ABSTRACT
BACKGROUND: Chronic kidney disease (CKD) is a highly prevalent condition. Urologic disorders are known causes of CKD, but often remain undiagnosed and underestimated also for their insidious onset and slow progression. We aimed to evaluate the prevalence of urological unrecognized diseases in CKD patients by uroflowmetry. METHODS: We enrolled consecutive stable CKD outpatients. The patients carried out two questionnaires, the International Prostate Symptom Score and Incontinence Questionnaire-Short Form, and they also underwent uroflowmetry, evaluating max flow rate (Q max), voiding time and voided volume values. RESULTS: A total of 83 patients (43 males, mean age of 59.8 ± 13.3 years) were enrolled. Our study showed 28 males and 10 females with a significant reduction of Q max (P < 0.001) while 21 females reported a significant increase of Q max (P < 0.001) with a prevalence of 49.5% of functional urological disease. Moreover, we showed a significant association between Q max and creatinine (P = 0.013), estimated glomerular filtration rate (P = 0.029) and voiding volume (P = 0.05). We have not shown significant associations with age (P = 0.215), body mass index (P = 0.793), systolic blood pressure (P = 0.642) or diastolic blood pressure (P = 0.305). Moreover, Pearson's chi-squared test showed a significant association between Q max altered with CKD (χ2 = 1.885, P = 0.170) and recurrent infection (χ2 = 8.886, P = 0.012), while we have not shown an association with proteinuria (χ2 = 0.484, P = 0.785), diabetes (χ2 = 0.334, P = 0.563) or hypertension (χ2 = 1.885, P = 0.170). CONCLUSIONS: We showed an elevated prevalence of urological diseases in nephropathic patients; therefore, we suggest to include uroflowmetry in CKD patient assessment, considering the non-invasiveness, repeatability and low cost of examination. Uroflowmetry could be used to identify previously unrecognized urological diseases, which may prevent the onset of CKD or progression to end-stage renal disease and reduce the costs of management.
ABSTRACT
Hypertension is commonly associated with autosomal dominant polycystic kidney disease (ADPKD), often discovered before the onset of renal failure, albeit the pathogenetic mechanisms are not well elucidated. Hyperaldosteronism in ADPKD may contribute to the development of insulin resistance and endothelial dysfunction, and progression of cardiorenal disease. The aim of study was to evaluate the prevalence of primary aldosteronism (PA) in ADPKD patients and identify some surrogate biomarkers of cardiovascular risk.We have enrolled 27 hypertensive ADPKD patients with estimated glomerular filtration rate (eGFR) ≥ 60âmL/min, evaluating the renin-angiotensin-aldosterone system (RAAS), inflammatory indexes, nutritional status, homocysteine (Hcy), homeostasis model assessment-insulin resistance (HOMA-IR), mineral metabolism, microalbuminuria, and surrogate markers of atherosclerosis [carotid intima media thickness (cIMT), ankle/brachial index (ABI), flow mediated dilation (FMD), renal resistive index (RRI) and left ventricular mass index (LVMI)]. Furthermore, we have carried out the morpho-functional magnetic resonance imaging (MRI) with high-field 3 T Magnetom Avanto.We have divided patients into group A, with normal plasma aldosterone concentration (PAC) and group B with PA, present in 9 (33%) of overall ADPKD patients. Respect to group A, group B showed a significant higher mean value of LVMI, HOMA-IR and Hcy (Pâ=â0.001, Pâ=â0.004, Pâ=â0.018; respectively), and a lower value of FMD and 25-hydroxyvitamin D (25-OH-VitD) (Pâ=â0.037, Pâ=â0.019; respectively) with a higher prevalence of non-dipper pattern at Ambulatory Blood Pressure Monitoring (ABPM) (65% vs 40%, Pâ<â0.05) at an early stage of the disease.In this study, we showed a high prevalence of PA in ADPKD patients, associated to higher LVMI, HOMA-IR, Hcy, lower FMD, and 25-OH-VitD, considered as surrogate markers of atherosclerosis, compared to ADPKD patients with normal PAC values. Our results indicate a higher overall cardiovascular risk in ADPKD patients with inappropriate aldosterone secretion, and a screening for PA in all patients with ADPKD is recommended.
Subject(s)
Cardiovascular Diseases/etiology , Hyperaldosteronism/etiology , Polycystic Kidney, Autosomal Dominant/complications , Adult , Antihypertensive Agents/therapeutic use , Biomarkers/blood , Brachial Artery/diagnostic imaging , Brachial Artery/physiopathology , Cardiovascular Diseases/physiopathology , Carotid Intima-Media Thickness , Echocardiography , Female , Glomerular Filtration Rate , Humans , Hyperaldosteronism/epidemiology , Hyperaldosteronism/physiopathology , Hypertension/drug therapy , Hypertension/physiopathology , Insulin Resistance , Magnetic Resonance Imaging , Male , Polycystic Kidney, Autosomal Dominant/physiopathology , Prevalence , Renin-Angiotensin System , Risk FactorsABSTRACT
BACKGROUND: Erectile dysfunction (ED) is not only evidence of diffuse atherosclerosis but also an index of early endothelial damage. We investigated cerebrovascular reactivity, expression of early arterial damage, in patients with isolated ED (ED+) and controls (ED-). MATERIALS AND METHODS: Fifteen ED+ and 15 ED- subjects, matched for age (ED+: 58+/-6, ED-: 59 +/- 4 years) and vascular risk factors, were submitted to carotid duplex ultrasound and transcranial Doppler. Cerebrovascular reactivity was assessed on both middle cerebral arteries simultaneously calculating (a) the total vasomotor range (VMR) measured after breath holding and hyperventilation and (b) the rate of change (VMR/CO(2)) after breath holding. RESULTS: Carotid Duplex scanning showed a light carotid stenosis only in 3 (2 in the ED+ and 1 in the ED- group). No differences were observed in intima-media thickness between ED+ and ED-. Slightly slower mean middle cerebral artery flow velocities were observed in ED+ with respect to ED-. ED+ patients showed a reduced VMR (p < 0.001) and a slower VMR/CO(2) rate of change (p < 0.001) compared to ED-. CONCLUSIONS: The reduced reactivity in patients with isolated ED may represent a marker of early cerebral vasomotor dysfunction due to subclinical endothelial damage.