SEARCH · Search PubMed

Results for “kidney function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

PubMed1992

Maillard reaction products and lysinoalanine: urinary excretion and the effects on kidney function of preterm infants fed heat-processed milk formula.

Heat processing is essential for the preservation of milk-based infant formulas. Heating, however, induces a number of chemical changes during which lysine in the milk proteins reacts with reducing sugars to form Maillard reaction products (MRPs) and also reacts with the dehydroalanine resulting from cystine degradation to form lysinoalanine (LAL). Both products have been reported to induce histological changes in the straight portion of the proximal tubule in the rat kidney. This pilot study was made to investigate the urinary excretion by healthy preterm babies of MRPs and LAL contained in infant formula and to determine their influence on kidney function. Twelve healthy male preterm babies were first fed for 10 days with pooled human milk and then for 5 days with each of two experimental premature infant formulas in a cross-over design. The infant formulas were sterilized either by ultra-high temperature (UHT) treatment or by a conventional retort process to give products with low and high levels of MRPs and LAL, respectively. In total, some 15.6% of the initial lysine had been modified in the in-can-sterilized product, compared to 6.2% in the UHT product. Urinary excretion of MRP lactulosyllysine ranged from 1.3 to 3.9% of the ingested amount, whereas that of LAL ranged from 6.2 to 9.3%. The higher level of MRPs and LAL in the formulas compared to breast milk had no influence on creatinine clearance or electrolyte excretion. There was no evidence of tubular damage as determined by the urinary excretion of four kidney-derived enzymes. Feeding of formula, however, did result in a general increase in urinary microprotein levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed2000

Fetal compensatory renal hypertrophy with a unilateral functioning kidney.

OBJECTIVE: To evaluate the possibility of fetal compensatory renal hypertrophy with a unilateral functioning kidney. METHODS: A nomogram of renal length was established from 254 normal fetuses. Renal length was also obtained in 14 fetuses with unilateral renal agenesis and 22 fetuses with a unilateral multicystic kidney. RESULTS: Compensatory renal hypertrophy, defined as a renal length > 95th percentile for gestational age, occurred in 16 of 36 cases (44.4%). CONCLUSIONS: Compensatory renal hypertrophy is detectable in utero and may occur as early as 22 weeks' gestation.

Adaptation, Physiological↗

PubMed1981

Kidney function and size in normal subjects before and during growth hormone administration for one week.

Kidney function and size were studied in seven normal male subjects before and after administration of highly purified human growth hormone for 1 week. Glomerular filtration rate, renal plasma flow (steady-state infusion technique with urinary collections using 125I-iothalamate and 131I-hippuran) kidney size (ultrasonic scanning) and urinary excretion rates of albumin and beta 2-microglobulin (radioimmunoassays) were measured. Highly purified growth hormone was injected subcutaneously, 2 IU in the morning and 4 IU in the evening. Glomerular filtration rate increased from (mean +/- SEM) 114 +/- 5 to 125 +/- 4 ml/min x 1.73 m2 (P less than 0.01) and renal plasma flow increased from 554 +/- 30 to 601 +/- 36 ml/min x 1.73 m2 (P less than 0.01). Kidney size and urinary excretion rates of albumin and beta 2-microglobulin did not change significantly. Our results show that raising plasma growth hormone into a range similar to that found in insulin-dependent diabetics enhances glomerular filtration rate and renal plasma flow, while kidney size remains unchanged. Increased renal plasma flow is the major determinant of growth hormone induced elevation in glomerular filtration rate. Growth hormone may thus contribute to the enhancement of glomerular filtration rate and renal plasma flow typically found in insulin-dependent diabetics.

Adult↗

PubMed1980

Effects of obstruction on single-kidney function: clinical and experimental results with 131I-hippurate and 99mTc-DMSA.

In 35 patients, renography with 131I-o-hippurate (OIH) and static renal imaging with 99mTc-dimercaptosuccinic acid (DMSA) were used to measure differential renal function (DRF). The results were compared. Depth correction was applied in both methods. In non-obstructed kidneys (19 patients), both methods revealed nearly identical kidney function (r = 0.98). For completely obstructed kidneys (16 patients), OIH gave a significantly better DRF (14 ml/min) than DMSA. This small difference was of no clinical value. Because DMSA is reported to give unreliable results in unilateral obstructed kidneys, the right ureter was ligated in 8 dogs for 10 days and DRF was measured before and after opening an ureteral fistula. The difference in DRF was about 1% and could be accounted for by the amount of urinary radioactivity collected from the pelvic system after the ligature had been opened. Although DMSA appears to give reliable values in determining DRF, even in obstructed kidneys, OIH is preferred since total clearance values and postrenal urinary dynamics can be determined simultaneously.

Animals↗

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↗

PubMed1959