scholarly journals Loss of nocturnal decline of blood pressure in non-diabetic patients with nephrotic syndrome in the early and middle stages of chronic kidney disease

2009 ◽  
Vol 32 (5) ◽  
pp. 364-368 ◽  
Author(s):  
Daisaku Andoh ◽  
Mayumi Kobayashi ◽  
Gen Yasuda ◽  
Nobuhito Hirawa ◽  
Sanae Saka ◽  
...  
1970 ◽  
Vol 28 (6) ◽  
Author(s):  
Shewaneh Damtie ◽  
Belete Biadgo ◽  
Habtamu Wondifraw Baynes ◽  
Sintayehu Ambachew ◽  
Tadele Melak ◽  
...  

BACKGROUND: The prevalence of chronic kidney disease, particularly in diabetic patients, is increasing rapidly throughout the world. Nowadays, many individuals in developing nations are suffering from diabetes which is one of the primary risk factors of chronic kidney disease.METHODS: Institution based cross-sectional study was conducted at the University of Gondar Hospital from February to April 2016. A total of 229 study participants were selected using systematic random sampling technique. Urine sample was collected for albumin determination by dipstick. The Simplified Modification of Diet in Renal Disease study equation was used to estimate glomerular filtration rate. Binary logistic regression model was used to identify risk factors.RESULTS: Of the total 229 study participants, 50.2% were females and the mean age was 47±15.7 years. Among study participants, the prevalence of chronic kidney disease (CKD) was found to be 21.8% (95% CI: 16% - 27%). Of all study participants, 9(3.9%) had renal impairment (eGFR < 60 ml/min/ 1.73 m2) and 46 (20.1%) had albuminuria. Older age (AOR: 5.239, 95% CI: 2.255-12.175), systolic blood pressure ≥140mmHg (AOR: 3.633, 95% CI: 1.597-8.265), type 2 diabetes mellitus (AOR: 3.751, 95% CI: 1.507-9.336) and longer duration of diabetes (AOR: 3.380, 95% CI: 1.393-8.197) were independent risk factors of CKD.CONCLUSIONS: The study identified high prevalence (21.8%) of CKD among diabetic adults. CKD was significantly associated with older age, systolic blood pressure, type 2 DM and longer duration of DM. Thus, DM patients should be diagnosed for chronic kidney disease and then managed accordingly. 


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Oliva Mejía-Rodríguez ◽  
Jorge E. Herrera-Abarca ◽  
Guillermo Ceballos-Reyes ◽  
Marcela Avila-Diaz ◽  
Carmen Prado-Uribe ◽  
...  

Objective. The objective of this study was to investigate the effect of bromocriptine (BEC) on left ventricular mass index (LVMI) and residual renal function (RRF) in chronic kidney disease (CKD) patients with type 2 diabetes (T2D).Research Design and Methods. A 6-month double-blind randomized controlled trial was conducted in 28 patients with T2D and stage 4 CKD with increased LVMI. Fourteen patients received BEC (2.5 mg, initially 1 tablet with subsequent increase to three times a day) and 14 received a placebo (PBO; initially 1 tablet with subsequent increase to three times a day). Cardiovascular changes were assessed by monitoring 24 h ambulatory blood pressure, two-dimensional-guided M-mode echocardiography, and N-terminal brain natriuretic peptide (NT-proBNP) plasma levels. RRF was evaluated by creatinine clearance and cystatin-C plasma levels.Results. Both BEC and PBO groups decreased blood pressure—but the effect was more pronounced in the BEC group. Average 24 h, diurnal and nocturnal blood pressures, and circadian profile showed improved values compared to the PBO group; LVMI decreased by 14% in BEC and increased by 8% in PBO group. NT-proBNP decreased in BEC (0.54±0.15to0.32±0.17 pg/mL) and increased in PBO (0.37±0.15to0.64±0.17 pg/mL). Creatinine clearance did not change in the BEC group and decreased in the PBO group.Conclusions. BEC resulted in a decrease on blood pressure and LVMI. BEC also prevented the progression of CKD while maintaining the creatinine clearance unchanged.


2021 ◽  
Author(s):  
Mahya Daniyali ◽  
Leila Mahmoudieh ◽  
Golnaz Afzal ◽  
Farzaneh Hematian ◽  
Omid Moradi ◽  
...  

Abstract Background: Diabetic nephropathy is the most prevalent cause of end-stage kidney disease (ESRD). Besides, factors such as; pro-fibrotic, cytokines, vascular endothelial growth factor, inflammatory factor, and uric acid may play a role in creating and progressing diabetic nephropathy. Decreasing the serum level of inflammatory factors can be useful in the treatment of diabetic nephropathy. Therefore, this study aimed to evaluate allopurinol's anti-inflammatory effects in diabetic patients with chronic kidney disease.Methods: In this clinical trial, 60 diabetic patients with chronic kidney disease and normal uric acid level were enrolled into the study with certain inclusion and exclusion criteria. Patients received allopurinol at a dose of 100 mg daily. Demographic parameters, laboratory results in blood urea nitrogen (BUN), serum creatinine (sCr), glomerular filtration rate (GFR), 24-hour urine protein (PrUrine24h), uric acid, serum albumin (Alb), systolic blood pressure (SBP), diastolic blood pressure (DBP), glycosylated hemoglobin (HbA1C) and high sensitivity C reactive protein (HSCRP), as well as adverse reactions, were recorded at baseline, ones and three months after.Results: The results showed that patients were not different in point of demographic parameters at baseline. Laboratory results such as; BUN, sCr, GFR, PrUrine24h, Alb, SBP, DBP, and HbA1C did not change significantly over study duration (P>0.05), except uric acid and HSCRP, which were significantly decreased in patients (P=0.024 and P=0.016, respectively). There was not any notable adverse reaction among patients.Conclusion: Low dose Allopurinol (100 mg/day) reduced uric acid and inflammatory biomarker (HSCRP) after three administration months. According to the present study results, Allopurinol can be considered an auxiliary, inexpensive, and low side-effect therapy in diabetic patients with chronic kidney disease.


2018 ◽  
Vol 24 (4) ◽  
pp. 478-489 ◽  
Author(s):  
O. A. Koshelskaya ◽  
O. A. Zhuravleva ◽  
R. S. Karpov

Objective. To determine the frequency of markers of chronic kidney disease (CKD) in hypertensive patients, and to assess their relationship with the circadian blood pressure (BP) profile and intrarenal vascular resistance.Design and Methods. We studied 70 patients with medically-controlled hypertension (63,2 ± 8,3 years, m — 48,6 %, office BP was 130,5 ± 13,7 / 78,1 ± 8,5 mm Hg), 40 patients were recruited from the Russian multicentre program CHRONOGRAF. Measurement of the office BP, ambulatory BP monitoring were performed. Glomerular filtration rate (GFR) was calculated using the CKD-EPI formula, and albuminuria (AU) was determined as albumin/creatinine (A/Cr) ratio in the morning portion of urine (n = 40) or 24-hour urinary albumin excretion (UAE) (n = 22). Intrarenal vascular resistance was estimated by renal duplex Doppler ultrasound. The resistive index (RI) levels in the main renal arteries (MRA) and intrarenal arteries (IRA) were calculated.Results. Markers of CKD (GFR < 60 ml/min/1,73 m2and/or A/Cr > 30 mg/g and/or UAE > 30 mg/day) were detected in 31,4 % of patients with well-medically-controlled hypertension: average values of BP-day and BP-night were normal. The frequency of markers of CKD was 44,4 % in patients with BP-night ≥ 120/70 mm Hg (40,9 %) and 28,2 % in patients with BP-night < 120/70 mm Hg (58,1 %). A/Cr ratio was positively associated (Rs = 0,3550, р = 0,0266), GFR was negatively associated (Rs = –0,3795, р = 0,002) with systolic BP-night. RI in the segmental intrarenal arteries correlated with GFR (Rs = –0,4232, p = 0,0005). Renal RI were higher in CKD-patients vs. non-CKD-patients. During the ROC-analysis, the threshold value of RI in segmental IRA 0,725 to the detection of CKD markers (sensitivity of 71,4 %, specificity of 68,9 %, AUC = 0,699) was established. Among the diabetic patients, there were more marked disturbances of renal hemodynamic in the presence of CKD markers: RI in arcuate IRA reached 0,73 (0,68–0,75).Conclusions. The high frequency of markers of CKD (31,4 %) was identified even in patients with well-medically-controlled hypertension, it was associated with systolic BP-night. The negative correlation was found between GFR and RI. Renal hemodynamics was significantly disturbed in the presence of CKD markers, especially in patients with type 2 diabetes mellitus. The cut-off point of RI in segmental IRA indicating the CKD markers is 0,725.


2010 ◽  
Vol 57 (1) ◽  
Author(s):  
Marcin Renke ◽  
Leszek Tylicki ◽  
Przemysław Rutkowski ◽  
Narcyz Knap ◽  
Marcin Zietkiewicz ◽  
...  

Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) is a common strategy used in the management of patients with chronic kidney disease (CKD). However, there is no universal therapy that can stop progression of CKD. Pentoxifylline (PTE) is a non-specific phosphodiesterase inhibitor with anti-inflammatory properties. It has been reported to have promising effects in CKD treatment. In a placebo-controlled, randomized, cross-over study we evaluated the influence of PTE (1200 mg/day) added to RAAS blockade on proteinuria, surrogate markers of tubular injury and oxidative stress-dependent products in 22 non-diabetic patients with proteinuria (0.4-4.3 g per 24 h) with normal or declined kidney function [eGFR 37-178 mL/min]. In an eight-week run-in period, therapy using ACEI and/or ARB was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: PTE/washout/placebo or placebo/washout/PTE. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. The PTE therapy reduced proteinuria (by 26%) as compared to placebo. There were no differences in alpha(1)-microglobulin, urine excretion of N-acetyl-beta-d-glucosaminidase (NAG), hsCRP, the urinary excretion of 15-F(2)t-isoprostane, blood pressure (BP), eGFR and serum creatinine between the PTE and placebo groups. Pentoxifylline may decrease proteinuria in non-diabetic patients with CKD.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Silverio Rotondi ◽  
Lida Tartaglione ◽  
Marzia Pasquali ◽  
Maria Luisa Muci ◽  
Sandro Mazzaferro ◽  
...  

Abstract Background and Aims DMT2 and its complications such as chronic kidney disease (CKD) lead to increase vascular stiffness, measurable with CAVI, and biochemical alterations in substances implicated in vascular damage like Klotho, FGF23, and Sclerostin. The aim of the study was to evaluate the role of CKD stage 1-2 and possible alterations of 25 (OH)Vitamin-D, FGF23, Klotho, and Sclerostin on early vascular damage in DMT2 patients Method Patients included: DMT2 from &lt;10 years, age &lt;60 years, no insulin therapy, eGFR≥60 ml/min/1.73m2, absence of vascular complications. We have evaluated CAVI, albumin-excretion-rate (ACR), 25(OH)Vitamin-D, Klotho, FGF23, and Sclerostin. 30 healthy subjects were the control for CAVI, Klotho, FGF23 and Sclerostin. Results We enrolled 40 women and 60 men, average age 56 years (IQR: 52-59), 5-year DMT2 (IQR: 2.7-7), HbA1c 6.3% (5.8-6.7), eGFR of 95 ml/min/1.73m2. FGF23 (42±10 vs controls 29.8±11 pmol/l, p&lt;.05) and Sclerostin (36.2±7 vs 26.6±1 pmol/l, p&lt;.05) were increased and Klotho reduced (673±300 vs 845±330 pg/ml, p&lt;.05). CKD (ACR≥30mg/gr; eGFR between 60-90 ml/min /1.73m2) was present in 12.6%. The mean CAVI value was normal. Patients with borderline (≥8, 33%) and pathological (≥9, 13%) CAVI were older (p.001), with longer duration of DMT2 (p.022) and lower 25(OH)Vitamin-D (p.041). CAVI correlated positively with age (p.001), Hb1Ac (p.036), systolic blood pressure (SBP) (p.012) and diastolic blood pressure (DBP) (p.001) and correlated negatively with 25(OH)Vitamin-D (p.046). The multivariate analysis showed positive predictors of CAVI age (p.001), DBP (p.0001), ACR (p.008) and Klotho (p.017). Conclusion In our DMT2 population, borderline and pathological CAVI is associated with increased ACR, elevated DBP and reduced 25(OH)Vitamin-D. Furthermore the alterations of FGF23, Sclerostin and Klotho, secondary to CKD, are an early sign of possible vascular damage. ACR, 25(OH)Vitamin-D and DBP can be modifiable risk factors for early vascular damage in DMT2


2010 ◽  
Vol 57 (4) ◽  
Author(s):  
Marcin Renke ◽  
Leszek Tylicki ◽  
Przemysław Rutkowski ◽  
Alexander Neuwelt ◽  
Wojciech Larczyński ◽  
...  

There is evidence that dyslipidemia is associated with chronic kidney disease (CKD) and it has been implicated in the progression of renal damage. Optimal management of dyslipidemia should therefore lead to renal benefits. A number of experimental models demonstrate a beneficial effect of statins in ameliorating renal damage. However, the exact mechanism by which statins protect against renal damage remains unclear. In a placebo-controlled, randomized, cross-over study we evaluated the influence of atorvastatin (ATO) 40 mg/day added to the renin-angiotensin-aldosterone systeme (RAAS) blockade on proteinuria and surrogate biomarkers of tubular damage or injury in 14 non-diabetic patients with proteinuria (0.4-1.8 g per 24 h) with normal or declined kidney function (eGFR 55-153 ml/min). In the eight-week run-in period, therapy using angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: ATO/washout/placebo or placebo/washout/ATO. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. The primary end point of this study was a change in proteinuria measured as 24-h urine protein excretion (DPE). Secondary end points included urine N-acetyl-β-D-glucosaminidase (NAG) and α1-microglobulin (α1m) excretion. The ATO therapy significantly reduced urine excretion of α₁m (p=0.033) and NAG (p=0.038) as compared to placebo. There were no differences in proteinuria, blood pressure, eGFR and serum creatinine between the ATO and placebo groups. Atorvastatin treatment is safe and improves biomarkers of tubular damage or injury in non-diabetic patients with CKD.


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