scholarly journals Early diagnosis of renal dysfunction in hypertensive patients with type 2 diabetes mellitus

2020 ◽  
Vol 11 (4) ◽  
pp. 102-109
Author(s):  
Oleksandr M Bilovol ◽  
Iryna I. Kniazkova ◽  
Oleksandr M. Kirienko ◽  
Vladyslav. I. Korniichuk ◽  
Denis A. Kirienko ◽  
...  
2019 ◽  
Vol 19 (20) ◽  
pp. 1818-1849 ◽  
Author(s):  
Ban Liu ◽  
Yuliang Wang ◽  
Yangyang Zhang ◽  
Biao Yan

: Type 2 diabetes mellitus is one of the most common forms of the disease worldwide. Hyperglycemia and insulin resistance play key roles in type 2 diabetes mellitus. Renal glucose reabsorption is an essential feature in glycaemic control. Kidneys filter 160 g of glucose daily in healthy subjects under euglycaemic conditions. The expanding epidemic of diabetes leads to a prevalence of diabetes-related cardiovascular disorders, in particular, heart failure and renal dysfunction. Cellular glucose uptake is a fundamental process for homeostasis, growth, and metabolism. In humans, three families of glucose transporters have been identified, including the glucose facilitators GLUTs, the sodium-glucose cotransporter SGLTs, and the recently identified SWEETs. Structures of the major isoforms of all three families were studied. Sodium-glucose cotransporter (SGLT2) provides most of the capacity for renal glucose reabsorption in the early proximal tubule. A number of cardiovascular outcome trials in patients with type 2 diabetes have been studied with SGLT2 inhibitors reducing cardiovascular morbidity and mortality. : The current review article summarises these aspects and discusses possible mechanisms with SGLT2 inhibitors in protecting heart failure and renal dysfunction in diabetic patients. Through glucosuria, SGLT2 inhibitors reduce body weight and body fat, and shift substrate utilisation from carbohydrates to lipids and, possibly, ketone bodies. These pleiotropic effects of SGLT2 inhibitors are likely to have contributed to the results of the EMPA-REG OUTCOME trial in which the SGLT2 inhibitor, empagliflozin, slowed down the progression of chronic kidney disease and reduced major adverse cardiovascular events in high-risk individuals with type 2 diabetes. This review discusses the role of SGLT2 in the physiology and pathophysiology of renal glucose reabsorption and outlines the unexpected logic of inhibiting SGLT2 in the diabetic kidney.


Author(s):  
GA Amusa ◽  
SU Uguru ◽  
BI Awokola

Cardiovascular disease (CVD) is a common cause of morbidity/mortality in patients with type 2 diabetes mellitus (T2DM). Echocardiography can detect changes in cardiac geometry/function before overt CVD symptoms. This study aimed to evaluate left ventricular (LV) geometry and function in normotensive/hypertensive patients with T2DM without overt cardiac symptoms. A cross-sectional study in which fifty normotensives and fifty hypertensive adults with DM without overt cardiac symptoms were enrolled from the cardiology/diabetes clinics of Jos University Teaching Hospital (JUTH) in a simple random manner. Relevant history, physical examination and biochemical investigations were performed. 12-lead electrocardiography and echocardiograph assessment of LV geometry and function were also performed. Data was analyzed using Epi-info 7 statistical software; p value < 0.05 was considered significant. There were 27 females and 29 females in both groups. The prevalence of abnormal LV geometry was 36.0%, 95% CI 33.2-38.8% and 58.0%, 95% CI 55.2-60.8% in the normotensive and hypertensive groups respectively, P=0.028. Similarly, the prevalence of LV dysfunction was 38.0%, 95%CI 35.2-40.8% and 62.0%, 95%CI 59.2-64.8% respectively, P=0.017. The independent predictors of LV dysfunction were found to be duration of diabetes (OR 7.74, 95%CI 4.46-10.46), duration of hypertension ≥5years (OR 4.15, 95%CI 4.01-9.27), smoking (OR 4.34, 95%CI 1.32-6.23), body mass index ≥25 (OR 5.53, 95%CI 1.38-2.09) and glycosylated haemoglobin ≥7 (OR 7.11, 95%CI 2.15-0.81).  There is high prevalence of LV dysfunction/abnormal LV geometry in T2DM patients without overt cardiac symptoms; co-morbid hypertension worsens these abnormalities. Early and periodic echocardiography is recommended with appropriate intervention in these patients.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Viktoria Chernomorets ◽  
Elena Troitskaya ◽  
Zhanna Kobalava

Abstract Background and Aims 24-h blood pressure (BP) may be superior to office BP in the prediction of cardiovascular mortality and also central aortic BP may better predict outcomes than brachial one. Hypertensive patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) have higher risk and poorer BP control than patients with normal glycemic state and renal function. 24-h profile of central BP and arterial stiffness according to CKD phenotypes are not well described in this population. The aim of the study was to evaluate the associations of kidney function and proteinuria with 24-h central BP and parameters of arterial stiffness in hypertensive patients with T2DM and CKD. Method 90 patients with hypertension (HTN), T2DM and CKD (eGFR 30-60 ml/min/1.73 m2 and morning spot urine albumin–creatinine ratio (UACR) &lt;300 mg/g) were included. 66% of them were females, median age was 60 years, 69% were smokers, 53% obese, 77% with dyslipidemia. Median duration of T2DM and HTN was 7.5 years and 18 years, respectively. All received antihypertensive drugs (77% – combinations of 2 or 3 drugs) and glucose lowering therapy (insulin in 58%). The analysis was performed according to CKD phenotype: proteinuric (UACR 30-300 mg/g) and non-proteinuric (UACR &lt;30 mg/g) and according to CKD stage assessed by GFR (G3a and G3b, KDIGO (2012)). Office brachial BP was measured with a validated oscillometric device. Office aortic BP and arterial stiffness were assessed with applanation tonometry (SphygmoCor AtCor). 24-hour ABPM of brachial and aortic BP was performed with BPLab Vasotens. All results are presented as median values. P&lt;0.05 was considered significant. Results Median brachial BP was 156/83 mmHg, aortic BP 139/90 mmHg. Median eGFR was 53 ml/min/1.73 m2, UACR – 62.2 mg/g. Phenotypes of CKD were as follows: proteinuric in 78% (GFR 50 ml/min/1.73 m2, UACR 62 mg/g) and non-proteinuric in 22 % (GFR 54 ml/min/1.73 m2, med UACR 5 mg/g, p&lt;0.01 for trend compared non-proteinuric). Patients with proteinuric phenotype compared to non-proteinuric were characterized by higher rate of dyslipidemia (85% vs 45%, p&lt;0.001), longer duration of HTN and DM (19.5 vs 7.5 years and 8 vs 3 years, respectively, p &lt;0.01 for trend) and lower HDL-C (1.2 vs 1.9, p=0.02). Both groups had similar office brachial SBP (156 vs 157 mmHg; p=0.48), but patients with proteinuric phenotype had higher office central SBP (147 vs 137 mmHg, p=0.007) and worse 24-h profile of central SBP (daytime 147 vs 138 mmHg, p=0.008; night-time 143 vs 130 mmHg, p=0.04). Proteinuric phenotype significantly correlated with office aortic SBP (r=0.28; p=0.01) and daytime and night-time aortic SBP (r=0.28 and 0.21 respectively, p &lt;0.05 for trend). The eGFR phenotypes were as follows: G3a in 82.2% (GFR 54 ml/min/1.73 m2, UACR 20 mg/g) and G3b in 17.8% (GFR 38 ml/min/1.73 m2, med UACR 46 mg/g, p&lt;0.01 for trend compared to G3a). Patients with worse kidney function had longer duration of HTN and DM (16 vs 11 years and 10 vs 6 years, respectively, p &lt;0.01 for trend), higher median brachial and aortic BP levels (158/90 vs 146/82 mmHg and 150/95 vs 138/80 mmHg, respectively, p&lt;0.01 for trend), worse 24-h profile of central SBP (daytime 148 vs 138 mmHg, p=0.008; night-time 146 vs 130 mmHg, p=0.006), higher central pulse pressure (56 vs 49 mmHg, p=0.007), augmentation index (33 vs 14%, p=0.007). Conclusion Hypertensive patients with T2DM and CKD G3b and proteinuria were characterized by worse 24-profile of central BP and higher arterial stiffness.


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