Cardiovascular risk independently predicts small functional bladder storage capacity

Monaghan, Thomas F.; Miller, Connelly; Agudelo, Christina W.; Rahman, Syed N.; Everaert, Karel; Birder, Lori A.; Wein, Alan J.; Weiss, Jeffrey P.; Lazar, Jason

doi:10.1007/s11255-020-02616-6

Cited by 9 publications

(8 citation statements)

References 29 publications

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“…An alternative hypothesis to the DM milieu being directly harmful to bladder cells is that DM-induced arteriosclerosis causes bladder ischaemia and subsequent bladder cell damage. It has been reported that experimental models of atherosclerosis in rabbits and rats are associated with bladder ischaemia and altered mechanical properties 45 , 46 that cardiovascular risk factors in human populations correlate with urinary tract symptoms and bladder storage capacity 47 , 48 These studies, however, do not primarily address DM per se. Moreover, as recently reviewed 49 , rats are resistant to acquiring atherosclerosis unless they have undergone, as examples, physical vascular damage and/or exposure to special diets to increase blood lipids.…”

Section: Discussionmentioning

confidence: 99%

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder

Hindi

Williams

Zeef

et al. 2021

Sci Rep

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Diabetes mellitus (DM) is the leading cause of chronic kidney disease and diabetic nephropathy is widely studied. In contrast, the pathobiology of diabetic urinary bladder disease is less understood despite dysfunctional voiding being common in DM. We hypothesised that diabetic cystopathy has a characteristic molecular signature. We therefore studied bladders of hyperglycaemic and polyuric rats with streptozotocin (STZ)-induced DM. Sixteen weeks after induction of DM, as assessed by RNA arrays, wide-ranging changes of gene expression occurred in DM bladders over and above those induced in bladders of non-hyperglycaemic rats with sucrose-induced polyuria. The altered transcripts included those coding for extracellular matrix regulators and neural molecules. Changes in key genes deregulated in DM rat bladders were also detected in db/db mouse bladders. In DM rat bladders there was reduced birefringent collagen between detrusor muscle bundles, and atomic force microscopy showed a significant reduction in tissue stiffness; neither change was found in bladders of sucrose-treated rats. Thus, altered extracellular matrix with reduced tissue rigidity may contribute to voiding dysfunction in people with long-term DM. These results serve as an informative stepping stone towards understanding the complex pathobiology of diabetic cystopathy.

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Section: Discussionmentioning

confidence: 99%

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder

Hindi

Williams

Zeef

et al. 2021

Sci Rep

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“…[51][52][53][54][55][56][57] Further, sleep-related complaints are highly prevalent across multiple common medical conditions, 58 and growing evidence also supports small functional bladder storage capacity in nocturia patients as a potential hallmark of chronic bladder ischemia. [59][60][61][62] Consistent with the diverse adverse effects of medical disease on nocturnal urine production, storage, and sleep architecture, nocturia may even be an important early sign of medical disease states, including undiagnosed hypertension, 63,64 endorgan damage in diabetes mellitus, 65 and underlying structural cardiac abnormalities. 66 As a potential harbinger of undiagnosed medical disease, consideration of systems beyond the urinary tract in the evaluation of nocturia has important implications for the patient's overall health and preventative medicine, 67 but also directly relates to the primary treatment of nocturia.…”

Section: Comorbiditiesmentioning

confidence: 99%

“…These conditions have been associated with excess nocturnal urine production through a variety of well‐described pathophysiological mechanisms 51–57 . Further, sleep‐related complaints are highly prevalent across multiple common medical conditions, 58 and growing evidence also supports small functional bladder storage capacity in nocturia patients as a potential hallmark of chronic bladder ischemia 59–62 . Consistent with the diverse adverse effects of medical disease on nocturnal urine production, storage, and sleep architecture, nocturia may even be an important early sign of medical disease states, including undiagnosed hypertension, 63,64 end‐organ damage in diabetes mellitus, 65 and underlying structural cardiac abnormalities 66 …”

Section: Introductionmentioning

confidence: 99%

Sleep Disorders, Comorbidities, Actions, Lower Urinary Tract Dysfunction, and Medications (“Sleep C.A.L.M.”) in the evaluation and management of nocturia: A simple approach to a complex diagnosis

Monaghan

Weiss

Wein

et al. 2023

Neurourology and Urodynamics

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Introduction Nocturia arises from a fundamental mismatch between nocturnal urine production, storage capacity, and sleep architecture, which may be driven by abnormalities of the genitourinary tract, but also by sleep disorders, medical diseases, patient actions/lifestyle factors, or medications. This article introduces a novel system for organizing the complex differential diagnosis for nocturia, as proposed by an international collective of practicing urologists, physician specialists, and sleep experts: “Sleep CALM”—Sleep Disorders, Comorbidities, Actions, Lower Urinary Tract Dysfunction, and Medications. Methods Narrative review of current evidence regarding the relevance of each “Sleep CALM” factor to nocturia pathogenesis, evaluation, and management. Results Nocturia and sleep disorders are highly intertwined and often bidirectional, such that nocturnal awakenings for reasons other than a sensation of bladder fullness should not be used as grounds for exclusion from nocturia treatment, but rather leveraged to broaden therapeutic options for nocturia. Nocturia is an important potential harbinger of several serious medical conditions beyond the genitourinary tract. Urologists should have a low threshold for primary care and medical specialty referral for medical optimization, which carries the potential to significantly improve nocturnal voiding frequency in addition to overall health status. Adverse patient actions/lifestyle factors, lower urinary tract dysfunction, and medication use commonly coexist with disordered sleep and comorbid medical conditions, and may be the primary mediators of nocturia severity and treatment response, or further exacerbate nocturia severity and complicate treatment. Conclusion “Sleep CALM” provides a memorable and clinically relevant means by which to structure the initial patient history, physical exam, and clinical testing in accordance with current best‐practice guidelines for nocturia. Although not intended as an all‐encompassing diagnostic tool, the “Sleep CALM” schema may also be useful in guiding individualized ancillary testing, identifying the need for specialty referral and multidisciplinary care, and uncovering first‐line treatment targets.

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“…Although classically considered a urological condition, nocturia has been increasingly recognized as a manifestation of systemic disease, and multiple studies have shown the presence and severity of nocturia to be associated with hypertension 2–5 . Pathophysiologic mechanisms underlying this association have not been fully characterized, but may involve nocturnal polyuria owing to dysregulation of the renin‐angiotensin‐aldosterone axis and a corresponding increase in nocturnal natriuresis, 6 as well as diminished functional bladder capacity from chronic vascular insufficiency mediated by hypertension and other atherosclerotic risk factors 7–9 . Notably, hypertension is associated with a number of electrocardiographic (ECG) abnormalities including left ventricular hypertrophy (LVH), left atrial enlargement (LAE), and prolonged QTc and, in turn, ECG abnormalities independently confer an increased risk for cardiovascular events 10 .…”

Section: Introductionmentioning

confidence: 99%

“…[2][3][4][5] Pathophysiologic mechanisms underlying this association have not been fully characterized, but may involve nocturnal polyuria owing to dysregulation of the reninangiotensin-aldosterone axis and a corresponding increase in nocturnal natriuresis, 6 as well as diminished functional bladder capacity from chronic vascular insufficiency mediated by hypertension and other atherosclerotic risk factors. [7][8][9] Notably, hypertension is associated with a number of electrocardiographic (ECG) abnormalities including left ventricular hypertrophy (LVH), left atrial enlargement (LAE), and prolonged QTc and, in turn, ECG abnormalities independently confer an increased risk for cardiovascular events. 10 However, the relationship between nocturia and ECG abnormalities has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Nocturia and electrocardiographic abnormalities among patients at an inner‐city cardiology clinic

Mekki

Monaghan

Lee

et al. 2020

Neurourology and Urodynamics

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Aims: Nocturia has been increasingly recognized as a potential manifestation of cardiovascular disease. However, the relationship between nocturia and electrocardiographic (ECG) abnormalities has not been studied. This study aims to characterize the diagnostic utility of nocturia in identifying left ventricular hypertrophy (LVH), left atrial enlargement (LAE), and prolonged QTc on ECG. Methods: Retrospective analysis of nocturnal voiding frequency and contemporaneous ECG data from consecutive patients evaluated at a university-based outpatient cardiology clinic. Three sets of three incremental binary multiple logistic regression models controlling for (1) age, (2) sex and race, and (3) body mass index, hypertension, diabetes mellitus, and diuretic utilization were performed to determine whether nocturia was predictive of LVH, LAE, and prolonged QTc. Results: Included patients (n = 143, 77.6% nocturia) were predominantly African-American (89.5%), female (74.1%), and obese (61.5%), of whom 44.1%, 41.3%, and 27.3% had LVH, LAE, and prolonged QTc, respectively. Older age, African-American race, obesity, hypertension, diuretic use, LVH, and LAE were significantly associated with nocturia on univariate analysis. No significant differences were observed in the strength of associations between nocturia and LVH, LAE, or QTc prolongation based on age. Nocturia independently predicted LVH in Models I-III (odds ratios [ORs], 2.99-3.20; relative risks [RRs], 1.18 for all, p ≤ .046) and LAE in Models I-III (ORs, 4.24-4.72; RRs, 1.21 for all, p ≤ .015). No significant associations were observed between nocturia and prolonged QTc. Conclusions: Nocturia may be a risk marker for underlying structural cardiac abnormalities.

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Cardiovascular risk independently predicts small functional bladder storage capacity

Cited by 9 publications

References 29 publications

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder

Sleep Disorders, Comorbidities, Actions, Lower Urinary Tract Dysfunction, and Medications (“Sleep C.A.L.M.”) in the evaluation and management of nocturia: A simple approach to a complex diagnosis

Nocturia and electrocardiographic abnormalities among patients at an inner‐city cardiology clinic

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