Influence of angiotensin-converting enzyme inhibitor ramipril on indicators of tubular kidney lesion in patients with chronic glomerulonephritis

2020 ◽  
Vol 33 (1) ◽  
pp. 17-20
Author(s):  
Mariia O. Dolinna ◽  
Oleksandr O. Svyntozelskyi

AbstractTo research and deepen the understanding of the links between morphological tubular kidney lesion parameters and serum markers – neutrophil gelatinase-associated lipocalin (NGAL) and interleukin-18 (IL-18), in patients with chronic glomerulonephritis (CGN) with saved renal function, as well as to estimate therapeutic correction of identified changes using ACE inhibitor ramipril. The diagnosis of “chronic glomerulonephritis” was verified based on clinical, laboratory and morphological data. Patients were divided into 2 clinical groups: patients with CGN and arterial hypertension (AH) and without AH. We used the data of renal biopsies to analyze the indicators of tubular kidney lesion in patients with CGN. Levels of serum NGAL and IL-18 were measured by means of ELISA kits. Treatment of patients was carried out over 24 weeks using the ACE inhibitor ramipril. The average daily dose of ramipril for the entire treatment period for patients with AH was 12.8±5.6 mg, patients of the second group – without AH, were treated with ramipril at a dose of 2.5 mg. On the basis of rank correlation analysis, we demonstrated that the level of serum NGAL is directly correlated with interstitial fibrosis (r=0.65; p<0.05), serum IL-18 – with dystrophic changes in the epithelium of renal tubules (r=0.81; p<0.05).Conclusion. Serum levels of NGAL and IL-18 are one of the most sensitive markers of tubular kidney lesion and have diagnostic efficiency up to 97%. A 24-week treatment with ACE inhibitor ramipril in patients with CGN with and without AH leads to a decrease in the levels of tubular kidney lesion markers.

Author(s):  
M.A. Dolinnayä ◽  
T.G. Shekhovtseva

The aim: to examine the relations between morphological tubulointerstitial (TIT) parameters of kidney damage and neutrophil gelatinase-associated lipocalin (NGAL) and interleukin-18 (IL-18) of blood serum in patients with chronic glomerulonephritis (CGN) with saved renal function, and to estimate the therapeutic correction of identified changes using ACE inhibitor ramipril.. Materials and methods. The study included 81 patients with CGN. Patients were divided into 2 clinical groups: CGN patients with arterial hypertension (AH), CGN without AH. The average daily dose of ramipril in patients with AH was 12,8 ± 5,6 mg, in patients without hypertension – 2,5 mg. We used kidney biopsy data for the analysis of renal damage on the following parameters: dystrophic and necrotic changes in tubular epithelium, thickening and/or cleavage of tubular basement membrane, presence ofcellular infiltration, interstitial fibrosis (IF). The level of NGAL and IL-18 in serum were determined by ELISA. Results. We statistically confirmed a direct link between blood NGAL and IF (r=+0,65;p<0,05), blood IL-18 and dystrophic changes in tubular epithelium (r=+0,81;p<0,05). It was established that the kidney IF diagnostic using NGAL determination in serum is highly sensitive and specific, with an efficiency of 95,3 %, and dystrophic changes in tubular epithelium via serum IL-18 – 96,6 %. Conclusion: serum levels of NGAL and IL-18 are sensitive markers of kidney TIT damage in patients with CGN with diagnostic efficiency up to 97 %. Under the influence of 24 weeks treatment with an ACE inhibitor ramipril we observed a significant decrease in levels of markers of kidney TIT damage, that confirmed nephroprotective effect of the drug.


2020 ◽  
Vol 19 (3) ◽  
pp. 2491
Author(s):  
E. S. Levitskaya ◽  
M. M. Batyushin ◽  
O. K. Bondarenko ◽  
E. S. Kekukh ◽  
D. B. Bondarenko ◽  
...  

Aim. To study clinical, laboratory, and morphological risk factors for small-diameter renal arterial fibrosis in patients with hypertension (HTN) and primary chronic glomerulonephritis (CGN).Material and methods. The study included 102 patients with primary CGN. The first group consisted of 62 patients with small-diameter renal arterial fibrosis according to renal biopsy; the second group included 40 patients without vascular fibrosis. All patients signed informed consent.Results. A comparative analysis revealed the most significant differences between groups 1 and 2: mean systolic blood pressure (SBP)  — 131,85±17,56 mm Hg and 119,65±22,2 mm Hg, respectively (p=0,0008); mean diastolic blood pressure (DBP) — 84,11±10,7 and 79,63±9,7 mm Hg (p=0,03), respectively; peak SBP — 158,61±23,76 mm Hg and 144,25±23,56 mm Hg (p=0,002), respectively; peak DBP  — 95,66±10,33 mm Hg and 90,63±10,74 mm Hg (p=0,02), respectively; HTN stage — 1,85 [1; 3] and 1,38 [1; 3] (p=0,03), respectively; HTN grade  — 1,73 [1; 3] and 1,13 [1; 3] (p=0,004), respectively; left ventricular hypertrophy  — 15 patients and 2 patients (p=0,006), respectively; blood urea nitrogen  — 8,98±7,31 and 6,42±4,02 mmol/L (p=0,03), respectively. Significant morphological differences between first and second groups were as follows: tubulointerstitial fibrosis — 56% and 21% (p<0,001), respectively; tubulointerstitial inflamemation — 44% and 16% (p=0,002), respectively; interstitial fibrosis — 24,9±20,5% and 9,89±19,8% (p=0,001), respectively.Conclusion. The presented analysis emphasizes a significant contribution of hemodynamics in small-diameter renal arterial fibrosis in patients with HTN and CGN. It manifested by a persistent increase of SBP and involvement of target organs. Systemic hemodynamic changes are fundamental in the development of small-diameter renal arterial fibrosis in patients with HTN and primary CGN, while the isolated progression of CGN does not significantly affect the structure of small-diameter renal arteries.


2019 ◽  
pp. 57-67
Author(s):  
A. N. Katrich ◽  
V. A. Porkhanov ◽  
N. S. Ryabin

Objective: efficacy evaluation of the CEUS LI RADS v2017® system for differential diagnosis of liver tumors in patients with and without cirrhosis.Materials and methods. Retrospective analysis of diagnostic results of the 165 patients with liver tumors (177 nodules) was done. All patients underwent CEUS with results interpretation in accordance to the CEUS LIRADSv2017 ® criteria. Patients were divided into 2 groups based on clinical and morphological data. Group 1 included 62 patients with cirrhosis and/or CVH. Group 2 included 110 patients without risk factors for HCC.Results. Diagnostic efficiency of CEUS LI RADS v2017® for HCC identification was: group 1 – Se – 100%, Sp – 88%, Ac – 95.5%; group 2 – Se – 100%, Sp – 68.8%, Ac – 72.7%; general group Se – 100%, Sp – 72.2%, Ac – 81.4%. In the 2nd group, 21 out of 22 neoplasms, confirmed morphologically as FNH, we classified as LR 4. By applying benign character and specific contrasting patterns of FNG, they were transferred from LR 4 to LR 3. This allowed to increase sensitivity and specificity of differential diagnosis in group 2 (Se – 100%, Sp – 90.6%, Ac – 91.8%) and in general group (Se – 100%, Sp – 90.1%, Ac – 93.2%). Diagnostic efficiency of the criteria for non hepatocellular malignant neoplasms (LR M) was: group 1 – Se – 77.8%, Sp – 100%, Ac – 97%; group 2 – Se – 90%, Sp – 96.7%, Ac – 93.6%; general group- Se – 88.1%, Sp – 98.3%, Ac – 94.9%.Conclusion. Our study confirmed high accuracy of the CEUS LI RADS v2017® system in the differential diagnosis of focal liver tumors. Modification of the system (in particular, transfer of typical FNG forms from the LR 4 category) will make it possible to increase the accuracy of diagnostics by 20%. It will allow to use the LI RADS v2017® system for interpretation CEUS not only among patients with liver cirrhosis, but also in a general group without risk factors of GCC.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gonjin Song ◽  
Ji Yea Kim ◽  
Ha Young Yoon ◽  
Jeong Yee ◽  
Hye Sun Gwak

AbstractAlthough a considerable volume of data supporting induction or aggravation of psoriasis because of angiotensin-converting enzyme (ACE) inhibitor use exists, it remains insufficient for definitive conclusions. Therefore, we aimed to evaluate the association between ACE inhibitor use and psoriasis incidence through a systematic literature review and meta-analysis. We searched for qualifying studies across PubMed, Web of Science, and Embase. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the strength of the association between ACE inhibitor use and psoriasis incidence. Eight studies with a total of 54,509 patients with a psoriasis diagnosis were included in this meta-analysis. The pooled OR for psoriasis incidence among ACE inhibitor users was 1.52 (95% CI, 1.16–2.00) compared to that among non-users. From subgroup analysis by continent, the OR for ACE inhibitor users versus non-users was 2.37 (95% CI 1.28–4.37) in Asia. Per the subgroup analysis by climate, the OR for ACE inhibitor users vs non-users in dry climate was 3.45 (95% CI: 2.05–5.79) vs 1.32 (95% CI 1.01–1.73) in temperate climate. Our results reveal a significant association between ACE inhibitor use and psoriasis incidence.


2019 ◽  
Vol 11 (3) ◽  
pp. 37-48
Author(s):  
O. V. Azovtseva ◽  
E. A. Viktorovа ◽  
V. V. Murochkin ◽  
A. S. Shelomov ◽  
E. G. Bakulina ◽  
...  

A feature of the HIV epidemic is currently a large number of comorbid and severe forms of the disease, with frequent involvement in the pathological process of the brain. Methods of in vivo verification of brain damage in clinical practice is sufficient, but in some cases they are limited by financial availability and time factor. Correct and timely deciphering of the nature of brain damage is necessary for the choice of treatment tactics, and as a consequence, reducing mortality. Objective: to study the epidemiology, clinic and pathomorphology of brain damage in HIV infection in conditions of urgent and planned admission of patients to a specialized hospital. Materials and methods. Clinical and pathomorphological studies of HIV-infected patients (n=85) receiving specialized medical care were carried out. The final diagnosis was made taking into account clinical, laboratory and morphological data on the classification of ICD-10 in accordance with the domestic requirements of the formulation of comorbid diagnosis. Conclusion. Brain lesions are clinically and morphologically detected in most HIV-infected patients. Opportunistic and secondary diseases with brain damage have their clinical picture, but it is not specific. From the timely decoding of the nature of brain damage depends on the choice of treatment tactics and, as a consequence, reducing the risk of death. Therefore for verification of the etiological agent, you need to conduct a comprehensive examination: clinical (neurological, psychological distress) and laboratory (cellular composition of CSF protein level and glucose) and bacteriological (seeding of CSF on the flora, on Wednesday Saburo to identify mushrooms on medium Bactec and Lowenstein-Jensen medium for detection of M.tuberculesis); immunological (number of CD4-lymphocytes, at.gondii IgM, at.gondii IgG antibodies), molecular genetic (HIV RNA; DNA HSV1, 2; VZV DNA; DNA EBV; CMV DNA; DNA ВГЧ6; T.gondii DNA; DNA of M.tuberculesis; DNA Cr.neoformans; JC virus DNA) and radiological (MRI brain) research methods. The structure of brain damage in deceased patients was dominated by toxoplasmosis in 28,8% of cases; neuroinfection of unspecified etiology in 28,8% and herpesvirus lesion in 11,9%. Rarely met: tuberculosis 8,47%; candidiasis 8,47%; PML 3,39%; cryptococcosis 3,39%; b-cell lymphoma with brain metastases 3,39%. 


Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Vidya K Nagalakshmi ◽  
Minghong Li ◽  
R. A Gomez ◽  
Maria Luisa S Sequeira-Lopez

Tubular degeneration, loss of renal tubules and interstitial fibrosis due to kidney injury lead to chronic renal disease and hypertension. Using a partial unilateral ureteral obstruction (pUUO) model in neonatal mice, we analyzed the fate cell changes that occur during obstruction and during recovery following the release of UUO. We traced the fate of cells derived from the renal stroma, cap mesenchyme and ureteric bud epithelium using Foxd1-Cre, Six2-Cre and HoxB7-Cre mice respectively, crossed with double fluorescent reporter (mT/mG) mice. pUUO was performed 24-36h after birth (n=84). In a group of pups (n=37), the obstruction was released after seven days. Sham operated animals (n=35) were used as controls. Lineage tracing revealed that Foxd1-derived interstitial pericytes acquired α-smooth muscle actin expression and underwent significant expansion due to pUUO (fibrotic area 91.06+/-6.77 %). Release of obstruction resulted in complete resolution of fibrotic areas (0.00%; p<0.005). Further, loss of Six2-derived cells at the glomerular-tubular junction in pUUO kidneys resulted in the formation of atubular glomeruli (39%). Atubular glomeruli were not observed after release. In addition, a significant loss of HoxB7-derived collecting duct tubules was observed during pUUO. Most collecting ducts recovered following release. Our study indicates that obstruction leads to significant tubular damage, expansion of interstitial pericytes, fibrosis, tubular loss and formation of atubular glomeruli. The striking recovery observed after release of ureteral obstruction suggests a reversal of cell fate changes and tubular regeneration. Elucidation of the cellular and molecular mechanisms mediating these events may be of use in the design of strategies for the prevention and/or treatment of kidney diseases and secondary hypertension.


2020 ◽  
Vol 21 (8) ◽  
pp. 2951 ◽  
Author(s):  
Masahiro Nezu ◽  
Norio Suzuki

Over 10% of the global population suffers from kidney disease. However, only kidney replacement therapies, which burden medical expenses, are currently effective in treating kidney disease. Therefore, elucidating the complicated molecular pathology of kidney disease is an urgent priority for developing innovative therapeutics for kidney disease. Recent studies demonstrated that intertwined renal vasculature often causes ischemia-reperfusion injury (IRI), which generates oxidative stress, and that the accumulation of oxidative stress is a common pathway underlying various types of kidney disease. We reported that activating the antioxidative transcription factor Nrf2 in renal tubules in mice with renal IRI effectively mitigates tubular damage and interstitial fibrosis by inducing the expression of genes related to cytoprotection against oxidative stress. Additionally, since the kidney performs multiple functions beyond blood purification, renoprotection by Nrf2 activation is anticipated to lead to various benefits. Indeed, our experiments indicated the possibility that Nrf2 activation mitigates anemia, which is caused by impaired production of the erythroid growth factor erythropoietin from injured kidneys, and moderates organ damage worsened by anemic hypoxia. Clinical trials investigating Nrf2-activating compounds in kidney disease patients are ongoing, and beneficial effects are being obtained. Thus, Nrf2 activators are expected to emerge as first-in-class innovative medicine for kidney disease treatment.


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