P5731Optimal blood pressure in diabetic hypertensive patients with overt proteinuria

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C J Lee ◽  
J Hwang ◽  
C Y Kang ◽  
H Kim ◽  
J Ha ◽  
...  

Abstract Background Evidence for the benefit of intensive blood pressure lowering in diabetic nephropathy is not clear at this time. The objective of this study was to demonstrate whether lower mean blood pressure (BP) in treated hypertensive patients with diabetic nephropathy is associated with better prognosis. Methods From the National Health Insurance Service (NHIS) Health Examination Database, diabetic hypertensive subjects with proteinuria between 2009 and 2010 were selected and followed-up until 2015 (N=8,663). Mean of the recorded systolic and diastolic BP during follow-up health examinations were stratified into five categories (SBP: <120, 120 to <130, 130 to <140, 140 to <150, and ≥150 mmHg; DBP: <70, 70 to <80, 80 to <90, 90 to <100, and ≥100 mmHg). All-cause death, myocardial infarction (MI), stroke, and renal outcome (progression to end stage renal disease or doubling of serum creatinine) were examined by Cox proportional hazard models with the propensity scores adjusted method. Results Compared to SBP of 130 to <140 mmHg, SBP of 120 to <130 mmHg was associated with lower risk of all-cause death (HR=0.78; 95% CI, 0.64–0.95), stroke (HR: 0.65; 95% CI, 0.45–0.94), and renal outcome (HR: 0.81; 95% CI, 0.68–0.97). SBP of <120 mmHg was associated with benefit for renal outcomes (HR: 0.69; 95% CI 0.55–0.88) but not with elevated risk of other outcomes. Compared to DBP of 80 to <90 mmHg, DBP of 70 to <80 mmHg were associated with lower risk of all-cause death (HR: 0.75; 95% CI, 0.64–0.88) but with higher risk of MI (HR: 1.52; 95% CI, 1.05–2.21). DBP of <70 mmHg was associated with reduced risk of all-cause death (HR: 0.79; 95% CI, 0.64–0.98). Conclusion In diabetic hypertensive subjects with overt proteinuria, deterioration of renal function decreased with decreasing SBP and the lowest risk of all-cause death and stroke were observed in SBP <130 mmHg. Low DBP was associated with low risk of all-cause death but there was a J curve phenomenon for MI in DBP of 70 to <80 mmHg.

1995 ◽  
Vol 6 (6) ◽  
pp. 1523-1529
Author(s):  
J A Breyer

Diabetic nephropathy is the single most common cause of end-stage renal disease in the United States. Recently, several major therapeutic interventions have been developed and demonstrated to slow or halt the progression of renal failure in patients with diabetes and diabetic kidney disease. The Diabetes Control and Complications Trial demonstrated that microalbuminuria developed in fewer patients in the intensive blood sugar control group than in the conventional therapy group. Similarly, the risk of developing proteinuria was reduced by intensive blood sugar control. Multiple studies have demonstrated that in patients with insulin-dependent diabetes and proteinuria, lowering the systemic blood pressure slows the rate of decline in renal function and improves patients' survival. In the recently completed trial of ACE inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death. In studies in small numbers of patients with insulin-dependent diabetes and established diabetic nephropathy, dietary protein restriction has also been demonstrated to slow the rate of decline of renal function. New potential interventions currently undergoing study include the use of aldose reductase inhibitors, the use of drugs that prevent the formation of advanced glycosylation end-products, and the use of angiotensin II receptor antagonists. Thus, several established benefits have recently been demonstrated to help prevent the development of or slow the progression of diabetic nephropathy, including blood pressure control, blood sugar control, and treatment with ACE inhibitors. Dietary protein restriction may also be of benefit. Multiple new interventions are undergoing clinical trials currently.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Valentin Calvez ◽  
Marco Palladino ◽  
Giulio Montefusco ◽  
Vincenzo Cesario ◽  
Claudia Fofi ◽  
...  

Hemodialysis (HD) may induce vascular stiffness through several mechanisms. We sought to determine the role of dialysis vintage (DV) on the development of cardiovascular alterations. We studied 14 patients in chronic HD and 24 newly diagnosed never treated hypertensive patients and 16 normotensive controls. The patients in HD were divided in two groups according to DV: <60-months (DV<60,n=7) or >60-months (DV>60,n=7). After HD session, when dry weight was reached, we evaluated peripheral blood pressure (pBP), the parameters derived by tonometric analysis of the pulse waveform (central blood pressure-cBP-, Subendocardial Viability Ratio-SEVR-, carotid-femoral pulse wave velocity-cf-PWV-) and those derived from echocardiography: ejection fraction (EF-for systolic function) and E/e’ (for diastolic function), and the ultrafiltration volume (UV). Calcium/phosphate (Ca/P) levels, serum albumin, and Kt/V were evaluated retrospectively on repeated measurements over the past 5 years. All the groups were similar for sex and BMI, both DV<60 and DV>60 were older than hypertensives and controls (58.33±3.71 and 59.83±7.98 vs 44.14±1.28 and vs 40.63±2.05 years, respectively, P<0.05). Both DV<60 and DV>60 presented similar levels of Ca/P, serum albumin, Kt/V and UV. pBP was increased and similar to hypertensives in DV>60 vs DV<60 (systolic-pBP: 154.2±4.5 vs 132.5±5.18 mmHg, P<0.01 and diastolic-pBP: 90.4±49 vs 78.5±3.3 mmHg, P<0.01). Likewise cBP was increased and similar to hypertensive patients in DV>60 vs DV<60 (systolic-cBP: 140.8±8.4 vs 111.2±3.36 mmHg, P<0.001 and diastolic-cBP: 88.2±3.73 vs 72.33±7.78 mmHg, respectively, P<0.05). cf-PWV was similar in normotensives, hypertensives and DV<60, and increased only in DV>60 vs DV<60 (9.6±1.4 vs 7.13±1.4 m/s, p<0.05). SEVR and EF were preserved and similar in all the groups. E/e’ was significantly increased only in the groups in HD, however it was higher in DV>60 vs DV<60 (9.16±1.14 vs 6.96±0.72, P<0.01). In conclusion, only patients with DV>60 presented increased aortic stiffness. This was associated to higher BP and diastolic dysfunction. Hence, chronic HD, particularly after 60 months, may play a putative role in developing cardiovascular alterations in patients with end-stage renal disease.


Author(s):  
L. Zhao ◽  
Y. Zhang ◽  
F. Liu ◽  
H. Yang ◽  
Y. Zhong ◽  
...  

Abstract Purpose To investigate the association between urinary complement proteins and renal outcome in biopsy-proven diabetic nephropathy (DN). Methods Untargeted proteomic and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional analyses and targeted proteomic analysis using parallel reaction-monitoring (PRM)-mass spectrometry was performed to determine the abundance of urinary complement proteins in healthy controls, type 2 diabetes mellitus (T2DM) patients, and patients with T2DM and biopsy-proven DN. The abundance of each urinary complement protein was individually included in Cox proportional hazards models for predicting progression to end-stage renal disease (ESRD). Results Untargeted proteomic and functional analysis using the KEGG showed that differentially expressed urinary proteins were primarily associated with the complement and coagulation cascades. Subsequent urinary complement proteins quantification using PRM showed that urinary abundances of C3, C9, and complement factor H (CFAH) correlated negatively with annual estimated glomerular filtration rate (eGFR) decline, while urinary abundances of C5, decay-accelerating factor (DAF), and CD59 correlated positively with annual rate of eGFR decline. Furthermore, higher urinary abundance of CFAH and lower urinary abundance of DAF were independently associated with greater risk of progression to ESRD. Urinary abundance of CFAH and DAF had a larger area under the curve (AUC) than that of eGFR, proteinuria, or any pathological parameter. Moreover, the model that included CFAH or DAF had a larger AUC than that with only clinical or pathological parameters. Conclusion Urinary abundance of complement proteins was significantly associated with ESRD in patients with T2DM and biopsy-proven DN, indicating that therapeutically targeting the complement pathway may alleviate progression of DN.


2021 ◽  
Vol 8 ◽  
Author(s):  
Michele Provenzano ◽  
Maria Chiara Pelle ◽  
Isabella Zaffina ◽  
Bruno Tassone ◽  
Roberta Pujia ◽  
...  

Diabetic nephropathy is the most common cause of end-stage renal disease worldwide. Control of blood glucose and blood pressure (BP) reduces the risk of developing this complication, but once diabetic nephropathy is established, it is then only possible to slow its progression. Sodium-glucose cotransporter-2 inhibitors (SGLT2is) are a novel class of oral hypoglycemic agents that increase urinary glucose excretion by suppressing glucose reabsorption at the renal proximal tubule. SGLT2is lower glycated hemoglobin (HbA1c) without increasing the risk of hypoglycemia, induce weight loss and improve various metabolic parameters including BP, lipid profile, albuminuria and uric acid. Several clinical trials have shown that SGLT2is (empagliflozin, dapagliflozin canagliflozin, and ertugliflozin) improve cardiovascular and renal outcomes and mortality in patients with type 2 diabetes. Effects of SGLT2is on the kidney can be explained by multiple pathways. SGLT2is may improve renal oxygenation and intra-renal inflammation thereby slowing the progression of kidney function decline. Additionally, SGLT2is are associated with a reduction in glomerular hyperfiltration, an effect which is mediated by the increase in natriuresis, the re-activation of tubule-glomerular feedback and independent of glycemic control. In this review, we will focus on renal results of major cardiovascular and renal outcome trials and we will describe direct and indirect mechanisms through which SGLT2is confer renal protection.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Boukhtioua Mariem ◽  
Mami Ikram ◽  
Tlili Syrine ◽  
Ghabi Hiba ◽  
Hela Jbali ◽  
...  

Abstract Background and Aims Diabetic nephropathy (DN) is associated with a high incidence of cardiovascular morbidity and mortality. The relationship between hypertension and diabetic nephropathy is complex and blood pressure (BP) control is an important management strategy in the prevention of its onset and progression .The aim of this study was to determine whether blood pressure control delays the progression of DN and prevents macrovascular complications in patients with diabetes mellitus. Method Hypertension guidelines advocate treating systolic blood pressure to less than 130 mm Hg and diastolic blood pressure to less than 80 mmHg for patients with diabetes mellitus and overt nephropathy.The relationship between blood pressure and progression of nephropathy was studied in 120 diabetic and hypertensive patients with established diabetic nephropathy. We divided hypertensive patients with stage 1 to 3 CKD already treated with antihypertensive therapy into 2 groups: those with BP &lt; 130/80 mmHg were designated as Group A (n=66) and those with BP&gt; 130/80 as Group B (n=54). Serum creatinine level as well as urinary albumin excretion were measured at 3 months,6 months, one year,2 years and at last visit during follow-up.The GFR was calculated using the Modification of diet in renal disease formula.The kidney disease outcome was defined as time to end-stage renal disease. The cardiovascular outcome was defined as time to myocardial infarction, stroke,ischemic stroke, hospitalization for heart failure, or revascularization. Results During the mean follow up period of 33,8 ± 11,7 months, the primary end point of end-stage renal disease occured in 9 patients (7 patients in Group B versus 2 patients in groupe A) while 11 hypertensive patient experienced a cardiovascular event.  The decline rate in GFR was significantly more important in groupe B (p&lt;0,05). However, little difference existed between the two groups in urinary albumin excretion. Blood pressure control was not associated with improved cardiovascular outcomes when comparing the two groups. Conclusion The results of our study indicate that an uncontrolled hypertension is associated with a rapid progression of kidney impairment in diabetic patients with overt nephropathy but no relationship with the incidence of cradiovascular events was seen in our population.


2005 ◽  
Vol 00 (01) ◽  
pp. 39
Author(s):  
Steven Cheng ◽  
Daniel Coyne

In the US, diabetic nephropathy accounts for the majority of chronic kidney disease (CKD). It contributes significantly to morbidity and mortality among the diabetic population1,2and accounts for approximately 40% of patients with end-stage renal disease.3The earliest manifestation of renal involvement in diabetes is the presence of microalbuminuria, as defined by urine albumin excretion of 30–300mg/day.4Progression to overt proteinuria (urine albumin excretion greater than 300mg/day) and diabetic nephropathy occur more frequently in those with poor glycemic control, glomerular hyperfiltration, and hypertension.5


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Hea Eun Kim ◽  
HO JUN CHIN

Abstract Background and Aims Hypertensive nephrosclerosis (HT-N) is known as the second common cause of end stage renal disease (ESRD) in Korea as well as in other countries. However, the HT-N is assumed by clinical findings which are not well correlated to the pathologic findings. Therefore, we report the clinical characteristics of HT-N diagnosed by renal biopsy and compare the prognosis between patients with HT-N and hypertensive patients with focal segmental nephrosclerosis (FSGS) without pathologic HT-N. Method We enrolled 21,617 patients having native kidney biopsy for diagnosis of nephritis between 1979 and 2018, retrospectively. Among them, we selected 267 adult hypertensive patients with only HT-N and 984 hypertensive patients with FSGS without HT-N or other diagnoses (FSGS-HT). The estimated glomerular filtration rate (GFR) was calculated by original MDRD equation. The final outcomes were incidences of end stage renal disease (ESRD) and death. We matched blood pressures and GFR between two groups and analyzed the difference of outcomes within the matched cohort (mHT-N and mFSGS-HTN), also. Results The age of patients with HT-N was 49.5 ± 15.3 years at renal biopsy. There were 175 (65.5 %) men. Systolic blood pressure (SBP) was 139.1 ± 24.0 mmHg and diastolic blood pressure (DBP) was 83.7 ± 15.6 mmHg at renal biopsy. Levels of serum creatinine, GFR, and urine protein to creatinine ratio were 3.17 ± 3.05 mg/dl, 40.7 ± 32.5 ml/min/1.73 m2, and 2.277 ± 2.803 g/g cr, respectively. During follow-up period of 64.1 months (median), there were 52 (22.7%) patients progressed to ESRD and 8 (3.1%) patients were dead. Age, SBP, and hemoglobin were risk factors to mortality by Cox’s hazard proportional model adjusted with related factors to mortality. With increase of 10 mmHg in the level of SBP at renal biopsy, hazard ratio(HR) of mortality was increase by 1.645 folds (95% CI: 1.192-2.270, P=0.002). Presence of diabetes mellitus, serum albumin, and GFR were risk factors to incident ESRD. Compared to patients with FSGS-HT, patients with HT-N showed higher levels of SBP, DBP, and serum creatinine and lower levels of GFR, serum albumin, hemoglobin, and UPCR (all p-values &lt;0.05), however, the risk of incident ESRD and mortality was not different. Therefore, we matched BP and GFR between groups and selected 235 patients in each group. The matched groups were not different in the values of age, SBP, DBP, and GFR. The risk of mortality was not different between groups (p-value =0.502), however, HR of incident ESRD was 1.558-fold higher (95% CI: 1.004-2.419, P=0.048) in mFSGS-HT compared to mHT-N by Cox’s hazard proportional model adjusted by factors related to ESRD. Conclusion Hypertensive nephrosclerosis was diagnosed in more advanced stage of CKD compared to hypertensive FSGS. Considering levels of GFR and SBP as risk factors to hard outcomes, we should consider early pathologic diagnosis for proteinuric and/or azotemic hypertensive patients and control blood pressures and renal dysfunction in more aggressive manners.


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