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Results for “kidney function”

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At least 595 records · Page 33Linked to original sources
PubMed1995

[Urinary diversion surgery of the ureter of a single functioning kidney].

During a 10 years period at the Department of Urology of the Surgical Clinic KBC "Bezanijska kosa" 32 patients were hospitalised with a single functional kidney, who were operated on and derivation operations of the ureter were performed. The reason for a derivating operation on the ureter was an infiltrative cancer of the urinary bladder in 24 patients. In 6 patients there was a recurrent vesico-vaginal fistula and in two multiple purulent ureterocutaneous fistulas. Derivant operations on the level of the ureter with a bowel loop of the ileum was performed in 24 patients, by ileocoecal conduit in 6; a ureterosigmoidostomy was performed in two patients. The complications of these surgical interventions and the remaining life span of these patients after the operation are presented.

Adolescent↗
PubMed1988

Kidney function in response to salt feeding in rainbow trout (Salmo gairdneri Richardson).

1. The effect of high levels of dietary salt up to 12% NaCl on kidney function in freshwater rainbow trout was investigated. 2. Renal response to dietary NaCl load includes increases in urinary flow rate and glomerular filtration rate, together with a slight reduction in ionic reabsorption capacity. 3. The renal salt excretion rate, which was doubled to about 100 microM/kg/hr, in fish fed the high salt diet, is not entirely a consequence of a reduction in tubular ionic reabsorption but also of increased glomerular filtration. 4. The role of the endocrine system in control of renal salt excretion is discussed.

Animals↗
PubMed1998

Interactions of cyclosporin A and amlodipine: blood cyclosporin A levels, hypertension and kidney function.

The introduction of cyclosporin A has led to improved survival of allografts in humans. However, the use of cyclosporin A is associated with an increased prevalence of hypertension in kidney transplant recipients. Renal vasoconstriction and enhancement of tubular reabsorption contribute to this hypertensive effect. Concomitant treatment with calcium channel blockers blocks or ameliorates most of these adverse effects. This paper reviews the short-term effects of the calcium channel blocker amlodipine on plasma levels of cyclosporin A and its interaction with blood pressure and kidney function.

Amlodipine↗
PubMed2005

Kidney function in mice lacking aldosterone.

To explore the effects of decreased amounts or absence of aldosterone, we have disrupted the gene coding for aldosterone synthase (AS) in mice and investigated blood pressure and kidney function in AS+/+, AS+/-, and AS-/- mice. AS+/- mice have normal blood pressures and show no abnormalities in electrolytes or kidney gene expression, but they have significantly higher than normal urine volume and lower urine osmolality. In contrast, the AS-/- mice have low blood pressure, abnormal electrolyte homeostasis (increased plasma concentrations of K+, Ca2+, and Mg2+ and decreased concentrations of HCO3(-) and Cl- but no difference in the plasma Na+ level), and disturbances in water metabolism (higher urine output, decreased urine osmolality, and impaired urine concentrating and diluting ability). Absence of aldosterone in the AS-/- mice induced several compensatory changes: an increased food intake-to-body weight ratio, an elevated plasma concentration of glucocorticoids, and strong activation of the renin-angiotensin system. Parallel with the markedly increased synthesis and release of renin, the AS-/- mice showed increased expression of cyclooxygenase-2 (COX-2) in macula densa. On salt supplementation, plasma electrolyte concentrations and kidney renin and COX-2 levels became similar to those of wild-type mice, but the lower blood pressure of the AS-/- mice was not corrected. Thus absence of aldosterone in AS-/- mice results in impairment of Na+ reabsorption in the distal nephron, decreased blood pressure, and strong renin-angiotensin system activation. Our data show the substantial correction of these abnormalities, except the low blood pressure, by high dietary salt does not depend on aldosterone.

Acid-Base Equilibrium↗
PubMed1993

Calcium citrate without aluminum antacids does not cause aluminum retention in patients with functioning kidneys.

It has been suggested that calcium citrate might enhance aluminum absorption from food, posing a threat of aluminum toxicity even in patients with normal renal function. We therefore measured serum and urinary aluminum before and following calcium citrate therapy in patients with moderate renal failure and in normal subjects maintained on constant metabolic diets with known aluminum content (967-1034 mumol/day, or 26.1-27.9 mg/day, in patients and either 834 or 1579 mumol/day, or 22.5 and 42.6 mg/day, in normal subjects). Seven patients with moderate renal failure (endogenous creatinine clearance of 43 ml/min) took 50 mmol (2 g) calcium/day as effervescent calcium citrate with meals for 17 days. Eight normal women received 25 mmol (1 g) calcium/day as tricalcium dicitrate tablets with meals for 7 days. In patients with moderate renal failure, serum and urinary aluminum were normal before treatment at 489 +/- 293 SD nmol/l (13.2 +/- 7.9 micrograms/l) and 767 +/- 497 nmol/day (20.7 +/- 13.4 micrograms/day), respectively. They remained within normal limits and did not change significantly during calcium citrate treatment (400 +/- 148 nmol/l and 600 +/- 441 nmol/day, respectively). Similarly, no significant change in serum and urinary aluminum was detected in normal women during calcium citrate administration (271 +/- 59 vs 293 +/- 85 nmol/l and 515 +/- 138 vs 615 +/- 170 nmol/day, respectively). In addition, skeletal bone aluminum content did not change significantly in 14 osteoporotic patients (endogenous creatinine clearance of 68.5 ml/min) treated for 24 months with calcium citrate, 10 mmol calcium twice/day separately from meals (29.3 +/- 13.9 ng/mg ash bone to 27.9 +/0- 10.4, P = 0.727). In them, histomorphometric examination did not show any evidence of mineralization defect. Thus, calcium citrate given alone without aluminum-containing drugs does not pose a risk of aluminum toxicity in subjects with normal or functioning kidneys, when it is administered on an empty stomach at a recommended dose of 20 mmol calcium/day.

Absorption↗
PubMed2000

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function.

Disruption of the atrial natriuretic peptide (ANP) receptor [guanylyl cyclase-A (GC-A)] gene yields mice with a salt-resistant form of hypertension, raising fundamental questions on the role of ANP in acute regulation of the kidney. Here, we show that water intake, food consumption, stool weight, urine volume, and sodium excretion are not significantly different between wild-type and GC-A null mice on standard rodent chow (0.7% NaCl) or a high-salt diet (8% NaCl). In conscious mice with an indwelling catheter, the infusion of a physiological saline solution containing 4% BSA resulted in a marked natriuresis/diuresis in wild-type mice but no response in GC-A null animals. When physiological saline was given by gavage, however, the kidney response of wild-type and null mice was equivalent, raising the possibility that the gastrointestinal tract can directly regulate kidney function. However, administration of 0.9% saline through an intraperitoneal route also resulted in equal kidney responses in wild-type and null mice. When 0.9% NaCl lacking protein was infused i.v., wild-type and null mice both responded at the kidney level. Thus, GC-A appears dispensable for regulation of sodium/water excretion in response to changes in dietary sodium concentration, but likely becomes critical in volume expansions where the isooncotic pressure remains constant, such as head-out immersion or the initial and correctable stages of congestive heart failure.

Animals↗
PubMed2004

Effects of COX inhibition on blood pressure and kidney function in ACE inhibitor-treated blacks and hispanics.

Cyclo-oxygenase (COX) inhibitors attenuate the antihypertensive effects of angiotensin-converting enzyme (ACE) inhibitors and reduce kidney function. The study tests the hypothesis that these two classes of drugs have similar effects on glomerular filtration rate (GFR) and 24-hour blood pressure. The primary endpoint was change in 24-hour systolic blood pressure. Using a randomized crossover design, 25 black and Hispanic hypertensive participants (mean age 58+/-3 years) with osteoarthritis were studied. All participants received an ACE inhibitor at baseline. Once systolic blood pressure was <140 mm Hg, either celecoxib 200 mg/d or diclofenac 75 mg twice daily for 4 weeks was started. After measurements were obtained, all participants underwent a 2-week washout period and crossed over to the other drug for 4 weeks. A significant difference in mean 24-hour systolic blood pressure was noted between groups at 4 weeks (+4.1+/-1.1 mm Hg diclofenac versus +0.6+/-0.6 mm Hg celecoxib; P=0.01). However, because celecoxib has duration of action shorter than 24 hours, we compared ambulatory values at celecoxib trough and peak activities. At peak, no difference in systolic blood pressure was noted between agents (+3.6+/-0.04 mm Hg diclofenac versus +4.2+/-1.9 mm Hg celecoxib; P=0.67). GFR was also differentially affected at 24 hours (-9.9+/-2.4 mL/min diclofenac versus -0.4+/-1.2 mL/min celecoxib; P=0.01). We conclude that diclofenac and celecoxib increase systolic blood pressure at peak levels; however, these agents differ in their 24-hour effects. Differences observed in blood pressure response between COX inhibitors may not be related in their sensitivity but rather their dosing frequency.

Adult↗
PubMedDate not supplied

Myo-inositol clearance in renal failure and in patients with normal kidney function.

In order to determine the mechanism of elevated serum inositol in renal failure, the clearance values of inositol and of creatinine were measured in patients with normal kidney function and in those whose renal function was impaired due to varying causes. Mean serum inositol level in controls was 5.6 microgram/ml, and in patients with renal failure 28.6 microgram/ml. In control patients, inositol clearance was 2.8 ml/min, and tubular reabsorption of inositol was found to be over 97 percent. The inositol clearance of patients in renal failure varied from 0.62 to 17 ml/min. The ratio inositol clearance/creatinine clearance was elevated in uremic patients. Total amounts of inositol excreted in the urine of uremic patients were consistently higher than those excreted by control patients. The elevated serum inositol levels seen in renal failure were therefore not primarily caused by inability of the diseased kidney to excrete inositol.

Creatinine↗