[The significance of cryoscopy as a clinical kidney function test].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The aim of our study was to evaluate whether inhibition of ACE (lisinopril 10-20 mg/day) can reduce the rate of decline in kidney function more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg/day), usually in combination with a diuretic. We performed a prospective, randomized, parallel study for 42 months, double blind for the first 12 months and single blind thereafter. Forty-three (21 lisinopril and 22 atenolol) hypertensive NIDDM patients with diabetic nephropathy were enrolled. Data from 36 patients (17 lisinopril and 19 atenolol, 60 +/- 7 years of age, 27 men) who completed at least 12 months of the study period are presented. At baseline, the two groups were comparable: glomerular filtration rate (51Cr-EDTA plasma clearance) was 75 +/- 6 and 74 +/- 8 ml x min(-1) x 1.73 m(-2), mean 24-h ambulatory blood pressure (A&D TM2420) was 110 +/- 3 and 114 +/- 2 mmHg, and 24-h urinary albumin excretion rate was 961 (range 331-5,727) and 1,578 (476-5,806) mg/24 h in the lisinopril and atenolol groups, respectively. The mean follow-up time was similar, 37 and 35 months in the lisinopril and atenolol groups, respectively. Mean ambulatory blood pressure was equally reduced in the two groups, 12 +/- 2 and 10 +/- 2 mmHg in the lisinopril and atenolol groups, respectively. Glomerular filtration rate declined in a biphasic manner with a faster initial (0 to 6 months) change of 1.25 +/- 0.49 and 0.81 +/- 0.29 ml x min(-1) x month(-1) followed by a slower sustained decline (6 to 42 months) of 0.59 +/- 0.10 and 0.54 +/- 0.13 ml x min(-1) x month(-1) in the lisinopril and atenolol groups, respectively. No significant differences were observed in either initial or sustained decline in glomerular filtration rate between the two groups. Urinary albumin excretion was reduced (% reduction of baseline) more in the lisinopril than in the atenolol group, at 55 (95% CI 29-72) and 15% (-13 to 34), respectively (P = 0.01). In conclusion, the relentless decline in kidney function characteristically found in hypertensive NIDDM patients with diabetic nephropathy can be reduced equally effectively by two antihypertensive treatments, the beta-blocker atenolol and the ACE inhibitor lisinopril.
PURPOSE: To evaluate three methods for digoxin dose adjustment in aged patients. METHODS: We determined the plasma digoxin levels that would be attained in 87 old patients with doses adjusted to the kidney function by means of three separate procedures. RESULTS: Age: 79.0 "6.3 years of age; creatinin clearance (Clc): 0.70" 0.23 ml/Kg of lean body weight and minute. Only the methods that adjust both the digoxin clearance and the volume of distribution to the Clc achieve the independence between the digoxinemia and the kidney function. The best of them, by calculating the elimination constant (K) and the volume of distribution (V) as linear functions of the Clc, so that K ranges between 0.173 and 0.462 days-1 and V between 4 and 10 l/Kg of lean body weight when the Clc varies from 0 to 110 ml/minute, achieve digoxinemia figures between 0.8 y 2.0 ng/ml and above 2.0 ng/ml in the 81.6% and 0.0% of the patients (95% confidence intervals (95% CI): 72.2% to 88.4 and 0.0% to 4.6%), respectively; with a precision and a bias of 0.43 and -0.06 ng/ml (95% CI: 0.38 to 0.48 and -0.16 to 0.03 ng/ml), respectively. CONCLUSION: The described method would lead to good results if digoxin has not been prescribed in order to control the cardiac frequency in the setting of auricular fibrilation.
In 10 pigs with reno-scintigraphically proven normal upper urinary tracts, a standardized partial obstruction of the left ureter was created at the lower kidney pole level. Three weeks later kidney function was scintigraphically reassessed and the pressure flow relationship in the flow range 0-20 ml/min outlined. The partially obstructed pelvic baseline pressure varied from 9.0 to 32.0 cmH2O. During perfusion small increases in pelvic pressure were seen at all flow rates in the individual cases and there was a linear relationship between pressure and flow. Compared to previous results of a similar but acute obstruction the results were identical in pressure ranges and pressure flow profile. This demonstrates, that a longitudinal stability in transport mechanism qualities is present also during the course of obstruction. The pelvic pressure at low flow rates was significantly correlated to kidney function depression, whereas perfusion pressures at high flow rates did not show any correlation, except at 20 ml/min. This clearly indicates, that the pelvic pressure at normal urine flow rate is an important factor in the pathogenesis of obstructive nephropathy.
BACKGROUND: Acute infections, including diarrhea, are associated with an increased risk of vitamin A deficiency. Urinary retinol excretion during such infections may contribute to this risk. The mechanism accounting for urinary retinol loss has not been clearly defined. OBJECTIVE: This study attempted to determine whether urinary retinol loss in children with acute infection is associated with impaired kidney function, particularly impaired tubular protein reabsorption. DESIGN: Urinary retinol excretion and kidney function were examined in 66 hospitalized children 5 mo to 5 y of age with acute Shigella dysentery. RESULTS: Urinary retinol loss occurred in 59% of children and was substantial (>0.1 micromol/d) in 8% of them. Children with more severe disease excreted higher concentrations of urinary retinol; those with a body temperature > or =40 degrees C excreted a mean of 0.10 +/- 0.18 micromol/d compared with 0.005 +/- 0.008 micromol/d for other children (P < 0.0001). Children with more severe disease also had impaired tubular reabsorption of low-molecular-weight proteins beta2-microglobulin and retinol binding protein (RBP)], although other measures of tubular and glomerular function were not similarly impaired. In multiple regression analysis, severity of disease indicators were the best predictors of tubular reabsorption of beta2-microglobulin (R2 = 0.53) whereas tubular reabsorption of beta2-microglobulin and RBP were found to be the best predictors of urinary retinol loss (R2 = 0.69). CONCLUSIONS: A significant amount of retinol was excreted in the urine in children with shigellosis: 8% excreted >0.10 micromol/d (15% of the daily metabolic requirement). Impaired tubular reabsorption of low-molecular-weight proteins, such as RBP transporting retinol, appeared to be the cause of this urinary retinol loss.
BACKGROUND: The burden of chronic kidney disease (CKD) is high, but its natural history and the benefit of routine nephrology care is unclear. This study investigated the decline in kidney function prior to and following nephrology referral and its association with mortality. METHODS: This study provides a retrospective review of the individual rates of glomerular filtration rate (GFR) decline (millilitre per minute per 1.73 m(2)/year) for the 5 years before and after referral in 726 new referrals with stages 3-5 CKD to one renal unit between 1997 and 2003. Blood pressures are averages at referral, 1 and 3 years post referral. Logistic regression and Cox's models tested factors predicting post-referral GFR decline and the impact on mortality. RESULTS: Mean (SD) age was 72 (14), and 389 (54%) patients had stages 4-5 CKD. GFR decline slowed significantly from -5.4 ml/min/1.73 m(2)/year (-13. to -2) before to -0.35 ml/min/1.73 m(2)/year (-3 to +3) after referral (P < 0.001). Blood pressure also reduced significantly (155/84 to 149/80, P < 0.05) with most changes occurring within 1 year of referral. Factors predicting a non-progressive post-referral decline included a lower systolic blood pressure at referral and 1 year after referral, a CKD diagnosis other than diabetic nephropathy, less baseline proteinuria and a non-progressive pre-referral GFR decline. A non-progressive post-referral GFR decline was independently associated with significantly better survival (hazard ratio 0.55, 95% CI 0.40-0.75, P <or = 0.001) after adjustment for known risk factors. CONCLUSIONS: Following nephrology referral, GFR decline slowed significantly and was associated with better survival. Earlier detection of patients with progressive CKD and interventions to slow progression may have benefits on both kidney and patient survival.
Explore the source record for details and available documents.
In end stage congestive heart failure activation of a series of compensatory mechanisms increase renal vascular resistance and impair renal function. Prostaglandin E1 is increasingly used in the treatment of severe heart failure for its vasodilating actions. In various experimental settings prostaglandin E analogues are known to improve renal function by modulating renal filtration pressure and redistribution of renal blood flow. However, prostaglandin E1 decreases systemic blood pressure and thus, also renal perfusion pressure, a fact by which renal function might be further compromized in heart failure patients. The aim of the study was to evaluate the effects of prostaglandin E1 on excretory renal function in patients with end stage heart failure and to prove the hypothesis, that the well known local actions of prostaglandins on renal microcirculation might outweigh the negative impact of an expected decrease in perfusion pressure. 25 patients with terminal congestive heart failure were investigated. 13 patients received prostaglandin E1 at a dose of 13.5 +/- 1.9 ng/kg/min in combination with constant rates of dopamine and dobutamine (group A), 12 patients received prostaglandin E1 at a dose of 10.3 +/- 1.7 ng/kg/min without catecholamines (group B). There was no significant difference in prostaglandin dosages between groups. Kidney function was assessed by measuring plasma creatinine and urea nitrogen, urinary output, creatinine clearance, osmotic and free water clearance at baseline and after 72 h of infusion therapy. Hemodynamic parameters were measured by using a balloon tipped pulmonary arterial catheter. Hemodynamic measurements during infusion showed a significant improvement in all patients. At the same time as expected mean arterial pressure decreased in both groups (p < 0.001). Nevertheless, in both groups a significant increase of creatinine clearance during infusion was observed (in group A from 45 ml/min to 78 ml/min., p < 0.05, in group B from 59 ml/min to 105 ml/min., p < 0.001). Creatinine clearance in group B (without catecholamines) reached higher levels than group A (p < 0.05). Urinary volumes did not change during infusion therapy, whereas free water clearance significantly decreased, as an indication of an improvement of renal concentrations ability. We conclude, that in patients with end stage heart failure continuous infusion of prostaglandin E1 improves excretory kidney function. These findings suggest that the local effects of prostaglandin E1 on renal microcirculation can counterregulate the negative impact of prostaglandins on renal perfusion pressure.
70 rats were subjected to tourniquet ischemia of a hind limb for a period of two and three hours. 12 rats served as controls. After release of the 3 hours tourniquets 20 rats were treated either with Ringer's solution or with hydroxyethyl starch. Kidney function and morphology, systolic blood pressure, hematocrit, serum electrolytes, creatinine and urea were studied as different times of recirculation. 1. Reduction in renal function was only observed after releasing the tourniquets. 2. The extent of reduction in renal function depended on the time of ischemia and time of recirculation. 3 hours of tourniquet with two hours of recirculation led to the largest extent of reduction in renal function and renal parenchymal lesions. 3. If the infusion of HES was applied at the beginning of recirculation, reduction in renal function was prevented, as well as parenchymal lesions. Ringer's infusion, however, did not improve kidney function to a normal range.
BACKGROUND: Recently developed clinical practice guidelines and calibration of the Third National Health and Nutrition Examination Survey (NHANES III) serum creatinine assay provide a basis for estimating the prevalence and distribution of chronic kidney disease (CKD) in the United States using standardized criteria based on estimated glomerular filtration rate (GFR) and persistent albuminuria. METHODS: A nationally representative sample of 15,625 noninstitutionalized adults aged 20 years and older from the NHANES III was analyzed. Kidney function (GFR), kidney damage (albuminuria), and stages of CKD (GFR and albuminuria) were estimated from calibrated serum creatinine level, spot urine albumin level, age, sex, and race. GFR was estimated using the simplified Modification of Diet in Renal Disease Study equation and compared with the Cockcroft-Gault equation for creatinine clearance (CCr). RESULTS: The prevalence of CKD in the US adult population was 11% (19.2 million). By stage, an estimated 5.9 million individuals (3.3%) had stage 1 (persistent albuminuria with a normal GFR), 5.3 million (3.0%) had stage 2 (persistent albuminuria with a GFR of 60 to 89 mL/min/1.73 m(2)), 7.6 million (4.3%) had stage 3 (GFR, 30 to 59 mL/min/1.73 m(2)), 400,000 individuals (0.2%) had stage 4 (GFR, 15 to 29 mL/min/1.73 m(2)), and 300,000 individuals (0.2%) had stage 5, or kidney failure. Aside from hypertension and diabetes, age is a key predictor of CKD, and 11% of individuals older than 65 years without hypertension or diabetes had stage 3 or worse CKD. Compared with GFR estimates, CCr estimates showed a steeper decline with age and were lower in non-Hispanic blacks. CONCLUSION: CKD is common and warrants improved detection and classification using standardized criteria to improve outcomes. Am J Kidney Dis 41:1-12.
Morphometric data on glomerular size are presented on three patients with solitary functioning kidneys and one with bilateral oligomeganephronic hypoplasia. Renal biopsy of each of two patients with a congenitally absent kidney (unilateral renal agenesis) and a patient with oligomeganephronie, all with proteinuria and renal insufficiency, reveal increases of mean glomerular diameters of at least 1.75X and mean glomerular volumes greater than 5X. These dimensions, which are in the range of maximal increases recorded for man, are associated in all three biopsies with focal sclerosis of the hypertrophied glomeruli. By contrast, the functionally fully-compensated solitary kidney of a patient who lost function of the contralateral kidney from acquired disease, is characterized by the absence of focal glomerulosclerosis and by glomerular enlargement of significantly lesser degree (increased mean diameter 1.24X and mean volume less than 2X). These observations correlate glomerular injury with glomerular size and suggest that in the setting of reduced nephron numbers, nephron destruction via focal glomerulosclerosis may be initiated when compensatory glomerular hypertrophy has reached its limits.
Dog kidneys were perfused with a newly developed perfusate containing adenosine and PO4 for 48 hr, stored in the same perfusate for an additional 24 hr without perfusion (total preservation time:72 hr), and transplanted with immediate contralateral nephrectomy. Posttransplant renal function and biochemical analysis of the kidneys revealed practically no additional preservation-induced damage during the cold storage period. Serum creatinine levels reached normal between the third and eighth day posttransplant. This preservation method may be the method of choice for patients receiving postoperative cyclosporine therapy--and, in addition, facilitate organ sharing between transplant centers, thus reducing wastage of cadaveric kidneys.
The effect on urinary electrolyte excretion, renin release and plasma norepinephrine of single oral doses of 400 mg etozolin (E) and of 40 mg furosemide (F) were studied in hypertensive patients with normal (n = 6) and impaired kidney function (n = 6). E caused a marked saluresis up to 24 hours, showing its long duration of action. F, however, displayed a brief, brisk peak diuresis, followed by a rebound from the 4th to the 24th hours. The brisk peak diuresis induced by F was associated with pronounced release of renin, almost twice that induced by E. In chronic renal failure the renin release in relation to the magnitude of the diuresis was increased, i.e. the sensitivity of these patients to changes in water homeostasis was increased. E and F stimulated the sympathetic system to roughly the same extent. Patients with essential hypertension had higher plasma levels of norepinephrine than hypertensive patients with chronic renal failure. In addition, hypertensive patients with normal renal function (n = 4) and varying degrees of renal impairment (n = 11) were also given 400 mg daily for 2 weeks. Effects on blood pressure and electrolyte homeostasis were monitored, as well as the plasma kinetics of metabolite I, ozolinone. At the end of the 2 week treatment E had significantly lowered systolic (-12 mm Hg) and diastolic (-9 mm Hg) blood pressure, and had produced a significant loss of body weight, without altering plasma electrolytes or blood chemistry. There was no accumulation of the effective metabolite ozolinone under conditions of severe impairment of kidney function.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Oral bisphosphonates are prescribed for millions of men and women in the United States who have osteopenia or osteoporosis. However, there are limited data on the use of oral bisphosphonates in patients with kidney impairment. OBJECTIVE: The purpose of this study was to evaluate changes in calculated creatinine clearance (CrCl) and reported adverse events in elderly patients with varying degrees of kidney function who were taking oral bisphosphonate therapy. METHODS: The present study was a retrospective review of the medical records of elderly patients (age range, 65-89 years) who were prescribed oral bisphosphonates for a diagnosis of osteoporosis or osteopenia at the University of Colorado Hospital Seniors Clinic during the period January 1999 through March 2003. Data on age, sex, body weight, height, blood urea nitrogen and serum creatinine concentrations, and adverse-reaction history were collected. Clinic notes were reviewed to determine whether patients had taken an oral bisphosphonate previously or whether bisphosphonate therapy was initiated during the study period. The Cockcroft-Gault equation was used to calculate CrCl. Rates of drug-related adverse events were compared in patients with and without severe kidney impairment. For the purposes of this study, severe kidney impairment was defined as a CrCl <35 mL/min. RESULTS: Data from 181 patients (88.4% female, 11.6% male; mean age, 79.2 years) who received oral bisphosphonates were included in the analysis. One hundred fourteen (63.0%) patients began bisphosphonate therapy during the study period. The mean duration of bisphosphonate therapy was 22.3 months. Thirty-one (17.1%) patients taking bisphosphonates had severe kidney impairment. There was no change in calculated CrCl after the initiation of oral bisphosphonate therapy in patients who started therapy during the study period. Adverse drug events, 19 of them related to the gastrointestinal system, occurred in 24 (13.3%) patients. Overall, 19.4% (6/31) of patients with severe kidney impairment and 12.0% (18/150) of those without severe kidney impairment experienced adverse events; the difference between groups was not statistically significant. No reported adverse drug event required hospitalization or emergency treatment. CONCLUSIONS: When prescribed for elderly patients with varying degrees of kidney function, oral bisphosphonate therapy was well tolerated and was not associated with a decline in calculated CrCl.
The reactions of the mean systemic arterial blood pressure, arterial acid-base balance kidney function (clearance-technique), and plasma aldosterone concentration (radio-immunoassay) elicited by stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate were determined in chloralosed, non-vagotomized, spontaneously breathing cats in moderate mannitol-saline diuresis. The left renal nerves were cut; urine was collected separately from both the innervated and denervated kidneys. Intravenous injection of 0.2 mg/kg of the drug caused the expected long-lasting increase of the pO2 and pH and a decrease of pCO2 in the arterial blood, whereas the mean systemic arterial blood pressure slightly rose by an average of 2-4 mm Hg in the first hour of chemoreceptor stimulation but afterwards considerably decreased below the pre-injection values. The renal responses were characterized by a moderate vasoconstriction particularly in the innervated kidneys and a pronounced increase of sodium and urine excretion especially in the denervated kidneys. The inhibition of renal tubular sodium reabsorption underlying these natriuretic and diuretic reactions was fully demonstrable even at the end of the experiments, i. e. 4 h after the administration of the agent. Plasma aldosterone increased with the time of the experiments but did not show any clear relationships to the activity of the arterial chemoreceptors. The results show that the intravenous injection of almitrine bismesylate is connected with a renal response pattern which is typical for an excitation of the peripheral arterial chemoreceptors, i. e. moderate vasoconstriction (efferently mediated by the renal nerves) and an inhibition of renal tubular sodium reabsorption (efferently mediated by hormonal mechanisms). Furthermore, the data suggest that, on the one hand, under certain conditions these reactions of the kidney function could play the role of undesirable side effects but, on the other hand, the inhibition of renal tubular sodium reabsorption caused by almitrine bismesylate might possibly be used to treat diseases that are connected with a reduced ability of the kidneys to sufficiently excrete sodium.
We report the case of a 28-year-old female with type II Takayasu's arteritis affecting her single functioning kidney. Impaired renal function precluded the use of conventional contrast media. We used carbon dioxide-guided renal angioplasty to successfully treat the patient.
Anemia in persistent nephrotic syndrome (NS) has been described in a few case reports but has not been studied systematically. We present a group of 19 children with NS who developed anemia before the deterioration of kidney function. The aim of our study is to determine whether erythropoietin (EPO) and/or iron deficiency are causative factors and to evaluate the effect of EPO replacement therapy. Serum EPO levels, iron status, and vitamin B(12) concentrations were measured in nephrotic patients with anemia (NS-A) and compared with those of nephrotic children with normal hemoglobin (Hb) levels (NS-NHb; n = 13). Two control groups consisted of age-matched patients without kidney disease or hypoxemia with either iron deficiency anemia (IDA; n = 19) or normal Hb concentrations (NHb; n = 16). Most NS-A patients experienced persistent steroid-resistant NS, whereas most NS-NHb children had steroid-responsive NS. Although serum iron, ferritin, and B(12) levels were significantly lower in NS-A children, appropriate replacement therapy that resulted in normalization of ferritin and/or cobalamin levels did not lead to correction of the anemia. NS-A patients had greater EPO levels than those without anemia (21.6 +/- 3.3 versus 5.5 +/- 0.8 IU/L; P: < 0.001), but their response to anemia was inappropriately low compared with IDA children (EPO, 94.6 +/- 15.1 IU/L) despite similar Hb concentrations. EPO therapy for 4 to 9 months in 6 NS-A children with Hb levels less than 9 g/dL led to resolution of the anemia. In conclusion, anemia is a common feature of persistent NS that develops before the deterioration of kidney function. Depletion of iron stores may contribute to the development of anemia, but iron replacement therapy is ineffective. Nephrotic patients have EPO deficiency with a blunted response to anemia. The EPO deficiency is amenable to EPO therapy, which is recommended for this group of patients.