1,721,346 research outputs found
INTROITO di PROTEINE con la DIETA e INSUFFICIENZA RENALE CRONICA - Indicazioni pratiche per il MMG
No full text
Reduced calcium binding capacity is an intrinsic abnormality of red blood cell membrane in spontaneously hypertensive rats.
No full textDeterminants of kidney dysfunction: is vasopressin a new player in the arena?
No full textCopeptin is a marker of endogenous vasopressin secretion. Population-based data of the PREVEND Study show that men and women with high plasma copeptin have a highly prevalent microalbuminuria in addition to the low level of hydration typical of persons with high vasopressin secretion. The association of plasma copeptin with microalbuminuria suggests that vasopressin might have a role in kidney dysfunction via effects on the permselectivity of the glomerulus and/or on tubular albumin reabsorption
Elevated blood pressure and positive history of kidney stones: results from a population-based study.
No full textRationale, pros and cons of GFR estimation: the Cockcroft-Gault and MDRD equationsGIORNALE ITALIANO DI NEFROLOGIA
No full textCurrent guidelines suggest to evaluate kidney function by estimates of the
glomerular filtration rate (GFR) calculated using the Cockcroft-Gault equation
or the simplified equation of the Modification of Diet in Renal Disease (MDRD)
study. Cockcroft and Gault developed a method to predict an individual’s creatinine
clearance without urinary data but on the basis of average creatinine
clearance values corrected for age and body weight. The equation needs
information about gender, age, weight, and serum creatinine. The precision
of the equation is biased by overweight because the equation is based on the
assumption that creatinine clearance linearly reflects body weight. The MDRD
equation derives from a multiple regression used to analyze the relation of
GFR measurements by a radioisotope technique over serum creatinine after data linearization by logarithm transformation and with control for gender, age, ethnicity and other variables. The equation has not been validated for GFR >60 mL/min x 1.73 m2 because the study did not include healthy persons. The two equations often give conflicting estimates of GFR. Nephrologists have to understand the rationale of the two equations for the correct interpretation of these discrepancies. (G Ital Nefrol 2009; 26: 310-7
[Treatment of autosomal dominant polycystic kidney disease (ADPKD) - Tolvaptan].
No full textThe European Medicines Agency approved tolvaptan to slow cyst growth and renal failure progression in adults with ADPKD, glomerular filtration 60 mL/min x 1.73 m2 and rapidly progressive disease. In a multicenter 3-year study, conducted on 1,445 patients with non-genotyped ADPKD, ages 18-50 years, predicted creatinine clearance 60 mL/min and kidney total volume 750 mL, tolvaptan slowed kidney failure progression (-23%-46% for different objectives) and reduced kidney volume increase and pain without effects on hypertension and albuminuria.Tolvaptan induced reversible idiosyncratic hepatopathy in 4% of patients (1% in placebo). Tolvaptan antagonizes ADH effects, reduces cyclic-AMP generation in distal nephron, and induces water diuresis. It has high protein-binding and 8-hour half-life. Dosage is 60-120 mg/day in two different doses (for instance 45/15 or 60/30 mg). Treatment starts using lower dose and continues with cautious up-titolation. Data are insufficient for severe hepatopathy or nephropathy. There is no antidote against overdose. Dialysis should not remove tolvaptan. Aquaretic effects require high fluid intake to prevent dehydration. Treatment should be reduced or suspended in case of inadequate fluid intake or dehydration. Weight, natremia and plasma osmolality can inform on dehydration risks. Efficacy is not yet investigated on end-stage renal disease, non-renal ADPKD-related disorders, and mortality
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