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Relevant bibliographies by topics / Hypertensive Nephropathie

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Academic literature on the topic 'Hypertensive Nephropathie'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "Hypertensive Nephropathie"

1

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 The current definition of hypertensive nephropathy is non-specific, outdated and only allows a delayed diagnosis by exclusion.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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Dissertations / Theses on the topic "Hypertensive Nephropathie"

1

TRAN-VAN, PATRICIA. "Pathologie vasculo-renale chronique et grossesse : interet des examens complementaires ; a propos de 58 grossesses." Toulouse 3, 1992. http://www.theses.fr/1992TOU31553.

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Cheng, Sau-kong. "Diabetic end-stage renal disease (ESRD) : can health care costs be saved through blood pressure control? /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36887638.

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Lucas, Thierry. "Interet de la mesure ambulatoire de la pression arterielle dans le traitement de l'hypertendu a risque." Rennes 1, 1992. http://www.theses.fr/1992REN1M158.

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COUSTOLS, VALAT MAGALI. "Interet du dosage de l'activite de l'antiport sodium-proton dans la nephropathie diabetique." Toulouse 3, 1993. http://www.theses.fr/1993TOU31509.

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Thibodeau, Jean-François. "Prostaglandin E2 Signaling Through Kidney EP1 and EP4 Receptors; Implications in Diabetes and Hypertension." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32749.

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Chronic kidney disease is defined as the appearance of kidney functional or structural injury. Cyclooxygenase and prostaglandin E2 have been implicated in the pathogenesis of diabetic nephropathy, the leading cause of chronic kidney disease. Beneficial in certain settings, inhibition of the cyclooxygenase pathway can however be detrimental in patients with compromised cardiac or renal function. Moreover, the quest for new therapies to treat diabetic nephropathy is hampered by the lack of appropriate rodent models. This doctoral thesis is a culmination of three studies, the first to determine the role of the prostaglandin E2 EP1 receptor in diabetic nephropathy, the second to elucidate the vascular prostaglandin E2 EP4 receptor’s role in hypertension and lastly to establish and characterise a novel mouse model of diabetic nephropathy. The goal being to uncover new therapeutic avenues for the treatment of CKD, its causes and/or complications.

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Christiansen, Ingo [Verfasser]. "Muskuläre sympathische Nervenaktivität bei hypertensiven Patienten mit und ohne diabetische Nephropathie. Einfluss der AT1-Rezeptorblockade mit Valsartan / Ingo Christiansen." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2013. http://d-nb.info/1044609664/34.

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GAGNEUX, CHRISTELLE. "Une microalbuminurie persistante chez le diabetique de type ii hypertendu, predit une diminution de la filtration glomerulaire a court terme." Angers, 1994. http://www.theses.fr/1994ANGE1086.

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8

Torbjörnsdotter, Torun. "Glomerulopathy in normoalbuminuric adolescents with type 1 diabetes : relations between structure, function, metabolic control and ambulatory blood pressure /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-254-3/.

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Morales, Geneviève. "Profil tensionnel ambulatoire et néphropathie diabétique." Montpellier 1, 1991. http://www.theses.fr/1991MON11126.

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Bletsos, Vassili S. "The Role of CD40 Signaling in Chronic Renal Allograft Rejection in a Hypertensive Rat Model." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1532961455216765.

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Books on the topic "Hypertensive Nephropathie"

1

Tomson, C. R. V. Hypertensive Nephropathy. Science Press Ltd, 1996.

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Phipps, Lisa M., Titi Chen, and David C. H. Harris. Radiation nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0091_update_001.

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Radiation nephropathy usually arises after inadvertent exposure of kidneys to radiotherapy. It may manifest as acute nephropathy as early as 6 months after exposure, or later as chronic nephropathy, hypertension, or asymptomatic proteinuria. Glomerular and peritubular endothelium and renal tubular cells are especially radiosensitive. There are no pathognomonic histological features, but renal pathology may be similar to that of haemolytic uraemic syndrome. Radiation nephropathy may be prevented by renal shielding and mitigated by radiation dose fractionation. Control of hypertension is important and angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists appear to have protective effects beyond those of blood pressure control.

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Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. Boston: Nijhoff, 1988.

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Alderson, Helen, Constantina Chrysochou, James Ritchie, and Philip A. Kalra. Ischaemic nephropathy. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0212.

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Ischaemic nephropathy describes loss of renal function or renal parenchyma due to stenosis or occlusion of the renal artery or its branches. In the Western world, this is usually the result of atherosclerotic renovascular disease, but other aetiologies include arteritis, embolic disease, dissection, and fibromuscular disease.Chronic kidney disease is the most common manifestation of ischaemic nephropathy, but hypertension, flash pulmonary oedema, sensitivity to angiotensin blockade, and sensitivity of glomerular filtration rate to blood pressure reduction are all possible manifestations of occlusive diseases of the renal artery or its branches. Proteinuria may also occur.This chapter describes these clinical features and the outcomes of ischaemic nephropathy. It goes on to discuss the haemodynamics and mechanisms and what we understand of the pathophysiology of the condition.

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Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.

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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.

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Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0066_update_001.

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Immunoglobulin A (IgA) nephropathy characteristically causes haematuria and may present as a nephritic illness in older children and young adults. However, it may occur at any age and is commonly asymptomatic, associated first with haematuria alone, later progressing in some patients to hypertension, proteinuria, and progressive loss of glomerular filtration. While this evolution is characteristically slow, over decades, in some it is rapid, leading to early end-stage renal failure. It is common for the disease to present late, as advanced renal disease, or malignant hypertension. It may present with acute kidney injury caused by crescentic disease, but acute kidney injury caused by haematuria may be confused clinically with the same. Henoch–Schönlein purpura is a type of small vessel vasculitis that is most commonly seen in children, but which occurs at all ages, that is associated with IgA deposition. In older children and most adults it merges closely into IgA nephropathy after the acute event. Outcomes in adults are less good. IgA nephropathy is the most common type of glomerulonephritis in most developed countries. The disease is more common in men, and appears to be much less common in black people. The detected incidence is strongly influenced by biopsy policies; the lower your threshold to biopsy patients with haematuria, the more of this condition you discover. There are clear genetic tendencies but the strongest risk seems to come from genes in the human leucocyte antigen complex.

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Porush, J. G., and F. Faubert. Clinician's Manual on Hypertension, Diabetes Mellitus, and Nephropathy. Science Press, 2001.

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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus, Fourth. 4th ed. Springer, 1998.

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Mogensen, Carl Erik. The Kidney and Hypertension in Diabetes Mellitus, Sixth Edition. 6th ed. Informa Healthcare, 2004.

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Erik, Mogensen Carl, ed. The kidney and hypertension in diabetes mellitus. 3rd ed. Boston: Kluwer, 1997.

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Book chapters on the topic "Hypertensive Nephropathie"

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Segerer, Katja, and Christoph Wanner. "Hypertensive Nephropathie." In Springer-Lehrbuch, 99–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-28236-2_11.

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Ruiz-Hurtado, Gema, and Luis M. Ruilope. "Hypertension in Diabetic Kidney Disease." In Diabetic Nephropathy, 325–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-93521-8_20.

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Manis, Thomas, and Eli A. Friedman. "Contrast Media Induced Nephropathy in Diabetic Nephropathy." In The Kidney and Hypertension in Diabetes Mellitus, 251–58. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-1974-1_30.

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Cairns, Carolynn, and Bryan Conway. "Modeling Human Diabetic Kidney Disease by Combining Hyperglycemia and Hypertension in a Transgenic Rodent Model." In Diabetic Nephropathy, 41–52. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9841-8_4.

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Geiger, Helmut, U. Bahner, A. Andreae, W. Vaassen, and A. Heidland. "Effect of the ACE-Inhibitor Enalapril on Plasma Concentration of Atrial Natriuretic Peptide and on Glomerular Filtration Rate in Normotensive and Hypertensive Diabetic Rats." In Tubulo-Interstitial Nephropathies, 295–304. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3892-9_34.

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Marre, Michel, Samy Hadjadj, and Béatrice Bouhanick. "Genetics and Diabetic Nephropathy." In The Kidney and Hypertension in Diabetes Mellitus, 115–28. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4499-9_10.

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Kitzmiller, John L., and C. Andrew Combs. "Diabetic Nephropathy and Pregnancy." In The Kidney and Hypertension in Diabetes Mellitus, 487–500. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4499-9_38.

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Sawicki, Peter T. "Smoking and Diabetic Nephropathy." In The Kidney and Hypertension in Diabetes Mellitus, 133–40. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-6746-9_13.

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Kincaid-Smith, Priscilla, and Judith A. Whitworth. "Haematuria and Diabetic Nephropathy." In The Kidney and Hypertension in Diabetes Mellitus, 151–60. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-6746-9_15.

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Combs, C. Andrew, and John L. Kitzmiller. "Diabetic Nephropathy and Pregnancy." In The Kidney and Hypertension in Diabetes Mellitus, 389–400. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-6746-9_37.

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Conference papers on the topic "Hypertensive Nephropathie"

1

Nilsson, T., O. Johnson, and F. Lithner. "MOLECULAR MARKERS OF ENDOTHELIAL CELL DYSFUNCTION: OBSERVATIONS ON EXTRINSIC FIBRINOLYSIS IN SURVIVORS OF MYOCARDIAL INFARCTION AND IN TYPE-1 DIABETES MELLITUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643102.

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We have studied the extrinsic fibrinolytic system in survivors, below 70 years, from myocardial infarction (AMI) treated in Umeci during 1983; in 43 type-1 diabetics; and in controls. Elderly controls underwent chest x-ray, ECG, EEG, brain CT scan to verify their health. Tissue plasminogen activator (tPA) activity was measured with a fibrin-stimulated rate assay, before and after a 10 min venous occlusion test (VO), tPA antigen (Ag) with an ELISA, and plasminogen activator inhibitor (PAI) by incubating samples with purified tPA and measuring remaining tPA with a polylysine-stimulated rate assay.In the diabetics, PAI and tPA:Ag were similar to the controls. tPA:Ag correlated with age (r=0.6). Diabetics had much higher specific activity of tPA (61,300 vs 21,900), and had also much higher tPA activity after VO (2.2 vs 1.2 U/ml). The tPA activities after VO correlated well with HbA1c (r=0.39). A significant effect of smoking was disclosed. Smoking diabetics had higher PAI and tPA antigen but also lower specific activity of tPA (60,600 vs 115,700 U/mg). Ex-smokers were very similar to smokers, not to the non-smokers. Retinopathy, nephropathy, or hypertension didn’t appear to affect fibrinolysis independently.In the AMI survivors (sampled 3 months after discharge from hospital), PAI was 6-fold higher than in elderly controls (p less than 0.0001). tPA activity after VO was much higher (3.2 vs 1.2 U/ml), as was tPA:Ag. tPA specific activity was lower. Among AMI patients with PAI over 10 U/ml, PAI correlated with triglycerides (r=0.4) and negatively with age (r=™0.4): these relations were not seen in the patients with PAI less than 10. The effects of smoking seen in diabetics were not observed among the AMI patients, von Willebrand factor was not increased among AMI nor diabetic patients, except for those with retinopathy.The results suggest that the tPA/PAI system is a more sensitive indicator than vWF of endothelial cell dysfunction. It relates to effects of age, atherosclerotic vascular disease, and among diabetics also to degree of metabolic control and to tobacco smoking habits.

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