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PubMed1984

Effect of C10-C11 isoparaffinic solvent on kidney function in Fischer 344 rats during eight weeks of inhalation.

Two groups of 50 male and 50 female Fischer 344 rats were exposed by inhalation to either 5.48 g/m3 (900 ppm) or 1.83 g/m3 (300 ppm) of C10-C11 isoparaffin (IP) 6 hr/day, 5 days/week for 8 weeks to evaluate renal function and histologic effects. Another group of rats (50/sex) was air exposed and served as controls. Urine and blood were collected from 10 male and 10 female rats of each group after 1, 4, and 8 weeks, and following a 4-week period of recovery. The ability of males to concentrate urine was reduced at 4 and 8 weeks of exposure to either level of IP. Following the 4-week recovery period, the urine concentrating ability of the exposed groups showed evidence of recovery. Following 4 and 8 weeks of exposure, glucose, protein, and epithelial cell excretion in urine of males was higher in the exposed groups than in that of controls. Creatinine clearance decreased after 8 weeks in the male high exposure group. After 4 weeks of recovery, urine glucose, protein, epithelial cell exfoliation, and creatinine clearance returned to control levels in exposed male rats. Overall, the effect on kidney function in male rats was mild, with evidence of near complete recovery. Histologic changes in exposed male rats compared to controls included an increased incidence of regenerative tubular epithelia and tubules dilated at the corticomedullary junction with proteinaceous debris in the tubules. No functional or histologic changes were observed in exposed female rats.

Animals↗
PubMed1985

Mifentidine: evaluation of antiandrogen effects and kidney function studies.

Among a number of investigations aimed at evaluating the safety profile of a new antihistamine (H2), N1-[(4-imidazolyl)-phenyl]-N2-isopropyl-formamidine (mifentidine), its effects on male accessory sexual organs and on kidney function were studied in greater detail because of the known propensity of H2-antagonists to cause antiandrogenic activity and to alter renal function. Mifentidine (190 and 380 mg/kg p.o.) was compared to cimetidine (475 and 950 mg/kg p.o.) for its ability to affect growth of seminal vesicles and prostate of immature castrated rats treated either with testosterone (TP) or 5-alpha-dihydrotestosterone (DHT). Lower doses of mifentidine were investigated because, in terms of H2-antagonistic activity, it was shown to be several times (15 to 30) as potent as cimetidine. Cimetidine at the highest dose (950 mg/kg) reduced prostate growth sustained by TP, and the DHT-promoted growth of seminal vesicles and prostate. Mifentidine had no effect on hormone promoted growth of male accessory sexual organs. Renal function studies after repeated (7 days) administration of mifentidine (150 and 600 mg/kg p.o.) and cimetidine (1500 mg/kg p.o.) revealed a significant increase of the excreted fraction of filtered sodium (FeNa) and potassium (FeK) only after cimetidine, indicating altered tubular reabsorption. Creatinine and urea clearances were unchanged by either drug treatment. Thus mifentidine appears to be devoid of antiandrogenic activity and renal effects.

Androgen Antagonists↗
PubMed1994

Occupational exposure to lead, kidney function tests, and blood pressure.

In the present study we examined sensitive biochemical markers of kidney function and damage in 166 workers exposed to lead and in 60 control workers. The objective was to investigate the chronic renal toxicity of lead and its possible correlation with arterial pressure. Diastolic arterial pressure was higher in the exposed group (p < 0.05), but the two groups did not differ in systolic pressure. Median activity of urinary N-acetyl-beta-D-glucosaminidase was higher in the exposed group (p < 0.001), and correlated with blood lead levels (p < 0.001) and duration of exposure (p < 0.001), but not with arterial pressure. The other indicators studied, gamma-glutamyl-transpeptidase and alanine-aminopeptidase activity, urine albumin, and total urine protein, were not higher than in the control group and were not correlated with blood lead, duration of exposure, or arterial pressure.

Adolescent↗
PubMed1990

Hydrocarbon exposure, hypertension and kidney function tests.

Control and hydrocarbon exposed workers participated in a cross-sectional study about the nephrotoxicity of chronic hydrocarbon exposure. Different markers of glomerular and tubular function as well as the celluria were examined and compared. The results show that the interaction between hypertension and hydrocarbon exposure has an influence on the kidney function. For the clearance the interaction age-exposure seems to play a more important role than age or exposure alone. The most useful markers appear to be the albuminuria, the N-acetyl-beta-D-glucosaminidase activity, the retinol-binding-protein concentration and the creatinine clearance.

Adult↗
PubMed1986

Effect of captopril on kidney function in insulin-dependent diabetic patients with nephropathy.

The influence of angiotensin II on kidney function in diabetic nephropathy was assessed by studying the effect of 12 weeks' monotherapy with captopril (25-50 mg twice a day) in 16 hypertensive insulin dependent diabetic patients with persistent albuminuria. In an initial one week randomised single blind trial of captopril versus placebo, captopril (for nine patients) reduced arterial blood pressure from 148/94 (SD11/6) to 135/88 (8/7) mm Hg (p less than 0.05) and albuminuria from 1549 (range 352-2238) to 1170 (297-2198) micrograms/min (p less than 0.05), while glomerular filtration rate remained stable. No significant changes occurred in seven patients treated with placebo. During the 12 weeks of captopril treatment arterial blood pressure in all patients fell from 147/94 (11/6) to 135/86 (13/7) mm Hg (p less than 0.01), albuminuria fell from 1589 (range 168-2588) to 1075 (35-2647) micrograms/min (p less than 0.01), and glomerular filtration rate fell from 99 (SD19) to 93 (25) ml/min/1.73 m2 (p less than 0.01). The renin-angiotensin system showed suppressed plasma concentrations of angiotensin II and increased concentrations of angiotensin I and renin. The study showed that glomerular filtration rate is not dependent on angiotensin II, that captopril reduces albuminuria, probably by lowering glomerular hypertension, and that captopril represents a valuable new drug for treating hypertension in diabetics dependent on insulin with nephropathy.

Adult↗
PubMed2002

Kidney function and glomerulopathy over 8 years in young patients with Type I (insulin-dependent) diabetes mellitus and microalbuminuria.

AIMS/HYPOTHESIS: We aimed to investigate prospectively the interrelation between kidney function and glomerular morphological changes over 8 years in young patients with Type I (insulin-dependent) diabetes mellitus and microalbuminuria. METHODS: Kidney biopsies were taken at baseline and after 8 years in 18 subjects who were 20 years of age (19-29 mean and range), had duration of diabetes for 11 years (7-18), and who had an albumin excretion rate of 45 microg/min (15-194). The glomerular ultrastructural parameters were analysed using stereological methods. RESULTS: At the end of the study three patients had an increased albumin excretion rate of more than 25 % a year, two of whom developed overt nephropathy. Glomerular filtration rate declined 2.3 ml/min x 1.73 m(-2) x yr(-1). Glomerular volume, volume fractions of matrix and mesangium, and basement membrane thickness showed an increase over the 8 years. Multiple regression analysis showed that mean 8-years HbA(1 c), matrix volume fraction(baseline) and basement membrane thickness BMT(baseline) accounted for 70 % of the variation in AER at the end of the study. Mesangial volume fraction(baseline,) glomerular filtration fraction(baseline,) and mean 8-year HbA(1 c) accounted for 73 % of the change in glomerular filtration rate from baseline. Smoking was strongly associated with the glomerular filtration rate at baseline ( r = 0.65). When glomerular filtration rate(baseline) was omitted from the equation, smoking was the only significant parameter linked to the change in glomerular filtration rate from the baseline. CONCLUSION/INTERPRETATION: In patients who had diabetes for 20 years, long-term hyperglycaemia and glomerulopathy found 8 years prior to the study, and possibly smoking, affected renal function (i. e. albumin excretion rate and glomerular filtration rate).

Adult↗
PubMedDate not supplied

[Effect of nerobol on the water-electrolyte balance and kidney function in man during 120-day hypokinesia].

The influence of anabolic steroids on the fluid-electrolyte metabolism and renal function of man was studied during a prolonged bed rest experiment. Seven test subjects were kept under surveillance. Three test subjects were given nerobol and four subjects served as controls. The fluid-electrolyte metabolism and the osmoregulatory function of the kidneys were studied. Nerobol induced a decreased excretion of sodium, potassium, calcium, chlorides and osmotically active substances. Nerobol produced the most pronounced effect on the calcium and potassium metabolism. The effect of the drug used during the prolonged bed rest experiment depended on the time and dosage as well as on the state of fluid-eletrolyte metabolism and the renal function.

Adult↗
PubMed2001

Why is erythropoietin made in the kidney? The kidney functions as a critmeter.

Erythropoietin is distinct among the hematopoietic growth factors because it is produced primarily in the kidneys rather than the bone marrow. The kidney functions as a critmeter in that it senses oxygen tension and extracellular volume. By regulating red cell mass through erythropoietin and plasma volume through excretion of salt and water, the kidney sets the hematocrit at a normal value of 45%. This is not a random number, but a value that maximizes oxygen delivery to peripheral tissues. The ability of the kidney to coordinate these two volumes to generate a hematocrit of 45% establishes it as the logical site for erythropoietin production. The kidney has the unique ability to translate a measure of plasma volume as tissue oxygen pressure required to regulate erythropoietin production. I hypothesize that the critmeter is a functional unit that regulates the hematocrit. The critmeter is found at the tip of the juxtamedullary region of the cortical labyrinth in the kidney, where erythropoietin is made physiologically. Renal vasculature and nephron segment heterogeneity in sodium reabsorption generate the marginal tissue oxygen pressure required to trigger the production of erythropoietin. The balance of the oxygen consumption for sodium reabsorption and the oxygen delivery to the proximal tubule is reflected by the tissue oxygen pressure that determines red blood cell mass adjusted to plasma volume. Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter (eg, angiotensin II). Examples of clinical disorders caused by dysfunction or resetting of the critmeter are described.

Anemia↗
PubMed1995

Effect of pre-treatment with desferrioxamine and mannitol on radical production and kidney function after ischaemia-reperfusion. A study on rabbit kidneys.

The effects of pre-treatment with mannitol and the iron chelator desferrioxamine on oxygen radical formation and glomerular and tubular function after ischaemia in the rabbit kidney were studied. Radicals were measured with ESR and spin trapping. At reperfusion after 60 min of renal ischaemia there was a significant increase in the production of free radicals in the venous effluent from the kidney. Administration of either mannitol or desferrioxamine given before ischaemia and before recirculation reduced the radical production significantly. The iron chelator appeared to be more effective. Glomerular function measured 48 h after reperfusion was significantly better after pretreatment with desferrioxamine and mannitol compared with mannitol alone. Tubular function did not differ between the two pre-treatment groups.

Animals↗
PubMed2000

Do regular high protein diets have potential health risks on kidney function in athletes?

Excess protein and amino acid intake have been recognized as hazardous potential implications for kidney function, leading to progressive impairment of this organ. It has been suggested in the literature, without clear evidence, that high protein intake by athletes has no harmful consequences on renal function. This study investigated body-builders (BB) and other well-trained athletes (OA) with high and medium protein intake, respectively, in order to shed light on this issue. The athletes underwent a 7-day nutrition record analysis as well as blood sample and urine collection to determine the potential renal consequences of a high protein intake. The data revealed that despite higher plasma concentration of uric acid and calcium, Group BB had renal clearances of creatinine, urea, and albumin that were within the normal range. The nitrogen balance for both groups became positive when daily protein intake exceeded 1.26 g.kg but there were no correlations between protein intake and creatinine clearance, albumin excretion rate, and calcium excretion rate. To conclude, it appears that protein intake under 2. 8 g.kg does not impair renal function in well-trained athletes as indicated by the measures of renal function used in this study

Adult↗
PubMed1988

Iloprost preserves kidney function against anoxia.

Tissue protective activity of iloprost against anoxia was studied in the isolated perfused rabbit kidney. Addition of iloprost to the perfusion medium at concentrations between 10(-9)-10(-7) M attenuated the release of noradrenaline due to periarterial stimulation and decreased urine outflow. Iloprost also caused a concentration-dependent decrease in perfusion pressure. The potentiation by angiotensin II of the vasoconstriction due to periarterial stimulation and increase in urine volume were also decreased by further addition of iloprost into the medium. Iloprost at concentrations below 10(-7) M did not alter the vasoconstrictor effect of exogenously applied noradrenaline. UK 38 485, a powerful thromboxane A2 synthetase inhibitor, significantly suppressed the vascular but greatly potentiated the diuretic effects of angiotensin II. In kidneys exposed to anoxia for 24 hours in Krebs medium, the vascular and diuretic effects of angiotensin II and the release of noradrenaline due to periarterial stimulation were significantly diminished. In addition, interation between UK 38 485 and angiotensin II in both perfusion pressure and urine volume was also reduced after anoxia for 24 hours. On the other hand, no significant loss was observed in all investigated parameters measured in this study, in kidneys exposed to anoxia for 48 hours in the presence of iloprost. From these results it was concluded that iloprost preserves kidneys functionally against anoxia and possible mechanisms of this effect are discussed.

Animals↗