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Carriazo, Sol, Maria Vanessa Perez-Gomez, and Alberto Ortiz. "Hypertensive nephropathy: a major roadblock hindering the advance of precision nephrology." Clinical Kidney Journal 13, no. 4 (August 1, 2020): 504–9. http://dx.doi.org/10.1093/ckj/sfaa162.
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Abstract In the 2017 Annual Report of the ERA-EDTA Registry, hypertension continues to be the second or third most common cause of renal replacement therapy (RRT) in Europe, tied with glomerulonephritis. There is, however, one little issue: hypertension-induced end-stage renal disease (ESRD) might not exist at all as currently understood, that is, as hypertensive nephrosclerosis. In this regard, the incidence of RRT due to hypertensive nephropathy is related to the incidence of other causes of ESRD but not to the burden of hypertension per country. The current definition of hypertensive nephropathy is non-specific, outdated and only allows a delayed diagnosis by exclusion. It is not helpful that 80% of chronic kidney disease patients develop hypertension and kidney biopsy has no findings specific for hypertensive nephropathy. There is an urgent need to redefine the concept of hypertensive nephropathy with a clear and comprehensive set of criteria that at least should indicate how other nephropathies, including familial nephropathies, should be excluded. Correct causality assessment and aetiology-based therapy is a key to the progress of nephrology and it should no longer be accepted that ‘hypertensive nephropathy’ serves to disguise a suboptimal diagnostic workup. A diagnosis of nephropathy of unknown cause would be more honest when the full range of alternative aetiological diagnoses is not explored.
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Green, Siva Ranganathan, and Lavanya Vetrivel. "Hypertensive target organ damage and its relationship with platelet indices." International Journal of Advances in Medicine 8, no. 7 (June 23, 2021): 1002. http://dx.doi.org/10.18203/2349-3933.ijam20212415.
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Hypertension affects vascular endothelium of retina, kidney, and heart. These are called as target organ damage (TOD). Hypertension causes endothelial damage by shear mechanical stress which leads to platelet aggregation and activation. This article is a review for prediction of TOD in hypertensives by cost effective routine indicators like platelet indices [platelet distribution width (PDW), mean platelet volume (MPV) and platelet count]. Hypertension mediated target organ damage like left ventricular hypertrophy, hypertensive retinopathy and nephropathy is associated with increased platelet indices like MPV, PDW, and PLT. The use of these cost-effective platelet indicators in newly diagnosed hypertensives may need further studies to have clinical implications.
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Madubueze, George, and Emmanuel Ugwa. "A comparative ultrasonographic evaluation of intrarenal artery resistive index among hypertensive and normotensive adults in a black African population compared to a European population." Acta Radiologica Open 7, no. 1 (January 2018): 205846011775203. http://dx.doi.org/10.1177/2058460117752033.
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Background Hypertensive nephropathy is an important medical problem among the black African population. Early detection of renovascular changes using ultrasonography can provide opportunity for immediate intervention towards preventing or at least delaying the irreversible hypertensive nephropathy. Purpose To compare intrarenal resistive index (RI) in healthy normotensive and hypertensive adults in Kano, Nigeria. Material and Methods A prospective comparative study of intrarenal RI using ultrasound in 150 hypertensives and 150 normotensive controls. The mean renal RI of the interlobar arteries of both kidneys were measured and recorded. The data were analyzed with the aid of computer-based SPSS 16.0 software for Windows. Results The age range of the study participants was 35–70 years. The mean interlobar artery RI values were 0.59 ± 0.04 and 0.59 ± 0.03 on the right and left sides, respectively, in normotensive control individuals while those of hypertensive individuals were 0.73 ± 0.03 and 0.73 ± 0.03 for the mean interlobar artery RI values on the right and left sides, respectively. Conclusion The intrarenal RIs were lower in normotensives when compared with the hypertensive participants, which were statistically significant. These showed that hypertension has significant effects on the kidneys, and with early detection and intervention, irreversible renal damage may be prevented.
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Aryee, Christiana, William K. B. A. Owiredu, James Osei-Yeboah, Ellis Owusu-Dabo, Edwin F. Laing, and Isaac K. Owusu. "An Analysis of Anthropometric Indicators and Modifiable Lifestyle Parameters Associated with Hypertensive Nephropathy." International Journal of Hypertension 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/6598921.
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The surge in prevalence of chronic noncommunicable diseases like hypertension and chronic kidney disease has been linked with modifiable lifestyle practices and increased body fat. This study sought to compare the association between different modifiable lifestyle practices, adiposity indices, renal function parameters, and hypertension as well as the predictive implications for levels of these parameters in target cardiac organ damage among an urban Ghanaian hypertensive population. Using a hospital-based case-control study design, 241 Ghanaian indigenes from the Kumasi metropolis were recruited for this study. The case group was made up of 180 hypertensives and 61 normotensives served as controls. In addition to sociodemographic data, standard haemodynamic, anthropometric, renal function, and cardiac organ damage assessments were done. The prevalence of chronic kidney disease (CKD) ranged from 13.3% to 16.6% depending on the equation used in estimating the glomerular filtration rate (eGFR). Percentage cluster distribution by chronic kidney disease was observed to be significantly tilted toward the upper quartiles (3rd and 4th) of the haemodynamic parameters measured. Chronic kidney disease was significantly higher among self-reported smokers and alcoholic hypertensives. In this urban population, adiposity was associated with hypertension and renal insufficiency. Chronic kidney disease was associated with hypertension and cardiac abnormalities.
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Ng, L. L., and J. E. Davies. "Abnormalities in Na+/H+ antiporter activity in diabetic nephropathy." Journal of the American Society of Nephrology 3, no. 4 (October 1992): S50. http://dx.doi.org/10.1681/asn.v34s50.
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In hypertensive humans and the spontaneously hypertensive rat, increased cellular Na+/H+ antiport activity has been demonstrated in leukocytes, platelets, skeletal muscle, and vascular smooth muscle cells. This membrane abnormality may be associated with medial thickening of resistance vessels. A similar membrane transport abnormality has also been demonstrated in leukocytes and fibroblasts from type 1 diabetic patients with nephropathy. This membrane transport marker of hypertension may indicate a predisposition to essential hypertension in such patients and may lead to diabetic nephropathy, possibly from mesangial expansion.
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Schiffl, Helmut, and Susanne Lang. "Übergewicht und Nierenerkrankungen – renale Risiken einer „Epidemie“." DMW - Deutsche Medizinische Wochenschrift 142, no. 19 (September 2017): 1466–72. http://dx.doi.org/10.1055/s-0043-110659.
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AbstractOverweight and obesity are widespread in the German population, affecting not only adults but also a significant number of children and adolescents. The risk to develop chronic kidney disease is markedly increased in overweight or adipose children, adolescents and adults.Overweight and obesity induced risk factors have a direct impact on the development of chronic renal disease (obesity-associated focal segmental glomerulosclerosis). They accelerate the progression of coexistent nephropathies (diabetic or hypertensive nephropathy, primary glomerulonephritides) and are independent risk factors for the development of acute kidney injury in critically ill patients.Obesity induced nephropathies are basically preventible. Marked weight reduction, normoglycemia and control of hypertension may contribute to an improved glomerular filtration rate and/or reduced proteinuria in early stages of renal damage.The prevalence of kidney diseases in Germany is 13 % and estimated 80 000 patients need renal replacement therapy. In order to avoid a further rapid increase in numbers, preventive measures should be enforced more rigorously.It is necessary to raise the awareness of the negative consequences of obesity in the general public, to motivate the public to adopt a healthier lifestyle and to install nephrological surveillance to contain the obesity „epidemic“.
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Ghorbani, Ali, Mahmoud Rafieian-Kopaie, and Hamid Nasri. "Lipoprotein (a): More than a bystander in the etiology of hypertension? A study on essential hypertensive patients not yet on treatment." Journal of Nephropathology 2, no. 1 (January 1, 2013): 67–70. http://dx.doi.org/10.5812/nephropathol.9092.
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Kumar, Pradeep, Preeti Sharma, Rachna Sharma, Tripathi Gk, and Gaurav Gupta. "ASSESSMENT OF MICROALBUMINURIA IN ESSENTIAL HYPERTENSIVES AND ITS RESPONSE TO ANGIOTENSIN-CONVERTING ENZYME INHIBITOR THERAPY." Asian Journal of Pharmaceutical and Clinical Research 9, no. 9 (December 1, 2016): 32. http://dx.doi.org/10.22159/ajpcr.2016.v9s3.13618.
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ABSTRACTObjective: Objective is to study the prevalence of microalbuminuria among patients suffering from essential hypertension and also to evaluate theresponse of microalbuminuria to angiotensin-converting enzyme (ACE) inhibitors therapy.Methods: The study conducted at Santosh Medical College and Hospital, Ghaziabad, on 300 patients with essential hypertension. After attainingbaseline parameters in all patients, those newly diagnosed essential hypertensives with microalbuminuria not on any treatment were started on anACE inhibitor (ramipril), for 8 weeks, after which all parameters were reassessed and comparison and statistical analysis were done to establish theprevalence of microalbuminuria and its response to therapy.Results: In our study, mean microalbuminuria excretion was 101.79 mcg/mg creatinine at the beginning of the study and 80.20 mcg/mg creatinineafter 8 weeks of ACE inhibitor therapy, with 21.2% fall rate.Conclusion: Microalbuminuria is an independent risk factor for the development or worsening of hypertensive nephropathy and endothelialdysfunction, thereby increasing the risk of micro- and macro-vascular complications.Keywords: Microalbuminuria, Essential hypertension, Angiotensin-converting enzyme inhibitor therapy.
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Fontana, Fiorella, Pasquale Bernardi, Carmine Pizzi, Rosanna Toro, and Santi Spampinato. "β-Endorphin in pressor response to hyperventilation in elderly patients with essential and secondary hypertension." Open Medicine 3, no. 1 (March 1, 2008): 55–63. http://dx.doi.org/10.2478/s11536-007-0071-x.
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AbstractIt has been observed that a distinct blood pressure (BP) response to prolonged and forced hyperventilation in adult patients with essential hypertension is associated with significant changes in plasma catecholamine and β-endorphin levels. This paper investigated whether hemodynamic and neuro-endocrine responses to hyperventilation in elderly patients with essential hypertension (n = 39, mean age 81 ± 3 years) differ from those in elderly patients with secondary hypertension (isolated systolic hypertension, bilateral chronic nephropathy, nephroangiosclerosis, diabetic nephropathy and hyperparathyroidism) (n = 39, mean age 80 ± 1 years). Plasma β-endorphin levels were normal in patients with essential hypertension and increased in patients with secondary hypertension. Plasma norepinephrine levels were normal in both populations. Hyperventilation decreased BP and norepinephrine levels and increased β-endorphin levels in essential hypertensive patients, whereas it did not significantly change BP or neuro-hormonal levels in secondary hypertensive patients. Hierarchical cluster analysis based on BP response to hyperventilation disclosed a sub-group of essential hypertensive patients with the highest basal levels of norepinephrine and the lowest β-endorphin levels, in whom the BP decrease following hyperventilation was correlated with the decrease in norepinephrine and increase in β-endorphin levels. This suggests that b-endorphin may be involved in modulating sympatho-adrenergic activity in elderly patients with essential hypertension.
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Welker, Pia, Stephanie Krämer, David A. Groneberg, Hans H. Neumayer, Sebastian Bachmann, Kerstin Amann, and Harm Peters. "Increased mast cell number in human hypertensive nephropathy." American Journal of Physiology-Renal Physiology 295, no. 4 (October 2008): F1103—F1109. http://dx.doi.org/10.1152/ajprenal.00374.2007.
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Mast cells have recently been related to nonallergic chronic organ damage and fibrosis. In the present study, we analyzed mast cell number, localization, and maturation in the kidney of a relatively unique group of middle-aged accident victims with primary essential hypertension and in normotensive controls ( n = 8 per group, Caucasians, predominantly male). Hypertensive kidneys showed a significantly higher degree of arteriolosclerosis. However, glomerular and tubulointerstitial matrix accumulation did not differ significantly to normotensive controls indicating a relatively early stage of hypertensive nephropathy. Using toluidine blue staining, renal mast cell number was found to be fivefold higher in hypertensive subjects compared with normotensive controls. Mast cells were primarily located in the peritubular interstitial spaces, some perivascular, but not in glomeruli. In a series of immunohistological staining studies, mast cell maturation grading showed that expression of early hematopoietic precursor cell marker CD34 did not differ between both groups. In contrast, mast cells were mostly positive for IgE receptor, tryptase, and chymase indicating a mature, differentiated cell phenotype in hypertensive nephropathy. Renal expression of stem cell factor was markedly upregulated in primary hypertension. Kidney macrophage and lymphocyte numbers were similar in both groups. In conclusion, human hypertensive kidney disease shows an early and conspicuous upregulation of stem cell factor along with an increased number of mature mast cells. The results suggest that renal mast cell accumulation may play a role in the pathogenesis of human hypertensive nephropathy.
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Karam, Sabine. "Hypertensive nephropathy and cancer: Is it the hypertension, the nephropathy, or both?" Journal of Clinical Hypertension 21, no. 6 (May 24, 2019): 792–93. http://dx.doi.org/10.1111/jch.13562.
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Palabıyık, Şaziye Sezin, Ali Aşçı, Gözde Girgin, Gönül Şahin, Ramazan Çetinkaya, and Terken Baydar. "Evaluation of dihydropteridine reductase activities in patients with kidney failure." Pteridines 24, no. 3 (December 1, 2013): 219–23. http://dx.doi.org/10.1515/pterid-2013-0030.
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AbstractEnd-stage renal disease (ESRD) is the inability of the kidneys to remove waste products from the blood. The most important factors causing ESRD that require hemodialysis are diabetes and hypertension. There are limited numbers of studies to evaluate tetrahydrobiopterin pathway in these patients. The aim of the study was to evaluate tetrahydrobiopterin pathway by measuring its important components, biopterin to creatinine concentrations and dihydropteridine reductase activities in diabetes and hypertension patients treated with/without hemodialysis. The patients undergoing hemodialysis were classified as diabetic nephropathy (n=21), hypertensive nephropathy (n=20) and others (n=30), while the controls consisted of healthy subjects (n=21), diabetic subjects (n=23) and hypertensive subjects (n=22) without any renal disorder. It was found that urinary biopterin to creatinine concentrations significantly increased in kidney failure patients undergoing hemodialysis compared to the healthy control group (p<0.05). Additionally, there were significant differences in urinary biopterin to creatinine concentrations between diabetes or hypertension patients and their hypertensive or diabetic control counterparts (both p<0.05). Our results indicated an alteration in tetrahydrobiopterin pathway in ESRD, and in the presence of secondary pathologies such as diabetes and hypertension in the patients undergoing hemodialysis, more considerable changes are observed in the pathway.
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Ullah, Mohammad, and Suman Kumar Saha. "Modifiable Cardiovascular Risk Factors in Hypertensive Patients." Cardiovascular Journal 11, no. 1 (September 14, 2018): 10–16. http://dx.doi.org/10.3329/cardio.v11i1.38236.
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Background: Hypertension is one of the most important noncommunicable diseases. Presence of other cardiovascular risk factors in hypertensive patients increases the risk of ischaemic heart disease and cerebrovascular diseases. We evaluated the prevalence of cardiovascular risk factors among the hypertensive patients.Methods: Patients presenting to the outpatient department of a secondary hospital were included in the study. The prevalence of diabetes mellitus, current smoking, family history of ishaemic heart disease, dyslipidaemia and nephropathy were evaluated.Results: A total of 144 patients were included in the study (male 66 & female 78). 29.8% patients were smoker (57% of male patients and 6% of female patients); 34% patients were diabetic; 27% patients had raised total cholesterol, 40.3% had reduced HDL, 22% had raised LDL, 36.8% had raised triglyceride and 33.3% patients had nephropathy (proteinuria/ raised serum creatinine).Conclusion: The prevalence of cardiovascular risk factors, specifically smoking, diabetes mellitus, raised LDL and nephropathy were more among the hypertensive patients. All the hypertensive patients should be evaluated for modifiable cardiovascular risk factors during diagnosis and follow up. Treatment of these risk factors can improve the prognosis of the hypertensive patients.Cardiovasc. j. 2018; 11(1): 10-16
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Huan, Jia-Ming, Wen-Ge Su, Wei Li, Chao Gao, Peng Zhou, Chun-Sheng Fu, Xiao-Feng Wang, Yi-Min Wang, and Yi-Fei Wang. "Summarizing the Effective Herbs for the Treatment of Hypertensive Nephropathy by Complex Network and Machine Learning." Evidence-Based Complementary and Alternative Medicine 2021 (June 11, 2021): 1–12. http://dx.doi.org/10.1155/2021/5590743.
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Hypertensive nephropathy is a common complication of hypertension. Traditional Chinese medicine has been used in the clinical treatment of hypertensive nephropathy for a long time, but the commonly used prescriptions have not been summarized, and the basic therapeutic approaches have not been discussed. Based on data from 3 years of electronic medical records of traditional Chinese medicine used at the Affiliated Hospital of Shandong University of Traditional Chinese Medicine, a complex network and machine learning algorithm was used to explore the prescribed herbs of traditional Chinese medicine in the treatment of hypertensive nephropathy (HN). In this study, complex network algorithms were used to describe traditional Chinese medicine prescriptions for HN treatment. The Apriori algorithm was used to analyze the compatibility of these treatments with modern medicine. Data on the targets and regulatory genes related to hypertensive nephropathy and the herbs that affect their expression were obtained from public databases, and then, the signaling pathways enriched with these genes were identified on the basis of their participation in biological processes. A clustering algorithm was used to analyze the therapeutic pathways at multiple levels. A total of 1499 prescriptions of traditional Chinese medicines used for the treatment of hypertensive renal damage were identified. Fourteen herbs used to treat hypertensive nephropathy act through different biological pathways: huangqi, danshen, dangshen, fuling, baizhu, danggui, chenpi, banxia, gancao, qumai, cheqianzi, ezhu, qianshi, and niuxi. We found the formulae of these herbs and observed that they could downregulate the expression of inflammatory cytokines such as TNF, IL1B, and IL6 and the NF-κB and MAPK signaling pathways to reduce the renal inflammatory damage caused by excessive activation of RAAS. In addition, these herbs could facilitate the deceleration in the decline of renal function and relieve the symptoms of hypertensive nephropathy. In this study, the traditional Chinese medicine approach for treating hypertensive renal damage is summarized and effective treatment prescriptions were identified and analyzed. Data mining technology provided a feasible method for the collation and extraction of traditional Chinese medicine prescription data and provided an objective and reliable tool for use in determining the TCM treatments of hypertensive nephropathy.
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Olearczyk, Jeffrey J., Jeffrey E. Quigley, Bradford C. Mitchell, Tatsuo Yamamoto, In-Hae Kim, John W. Newman, Ayala Luria, Bruce D. Hammock, and John D. Imig. "Administration of a substituted adamantyl urea inhibitor of soluble epoxide hydrolase protects the kidney from damage in hypertensive Goto–Kakizaki rats." Clinical Science 116, no. 1 (November 28, 2008): 61–70. http://dx.doi.org/10.1042/cs20080039.
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Hypertension and Type 2 diabetes are co-morbid diseases that lead to the development of nephropathy. sEH (soluble epoxide hydrolase) inhibitors are reported to provide protection from renal injury. We hypothesized that the sEH inhibitor AUDA [12-(3-adamantan-1-yl-ureido)-dodecanoic acid] protects the kidney from the development of nephropathy associated with hypertension and Type 2 diabetes. Hypertension was induced in spontaneously diabetic GK (Goto–Kakizaki) rats using AngII (angiotensin II) and a high-salt diet. Hypertensive GK rats were treated for 2 weeks with either AUDA or its vehicle added to drinking water. MAP (mean arterial pressure) increased from 118±2 mmHg to 182±20 and 187±6 mmHg for vehicle and AUDA-treated hypertensive GK rats respectively. AUDA treatment did not alter blood glucose. Hypertension in GK rats resulted in a 17-fold increase in urinary albumin excretion, which was decreased with AUDA treatment. Renal histological evaluation determined that AUDA treatment decreased glomerular and tubular damage. In addition, AUDA treatment attenuated macrophage infiltration and inhibited urinary excretion of MCP-1 (monocyte chemoattractant protein-1) and kidney cortex MCP-1 gene expression. Taken together, these results provide evidence that sEH inhibition with AUDA attenuates the progression of renal damage associated with hypertension and Type 2 diabetes.
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Wang, Liping, Yong Zhang, Shanyuan Chen, Jian Chen, Yongze Zhuang, and Jinhua Chen. "Association of metabolic syndrome and IgA nephropathy." Journal of Clinical Pathology 63, no. 8 (August 2010): 697–701. http://dx.doi.org/10.1136/jcp.2009.074278.
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BackgroundThe disorders associated with metabolic syndrome (MS) can lead to renal disease. IgA nephropathy is the most common form of glomerulonephritis, and many patients with this disorder progress to renal failure.AimsTo identify the effect of MS on IgA nephropathy by retrospectively comparing patients who had IgA nephropathy and MS with those who had IgA nephropathy alone.Methods30 patients with MS and IgA nephropathy (MS group), and 30 matched controls with IgA nephropathy alone (non-MS group) were enrolled. IgA nephropathy was diagnosed by renal biopsy; activity and severity was graded by two classification systems. MS was diagnosed by criteria of the Diabetes Society of the Chinese Medical Association.ResultsSimple and multiple linear regression models (which adjusted for age, gender and body surface area) showed that only hypertension significantly affected serum creatinine, an indicator of the clinical severity of renal disease. Simple and multiple linear regression models (which adjusted for age, gender and body surface area) also showed that hypertensive patients had higher Katafuchi scores, an indicator of the pathological severity of renal disease.ConclusionAmong the disorders associated with MS, hypertension is the most important factor for renal disease.
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Nordbø, O. P., E. Koch, Ø. Eikrem, L. Landolt, A. Scherer, J. Palmer, T. Apeland, N. Delaleu, and H. P. Marti. "HYPERTENSIVE NEPHROPATHY." Journal of Hypertension 37 (July 2019): e89. http://dx.doi.org/10.1097/01.hjh.0000570304.08739.c0.
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Kostovska, Irena, Katerina Tosheska Trajkovska, Svetlana Cekovska, Goce Spasovski, and Danica Labudovic. "Nephrin and Podocalyxin - New Podocyte Proteins for Early Detection of Secondary Nephropathies." BANTAO Journal 14, no. 1 (June 27, 2016): 11–16. http://dx.doi.org/10.1515/bj-2016-0003.
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AbstractIn the last two decades a great progress was observed in understanding of podocytes, their specific structure and function identifying many specific podocyte proteins, such as nephrin and podocalyxin. Podocytes form the final barrier to plasma proteins leakage. Nephrin as a main component of the filtration diaphragm forms a physical barrier while podocalyxin as sialoglycoprotein forms an electrostatic barrier. Podocyte damage, i.e. podocytopathies and their loss through urine-podocyturia, are crucial in pathogenesis and progression of nephropathies with proteinuria as main clinical manifestation. In podocytopathies, nephrin and podocalyxin appear in the urine before proteinuria and microalbuminuria which were previously considered as earliest markers of nephropathies. Nephrinuria and podocalyxuria indicate damage of the podocytes on glomerular level and/or presence of apoptotic and necrotic podocytes in urine. These urinary markers are also important in early diagnosis of secondary nephropathies such as diabetic, lupus and hypertensive nephropathy as the most common causes of end-stage renal failure (ESRF). These markers are also important in the prediction of preeclampsia, which is the most common complication in pregnancy. In this review we elaborate in dept the main structural and functional features of podocytes and their specific proteins, nephrin and podocalyxin, summarizing the recent literature data on their importance in the early diagnosis of the most common secondary nephropathies.
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Rahman, Md Anisur, Md Mostarshid Billah, Palash Mitra, Md Emtiaz Hossan, Md Jakir Hossain, Wasim Md Mohosin Ul Haque, and Md Abul Mansur. "Raised Arterial Pressure and Microalbuminuria in Type 2 Diabetic Subjects with Familial Hypertension." Bangladesh Critical Care Journal 4, no. 1 (June 1, 2016): 14–18. http://dx.doi.org/10.3329/bccj.v4i1.27973.
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Background and Aims : Microalbuminuria is claimed to be an early marker of nephropathy in type 2 diabetes.The raised arterial pressure is an important factor in the progression of diabetic nephropathy. There is a significant correlation between blood pressure and the progression of albuminuria in both type 1 and type 2 diabetes. This study in Bangladeshi type 2 diabetic patients was to evaluate whether microalbuminuria and raised arterial pressure are influenced by familial predisposition to hypertension.Methods : Sixty three newly diagnosed Bangladeshi type 2 diabetic patients were investigated. The diabetic subjects were divided into two groups as diabetes with family history of hypertension (n=37) and diabetes without family history of hypertension (n=26). Diabetic subjects were further divided into normotensive (n= 46) and hypertensive (n= 17); diabetic normoalbuminuric (n 44) and diabetic microalbuminuric (n 19) subgroups. Serum glucose was measured by glucose-oxidase; blood urea, serum creatinine and urinary creatinine by enzymatic-colorimetric method and urinary albumin by immunoturbidimetry method.Results : systolic blood pressure (SBP), diastolic blood pressure (DBP) and microalbuminuria were significantly elevated in diabetic subjects with familial predisposition to hypertension when compared to diabetic subjects without familial predisposition to hypertension [SBP (127±16 vs 110±14) mmHg P= 0.001; DBP (81±9 vs 72±11) mmHg P= 0.001; Microalbuminuria 2.23(0.28-9.43) vs 1.52(.29-3.91) mg/mmol p<0.03]. When diabetic normotensive subjects were compared with diabetic hypertensive subjects for microalbuminuria, no significant difference was found among themselves [median (range) 1.67(0.17-8.62) vs 1.70(.28-9.43) mg/mmol p = NS]. Comparison of blood pressure was found no significant difference between diabetic normoalbuminuric and diabetic microalbuminuric subjects [systolic blood pressure (117±17 vs 125±17) mmHg p= NS ; diastolic blood pressure (76±11 vs 82±10) mmHg p= NS ].Conclusion : Microalbuminuria, a marker of early diabetic nephropathy and raised arterial pressure, a progression factor of nephropathy are more influenced by familial predisposition to hypertension in diabetic population irrespective of presence or absence of microalbuminuria and hypertension.Bangladesh Crit Care J March 2016; 4 (1): 14-18
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Hartner, Andrea, Nada Cordasic, Bernd Klanke, Michael Wittmann, Roland Veelken, and Karl F. Hilgers. "Renal injury in streptozotocin-diabetic Ren2-transgenic rats is mainly dependent on hypertension, not on diabetes." American Journal of Physiology-Renal Physiology 292, no. 2 (February 2007): F820—F827. http://dx.doi.org/10.1152/ajprenal.00088.2006.
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Induction of streptozotocin (STZ) diabetes in hypertensive rats transgenic for the mouse ren-2 gene (TGR) has been described as a model of progressive diabetic nephropathy. We investigated the long-term course of STZ diabetes in TGR and appropriate Sprague-Dawley control rats (SD) and tested the role of angiotensin-dependent hypertension by treating rats with the angiotensin II type 1 receptor blocker losartan (1 mg·kg−1·day−1) via osmotic minipumps. Five weeks after STZ injection, diabetes developed in TGR and SD. Urinary albumin excretion was increased by diabetes and, to a much higher degree, by hypertension. The effects of hypertension and diabetes were not additive, and only the effects of hypertension were ameliorated by losartan. A similar pattern was observed for cell proliferation and macrophage infiltration in the kidney. In contrast, the effects of hypertension and diabetes on glomerular collagen IV accumulation were additive 5 wk after STZ injection. In a long-term study for 20 wk after STZ, survival was better in STZ-treated TGR than in normoglycemic TGR, whereas all SD survived. Impaired creatinine clearance and increased macrophage infiltration as well as glomerular and interstitial matrix deposition were prominent in TGR compared with SD, regardless of the presence or absence of diabetes. In conclusion, STZ diabetes in TGR may be useful to study glomerular and interstitial matrix deposition early in the course of diabetes. However, the long-term course of this animal model resembles severe hypertensive nephrosclerosis, rather than progressive diabetic nephropathy.
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Liu, Mei-Li, Hai-Xu Song, Xiao-Xiang Tian, Yan-Xia Liu, Dan Liu, Zhi-Wei Hou, Jia-Yin Li, Cheng-Hui Yan, and Ya-ling Han. "Recombinant Cellular Repressor of E1A-Stimulated Genes Protects against Renal Fibrosis in Dahl Salt-Sensitive Rats." American Journal of Nephrology 51, no. 5 (2020): 401–10. http://dx.doi.org/10.1159/000506411.
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Background: Human cellular repressor of E1A-stimulated genes (CREG) is a secreted glycoprotein that attenuates angiotensin II-induced hypertension, alleviates myocardial fibrosis, and improves heart function. However, the role of CREG in high-salt (HS) diet-induced hypertensive nephropathy is unclear. Methods: To determine the effects and molecular mechanisms of CREG in HS diet-induced hypertensive nephropathy, we established a hypertensive nephropathy animal model in Dahl salt-sensitive (SS) rats fed a HS diet (8% NaCl, n = 20) for 8 weeks. At week 4 of HS loading, these rats were administered recombinant CREG (reCREG; 35 µg/kg·day, n = 5) and saline (n = 5) via subcutaneously implanted pumps and were also administered the vasodilator hydralazine (20 mg/kg·day, n = 5) in drinking water. We used hematoxylin and eosin staining, Masson’s trichrome staining, immunohistochemical labeling, western blotting, RT-PCR, and Tunel staining to determine the signaling pathways of CREG in HS diet-induced hypertensive nephropathy. Results: After 8 weeks of HS intake, the Dahl SS rats developed renal dysfunction and severe renal fibrosis associated with reductions of 78 and 67% in CREG expression, respectively, at both mRNA and protein levels in the kidney. Administration of reCREG improved renal function and relieved renal fibrosis. Administration of CREG also inhibited monocyte infiltration and reduced apoptosis in the kidney cells. CREG overexpression upregulated forkhead box P1 expression and inhibited the transforming growth factor-β1 signaling pathway. Conclusion: Our study shows that CREG protected the kidney against HS-diet-induced renal damage and provides new insights into the mechanisms underlying kidney injury.
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Cavalcante, Paula Andréa Malveira, Natalia Alenina, Alexandre Budu, Leandro Ceotto Freitas-Lima, Thaís Alves-Silva, Juan Sebastian Henao Agudelo, Fatimunnisa Qadri, Niels Olsen Saraiva Camara, Michael Bader, and Ronaldo Carvalho Araújo. "Nephropathy in Hypertensive Animals Is Linked to M2 Macrophages and Increased Expression of the YM1/Chi3l3 Protein." Mediators of Inflammation 2019 (July 10, 2019): 1–14. http://dx.doi.org/10.1155/2019/9086758.
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Macrophages contribute to a continuous increase in blood pressure and kidney damage in hypertension, but their polarization status and the underlying mechanisms have not been clarified. This study revealed an important role for M2 macrophages and the YM1/Chi3l3 protein in hypertensive nephropathy in a mouse model of hypertension. Bone marrow cells were isolated from the femurs and tibia of male FVB/N (control) and transgenic hypertensive animals that overexpressed the rat form of angiotensinogen (TGM(rAOGEN)123, TGM123-FVB/N). The cells were treated with murine M-CSF and subsequently with LPS+IFN-γ to promote their polarization into M1 macrophages and IL-4+IL-13 to trigger the M2 phenotype. We examined the kidneys of TGM123-FVB/N animals to assess macrophage polarization and end-organ damage. mRNA expression was evaluated using real-time PCR, and protein levels were assessed through ELISA, CBA, Western blot, and immunofluorescence. Histology confirmed high levels of renal collagen. Cells stimulated with LPS+IFN-γ in vitro showed no significant difference in the expression of CD86, an M1 marker, compared to cells from the controls or the hypertensive mice. When stimulated with IL-4+IL-13, however, macrophages of the hypertensive group showed a significant increase in CD206 expression, an M2 marker. The M2/M1 ratio reached 288%. Our results indicate that when stimulated in vitro, macrophages from hypertensive mice are predisposed toward polarization to an M2 phenotype. These data support results from the kidneys where we found an increased infiltration of macrophages predominantly polarized to M2 associated with high levels of YM1/Chi3l3 (91,89%), suggesting that YM1/Chi3l3 may be a biomarker of hypertensive nephropathy.
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Krutikov, E., S. Chistyakova, S. Gorbatyuk, and V. Cvetkov. "EARLYDIAGNOSIS OFINTRARENAL BLOOD FLOW DISORDERSIN PATIENTS WITH ESSENTIAL ARTERIAL HYPERTENSION." Ukrainian Journal of Nephrology and Dialysis, no. 2(42) (March 6, 2014): 30–35. http://dx.doi.org/10.31450/ukrjnd.2(42).2014.06.
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Summary. Among the causes of end-stage renal failure essential arterial (EAH) hypertension has a leading place. One of thepathogenic mechanisms of hypertensive nephropathy is a violation of intrarenal blood flow. The purpose of this study was to conduct an early diagnosis of intrarenal blood flow disorders using Doppler examination and comparison of these data with the standard criteria of nephropathy in EAH.
Materials and methods. 80patients with stage II EAH were examined.
Results. In patients with grade II and III EAH noted depletion of intrarenal blood flow, characterized by low Vmax and Vmin, while there was an increase IR characterizing renal vascular resistance. Hyper phase in hypertensive nephropathy was characterized by a relative increase in hemodynamic indices at the level of the trunk of the renal artery and segmental artery with a reduction in the small arteries to the level in healthy people. Hypofiltration phase was characterized by a significant reduction of velocity indexes that accompanied by a decreasing of vascular resistance (theirpseudonormalization). In assessing renal hemodynamics in patients with EAH and microalbuminuria showed a decreasening of Vmin and increasening of IR. A inverse correlation between the level of night BP decreasing and IR segmental artery (r = - 0,61, p<0,05).
Conclusions: 1. In patients with essential hypertension grade IIand IIImarked depletion of intrarenal blood flow characterized by a decrease in peak systolic and minimum diastolic velocity. At the same time there is increasing resistance indices characterizing renal vascular resistance. 2. Early stage of fypertensive nephropathy criteria before the development of microalbuminuria, hyperfiltration can be the increase in the indices at the level of resistance of main and segmental arteries according to Doppler examination of renal vessels. 3. In patients with essential hypertension and microalbuminuria there is a decrease in diastolic velocity and resistive index increase, indicating an increase in intrarenal vascular resistance and may also be a diagnostic criterion of nephropathy. 4. The inverse correlation between the level of nighttime decrease in blood pressure and segmental artery resistance index indicate the negative impact of the lack of night reduction in blood pressure to renal function in hypertension.
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Kang, Duk-Hee, Yoon-Goo Kim, Takeshi F. Andoh, Katherine L. Gordon, Shin-Ichi Suga, Marilda Mazzali, J. Ashley Jefferson, et al. "Post-cyclosporine-mediated hypertension and nephropathy: amelioration by vascular endothelial growth factor." American Journal of Physiology-Renal Physiology 280, no. 4 (April 1, 2001): F727—F736. http://dx.doi.org/10.1152/ajprenal.2001.280.4.f727.
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Recent studies have demonstrated a role for microvascular and tubulointerstitial injury in some models of salt-sensitive hypertension. We utilized a model of post-cyclosporin A (CsA) nephropathy and hypertension to test the hypothesis that treatment with an angiogenic factor aimed at ameliorating the microvascular and renal injury would prevent the development of hypertension. CsA was administered with a low-salt diet for 45 days, resulting in a renal lesion characterized by afferent arteriolopathy, focal peritubular capillary loss, and tubulointerstitial fibrosis. Rats were then placed on a high-salt diet and randomized to receive either vascular endothelial growth factor (VEGF121) or vehicle for 14 days. Placement of rats with established CsA nephropathy on a high-salt diet results in the rapid development of salt-sensitive hypertension. VEGF121 treatment resulted in lower blood pressure, and this persisted on discontinuing the VEGF. VEGF121 treatment was also associated with a decrease in osteopontin expression, macrophage infiltration, and collagen III deposition and markedly stimulated resolution of the arteriolopathy (20.9 ± 7.8 vs. 36.9 ± 6.1%, VEGF vs. vehicle, P < 0.05). In conclusion, CsA-associated renal microvascular and tubulointerstitial injury results in the development of salt-sensitive hypertension. Treatment of animals with established CsA nephropathy with VEGF reduces the hypertensive response and accelerates histological recovery. The vascular protective effect of VEGF may be due to the improvement of arteriolopathy. Angiogenic growth factors may represent a novel strategy for treating CsA-associated hypertension and renal disease.
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U., Ravi Kumar, Shashank J., and Narayana Swamy. "Study of clinical profile of chronic kidney disease in non-diabetic patients." International Journal of Advances in Medicine 8, no. 8 (July 23, 2021): 1113. http://dx.doi.org/10.18203/2349-3933.ijam20212809.
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Background: Chronic kidney disease (CKD) encompasses a spectrum of different pathophysiological processes associated with abnormal kidney function and a progressive decline in glomerular filtration rate. Cardiovascular disease is one of the major cause of morbidity and mortality in patients at every stage of CKD. Diabetes mellitus and hypertension together being major cause for CKD. Hypertension is a common cause for CKD and an independent risk factor for cardiovascular disease. This study mainly focused on the causes of CKD other than diabetes mellitus. An early detection and appropriate intervention of these patients will possibly help prevent progression of renal disease.Methods:We assessed 55 non diabetic CKD patients who presented to the OPD/IPD in Victoria hospital, Bowring and Lady Curzon hospital and other hospitals affiliated to Bangalore medical college and research institute during period June 2018 to December 2019. A detailed history and clinical examination was performed and patients were subjected to necessary investigations.Results: The commonest etiology for CKD was found to be hypertensive nephropathy followed by glomerulonephritis. Common symptoms were generalized weakness, lower limb swelling. Commonest signs are pallor, pedal edema and hypertension.Conclusions:CKD is a major health problem. Diabetic nephropathy is the commonest cause for CKD followed by hypertensive nephropathy and glomerulonephritis. Anaemia, pedal oedema, oliguria and generalised weakness were the major presenting clinical signs and symptoms in CKD. This condition when detected in early stages and managed can slow down the progression of CKDs and delay the need of renal replacement therapy.
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Seccia, Teresa, Brasilina Caroccia, Maria Piazza, and Gian Paolo Rossi. "The Key Role of Epithelial to Mesenchymal Transition (EMT) in Hypertensive Kidney Disease." International Journal of Molecular Sciences 20, no. 14 (July 21, 2019): 3567. http://dx.doi.org/10.3390/ijms20143567.
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Accumulating evidence indicates that epithelial-to-mesenchymal transition (EMT), originally described as a key process for organ development and metastasis budding in cancer, plays a key role in the development of renal fibrosis in several diseases, including hypertensive nephroangiosclerosis. We herein reviewed the concept of EMT and its role in renal diseases, with particular focus on hypertensive kidney disease, the second leading cause of end-stage renal disease after diabetes mellitus. After discussing the pathophysiology of hypertensive nephropathy, the ‘classic’ view of hypertensive nephrosclerosis entailing hyalinization, and sclerosis of interlobular and afferent arterioles, we examined the changes occurring in the glomerulus and tubulo-interstitium and the studies that investigated the role of EMT and its molecular mechanisms in hypertensive kidney disease. Finally, we examined the reasons why some studies failed to provide solid evidence for renal EMT in hypertension.
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Ostroumova, O. D., A. A. Zykova, and A. M. Batutina. "Treatment of arterial hypertension in patients with diabetes mellitus and nephropathy: current potentialities of renin-angiotensin-aldosterone system block." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 9, no. 6 (December 28, 2003): 191–95. http://dx.doi.org/10.18705/1607-419x-2003-9-6-191-195.
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Diabetes mellitus and arterial hypertension are major risk factors of cardiovascular complications. Diabetic nephropathy is the most common cause of end-stage chronic renal failure in the world; next is hypertensive nephropathy. Microalbuminuria is the earliest clinical marker of renal dysfunction. The basic clinical significance of microalbuminuria is that it is an independent risk factor of both end-stage chronic renal failure and cardiovascular complications. Controlling blood pressure with antihypertensive agents in patients with diabetes mellitus ensures diminished microalbuminuria and retards the development of chronic renal failure. Angiotensin II receptor blockers and angiotensin-converting enzyme (ACE) inhibitors are essential drugs for the treatment of patients with diabetes mellitus and nephropathy. A combination of these two classes of drugs offers new prospects for nephroprotection in this group of patients.
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Glazyrin, Yury E., Dmitry V. Veprintsev, Irina A. Ler, Maria L. Rossovskaya, Svetlana A. Varygina, Sofia L. Glizer, Tatiana N. Zamay, et al. "Proteomics-Based Machine Learning Approach as an Alternative to Conventional Biomarkers for Differential Diagnosis of Chronic Kidney Diseases." International Journal of Molecular Sciences 21, no. 13 (July 7, 2020): 4802. http://dx.doi.org/10.3390/ijms21134802.
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Diabetic nephropathy, hypertension, and glomerulonephritis are the most common causes of chronic kidney diseases (CKD). Since CKD of various origins may not become apparent until kidney function is significantly impaired, a differential diagnosis and an appropriate treatment are needed at the very early stages. Conventional biomarkers may not have sufficient separation capabilities, while a full-proteomic approach may be used for these purposes. In the current study, several machine learning algorithms were examined for the differential diagnosis of CKD of three origins. The tested dataset was based on whole proteomic data obtained after the mass spectrometric analysis of plasma and urine samples of 34 CKD patients and the use of label-free quantification approach. The k-nearest-neighbors algorithm showed the possibility of separation of a healthy group from renal patients in general by proteomics data of plasma with high confidence (97.8%). This algorithm has also be proven to be the best of the three tested for distinguishing the groups of patients with diabetic nephropathy and glomerulonephritis according to proteomics data of plasma (96.3% of correct decisions). The group of hypertensive nephropathy could not be reliably separated according to plasma data, whereas analysis of entire proteomics data of urine did not allow differentiating the three diseases. Nevertheless, the group of hypertensive nephropathy was reliably separated from all other renal patients using the k-nearest-neighbors classifier “one against all” with 100% of accuracy by urine proteome data. The tested algorithms show good abilities to differentiate the various groups across proteomic data sets, which may help to avoid invasive intervention for the verification of the glomerulonephritis subtypes, as well as to differentiate hypertensive and diabetic nephropathy in the early stages based not on individual biomarkers, but on the whole proteomic composition of urine and blood.
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Liu, Guan-Xian, You-Qi Li, Xiao R. Huang, Li Hua Wei, Yang Zhang, Min Feng, Xiao-Ming Meng, Hai-Yong Chen, Yong-Jun Shi, and Hui Y. Lan. "Smad7 inhibits AngII-mediated hypertensive nephropathy in a mouse model of hypertension." Clinical Science 127, no. 3 (April 3, 2014): 195–208. http://dx.doi.org/10.1042/cs20130706.
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SMAD7 treatment inhibits AngII-induced hypertensive kidney disease. Inhibition of the Sp1/TGFβ/SMAD3/NF-κB/miR-29 regulatory network may be a mechanism by which SMAD7 protects kidney from hypertensive kidney injury. Thus SMAD7 may be a novel therapeutic agent for hypertensive kidney disease.
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Hannedouche, T. P., L. P. Marques, P. Guicheney, B. Lacour, C. Boitard, and J. P. Grünfeld. "Predisposition to essential hypertension and renal hemodynamics in recent-onset insulin-dependent diabetic patients." Journal of the American Society of Nephrology 3, no. 4 (October 1992): S34. http://dx.doi.org/10.1681/asn.v34s34.
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The offspring of essential hypertensive parents have been found to exhibit abnormalities in renal hemodynamics and sodium handling before the eventual occurrence of hypertension. The reported abnormalities represent a wide spectrum of changes including increased GFR, normal or decreased RPF, slight increase in blood pressure (although within the normal range), and an exaggerated natriuresis response to a sodium load. The heterogeneity of these abnormalities may reflect the specific conditions of the studies, the lability of the changes, or different subgroups of subjects with genetic predisposition to essential hypertension. Several lines of evidence have suggested a relationship between hypertension and the development of diabetic nephropathy in insulin-dependent diabetics. This laboratory has found that recent-onset insulin-dependent diabetics can exhibit renal hemodynamics abnormalities very early in the course of diabetes according to a positive or negative family history of essential hypertension. These changes include increased GFR and mean arterial pressure, but no differences in renal sodium and lithium handling in diabetics with a genetic predisposition to essential hypertension. In addition, diabetics with a positive family history of essential hypertension exhibited a more-marked vasodilative response to an acute interruption of the renin-angiotensin system, further suggesting inadequate angiotensin modulation of renal vascular tone. The significance of these abnormalities in relation to the development of diabetic nephropathy requires further investigation.
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Makino, H., M. Haneda, T. Babazono, T. Moriya, S. Ito, Y. Iwamoto, R. Kawamori, M. Takeuchi, and S. Katayama. "The Telmisartan Renoprotective Study from Incipient Nephropathy to Overt Nephropathy – Rationale, Study Design, Treatment Plan and Baseline Characteristics of the Incipient to Overt: Angiotensin II Receptor Blocker, Telmisartan, Investigation on Type 2 Diabetic Nephropathy (INNOVATION) Study." Journal of International Medical Research 33, no. 6 (November 2005): 677–86. http://dx.doi.org/10.1177/147323000503300610.
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We planned the INNOVATION study to determine whether telmisartan, an angiotensin-2-receptor blocker, delays the progression of renal disease from incipient nephropathy to overt nephropathy in hypertensive or normotensive Japanese patients with type 2 diabetes mellitus. The INNOVATION study is a randomized, double-blind, placebo-controlled trial. Eligible patients must have incipient nephropathy (defined as a urinary albumin to creatinine ratio of 100-300 mg/g creatinine) and a serum creatinine concentration of < 1.5 mg/dl for men and < 1.3 mg/dl for women. Patients who need treatment with angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors are excluded. Eligible patients are randomly assigned to three groups: telmisartan titrated to 40 mg; telmisartan titrated to 80 mg; or placebo. The primary endpoint is the time from baseline visit to first detection of overt nephropathy (defined by a urinary albumin to creatinine ratio that is > 300 mg/g creatinine and 30% higher than the baseline on at least two consecutive visits). A total of 1855 patients have been enrolled from 160 study centres. In 527 randomized patients (28.4% of the enrolled patients), mean (SD) urinary albumin to creatinine ratio and serum creatinine concentration at baseline were 173.3 (47.2) mg/g creatinine and 0.78 (0.19) mg/dl. Sixty-eight per cent of the patients had hypertension at baseline. Mean (SD) systolic and diastolic blood pressures at baseline were 137.1 (14.6) and 77.5 (10.3) mmHg. The INNOVATION study will determine whether telmisartan, an angiotensin II receptor blocker, provides clinical benefits in hypertensive or normotensive patients with diabetes mellitus and diabetic nephropathy.
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Durst, Stephen W., and Deb Schering. "Hypertension Management in the Diabetes Patient." Journal of Pharmacy Practice 17, no. 1 (February 2004): 55–60. http://dx.doi.org/10.1177/0897190003261309.
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Approximately 11 million of the 17 million US citizens with type 2 diabetes mellitus also have hypertension. The development of diabetic nephropathy in patients with type 1 diabetes is frequently associated with hypertension, and both may present several years after the onset of diabetes. In type 2 diabetes, hypertension may precede the development of diabetes by several years. Differences that exist between type 1 and type 2 diabetes and the development of hypertension may indicate differences in the concomitant disease processes, yet the inevitable development of both diseases contributes to significant increases in risk of cardiovascular disease.The pharmacist must be familiar with blood pressure treatment goals in the hypertensive-diabetic patient and appropriate pharmacotherapeutic management. This article outlines treatment goals in the patient with diabetes and concurrent hypertension, reviews trials assessing pharmacologic treatments, and provides a summary of monitoring parameters to guide the pharmacist in the management of this population.
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Schmieder, Roland E., Roland Veelken, Christoph D. Gatzka, Heinz R??ddel, and Hartmut Sch??chinger. "Predictors for hypertensive nephropathy." Journal of Hypertension 13, no. 3 (March 1995): 357???366. http://dx.doi.org/10.1097/00004872-199503000-00012.
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Liu, Zhen, Xiao R. Huang, and Hui Y. Lan. "Smad3 mediates ANG II-induced hypertensive kidney disease in mice." American Journal of Physiology-Renal Physiology 302, no. 8 (April 15, 2012): F986—F997. http://dx.doi.org/10.1152/ajprenal.00595.2011.
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Although Smad3 is a key mediator for fibrosis, its functional role and mechanisms in hypertensive nephropathy remain largely unclear. This was examined in the present study in a mouse model of hypertension induced in Smad3 knockout (KO) and wild-type (WT) mice by subcutaneous angiotensin II infusion and in vitro in mesangial cells lacking Smad3. After angiotensin II infusion, both Smad3 KO and WT mice developed equally high levels of blood pressure. However, disruption of Smad3 prevented angiotensin II-induced kidney injury by lowering albuminuria and serum creatinine ( P < 0.01), inhibiting renal fibrosis such as collagen type I and IV, fibronectin, and α-SMA expression (all P < 0.01), and blocking renal inflammation including macrophage and T cell infiltration and upregulation of IL-1β, TNF-α, and monocyte chemoattractant protein-1 in vivo and in vitro (all P < 0.001). Further studies revealed that blockade of angiotensin II-induced renal transforming growth factor (TGF)-β1 expression and inhibition of Smurf2-mediated degradation of renal Smad7 are mechanisms by which Smad3 KO mice were protected from angiotensin II-induced renal fibrosis and NF-κB-driven renal inflammation in vivo and in vitro. In conclusion, Smad3 is a key mediator of hypertensive nephropathy. Smad3 promotes Smurf2-dependent ubiquitin degradation of renal Smad7, thereby enhancing angiotensin II-induced TGF-β/Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation. Results from this study suggest that inhibition of Smad3 or overexpression of Smad7 may be a novel therapeutic strategy for hypertensive nephropathy.
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Demikhova, Nadiia, Olga Chernatska, Tetiana Mazur, Svetlana Bokova, Tetiana Rudenko, Lina Bumeister, and Oleksii Demikhov. "Markers of cardiovascular complications in patients with type 2 diabetes mellitus and arterial hypertension." Bangladesh Journal of Medical Science 17, no. 2 (March 23, 2018): 319–22. http://dx.doi.org/10.3329/bjms.v17i2.35894.
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Background: Hypertensive patients with type 2 diabetes mellitus are also at increased risk for diabetes mellitus–specific complications, including nephropathy. Even the smallest degree of albuminuria increases risk for cardiovascular diseases and all-cause death. The common conditions coexisting with type 2 diabetes (e.g., hypertension and dyslipidemia) are clear risk factors for cardiovascular diseases.Methods and materials: The first (I) group consists of 99 obtained patients with type 2 and AH, the second (II) includes 49 practically healthy people. We evaluated such markers of cardiovascular complications as glycated hemoglobin, lipid profile components by biochemical method and albumin excretion rate with the help of enzyme immunoassay.Result: The positive correlation between the level of albumin excretion rate and glycated hemoglobin (r = 0,23, p < 0,001) is confirmed that albuminuria is a main marker of diabetic nephropathy. The positive correlation between albuminuria and low density lipoproteins (r = 0,34, p < 0,001), triglycerides (r = 0,04, p < 0,001) is the definition of the important role of dyslipidemia in diabetic nephropathy.Conclusion: Determination of albumin excretion rate, glycated hemoglobin as markers of nephropathy, lipid profile components is necessary for patients with type 2 diabetes mellitus and arterial hypertension for prevention cardiovascular complications.Bangladesh Journal of Medical Science Vol.17(2) 2018 p.319-322
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Zuccollo, Adriana, Monica Navarro, and Orlando Catanzaro. "The Diabetic Nephropathy and the Development of Hypertension in Rats." International Journal of Experimental Diabetes Research 2, no. 3 (2001): 195–99. http://dx.doi.org/10.1155/edr.2001.195.
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The present study was designed to examine the development of hypertension in diabetic rats treated with streptozotocin (STZ, 1mg/g bw). The rats were studied at 3, 6, 9, 12 and 15 weeks. From the third week the rats were divided in diabetic rats according their glycemias and controls, along 15 weeks. After the third week a group, of rats showed increased urinary protein excretion (93, 134, 155 and 191%) compared to controls. In this group of rats the urinary kallikrein excretion was lower than control and the systolic blood pressure became significantly elevated between 3 and 6 weeks and persisted up to 15 weeks. On the other hand a group of diabetic rats were normotensive with urinary protein excretion similar to controls and urinary kallikrein lower compared to control but significantly higher compared diabetic hypertensive rats. These data suggest that the association of progressive diabetic nephropathy with abnormal endothelium-dependent vasodilation may produce a high prevalence of hypertensive diabetes.
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Shah, Jay, and Avinash Balraj. "Drug utilization pattern of antihypertensive agents in patients of hypertensive nephropathy in a tertiary care hospital: a cross sectional study." International Journal of Basic & Clinical Pharmacology 6, no. 9 (August 22, 2017): 2131. http://dx.doi.org/10.18203/2319-2003.ijbcp20173636.
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Background: Objective of the study was to determine the drug utilization pattern of antihypertensive agents in patients of hypertensive nephropathy in a tertiary care teaching hospital.Methods: This was a prospective observational study carried out in Index medical college and Hospital, Indore over a period of three 4 months. A total of 60 patients aged 40-79 years taking treatment for hypertension with associated nephropathy were enrolled in the study. All the relevant data were collected and drug utilization pattern of antihypertensive agents was determined. The study evaluated the percentage of use of multidrug therapy, drugs prescribed from Essential Drug List (EDL) and prescriptions with generic name. The cost of antihypertensive drugs used per day was calculated and linked with socioeconomic status of the patients.Results: Evaluation of the prescriptions demonstrates that a total of 63.3% males and 36.7% females with mean age of 58.9±11.9 years were enrolled out of which 70% patients were on multidrug therapy while only 30% were on monotherapy. Though only 16.67% patients were prescribed generic drugs but it did not affect the economic condition of the patient as most of enrolled patients belong to upper middle class.Conclusions: The prescriptions analysed were in accordance to guidelines of JNC-8 (Joint National Committee - 8) and most of the prescriptions were found to be rational and it also shows that management of hypertensive nephropathy needs combination therapy.
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Kuzmin, O. B., V. V. Zhezha, and V. V. Belyanin. "Dihydropyridine calcium channel blockers for the renoprotective therapy of hypertensive patients with chronic kidney disease." Nephrology (Saint-Petersburg) 25, no. 2 (February 13, 2021): 27–34. http://dx.doi.org/10.36485/1561-6274-2021-25-2-27-34.
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Amlodipine and selective dihydropyridine Ca2+ channels blockers of the second generation in addition to ACE inhibitors or replacing them antagonists of AT1-angiotensin receptors don’t improve clinical renal outcomes in hypertensive patients with chronic kidney disease. These drugs don’t eliminate intraglomerular hypertension that underlies hypertensive nephropathy and can have an adverse effect on the neurohormonal status of the organism, triggering the activation of the sympathetic and renin-angiotensin-aldosterone systems. The review presents the results of clinical studies evaluating the effectiveness of the use in this patients population of a new dihydropyridine blocker L-Ca2+ channels third-generation lercanidipine, dual blocker T/L-Ca2+ channels benedipine and dual blocker N/L-Ca2+ channels cilnidipine, that differ from their predecessors expressed renoprotective properties.
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Titjaev, Igor I., Sergey S. Andreev, Svetlana V. Andreeva, Konstantin V. Udalov, and Denis S. Kas’janov. "Hypertensive nephropathy as an outcome of unilateral nephrectomy in kidney cancer." Urology reports (St. - Petersburg) 10, no. 3 (October 26, 2020): 229–34. http://dx.doi.org/10.17816/uroved42529.
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Aim. To study the adaptive mechanisms of structural and functional changes in a single kidney after nephrectomy for kidney cancer.
Materials and Methods. A total of 179 operations of two types were performed: nephrectomy and kidney resection in patients with cancerous lesions. Postoperative ultrasound was performed size control and dopplerography of the vessels of the contralateral single kidney, monitoring-control of blood pressure.
Results. In case of kidney resection, the adaptive mechanisms controlling the volume of functioning tissue are preserved. The load on the organ remains minimal and physiological, and is not redistributed, blood pressure remains close to baseline. Nephrectomy does not lead to functional changes in a single kidney, but to adaptive and pathophysiological structural damage as a result of increased plasma pressure, organ reboot, its vicarious hypertrophy, which is accompanied by venous edema of interstitium as a pressure factor on the tissue, increased tone of arterioles, the development of secondary organ ischemia, circulatory hypoxia and increased blood pressure. All this fits into the clinical picture of hypertensive nephropathy.
Conclusions. The potential risk of hypertension and hypertensive nephropathy in patients undergoing nephrectomy, compared with patients after organ-saving surgery, is significantly higher. One of the most important manifestations of hypertension in the elderly is a violation of the structure and function of target organs, which include: the brain, heart, blood vessels, kidney. Nephrectomy forms a pathological vicious circle, contributing to the development and further progression of renal and cardiovascular failure.
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CORDONNIER, DANIEL J., NICOLE PINEL, CLAIRE BARRO, CLAIRE MAYNARD, PHILIPPE ZAOUI, SERGE HALIMI, BRUNO HURAULT DE LIGNY, YVES REZNIC, DOMINIQUE SIMON, and RUDOLF W. BILOUS. "Expansion of Cortical Interstitium Is Limited by Converting Enzyme Inhibition in Type 2 Diabetic Patients with Glomerulosclerosis." Journal of the American Society of Nephrology 10, no. 6 (June 1999): 1253–63. http://dx.doi.org/10.1681/asn.v1061253.
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Abstract. Renal interstitial expansion is now considered a useful marker of progression of several nephropathies. This study describes a multicenter, prospective, double-blind, placebo-controlled, randomized trial of the effects of Perindopril (4 mg/d) on kidney structure and function over 2 yr in 26 type 2 diabetic patients with proteinuria ranging from 70 to 4210 mg/d and relatively preserved GFR (creatinine clearance >60 ml/min). All patients underwent baseline renal biopsy, but four (15%) were not randomized because of the presence of nondiabetic nephropathy. The remaining 22 were randomized (11 to Perindopril [PE], 11 to placebo [PO]), and 19 (9 PE, 10 PO) underwent follow-up biopsy at 2 yr. BP was controlled equally in both groups throughout. Proteinuria increased in PO patients (+1562 mg/d) but declined in PE patients (-156 mg/d) (P < 0.05). Morphometric analysis was performed by light microscopy using a Biocom computer. Over the 2 yr, mean cortical interstitial fractional volume identical at baseline increased significantly in PO patients (31.7 ± 5.3 versus 40.2 ± 11.1%; P = 0.001) but was unchanged in PE patients (33.8 ± 4.9 versus 34.7 ± 6.6%; P = 0.50). It is concluded that: (1) nondiabetic nephropathy is present in approximately 15% of albuminuric type 2 diabetic patients; and (2) Perindopril prevents interstitial expansion in hypertensive patients with biopsy-proven diabetic glomerulopathy. These results support a role of angiotensin II in the progression of interstitial changes in type 2 diabetic patients with nephropathy.
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Nasri, Hamid. "Hypertension and renal failure with right arm pulse weakness in a 65 years old man." Journal of Nephropathology 1, no. 3 (October 1, 2012): 130–33. http://dx.doi.org/10.5812/nephropathol.8265.
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Patinha, Daniela, Carla Abreu, Carla Carvalho, Olga Mariana Cunha, Mariana Mota, Joana Afonso, Teresa Sousa, António Albino-Teixeira, Carmen Diniz, and Manuela Morato. "Adenosine A2A and A3 Receptors as Targets for the Treatment of Hypertensive-Diabetic Nephropathy." Biomedicines 8, no. 11 (November 23, 2020): 529. http://dx.doi.org/10.3390/biomedicines8110529.
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Diabetic nephropathy (DN) and hypertension are prime causes for end-stage renal disease (ESRD) that often coexist in patients, but are seldom studied in combination. Kidney adenosine levels are markedly increased in diabetes, and the expression and function of renal adenosine receptors are altered in experimental diabetes. The aim of this work is to explore the impact of endogenous and exogenous adenosine on the expression/distribution profile of its receptors along the nephron of hypertensive rats with experimentally-induced diabetes. Using spontaneously hypertensive (SHR) rats rendered diabetic with streptozotocin (STZ), we show that treatment of SHR-STZ rats with an agonist of adenosine receptors increases A2A immunoreactivity in superficial glomeruli (SG), proximal tubule (PCT), and distal tubule (DCT). Differently, treatment of SHR-STZ rats with a xanthinic antagonist of adenosine receptors decreases adenosine A3 immunoreactivity in SG, PCT, DCT, and collecting duct. There is no difference in the immunoreactivity against the adenosine A1 and A2B receptors between the experimental groups. The agonist of adenosine receptors ameliorates renal fibrosis, probably via A2A receptors, while the antagonist exacerbates it, most likely due to tonic activation of A3 receptors. The reduction in adenosine A3 immunoreactivity might be due to receptor downregulation in response to prolonged activation. Altogether, these results suggest an opposite regulation exerted by endogenous and exogenous adenosine upon the expression of its A2A and A3 receptors along the nephron of hypertensive diabetic rats, which has a functional impact and should be taken into account when considering novel therapeutic targets for hypertensive-diabetic nephropathy.
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Aumiller, Jochen. "HIV-Infektion: Hypertensive Nephropathien nehmen zu." CardioVasc 13, no. 6 (December 2013): 20. http://dx.doi.org/10.1007/s15027-013-0261-1.
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Khasan, SKh Mansur. "Features of pregnancy and delivery in patients with pregnancy-induced hypertension." Kazan medical journal 96, no. 4 (August 15, 2015): 558–63. http://dx.doi.org/10.17750/kmj2015-558.
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Pregnant women with hypertensive disorders have a high risk for premature birth and early delivery due to the increased severity of hypertension associated with low effect of treatment. Vaginal birth in patients with hypertensive disorders are often complicated by premature rupture of membranes, labor abnormalities, abnormal blood loss. Emergency abdominal delivery is performed together with complex intensive therapy. A common approach to the management of pregnancies with mild and moderate forms of hypertension is treatment associated with prolongation of pregnancy. Therapeutic and protective regimen in childbirth is created by phased long-term epidural analgesia. Indications for induced delivery - I-II degree of nephropathy in the absence of a positive therapeutic effect for 1-2 weeks. Regarding to severe forms of hypertensive disorders, many researchers tend to think of the need for early delivery, to avoid complications. At the same time, early delivery often leads to birth with premature fetus, which contributes to worsening of perinatal outcomes in patients with hypertensive disorders. Currently the possibility of conservative management of pregnant with hypertensive disorders at the gestation term of less than 32 weeks using glucocorticoids may significantly improve perinatal outcomes. Conservative management is only possible in large clinical settings with careful selection of patients. Currently, there are different approaches to the selection of methods and timing of delivery in hypertensive disorders. The optimal strategy is based on a differentiated approach that takes into account the severity of hypertensive disorders and the probability of complications for mother and fetus. At the same time, the diversity of the pathogenesis of hypertensive disorders determines the presence of different variants of its clinical manifestations, clinical course and complications, making it difficult to properly assess its severity.
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Bloomgarden, Z. T. "Hypertension and Nephropathy." Diabetes Care 19, no. 4 (April 1, 1996): 401–4. http://dx.doi.org/10.2337/diacare.19.4.401.
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Bakris, George L. "Hypertension and nephropathy." American Journal of Medicine 115, no. 8 (December 2003): 49–54. http://dx.doi.org/10.1016/j.amjmed.2003.08.013.
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MA, Rahim, Shahana Zaman, Samira Humaira Habib, Faria Afsana, Wasim Md Mohosin Ul Haque, and Sarwar Iqbal. "Evaluation of risk factors for diabetic nephropathy among newly diagnosed type 2 diabetic subjects: preliminary report from a tertiary care hospital of Bangladesh." BIRDEM Medical Journal 10, no. 2 (June 22, 2020): 88–91. http://dx.doi.org/10.3329/birdem.v10i2.47732.
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Background: Diabetes mellitus (DM) is the leading cause of chronic kidney disease through-out the world andhalf of the type 2 DM (T2DM) patients remain undiagnosed. During diagnosis, one-third to half of the T2DMpatients may have different macro- and micro-vascular complications including diabetic nephropathy. This studyaimed to evaluate selected risk factors for diabetic nephropathy among newly detected T2DM subjects.
Methods: A case-control study was done at out-patient department of BIRDEM General Hospital, Dhaka,Bangladesh from October 2016 to June 2017. Newly detected (<3 months) adult (³18 years) T2DM patientswere included in this study. Patients with diagnosed kidney diseases, features of glomerulonephritis, systemicdiseases like systemic lupus erythematosus and vasculitis, history of recent fever and exercise, urinary tractinfection and pregnancy were excluded. Patients with urine albumin-creatinine ratio (UACR) ³30 mg/g in atleast two (of three, if done) samples were cases and those with UACR <30 mg/g were controls.
Results: Total patients were 100, including 35 cases [microalbuminuria (UACR 30-299 mg/g) = 33 and overtproteinuria (UACR ³300 mg/g) = 2] and 65 controls. Mean age was 46.6±12.3 years and there was femalepredominance (male:female ratio was 1:2). One-fourth patients were smokers, half were hypertensive andtwo-fifths had dyslipidaemia. Three-fourths of the study participants had positive family history of DM andtwo-fifths had family history of diabetic nephropathy. Mean body mass index (BMI) was 26.26±2.97 kg/m2.Mean fasting blood glucose (mmol/L), 2-h post glucose value (mmol/L) and mean glycatedhaemoglobin(HbA1c) (%) were 9.2±2.9, 14.5±4.1 and 7.9±1.3 respectively. Eighty percent of the patients were asymptomaticregarding DM. Besides nephropathy, other chronic complications of DM were diabetic retinopathy (17%),neuropathy (11%), coronary artery disease (11%) and cerebrovascular disease (4%). Regarding risk factorsfor diabetic nephropathy, family history of DM (OR 1.62, p 0.0001) and diabetic nephropathy (OR 25.13,p 0.003), presence of hypertension (OR 4.93, p 0.001) and coexisting diabetic retinopathy (OR 14.18, p 0.046)were significant. On multivariate logistic regression, family history of DM (OR 1.77, p 0.001) and diabeticnephropathy (OR 24.31, p 0.001), higher BMI (>25 kg/m2) (OR 2.11, p 0.013), hypertension (OR 4.31,p 0.003) and diabetic retinopathy (OR 14.09, p 0.021) were significant.
Conclusions: One-third of the newly detected T2DM subjects had diabetic nephropathy in this study. Familyhistory of DM and nephropathy, higher BMI, presence of hypertension and diabetic retinopathy were significantrisk factors for diabetic nephropathy.
Birdem Med J 2020; 10(2): 88-91
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Patel, Swati, and Poonam Savlani. "Microalbuminuria in essential hypertension: A single centre study." IP Journal of Diagnostic Pathology and Oncology 6, no. 3 (September 15, 2021): 189–93. http://dx.doi.org/10.18231/j.jdpo.2021.041.
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To evaluate the prevalence of microalbuminuria in patients with essential hypertension and its relationship to severity of hypertension, to renal function and its association with coronary artery disease and target organ damage, present study was conducted. Total 100 primary hypertensive, non diabetic patients and 25 healthy normotensive, non diabetic patients (controls) admitted in S.S.G.H (Sir Sayajirao General Hospital) from June 2009 to November 2011. Patient's complete history, routine investigation along with microalbuminuria was measured by ACR by immunoturbidimetric method. In present study patient’s mean age was 52.7 years. Total 70% of patients selected for study were males and 30% were females. Total 50% to 75% of patients in the 61 -80 year age group were positive for microalbuminuria. Total 42.85% of males were positive for microalbuminuria as compared to 33.33% of females. Total 75% of patients having hypertension for more than 8 years had microalbuminuria. Total 67.5% of patients positive for microalbuminuria had associated target organ damage. Total 45% of patients positive for microalbuminuria had left ventricular hypertrophy and 40% of patients had hypertensive retinopathy. Microalbuminuria helps to identify incipient nephropathy and vascular changes. Its detection can thus help to prevent the development of complications by aggressive treatment to get down targeting blood pressure.
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Pandey, Sant, Sucheta Yadav, Suresh Babu, Ashutosh Kumar, Bhupendra P. Singh, Anupam Wakhlu, Atin Singhai, S. K. Sonkar, and Vishal Pooniya. "C4d deposition in native kidney disease and its correlation with proteinuria and serum urea/creatinine." International Journal of Research in Medical Sciences 6, no. 12 (November 26, 2018): 3935. http://dx.doi.org/10.18203/2320-6012.ijrms20184886.
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Background: C4d is a well-known biomarker of the complement cascade. It is derived from cleavage of the labile thioester bond of C4b. This cleavage provides C4d a covalent bond which helps C4d to anchor to nearby cells where immune complexes are deposited. Antibodies dissociate naturally because of relatively weak hydrostatic and Van der Waals forces between antigens and antibodies, whereas covalent bond of C4d has a much longer half-life. For this reason, C4d serves as a footprint of complement activation.Methods: This was a retrospective and prospective cross-sectional study, done at our tertiary care hospital.Results: Authors evaluated 50 cases and 10 controls to adjudge the significance of C4d deposits in native renal diseases. Majority of the patients (44%) were in the age group of 10-20 years followed by 20% in the age group of 31-40 years. 62% of study population were male. Majority of patients were diagnosed with FSGS (16%), followed by membranous nephropathy (14%), lupus nephropathy (14%) and IgA nephropathy (12%). There was correlation of intensity expression of glomerular C4d deposits with presenting 24 hours urinary protein level at the time of biopsy (p value=0.027) but no correlation with urea/creatinine.Conclusions: All patients diagnosed with membranous nephropathy, IgA nephropathy and hypertensive nephropathy showed glomerular C4d deposits, and also diagnosed with IgA nephropathy, post infectious glomerulonephritis, lupus nephritis, minimal change disease, acute/chronic tubulointerstitial nephritis, diabetic nephropathy, hypertensive nephropathy showed tubular C4d deposits. All patients diagnosed with diabetic nephropathy and hypertensive nephropathy showed arterial C4d deposits.
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Elumalai, Arumugam, Navin Boopathy, and Nivedha Balakrishnan. "A Comparative Cross-Sectional Study on Clinical and Laboratory Profile of Chronic Kidney Disease in Diabetic and Non-Diabetic Patients at a Tertiary Care Teaching Hospital, India." Journal of Evidence Based Medicine and Healthcare 8, no. 6 (February 8, 2021): 278–82. http://dx.doi.org/10.18410/jebmh/2021/54.
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BACKGROUND Diabetic nephropathy is the major cause for chronic kidney disease (CKD) in India, but there is plethora of non-diabetic causes of CKD. This study was conducted to analyse the aetiological profile of CKD, compare demographic details, clinical characteristics, laboratory parameters between diabetic and non-diabetic causes of CKD. METHODS This is a comparative cross-sectional study conducted in a tertiary centre at Maduranthagam, Tamil Nadu, on 250 subjects. The study population included all renal failure cases diagnosed in the study setting during the period December 2017 - December 2019. CKD grade is assessed as per National Kidney Foundation (NKF / KDOQI) staging system. The quantitative variables were analysed by mean, and standard deviation. Categorical variables were analysed by frequency and proportion. RESULTS 250 patients were included in the analysis; 49.20 % were diabetics with a mean age of 62.81 ± 10.44 years, and 50.80 % were non-diabetics with a mean age of 59.24 ± 10.46 years. Among the non-diabetics, 88.98 % had hypertension and 51.22 % among diabetics had hypertension. 55 subjects had both diabetes and hypertension. In the diabetes group, 39.84 % patients had trace proteinuria, 9.76 % had proteinuria +, 4.88 % had proteinuria ++ and 45.53 % participants had proteinuria +++. Among non-diabetics, 51.97 % had trace proteinuria and 40.94 % had proteinuria +++. In both groups, majority of patients had grade 5 renal failure with 57.72 % among diabetics and 56.69 % among non-diabetics. CONCLUSIONS The clinical and laboratory profile was significantly different among the two groups. In diabetic CKD, intensified risk factor control of blood glucose and HbA1c was needed, while in non-diabetic CKD, better blood pressure control measures was needed. KEYWORDS Chronic Kidney Disease, Aetiological Profile, Diabetes Mellitus, Laboratory Parameters, Diabetic Nephropathy, Hypertensive Nephropathy