renal failure [CRF] against sepsis and endotoxin-induced organ failure and mortality in ARF. The present study was undertaken to investigate apoptosis and endotoxin-induced total production and secretion of interleukin-IB [IL-1B] and secretion of tumor necrosis factor a [TNF alpha] by mononuclear cells in patients with acute versus chronic renal failure. Lipopolysaccharide [LPS] induced IL-1B total production and secretion and TNF alpha secretion by peripheral blood mononuclear cells [PBMC] cultured for 18 hours were determined in patients with advanced CRF but not yet on dialysis [n=13], ARF patients [n=10] and healthy controls [n=10]. In vitro spontaneous apoptosis of cultured PBMC [for 18 hours] was also determined in these subjects. Suppressed secretion of IL-1B [629 +/- 490 pg/ml] by LPS stimulated PBMS was found in patients with CRF compared to patients with ARF [1989 +/- 1209 pg/ml, P<0.05] and healthy controls [1543 +/- 107.3 pg/ml, P<0.05]. A decrease in the total [1346 +/- 998.6 pg/ml] and cell associated [717 +/- 534 pg/ml] LPS induced IL-IB production was also found in them compared to those with ARF [39005 +/- 2516 pg/ml, P<0.05 and 1917 +/- 1308 pg/ml, P<0.05 for total and cell associated levels respectively]. Total production and secretion [absolute value] of LPS induced IL-1B were similar in patients with ARF and healthy controls but with increased cell associated IL-1B production in patients with ARF [P<0.05] LPS-induced TNF alpha secretion by PBMC did not differ significantly in the three groups. Accelerated spontaneous apoptosis of PBMC was found in patients with CRF [30.6 +/- 6.2%] compared to healthy controls [15.8 +/- 9.9%, P<0.05] and to patients with ARF [16.4 +/- 4.7%, P<0.05]. Negative correlation was found between% apoptosis of PBMC and secretion of both LPS induced IL-1B [P<0.01] and TNF alpha [P<0.01] by PBMC in patients with CRF. The reduced capability of PBMC from patients with CRF to secrete adequate amounts of IL-1B in response to LPS together with the accelerated spontaneous apoptosis may be protective mechanisms that decrease the deleterious effect of tissue necrosis and may partly explain the reported fair prognosis of ARF and sepsis in cases with prior CRF

Chromosome aberrations in chronic renal failure

A high frequency of cancer appears among uremic patients. Meanwhile, occupational and environmental pollutants may have a role in the development of chronic renal failure [CRF] and some of these pollutants have a potential genotoxic and carcinogenic effects. The present study was undertaken to investigate the rate of chromosomal aberrations [CA] in patients with advanced CRF of known and unknown etiology. Chromosomes were analyzed in Peripheral blood lymphocytes of two groups of patients with CRF. Group I [n = 10] with known and group II [n = 10] with unknown etiology of CRF and the results were compared to those of 10 healthy controls [group III] of matched age, sex and region of residence [urban or countryside] to those in group I, II. Increased rate of CA of peripheral blood lymphocytes predominantly of chromatid break was noticed in patients with unknown etiology of CRF in comparison to the controls and to patients with known cause of CRF. Similar findings were obtained among farmers in group I, II in comparison to the controls and to other subjects with CRF. Increased rate of chromosomal damage occurs among patients with unknown etiology of CRF and also among farmers with CRF which may suggest a role of environmental exposure to genotoxic agent which may be nephrotoxic. The impact of these findings on the increased cancer incidence among uremic patients deserve further follow up studies

Bacteriuria in elderly women

Thirty-five ambulatory elderly women with a mean age of 64.6 +/- 4.2 years were examined for pyuria and bacteriuria and were questioned about urinary symptoms [dysuria, incontinence, frequency, urgency, suprapubic pain, flank pain and fever]. Attempts of localization of the site of urinary tract infection [UTI] were done for those with bacteriuria by detecting antibody coated bacteria in urinary specimens [using the direct immunofluorescent technique] and by estimating urinary N acetyl beta-D-glucosaminidase [NAG] urinary excretion [in units/g creatinine] as indicators of upper UTI. Bacteriuria was found in 22.8% of the elderly women in the present study of whom 62.5% were asymptomatic. No association was found between symptoms [dysuria, loin pain, incontinence] and bacteriuria. Absence of pyuria was a good predictor of absence of bacteriuria. Upper urinary tract infection represented 50% of cases with bacteriuria and all cases with upper UTI were asymptomatic. NAG urinary excretion is too sensitive to renal damage to be used to localize the site of UTI

Histological and enzymatic study of small intestine in patients with short stature of unknown etiology

Eleven patients with short stature [below the 3rd percentile in height] of undetermined cause and no gastrointestinal symptoms [group I: GI] and six subjects with short stature and growth hormone deficiency [group II: GII] underwent jejunal biopsy and estimation of intestinal disaccharidase activities [sucrase, maltase and lactase] for exclusion of intestinal damage as a cause of short stature. Jejunal biopsy was performed also in ten healthy age and sex matched controls. The controls were between the 30th and 70th percentile in height. Decreased intestinal lactase activity +/- diminished intestinal sucrase and maltase activities were found in 64 percent of cases in GI and in 33 percent of cases in GII. The altered enzyme activities were accompanied with mild, moderate or severe morphological lesions of the intestinal mucosa in 55 percent of the cases in GI and with mild lesion in the 33 percent of the cases in GII. We can conclude that short stature by itself in the complete absence of gastrointestinal tract symptoms and even in the presence of growth hormone deficiency is an indication for jejunal biopsy to exclude intestinal malabsorption as the primary etiology

Triglyceride clearance in chronic renal failure

The clearance of exogenous triglycerides from the blood was studied after intravenous infection of intralipid in three groups of subjects. The first group included seven healthy controls, the second group comprised ten patients with chronic renal failure [CRF] on conservative medical treatment [CMR] and the third group consisted of six patients with end stage renal disease [ESRD] on maintenance hemodialysis [MH]. All controls and patients had normal fasting serum triglyceride level except one patient with CRF on CMR who had hypertriglyceridemia with an incidence of 6.3%. This was planned to eliminate the effect of hypertriglyceridemia perse on the fractional turnover rate of intralipid [K2]. The present study has shown that CRF patients with normal fasting serum triglyceride [TG] level and on CMR have impaired TG clearance that correlated negatively with their fasting serum TG levels, while those on MH have a normal TG clearance. results were discussed and compared with previous studies done on the same topic