Academic literature on the topic 'Angiotensin converting enzyme Angiotensin II Proteinuria. Kidneys'

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Journal articles on the topic "Angiotensin converting enzyme Angiotensin II Proteinuria. Kidneys"

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BENIGNI, ARIELA, SUSANNA TOMASONI, ELENA GAGLIARDINI, et al. "Blocking Angiotensin II Synthesis/Activity Preserves Glomerular Nephrin in Rats with Severe Nephrosis." Journal of the American Society of Nephrology 12, no. 5 (2001): 941–48. http://dx.doi.org/10.1681/asn.v125941.

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Abstract. Angiotensin-converting enzyme inhibitors restore size-selective dysfunction of the glomerular barrier in experimental animals and humans with proteinuric nephropathies, although the structural and molecular determinants of such an effect are not completely understood. This study used an accelerated model of experimental nephrosis to assess nephrin gene and protein expression in the kidney and the possible modulating effect of drugs that block angiotensin II (AII) synthesis/activity. Passive Heymann nephritis (PHN) and control animals were studied at day 7, month 4, and month 8. Additional PHN rats were treated with lisinopril or AII receptor blocker L-158,809 and studied at 8 mo. Lisinopril and L-158,809 controlled BP, prevented proteinuria, and protected PHN animals from renal injury. An intense signal of nephrin mRNA was detected in glomeruli of control animals mainly restricted to podocytes. In PHN rats, nephrin staining progressively and remarkably decreased with time. Lisinopril and L-158,809 fully prevented the decrease in nephrin transcripts to levels comparable to those of control rats. Consistent with nephrin mRNA expression, immunostaining of the protein showed a progressive decrease in kidneys from PHN rats that was completely abolished by lisinopril and L-158,809. In summary, progressive renal injury was associated with downregulation of nephrin gene that was totally prevented by angiotensin-converting enzyme inhibitor and AII receptor blocker, suggesting that renoprotection afforded by drugs that interfere with AII synthesis/activity was related to an effect on nephrin assembly.
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Jung, F. F., T. M. Kennefick, J. R. Ingelfinger, J. P. Vora, and S. Anderson. "Down-regulation of the intrarenal renin-angiotensin system in the aging rat." Journal of the American Society of Nephrology 5, no. 8 (1995): 1573–80. http://dx.doi.org/10.1681/asn.v581573.

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Progressive deterioration of renal function occurs during normal aging. Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. Aging rats treated with angiotensin-converting enzyme inhibition have relatively less proteinuria and sclerosis, suggesting that age-related changes in renal function may be associated with alterations in the intrarenal renin-angiotensin system, which thus may play a major role in the pathogenesis of these maladaptations. To investigate this possibility, renal and systemic renin-angiotensin systems were examined at an early phase of the aging process (3 months) and at a later phase (12 months) in male Sprague-Dawley rats. Although plasma renin and serum angiotensin-converting enzyme concentrations did not differ significantly, the intrarenal system showed down-regulation of renin mRNA and angiotensin-converting enzyme levels with aging, whereas angiotensinogen levels remained stable. The decrease in renin mRNA appeared to precede the fall in plasma renin concentration in the aging process. Additional studies in 15-month-old rats confirmed that, by this time, both basal and stimulated renal renin release rates were impaired in older rats. Thus, both decreased renin synthesis and impaired renin release underlie the fall in plasma renin with normal aging. This decrease may act to lower intrarenal baseline levels of angiotensin II, an adaptation of likely importance in the modulation of intrarenal vascular tone and tubular function in the aging kidney.
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Mata-Greenwood, Eugenia, Arlin B. Blood, LeeAnna D. Sands, Shannon L. Bragg, Daliao Xiao, and Lubo Zhang. "A novel rodent model of pregnancy complications associated with genetically determined angiotensin-converting enzyme (ACE) activity." American Journal of Physiology-Endocrinology and Metabolism 315, no. 1 (2018): E52—E62. http://dx.doi.org/10.1152/ajpendo.00289.2017.

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Brown Norway (BN) and Lewis (LW) inbred rat strains harbor different angiotensin-converting enzyme ( Ace) polymorphisms that result in higher ACE activity in BN than LW rats. Thus we hypothesized that pregnant BN rats would show pregnancy complications linked to angiotensin II (AII) activity. We performed longitudinal and cross-sectional studies in pregnant LW and BN rats. We found that BN rats have significantly higher ACE activity and AII levels at prepregnancy and throughout pregnancy compared with LW rats, except at midgestation. BN placentas and maternal kidneys had significantly higher expression of AII receptor 1 (AGTR1) and lower expression of AGTR2 than the respective LW placentas and maternal kidneys. Renin-angiotensin system activation in BN rats correlated with hypertension and proteinuria at gestational days 17–21, which were resolved after delivery. In addition, BN rat pregnancies were characterized by significant fetal loss, restricted growth in surviving fetuses, decreased uteroplacental blood flows, and decreased trophoblast remodeling of uterine arteries compared with LW pregnancies. Short-term losartan treatment significantly increased uteroplacental blood flow and fetal weight and decreased maternal blood pressure (BP) and proteinuria in BN pregnancies. In contrast, losartan treatment significantly decreased uteroplacental blood flow and fetal weight but had no significant effect on maternal BP in LW pregnancies. We conclude that Ace polymorphisms play an important role in the reproductive phenotype of BN and LW rats and that BN rats are a novel model of pregnancy complications in association with genetically controlled, increased ACE activity.
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Gupta, Arvind, Upma Narain, and Aditya Sachan. "Comparison of the efficacy of triple blockade, double blockade and single blockade of RAAS in non diabetic chronic kidney disease." International Journal of Advances in Medicine 5, no. 4 (2018): 941. http://dx.doi.org/10.18203/2349-3933.ijam20183124.

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Background: Although dual blockade of the renin-angiotensin-aldosterone system with the combination of an angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker is generally well established as a treatment for nephropathy, this treatment is not fully effective in some patients.Methods: A prospective observational study was done on 600 chronic kidney disease patients during July 2012 to August 2014 to compare the efficacy of triple blockade, double blockade and single blockade of renin-angiotensin-aldosterone system in non diabetic chronic kidney disease.Results: At the end of the study, 24 hours urinary protein excretion rate of group I and group III were compared by using student t-test and p value (0.0268) was found significant. Similarly, on comparing group II and group III, p value (0.0160) was again found significant.Conclusions: Triple blockade of the renin-angiotensin-aldosterone system was effective for the treatment of proteinuria in patients with non-diabetic nephropathy whose increased urinary protein had not responded sufficiently to a dual blockade.
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Gupta, Arvind, Upma Narain, and Romar Dabu. "Nephro protection property of double blockade versus single blocked of RAAS in delaying the progression of CKD." International Journal of Advances in Medicine 5, no. 3 (2018): 748. http://dx.doi.org/10.18203/2349-3933.ijam20182135.

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Background: Dual renin angiotensin aldosterone system blockade using angiotensin receptor blockers in combination with angiotensin converting enzyme inhibitors is reported to improve proteinuria in non-diabetic patients.Methods: A prospective observational study was done on 810 non-diabetic chronic kidney disease patients during July 2012 to August 2014 to compare the nephro protection property of double blockade and single blocked of renin angiotensin aldosterone system in delaying the progression of chronic kidney disease.Results: At the end of 24 months urinary protein excretion rate of group I and group III were compared by using student t-test and p value (0.0001) was found significant. Similarly, on comparing group II and group III, p value (0.003) was again significant. Mean arterial blood pressure of group I and group III were statistically significant (<0.0496) while comparing group II and group III, p value (0.0419) was again significant.Conclusions: The study concludes that the use of double renin angiotensin aldosterone system blockade therapy is more effective than monotherapy at reducing albuminuria and proteinuiria, and in decreasing blood pressure at the same time not causing significant deterioration in glomerular filtration rate. Newer potassium lowering therapies can effectively and safely correct hyperkalemia and maintain normokalemia in patients receiving background treatment with renin angiotensin aldosterone system blockade. However, the use of new potassium binders for cardiovascular and renal risk reduction with combined renin angiotensin aldosterone system blockade therapy will require phase III trials.
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VAN DIJK, MARJAN A., DORIEN J. M. PETERS, MARTIJN H. BREUNING, and PETER C. CHANG. "The Angiotensin-Converting Enzyme Genotype and Microalbuminuria in Autosomal Dominant Polycystic Kidney Disease." Journal of the American Society of Nephrology 10, no. 9 (1999): 1916–20. http://dx.doi.org/10.1681/asn.v1091916.

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Abstract. Autosomal dominant polycystic kidney disease (ADPKD) has a variable clinical course. Clinical parameters associated with a worse prognosis are hypertension and proteinuria or microalbuminuria (MA). Because chronic stimulation of the renin-angiotensin system is likely to be present in ADPKD patients, the effect of the angiotensin-converting enzyme insertion/deletion (ACE I/D) genotype on the variability of these clinical parameters was examined in untreated ADPKD patients. Proteinuria and MA were determined in 24-h urine collections. BP measurements were performed with an ambulatory monitor, over 24 h. With analysis of covariance, the ACE genotype was found to be significantly associated with MA, corrected for age, gender, GFR, mean arterial pressure, body surface area, and urinary Na+ excretion (P < 0.05). The patients homozygous for the deletion (DD) had the highest rate of MA (P < 0.05) compared to the patients homozygous for the insertion (II). There was no relationship between the ACE genotype and BP or renal function. A significant positive correlation was found between MA and mean arterial pressure (r = 0.31, P < 0.05), whereas a significant negative correlation was found between MA and renal function (r = -0.28, P < 0.05). In conclusion, in ADPKD patients, MA is partly determined by the ACE I/D polymorphism. Because MA is associated with an enhanced progression toward renal failure, the ACE genotype could help in identifying patients at risk for a worse prognosis.
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Wu, L. L., A. Cox, C. J. Roe, M. Dziadek, M. E. Cooper, and R. E. Gilbert. "Secreted protein acidic and rich in cysteine expression after subtotal nephrectomy and blockade of the renin-angiotensin system." Journal of the American Society of Nephrology 8, no. 9 (1997): 1373–82. http://dx.doi.org/10.1681/asn.v891373.

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Secreted protein acidic and rich in cysteine (SPARC) is an extracellular matrix-associated protein with antiadhesive, antiproliferative, and matrix remodeling properties. SPARC gene and protein expression were investigated after subtotal nephrectomy (STNx), a model of noninflammatory progressive renal injury. In addition, the effect of blockade of the renin-angiotensin system by the angiotensin-converting enzyme inhibitor ramipril or by the angiotensin II receptor antagonist valsartan was examined. The STNx rats developed hypertension, proteinuria, and renal impairment. These changes were associated with a 2.4-fold increase in SPARC gene expression in STNx compared with SHAM kidneys (P < 0.001). In situ hybridization revealed increased SPARC mRNA in glomeruli and interstitial cells, as well as de novo expression by tubular epithelial cells at sites of renal injury. Immunofluorescence studies confirmed concordant changes in SPARC protein. Both ramipril and valsartan ameliorated renal injury and significantly reduced SPARC overexpression in the STNx animals. The findings of the present study suggest that SPARC, in the context of its known biological actions, may influence some of the pathological features associated with significant renal mass reduction.
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Park, Changhyun, Eun Kyoung Lee, So Mi Kim, et al. "Acute Kidney Injury after Administering Dapagliflozin to a Diabetic Patient with Acute Cerebral Infarction." Korean Journal of Medicine 95, no. 6 (2020): 404–8. http://dx.doi.org/10.3904/kjm.2020.95.6.404.

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Dapagliflozin is a recently developed oral anti-diabetic drug and SGLT2 inhibitor with well-known cardioprotective and renoprotective effects. Although a reduction of the glomerular filtration rate is induced by volume depletion and tubule-glomerular feedback during the early period after administering a SGLT2 inhibitor, the renal prognosis improves more with a decrease of proteinuria. However, the risk of acute kidney injury increases in heart failure and hypovolemia patients, and in those taking certain drugs, such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitor/angiotensin II receptor blockers, or diuretics. We report acute kidney injury after dapagliflozin administration in a diabetic patient with acute cerebral infarction accompanied by right hemiplegia, motor aphasia, and dysphagia.
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Binz-Lotter, Julia, Christian Jüngst, Markus M. Rinschen, et al. "Injured Podocytes Are Sensitized to Angiotensin II–Induced Calcium Signaling." Journal of the American Society of Nephrology 31, no. 3 (2020): 532–42. http://dx.doi.org/10.1681/asn.2019020109.

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BackgroundInhibition of angiotensin II (AngII) signaling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through regulating glomerular blood flow and reducing filtration pressure. Although extravascular actions of AngII have been suggested, a direct effect of AngII on podocytes has not been demonstrated in vivo.MethodsTo study the effects of AngII on podocyte calcium levels in vivo, we used intravital microscopy of the kidney in mice expressing the calcium indicator protein GCaMP3.ResultsIn healthy animals, podocytes displayed limited responsiveness to AngII stimulation. In contrast, in animals subjected to either adriamycin-induced acute chemical injury or genetic deletion of the podocin-encoding gene Nphs2, the consequent podocyte damage and proteinuria rendered the cells responsive to AngII and resulted in AngII-induced calcium transients in significantly more podocytes. The angiotensin type 1 receptor blocker losartan could fully inhibit this response. Also, responsiveness to AngII was at least partly mediated through the transient receptor potential channel 6, which has been implicated in podocyte calcium handling. Interestingly, loss of a single Nphs2 allele also increased podocytes’ responsiveness to AngII signaling. This direct effect of AngII on injured podocytes results in increased calcium transients, which can further aggravate the underlying kidney disease.ConclusionsOur discovery that podocytes become sensitized to AngII-induced calcium signaling upon injury might explain results from large, randomized, controlled trials in which improved renal outcomes occur only in the subgroup of patients with proteinuria, indicating podocyte damage. Our findings also emphasize the need to treat every patient with a glomerular disease with either an angiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor blocker.
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Severova-Andreevska, Galina, Ilina Danilovska, Aleksandar Sikole, Zivko Popov, and Ninoslav Ivanovski. "Hypertension after Kidney Transplantation: Clinical Significance and Therapeutical Aspects." Open Access Macedonian Journal of Medical Sciences 7, no. 7 (2019): 1241–45. http://dx.doi.org/10.3889/oamjms.2019.264.

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Most of the kidney transplanted patients develop arterial hypertension after renal transplantation. Together with very well-known and usual risk factors, post-transplant hypertension contributes to the whole cardiovascular morbidity and mortality in the kidney transplant population. The reasons of post-transplant hypertension are factors related to donors and recipients, immunosuppressive therapy like Calcineurin Inhibitors (CNI) and surgery procedures (stenosis and kinking of the renal artery and ureteral obstruction). According to Eighth National Committee (JNC 8) recommendations, blood pressure > 140/90 mmHg is considered as hypertension. The usual antihypertensive drugs used for the control of hypertension are Calcium channel blockers (CCB), Angiotensin-converting enzyme (ACE) inhibitors, Angiotensin –II receptor blockers (ARB), B- blockers and diuretics. Follow the KDIGO guidelines the target blood pressure < 140/90 mmHg for patients without proteinuria and < 125/75 mmHg in patients with proteinuria is recommended. Better control of post-transplant hypertension improves the long-term graft and patient’s survival.
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Dissertations / Theses on the topic "Angiotensin converting enzyme Angiotensin II Proteinuria. Kidneys"

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Ho, Kwun-wai. "Angiotensin converting enzyme inhibitor alone or in combination with angiotensin II type I receptor blocker in patients with chronic proteinuric nephropathies : a systemic review of clinical trials /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31684038.

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Ho, Kwun-wai, and 何冠威. "Angiotensin converting enzyme inhibitor alone or in combination with angiotensin II type I receptor blocker in patients with chronicproteinuric nephropathies: a systemic reviewof clinical trials." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010687.

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Hsu, Feng-Yi, and 徐鳳儀. "Renoprotective Effect of Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers in Diabetic Patients with Proteinuria." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/43750060782411415463.

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碩士<br>國立臺灣大學<br>藥學研究所<br>104<br>Background: Diabetes mellitus (DM) is a metabolic disease with high blood sugar levels over extended periods. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are the first-line medications for patients with diabetic nephropathy. While there are many ACEIs and ARBs available on the market, the differences in renoprotective effectiveness and safety among various ACEI and ARB drugs are unclear. Objective: 1. To compare the renal effectiveness and safety of ACEIs and ARBs. 2. To individually assess the renal effectiveness and safety of different ACEI and ARB agents. 3. To analyze the effectiveness and safety of ACEIs and ARBs individually for patients aged 65 years and older. Methods: The present study used the Longitudinal Health Insurance Database (LHID) to conduct a retrospective cohort analyses. We selected the new users of the monotherapy of ACEI or ARB with the diagnosis of diabetic nephropathy from July 1, 2002 through December 31, 2013, and required patients to have a second prescription within 100 days following the first prescription. The primary outcome was composited of the ESRD and renal transplant. The secondary and safety outcome were defined as the death from any cause and the hyperkalemia event respectively. The analyses were conducted on an intention-to-treat (ITT) basis and an as-treated (AT) basis. Propensity score weighting was used to balance the numerous important baseline covariates. All analyses were conducted by using SAS 9.4 (SAS Institute Inc., Cary, NC, USA). Results and Discussion: In Aim 1, ARBs seem to be a poorer treatment choice for the diabetic nephropathy patients compared with ACEIs due to the inferior renal protective effect (hazard ratio[HR], 1.44; 95% confidence intervals [CI], 1.26-1.64; P<0.01) and poorer safety outcome (HR, 1.20; 95% CI, 1.05-1.36; P<0.01). In Aim 2, captopril and fosinopril seem to be poorer treatment choices among the 7 ACEI drugs due to the poorer renal outcome (captopril: HR, 1.41; 95% CI, 1.05-1.90; P=0.02 / fosinopril: HR, 1.56; 95% CI, 1.05-2.32; P=0.03) and the higher mortality rate (captopril: HR, 1.35; 95% CI, 1.11-1.65; P<0.01 / fosinopril: HR, 1.37; 95% CI, 1.03-1.81; P=0.03). Additionally, on account of the less renal benefit, irbesartan seems to be an inferior treatment choice among the 4 ARB drugs (HR, 1.38; 95% CI, 1.05-1.82; P=0.02). On the contrary, losartan may be the better treatment choice due to the greater reduction in the mortality (HR, 0.28; 95% CI, 0.09-0.84; P=0.02). In Aim 3, the elderly patients seem to be even less suitable to use ARBs than ACEIs than the overall study sample owing to the higher risk of renal outcomes (HR, 1.79; 95% CI, 1.42-2.27; P<0.01) and hyperkalemia (HR, 1.28; 95% CI, 1.07-1.54; P<0.01). In addition, taking mortality into account, captopril may be inferior to other 6 ACEI drugs for the older diabetic patients with proteinuria (HR, 3.07; 95% CI, 1.10-8.58; P=0.03). On the other hand, losartan may be superior to other 3 ARB drugs for this population due to a higher decrease in mortality (HR, 0.12; 95% CI, 0.02-0.93; P=0.04). Conclusions: Our findings support the use of ACEIs as a relatively renoprotective and safe treatment as compare to ARBs in the diabetic nephropathy patients, especially in the elderly population. Fosinopril and irbesartan seem to poorer treatment choice for the adult population among 7 ACEI drugs and 4 ARB drugs respectively. Both in the adult population and elderly patients, captopril may be inferior to other 6 ACEI drugs, and, conversely, losartan may be superior to other 3 ARB drugs.
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Books on the topic "Angiotensin converting enzyme Angiotensin II Proteinuria. Kidneys"

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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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Schreuder, Michiel F. Renal tubular dysgenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0350.

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Renal tubular dysgenesis involves the absence or incomplete differentiation of proximal tubular nephron segments. Due to the lack of a patent nephron, it is characterized by (fetal) anuria and subsequent oligohydramnios, pulmonary hypoplasia, premature birth with severe and refractory arterial hypotension, and fetal or neonatal death. The main cause for renal tubular dysgenesis is a genetic mutation in the renin–angiotensin system, which has shown an autosomal recessive trait. Maternal use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers during pregnancy can have similar blocking effects on the fetal renin–angiotensin system, which may lead to renal tubular dysgenesis. Even though there is no actual renal function, ultrasound usually shows kidneys of normal size and architecture with an intact corticomedullary differentiation. Most patients with renal tubular dysgenesis do not survive beyond the neonatal period. A few patients have been described to survive with respiratory support, vasopressor treatment, and dialysis.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0338_update_001.

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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide (Gb3), which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. Proteinuria and estimated glomerular filtration rate (eGFR) are strongly associated with risk of progression, but this may be reduced by treatment with angiotensin-converting enzyme inhibitors as well as by enzyme replacement therapy (ERT). ERT was approved in 2001; it improves pain and other neuropathic symptoms, and well-being, and has been proven to clear deposits of Gb3 from tissues, at variable speeds. There is limited randomized controlled trial data but protective effects have been proven for renal outcomes, death, and better outcomes in some other organ systems. Renal function may be protected if ERT is commenced before there is heavy proteinuria or substantial loss of GFR. It is recommended to start ERT as soon as the diagnosis is made in those with very low or absent enzyme. For those with intermediate levels it is recommended to commence treatment only when signs or symptoms appear. Proteinuria and eGFR give most information from a renal point of view, but renal biopsy is also useful for confirming the renal diagnosis and staging the disease as well as monitoring progress in selected cases. Management should include regular screening for complications including myocardial and neurological assessments. It is likely that registries will show progressive rises in median survival with this condition.
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Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Alport syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0324.

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Management of Alport syndrome has in the past been expectant and supportive. Modern hearing aids have substantially improved the function of affected individuals. However, animal data and more recently observational data from Alport registries strongly suggest a protective effect of angiotensin-converting enzyme inhibitors. There is a suggestion that early commencement of treatment may slow progression substantially. These should now be recommended for all with proteinuria, and possibly even before then for those known to harbour mutations certain to cause end-stage renal failure. A very small minority develop the difficult post-transplant complication of Alport anti-glomerular basement membrane disease. This can rarely be treated successfully and leaves some patients on long-term dialysis. However, overall, patients with Alport syndrome have better than average survival and other outcomes than other patients with end-stage renal failure. Most are successfully transplanted. The question of risk to heterozygous carriers from donating kidneys to their affected relatives arises frequently. The risks may be felt acceptable in some circumstances. Additional therapies are under investigation.
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Book chapters on the topic "Angiotensin converting enzyme Angiotensin II Proteinuria. Kidneys"

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Bilous, Rudolf. "Diabetes mellitus and the kidney." In Oxford Textbook of Medicine, edited by John D. Firth. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0491.

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Diabetic nephropathy is the commonest cause of endstage renal disease in the developed world. Aetiology and pathology—causation is related to glycaemic control, hypertension, inflammation, genetic factors, and dietary and other environmental factors. Pathological hallmarks in the glomerulus are thickening of the glomerular basement membrane and mesangial expansion, with or without nodule formation, secondary to an accumulation of extracellular matrix. Many patients have a varying severity of tubulointerstitial inflammation and fibrosis. Staging and natural history—is classically described in terms of urinary albumin excretion rate (UAER). Clinical features—most patients (&gt;60%) will have a normal UAER throughout their diabetic life, but 1 to 2% of the remainder develop persistent moderately increased albuminuria each year. Once UAER exceeds 200 µg/min, there tends to be a relentless increase in proteinuria and glomerular filtration rate declines progressively at a rate that largely depends upon blood pressure control. Prevention—tight glycaemic control can prevent moderately increased albuminuria in both type 1 and type 2 diabetes. Whether intensive blood pressure control using angiotensin-converting enzyme (ACE) inhibitors can also prevent this remains controversial. In both type 1 and type 2 diabetes, intensive blood pressure control using ACE inhibitors or angiotensin II receptor blockers (ARBs) slows progression from moderately to severely increased albuminuria and also slows the rate of decline in glomerular filtration rate in those with severely increased albuminuria. Management—aims for (1) control of glycaemia, (2) control of hypertension (&lt;130/80 mmHg) using an ACE inhibitor or an ARB as first line; and (3) other interventions, including some or all of serum lipid lowering, smoking cessation, and reduction of dietary protein and salt.
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