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PubMed1981

The relationship between the renal clearance of creatinine and the apparent renal clearance of beta-2-microglobulin in patients with normal and impaired kidney function.

The renal clearances of creatinine and beta 2-microglobulin of patients with either normal or impaired kidney function were measured. The renal clearance of beta 2-microglobulin depends on the urinary pH and must be considered as an apparent renal clearance because after tubular reabsorption the compound is metabolized in the kidney. Impaired kidney function reduces the percentage of tubular reabsorption of beta 2-microglobulin.

Absorption↗
PubMed1998

Proteinuria, hypertension and chronic renal failure in X-linked Kallmann's syndrome, a defined genetic cause of solitary functioning kidney.

BACKGROUND: Anosmia and hypogonadotrophic hypogonadism are the classic features of X-linked Kallmann's syndrome, a disorder caused by mutations of KAL, a gene expressed during kidney and brain development. About a third of patients have a solitary functioning kidney, but little is known about their renal morbidity. METHODS: We studied seven patients aged 22-35 years with X-linked Kallmann's syndrome and a solitary functioning kidney. RESULTS: Two patients developed significant proteinuria associated with mild to moderate arterial hypertension in the second to third decades of life. In one, proteinuria and renal impairment preceded the appearance of hypertension, and the disorder progressed to chronic renal failure. The remaining five patients had normal plasma creatinine concentrations and no significant proteinuria although four had borderline systolic and/or diastolic hypertension. In two sets of patients from the same kindreds, there was a striking discordance for the occurrence of renal morbidity. CONCLUSIONS: All patients with X-linked Kallmann's syndrome should be screened for renal malformations, and those with solitary kidneys require life-long follow-up to detect hypertension, proteinuria and renal failure.

Adult↗
PubMed2006

Fetuin-A and kidney function in persons with coronary artery disease--data from the Heart and Soul Study.

BACKGROUND: Fetuin-A is a serum protein that inhibits ectopic vascular calcification and is present in lower concentrations in end-stage renal disease than in healthy controls. Whether fetuin-A concentrations are also lower in the setting of mild-to-moderate chronic kidney disease (CKD) is unknown. METHODS: We evaluated the associations of several parameters of kidney function including measured 24 h urinary creatinine clearance (CrCl), estimated glomerular filtration rate (GFR) by the Mayo Clinic quadratic GFR equation (qGFR), serum cystatin-C concentrations, and urinary albumin-to-creatinine ratio with serum fetuin-A concentrations in 970 outpatients with coronary artery disease. We used general linear models to determine the adjusted mean fetuin-A concentrations within each kidney function category. RESULTS: The mean age of the study sample was 67 years, 82% were male, 71% had hypertension and 26% had diabetes mellitus. In adjusted analysis, we observed no significant differences in mean fetuin-A concentrations across groups defined by CrCl, qGFR, or albumin-to-creatinine ratio groups. For example, adjusted mean fetuin-A concentrations were 0.66 g/l in participants with CrCl > 90, 60-90 and 45-60 ml/min/1.73 m(2), and 0.65 g/l in participants with CrCl < 45 ml/min/1.73 m(2). Higher serum cystatin-C (indicating worse kidney function) was associated with higher adjusted mean serum fetuin-A concentrations (lowest quartile 0.62 g/l, highest quartile 0.68 g/l; P for trend <0.001). CONCLUSIONS: Among ambulatory patients with coronary artery disease, there is no evidence that mild-to-moderate CKD is associated with lower concentrations of serum fetuin-A compared with persons with normal renal function. The mechanisms explaining the association between CKD and vascular calcification remain elusive.

Aged↗
PubMed1999

Natural course of kidney function in Type 2 diabetic patients with diabetic nephropathy.

AIMS: To determine the natural course of kidney function and to evaluate the impact of putative progression promoters in Caucasian Type 2 diabetes mellitus (DM) patients with diabetic nephropathy who had never received any antihypertensive treatment. METHODS: A long-term observational study of 13 normotensive to borderline hypertensive Type 2 DM patients with diabetic nephropathy. Glomerular filtration rate (GFR) was measured approximately every year (51Cr-EDTA plasma clearance technique). Albuminuria, blood pressure (BP) and haemoglobin A1c (HbA1c) was determined 2-4 times per year and serum cholesterol every second year. RESULTS: The patients (12 males/one female), age 56+/-9 (mean +/- SD) years, with a known duration of diabetes of 10+/-6 years, were followed for 55 (24-105) (median (range)) months. GFR decreased from 104 (50-126) to 80 (39-112) ml x min(-1) x 1.73 m(-2) (P = 0.002) with a median rate of decline of 4.5 (-0.4 to 12) ml x min(-1) x year(-1). During follow-up, albuminuria rose from 494 (301-1868) to 908 (108-2169) mg/24 h (P = 0.25), while BP, HbA1c and serum cholesterol remained essentially unchanged. In univariate analysis the rate of decline in GFR did not correlate significantly with neither baseline nor mean values during follow-up of BP, albuminuria, HbA1c and serum cholesterol. CONCLUSIONS: Our study suggests that normotensive to borderline hypertensive Type 2 DM patients with diabetic nephropathy have a rather slow decline in kidney function, but we did not unravel the putative progression promoters responsible for the variation in rate of decline in GFR.

Adult↗
PubMedDate not supplied

[Kidney function test].

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Kidney Function Tests↗
PubMed1976

Kidney function during hydropenia nad water diuresis in patients with idiopathic recurring nephrolithiasis.

The kidney function of 41 patients with idiopathic recurring kidney stones was investigated by inulin- and PAH-clearances and by measuring the excretion of electrolytes during hydropenia and water diuresis. All patients had normal inulin- and PAH-clearances and normal concentrating capacity as indicated by free water reabsorption (Tc H2O). Seven patients, all of whom had previously been found to have low excretion of magnesium in urine, were unable to dilute their urine. During water diuresis these patients also had lower osmolar clearance and lower excretion of sodium than the other patients. A defective dilution capacity may be of pathogenetic significance for stone formation; the causes of the defect, however, are not clear.

Adult↗
PubMed1986

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

Single-nephron and whole-kidney function were studied in female rats with corticomedullary nephrocalcinosis, and in animals where the lesion had been prevented either by a dietary magnesium supplement or by using a diet with a calcium:phosphorus ratio in excess of 1. At the single-nephron level, rats with nephrocalcinosis had prolonged tubular fluid transit times. Proximal transit time was 19.42 +/- 1.98 (mean +/- S.E. of mean) vs. 11.58 +/- 0.19 s for controls; distal transit time was 62.64 +/- 9.16 vs. 31.50 +/- 1.03 s for controls. Although single-nephron function is altered in nephrocalcinosis, data obtained from rats in metabolism cages indicate that whole-kidney function is largely unaffected by the lesion.

Animals↗
PubMed2006

Interaction of endothelin with renal nerves modulates kidney function in spontaneously hypertensive rats.

BACKGROUND AND METHODS: We investigated kidney function, renal endothelin-1 concentration, prepro-endothelin-1 mRNA as well as endothelin receptor A and B mRNA expression and receptor properties in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) with intact renal nerves and 7 days after renal denervation. In addition, responses of renal function to the non-selective ETA/ETB receptor blocker bosentan (10 mg/kg i.v. bolus injection) were studied. RESULTS: In SHR, renal papillary prepro-endothelin-1 mRNA expression, endothelin-1 tissue concentrations and endothelin receptor density were significantly lower than in normotensive rats. Renal denervation was associated with a decrease in papillary tissue prepro-endothelin-1 mRNA and in WKY rats also with a significant reduction in papillary endothelin-1 content without affecting ET receptor density. Bosentan did not alter renal blood flow or glomerular filtration rate but decreased urine flow rate in both intact normotensive and hypertensive rats, whereas it decreased urine sodium and potassium excretion only in intact WKY. Bosentan had no effects on renal function in renal denervated rats. CONCLUSION: Since renal papillary endothelin-1 appears to counteract the fluid and sodium retaining effects of renal nerve activity, an impaired renal endothelin-1 synthesis in SHR may contribute to excessive sodium retention and thus to the pathogenesis of hypertension in SHR.

Animals↗
PubMed1988

Creatinine excretion rates for evaluation of kidney function in children.

A protein load protocol for evaluation of kidney function was tested in normal children and pediatric renal patients. An overnight, timed urine collection was used for calculation of the baseline creatinine clearance and creatinine excretion rate. One hour following ingestion of a standardized protein meal (baked chicken), a 2-3 h urine collection was begun. The post-protein meal changes in creatinine clearance showed considerable variation in both the normal children and those with renal disorders. In contrast, the rate of excretion of creatinine was consistently increased in the normal children following the protein meal (73.4 +/- 18%; range 48.2%-122.4%). Of 33 renal patients, 14 showed less than a 48% increase in creatinine excretion rate, even though 9 of these children had baseline creatinine clearances within the normal range. These 9 patients have evidence of less than normal quantities of functioning renal tissue. Serial studies over a year on 2 children who presented with acute renal failure showed a progressive increase in creatinine clearance with scant increases in creatinine excretion rate. These studies provide indirect evidence that a less than normal enhancement of the rate of creatinine excretion following a protein load reflects the presence of adaptive glomerular hyperfiltration and hyperperfusion.

Adolescent↗
PubMed1999

Nitrite and nitrate levels in patients with cirrhosis of the liver: influence of kidney function and fasting state.

BACKGROUND: Increased serum nitrite/nitrate (NOx) levels, the stable metabolites of nitric oxide (NO), have been reported in patients with cirrhosis. NOx levels, however, are influenced not only by endogenous NO synthesis but also by urinary NOx excretion and dietary intake. We attempted to elucidate factors that influence NOx levels independently of endogenous NO production and to determine the conditions under which NOx levels reflect endogenous production in patients with cirrhosis and healthy controls. METHODS: NOx serum concentrations and urinary NOx excretion were determined by means of the Griess reaction in relation to Child-Pugh score, kidney function, fasting state, and after exposure to tap water. RESULTS: Multifactor regression analysis showed inulin clearance (P = 0.0074) and Child-Pugh score (P = 0.0001) to be independent factors predicting NOx levels in patients with cirrhosis. NOx serum levels correlated negatively with the inulin clearance (P < 0.0001), which deteriorated with progressive loss of liver function. NOx levels decreased by about 30% within a 24-h fasting period. After 24 h fasting urinary NOx excretion was not significantly increased in patients with advanced cirrhosis. CONCLUSION: NOx serum levels, taken as a surrogate for endogenous NO formation, have to be viewed with caution in patients with cirrhosis because they often have impaired kidney function. However, in steady-state conditions after an adequate fasting period NOx levels might be good prognostic markers in patients with cirrhosis since they reflect two possible sequelae of liver insufficiency-namely, increased NO formation and impaired kidney function.

Case-Control Studies↗
PubMed2026

Efficacy and safety of revascularization in patients with chronic limb-threatening ischemia by kidney function.

BACKGROUND: The optimal revascularization strategy for patients with chronic limb-threatening ischemia (CLTI) with chronic kidney disease (CKD) remains unknown. We evaluated whether the efficacy and safety of surgical vs endovascular revascularization differ by kidney function. METHODS: In this post hoc secondary analysis of BEST-CLI trial (NCT02060630), 1,704 patients with CLTI were stratified by baseline estimated glomerular filtration rate (eGFR, mL/min/1.73 m&#xb2;): non-CKD (eGFR &#x2265; 90), mild-moderate CKD (eGFR 45-89), advanced CKD (eGFR < 45 or dialysis). The primary outcome was a composite of major adverse limb events (MALE) or death. We estimated the difference in restricted mean time lost (RMTL, in days) adjusted for inverse probability treatment weights. RESULTS: Surgical revascularization was significantly associated with fewer days with MALE or death in non-CKD (RMTL difference: -127.8 days; 95% CI -176.1, -79.6) and mild-moderate CKD (-63.2 days; 95% CI -104.7, -21.8) but not in advanced CKD (-16.4 days; 95% CI -78.8, 46.0; P interaction = .02). This attenuation reflected a diminishing mortality benefit with more severe CKD (P interaction = .01), whereas the association with fewer days with MALE remained consistent across CKD strata (P interaction = .34). Major adverse cardiovascular events and serious adverse events were more common with more severe CKD but did not differ significantly by treatment. CONCLUSIONS: Surgical vs endovascular revascularization was consistently associated with fewer days with MALE across CKD strata. However, its association with mortality varied by kidney function, attenuating the overall benefit for the composite endpoint of MALE or death. These results support individualized revascularization strategies, but require prospective confirmation. TRIAL REGISTRATION: The BEST CLI trial is registered at ClinicalTrials.gov (NCT02060630).

Humans↗