Cardiovascular Disease, Chronic Kidney Disease, and Type 2 Diabetes Mellitus

Kanda, Takeshi; Wakino, Shu; Hayashi, Koichi; Plutzky, Jorge

doi:10.1681/asn.2007111182

Cited by 10 publications

(5 citation statements)

References 18 publications

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“…The high prevalence of LVH in CKD patients found in our study agrees with that of other studies 28-31. LVH in CKD is thought to result partly from uraemia-associated risk factors such as anaemia, calcium-phosphate products and hyperhomocysteinaemia 4.…”

Section: Discussionsupporting

confidence: 92%

Left ventricular hypertrophy and geometry in type 2 diabetes patients with chronic kidney disease. An echocardiographic study

Bayauli

Lepira

Kayembe

et al. 2012

Cardiovascular Journal of Africa

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ObjectiveWe assessed left ventricular structural alterations associated with chronic kidney disease (CKD) in Congolese patients with type 2 diabetes.MethodsThis was a cross-sectional study of a case series. We obtained anthropometric, clinical, biological and echocardiographic measurements in 60 consecutive type 2 diabetes patients (37 females, 62%) aged 20 years or older from the diabetes outpatient clinic, University of Kinshasa Hospital, DRC. We computed creatinine clearance rate according to the MDRD equation and categorised patients into mild (CrCl > 60 ml/min per 1.73 m2), moderate (CrCl 30–60 ml/min per 1.73 m2) and severe CKD (< 30 ml/min per 1.73 m2). Left ventricular hypertrophy (LVH) was indicated by a LV mass index (LVMI) > 51 g/m2.7 and LV geometry was defined as normal, or with concentric remodelling, eccentric or concentric hypertrophy, using relative wall thickness (RWT) and LVMI.ResultsCompared to patients with normal kidney function, CKD patients had higher uric acid levels (450 ± 166 vs 306 ± 107 μmol/l; p ≤ 0.001), a greater proportion of LVH (37 vs 14%; p ≤ 0.05) and longstanding diabetes (13 ± 8 vs 8 ± 6 years; p ≤ 0.001). Their left ventricular internal diameter, diastolic (LVIDD) was (47.00 ± 6.00 vs 43.00 ± 7.00 mm; p ≤ 0.001), LVMI was (47 ± 19 vs 36.00 ± 15 g/m2.7; p ≤ 0.05) and proportions of concentric (22 vs 11%; p ≤ 0.05) or eccentric (15 vs 3%; p ≤ 0.05) LVH were also greater. Severe CKD was associated with increased interventricular septum, diastolic (IVSD) (12.30 ± 3.08 vs 9.45 ± 1.94 mm; p ≤ 0.05), posterior wall thickness, diastolic (PWTD) (11.61 ± 2.78 vs 9.52 ± 1.77 mm; p ≤ 0.01), relative wall thickness (RWT) (0.52 ± 0.17 vs 0.40 ± 0.07; p ≤ 0.01) rate of LVH (50 vs 30%; p ≤ 0.05), and elevated proportions of concentric remodelling (25 vs 15%; p ≤ 0.05) and concentric LVH (42 vs 10%; p ≤ 0.05) in comparison with patients with moderate CKD. In multivariable adjusted analysis, hyperuricaemia emerged as the only predictor of the presence of LVH in patients with CKD (adjusted OR 9.10; 95% CI: 2.40–33.73).ConclusionIn keeping with a higher rate of cardiovascular events usually reported in patients with impaired renal function, CKD patients exhibited LVH and abnormal LV geometry.

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Section: Discussionsupporting

confidence: 92%

Left ventricular hypertrophy and geometry in type 2 diabetes patients with chronic kidney disease. An echocardiographic study

Bayauli

Lepira

Kayembe

et al. 2012

Cardiovascular Journal of Africa

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“…In six randomized, active-controlled trials up to 12 months in duration with either pioglitazone or rosiglitazone, significant 10%–30% reductions in albumin-to-creatinine ratio were demonstrated (74,75). …”

Section: Mechanisms Of Diabetic Microvascular Diseasementioning

confidence: 99%

The Pathologic Continuum of Diabetic Vascular Disease

Orasanu

Plutzky

2009

Journal of the American College of Cardiology

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408

321

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Hyperglycemia can promote vascular complications by multiple mechanisms, with formation of advanced glycation endproducts (AGEs) and increased oxidative stress proposed to contribute to both macrovascular and microvascular complications. Many of the earliest pathologic responses to hyperglycemia are manifest in the vascular cells that directly encounter elevated blood glucose levels. In the macrovasculature, these include endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). In the microvasculature, these include ECs, pericytes (in retinopathy), and podocytes (in renal disease). Additionally, neovascularization arising from the vasa vasorum may promote atherosclerotic plaque progression and contribute to plaque rupture, thereby interconnecting macro- and microangiopathy.

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“…Several clinical scenarios, including cardiac surgery (57), rhabdomyolysis (8), contrast exposure (20), and sepsis (59) cause AKI. Furthermore, the risk of CKD is increased in the setting of common comorbidities such as diabetes (1,42) and cardiovascular disease (9,22,29). In the clinic, CKD is often missed until disease is severe, as patients can demonstrate an insidious course with subclinical presentation until after significant structural kidney damage has occurred.…”

Section: Introductionmentioning

confidence: 99%

Divergent effects of AKI to CKD models on inflammation and fibrosis

Black

Lever

Traylor

et al. 2018

American Journal of Physiology-Renal Physiology

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Chronic kidney disease (CKD) is a condition with significant morbidity and mortality that affects 15% of adults in the United States. One cause of CKD is acute kidney injury (AKI), which commonly occurs secondary to sepsis, ischemic events, and drug-induced nephrotoxicity. Unilateral ischemia-reperfusion injury (UIRI) without contralateral nephrectomy (CLN) and repeated low-dose cisplatin (RLDC) models of AKI to CKD demonstrate responses characteristic of the transition; however, previous studies have not effectively compared the pathogenesis. We demonstrate both models instigate renal dysfunction, inflammatory cytokine responses, and fibrosis. However, the models exhibit differences in urinary excretory function, inflammatory cell infiltration, and degree of fibrotic response. UIRI without CLN demonstrated worsening perfusion and function, measured with Tc-mercaptoacetyltriglycine-3 imaging, and physiologic compensation in the contralateral kidney. Furthermore, UIRI without CLN elicited a robust inflammatory response that was characterized by a prolonged polymorphonuclear cell and natural killer cell infiltrate and an early expansion of kidney resident macrophages, followed by T-cell infiltration. Symmetrical diminished function occurred in RLDC kidneys and progressively worsened until day 17 of the study. Surprisingly, RLDC mice demonstrated a decrease in inflammatory cell numbers relative to controls. However, RLDC kidneys expressed increased levels of kidney injury molecule-1 (KIM-1), high mobility group box-1 ( HMGB1), and colony stimulating factor-1 ( CSF-1), which likely recruits inflammatory cells in response to injury. These data emphasize how the divergent etiologies of AKI to CKD models affect the kidney microenvironment and outcomes. This study provides support for subtyping AKI by etiology in human studies, aiding in the elucidation of injury-specific pathophysiologic mechanisms of the AKI to CKD transition.

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Cardiovascular Disease, Chronic Kidney Disease, and Type 2 Diabetes Mellitus

Cited by 10 publications

References 18 publications

Left ventricular hypertrophy and geometry in type 2 diabetes patients with chronic kidney disease. An echocardiographic study

Left ventricular hypertrophy and geometry in type 2 diabetes patients with chronic kidney disease. An echocardiographic study

The Pathologic Continuum of Diabetic Vascular Disease

Divergent effects of AKI to CKD models on inflammation and fibrosis

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