Objectives: One potential method of evaluating renin-angiotensin-aldosterone system (RAAS) activation involves the quantification of urinary aldosterone excretion. While blood concentrations of aldosterone are easily obtained, results may be misleading because of minute-to-minute variation in aldosterone secretion and subsequent blood concentrations. Urinary aldosterone concentration measurement represents a more consistent "pooled" index of aldosterone secretion, but obtaining 24-h urine samples is time-consuming, difficult, and fraught with potential error. We postulated that the urinary aldosterone:creatinine ratio, measured from spot urine samples, would correlate well with 24-h urinary aldosterone excretion, and would provide a simple index of aldosterone excretion that would eliminate the need for 24-h urine collection.
Animals, Materials And Methods: After validating an assay for aldosterone in canine urine, 24-h urinary aldosterone excretion was determined by radioimmunoassay from 8 normal, male beagle dogs under control conditions, after RAAS stimulation with amlodipine administration, and after RAAS attenuation with the addition of enalapril to amlodipine administration. Spot urine samples, each obtained at the same time of day, were used to determine the aldosterone:creatinine ratio during control conditions, RAAS stimulation, and RAAS attenuation.
Results: The aldosterone:creatinine ratio from spot-checked urine samples correlated well with 24-h urinary aldosterone excretion (r=0.77, P<0.0001).
Conclusions: A spot urinary aldosterone:creatinine ratio might be substituted for 24-h urinary aldosterone determination.
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http://dx.doi.org/10.1016/j.jvc.2006.11.001 | DOI Listing |
Nat Rev Nephrol
January 2025
AHEPA Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Diuretic drugs act on electrolyte transporters in the kidney to induce diuresis and are often used in chronic kidney disease (CKD), given that nephron loss creates a deficit in the ability to excrete dietary sodium, which promotes an increase in plasma volume. This rise in plasma volume is exacerbated by CKD-induced systemic and intra-renal activation of the renin-angiotensin-aldosterone-system, which further limits urinary sodium excretion. In the absence of a compensatory decrease in systemic vascular resistance, increases in plasma volume induced by sodium retention can manifest as a rise in systemic arterial blood pressure.
View Article and Find Full Text PDFArch Physiol Biochem
January 2025
Medical Physiology Department, Faculty of Medicine, Menoufia University, Shebin el Kom, Egypt.
Objective: This research assesses renoprotective effects of saracatinib (Src) in diabetic nephropathy (DN) and the potential underlying processes.
Materials And Methods: Rats were divided into: control, DN, DN + Met + Los, DN + Met + Src, and DN + Met + Los + Src. Rats' ABP, urinary albumin, urinary nephrin, and creatinine clearance were assessed.
Medicina (Kaunas)
December 2024
Unit of Nephrology and Dialysis, Department of Clinical and Experimental Medicine, A.O.U. "G. Martino", University of Messina, 98125 Messina, Italy.
Audits allow analysis of the delivery of care and the prevalence of diseases. This study investigated kidney diseases' impact on end-stage renal disease (ERSD) in patients younger than 30 years. : This analysis is retrospectively conducted on young dialysis-dependent patients included in the Sicilian Registry of Nephrology, Dialysis and Transplantation Participants.
View Article and Find Full Text PDFJ Diabetes Investig
December 2024
Department of Diabetes and Endocrine Medicine, Kagoshima University Graduate School of Medicine and Dental Sciences, Kagoshima, Japan.
Aims/introduction: We evaluated the 24-h ambulatory blood pressure monitoring data of patients to investigate the relationship between the progression of diabetic polyneuropathy and impaired circadian blood pressure variability.
Materials And Methods: This study included 154 patients with diabetes who were hospitalized for hyperglycemic control. Routine biochemical and hematological tests, ambulatory blood pressure monitoring, screening for diabetic complications, nerve conduction studies, and Holter electrocardiography were carried out on all patients.
BMJ Case Rep
December 2024
Faculty of Medical Sciences, The University of the West Indies at Cave Hill, Bridgetown, Barbados
Page kidney (Page phenomenon) is a rare and treatable cause of hypertension which can occur if a haematoma, leading to extrinsic compression, occurs after renal transplant biopsy. The renin-angiotensin-aldosterone system is activated leading to hypertension. This case report is that of a male in his 70s who had a renal transplant biopsy of his transplanted kidney and subsequently developed Page phenomenon as a result of an expanding haematoma.
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