Development Of Chronic Renal Failure Research Articles

#1852 When ‘pebbles’ affect the kidney: nephrolithiasis and chronic renal failure in Crohn's disease. The experience of a 3rd level centre

Abstract Background and Aims Nephrolithiasis is the most common expression of kidney involvement in chronic inflammatory bowel disease (IBD), especially in Crohn's disease (CD). Stone formation favoring factors are hyperoxaluria, dehydration, acidosis, common conditions in CD patient, who present a little higher incidence of renal stones, made of calcium oxalate, than the normal population. Only few studies focused on the relationship between CD activity (defined by CDAI score) and the development of nephrolithiasis and possible subsequent development of chronic renal failure (CRF). Materials and Method We conducted a retrospective study on a cohort of 1236 patients affected by CD referring to our Centre of IBD- Sant'Orsola between 2014 and 2021. We identified two cohorts from this population: 118 patients with nephrolithiasis and 118 patients without nephrolithiasis. Among these two groups, we identified variable clinical manifestations of CD and their relation with CRF and lithiasis. Results The prevalence of nephrolithiasis in all CD patients was 10.3%, a little higher than in the general population. The results of the analysis of patient and disease variables in the two groups are shown in Table 1. The mean age at diagnosis of CD was higher in the group without nephrolithiasis, so the treatment was started later. The presence of perianal disease, extraintestinal manifestations (MEI), like ankylosing spondylitis (APS), biliary tract involvement, or previous surgery, and presence of ileostomy correlate with the formation of stones in univariate regression analysis (Table 2). Perianal disease and MEI also maintained significance in multivariate analysis. Conclusion Our data suggest that a higher degree of disease activity, defined by the presence of perianal disease (a variable on CDAI score) and the presence of MEI, correlates with higher risk of lithiasis. It is advisable to start early the study of nephrolithiasis in these patients to adopt preventive strategies against formation and progression of renal stones. Future studies are required for a better definition of this deep relationship.

Renal complications of tuberculosis; a mini-review

Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis, which primarily affects the lungs but can also involve other organs, including the kidneys. TB has the potential to result in the development of chronic renal failure and requires prompt diagnosis and treatment for effective management. Renal TB can lead to various complications, including renal failure, perinephritis, perinephric abscesses, fistulae, psoas abscesses, and non-functioning kidneys. Additionally, TB-associated nephropathy is an infrequent variant of glomerulonephritis characterized by the deposition of immune complexes containing TB antigens in the kidney’s glomeruli.

The Second Case of Bardet-Biedl syndrome from Iraq: An educational article and expert opinion

Background: Bardet-Biedl syndrome and Laurence-Moon syndrome are rare autosomal recessive disorders with a similar phenotype. They are characterized by the gradual development of phenotype which includes cone-rod retinal dystrophy, obesity, and hypogonadism in males. Other associated abnormalities include learning disability and renal abnormalities. The two conditions are differentiated clinically by the presence of spasticity and the absence of polydactyly in Laurence-Moon syndrome. In 2002, we reported the first patient with Bardet-Biedl syndrome. The boy had polydactyly, obesity, retinal degeneration, and was hospitalized at the University Hospital in Al-Kadhimiyia because of the development of chronic renal failure. Patients and methods: The case of a 9-year-old obese Kurdish girl who had polydactyly of the hands and feet associated with reduced visual acuity is described.Results: A 9-year-old obese Kurdish girl had polydactyly of the hand and feet associated with reduced visual acuity that was attributed to myopia which was partially corrected with eye glasses. The parents were unrelated, and her younger 5-year sister had polydactyly of the feet only. No other family member known to have polydactyly. Both sisters had their extra-digits removed surgically. The girl was studying at fourth grade primary school and the parents reported no learning disability. Fundoscopy showed normal optic disc and periphery of the retina. The presence of retinitis pigmentosa was excluded. However, the foveal reflex was reported to be abnormal by the oophthalmologist. Electroretinography showed evidence of cone-rod dystrophy.Conclusion: The second case of Bardet-Biedl syndrome from Iraq is reported. The current evidence-based expert opinion suggests the use of long tem supplementation of citicoline, co-enzyme Q10 and lutein with hope of retarding the progression to blindness.

Comparative Analysis of the Fibrosis Factors Expression in the Heart Tissue of Sprague-Dawley and Wistar Rats during Development of Chronic Renal Failure

The severity of the development of uremic cardiomyopathy (UC) and fibrosis of cardiac tissue at chronic renal failure (CRF) was compared in the model experiments on male Sprague-Dawley and Wistar rats of the SPF category. To induce CRF in rats, subtotal nephrectomy (NE) was performed on the left, and after 2 weeks, total nephrectomy on the right. Sham-operated (Sham) animals served as controls. 4 weeks after the second surgery, blood pressure (BP) was measured in animals, and the expression of fibrotic factors (transcription factor Fli1, pro-collagen-I, collagen-I and collagen-IV) in the tissues of heart left ventricle was evaluated by real-time PCR and immunoblotting. After NE, Sprague-Dawley rats exhibited a significant increase in systolic blood pressure and left ventricular hypertrophy. In Wistar rats, the difference in BP between NE and Sham animals was smaller, and the ratio of left ventricular mass to body weight did not change. Experimental CRF in Sprague-Dawley rats was accompanied by a 1.5–2.5-fold suppression of the Fli1 gene expression and a decrease in the content of Fli1 protein in the cardiac tissue, while no significant differences were observed in Wistar rats. The levels of pro-collagen-I and collagen-I in the heart of rats of both lines did not change either at the levels of transcription or translation. Such difference in development of pathological processes indicates ineffectiveness of applied NE scheme for induction of UC and investigation of pro-fibrotic processes in Wistar rats.

Changes in Clinical Manifestations and Course of Systemic Lupus Erythematosus and Secondary Antiphospholipid Syndrome over Three Decades.

Systemic lupus erythematosus (SLE) is often associated with antiphospholipid syndrome (APS), which potentially results in a more severe disease course and reduced life expectancy. Since the therapeutic guidelines have been refined in the last 15 years, we assumed that the diseases course has become more favorable. In order to shed light on these achievements, we compared the data of SLE patients diagnosed before and since 2004. In our retrospective study, we assessed a wide spectrum of clinical and laboratory data of 554 SLE patients who received regular follow-up care and therapy at our autoimmune center. Among these patients, 247 had antiphospholipid antibodies (APAs) without clinical signs of APS, and 113 had definitive APS. In the APS group, among patients diagnosed since 2004, deep vein thrombosis (p = 0.049) and lupus anticoagulant positivity (p = 0.045) were more frequent, while acute myocardial infarction was less frequent (p = 0.021) compared with patients diagnosed before 2004. Among the APA positive patients without definitive APS, anti-cardiolipin antibody positivity (p = 0.024) and development of chronic renal failure (p = 0.005) decreased in patients diagnosed since 2004. Our study demonstrates that the disease course has changed in recent years; however, in the presence of APS, we have to expect repeated thrombotic events despite adequate anticoagulant therapy.

The second case of Bardet-Biedl syndrome from Iraq: An educational article and expert opinion

Background: Bardet-Biedl syndrome and Laurence-Moon syndrome are rare autosomal recessive disorders with a similar phenotype. They are characterized by the gradual development of phenotype which includes cone-rod retinal dystrophy, obesity, and hypogonadism in males. Other associated abnormalities include learning disability and renal abnormalities. The two conditions are differentiated clinically by the presence of spasticity and the absence of polydactyly in Laurence-Moon syndrome. In 2002, we reported the first patient with Bardet-Biedl syndrome. The boy had polydactyly, obesity, retinal degeneration, and was hospitalized at the University Hospital in Al-Kadhimiyia because of the development of chronic renal failure. Patients and methods: The case of a 9-year-old obese Kurdish girl who had polydactyly of the hands and feet associated with reduced visual acuity is described. Results: A 9-year-old obese Kurdish girl had polydactyly of the hand and feet associated with reduced visual acuity that was attributed to myopia which was partially corrected with eye glasses. The parents were unrelated, and her younger 5-year sister had polydactyly of the feet only. No other family member known to have polydactyly. Both sisters had their extra-digits removed surgically. The girl was studying at fourth grade primary school and the parents reported no learning disability. Fundoscopy showed normal optic disc and periphery of the retina. The presence of retinitis pigmentosa was excluded. However, the foveal reflex was reported to be abnormal by the oophthalmologist. Electroretinography showed evidence of cone-rod dystrophy. Conclusion: The second case of Bardet-Biedl syndrome from Iraq is reported. The current evidence-based expert opinion suggests the use of long tem supplementation of citicoline, co-enzyme Q10 and lutein with hope of retarding the progression to blindness.

Kidney diseases.

Dysregulation and accelerated activation of the alternative pathway (AP) of complement is known to cause or accentuate several pathologic conditions in which kidney injury leads to the appearance of hematuria and proteinuria and ultimately to the development of chronic renal failure. Multiple genetic and acquired defects involving plasma- and membrane-associated proteins are probably necessary to impair the protection of host tissues and to confer a significant predisposition to AP-mediated kidney diseases. This review aims to explore how our current understanding will make it possible to identify the mechanisms that underlie AP-mediated kidney diseases and to discuss the available clinical evidence that supports complement-directed therapies. Although the value of limiting uncontrolled complement activation has long been recognized, incorporating complement-targeted treatments into clinical use has proved challenging. Availability of anti-complement therapy has dramatically transformed the outcome of atypical hemolytic uremic syndrome, one of the most severe kidney diseases. Innovative drugs that directly counteract AP dysregulation have also opened new perspectives for the management of other kidney diseases in which complement activation is involved. However, gained experience indicates that the choice of drug should be tailored to each patient's characteristics, including clinical, histologic, genetic, and biochemical parameters. Successfully treating patients requires further research in the field and close collaboration between clinicians and researchers who have special expertise in the complement system.

Galectin 3 (LGALS3) Gene Polymorphisms Are Associated with Biochemical Parameters and Primary Disease in Patients with End-Stage Renal Disease in Serbian Population.

Galectin 3 plays a significant role in the development of chronic renal failure, particularly end-stage renal disease (ESRD). The aim of our study was to investigate the association between Gal-3 and biochemical parameters and primary disease in ESRD patients, by exploring the polymorphisms LGALS3 rs4644, rs4652, and rs11125. A total of 108 ESRD patients and 38 healthy controls were enrolled in the study. Genotyping of LGALS3 gene rs4644, rs4652, and rs11125 polymorphisms was performed by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP). By multivariate logistic regression analysis, we found that LGALS3 rs4644 CC and rs4652 AA genotypes were significantly associated with a higher risk for lower hemoglobin, higher level of parathyroid hormone, and also occurrence of diabetes mellitus and arterial hypertension. The CAA haplotype was significantly more common in patients with diabetes, low hemoglobin level, and normal PTH level. It has been observed as well that the ACT haplotype was more common in patients with low glomerular filtration, low PTH, and normal hemoglobin level. We found that the LGALS3 rs4644 and rs4652 gene polymorphism may be involved in the pathogenesis and appearance of complications in ESRD patients and thus could be considered a new genetic risk factor in this population.

IMMUNOHISTOPATHOLOGICAL CHARACTERISTICS OF OBSTRUCTIVE UROPATHY IN CHILDREN (LITERATURE REVIEW)

Despite advances in the early diagnosis of congenital obstructive uropathy, especially in prenatal diagnosis, and early surgical correction of this pathology, the problem of prognosis of obstructive uropathy in children currently comes out on top in terms of its relevance. In everyday clinical practice, the question constantly arises why, with the same type of uropathy in some children, kidney function recovers rather quickly after surgical treatment, while in others it continues to progressively decrease to the development of chronic renal failure.

Kidney Transplant in a Pediatric Patient With Congenital Abnormalities of the Urinary Tract.

Kidney transplant is the gold standard surgical treatment for patients with end-stage chronic kidney disease. Over the past decade, the frequency and prevalence of chronic kidney disease in children have been increasing, with it being a serious problem worldwide. Kidney transplant in Uzbekistan is still at an early stage, with the first successful kidney transplant performed in 2018. Here, we describe a successful kidney transplant in a pediatric female patient with a congenital abnormality of the urinary tract. The patient first showed symptoms at 7 years of age and was diagnosed with urolithic illness with inflammation of both kidneys. At presentation, she was 14 years of age with end-stage chronic kidney disease (diagnosed with stage 5 chronic kidney disease at age 13 years) caused by an anomaly in the development of the urinary tract. She received a kidney transplant from her mother as a living donor. There was vesicoureteral reflux on both sides and ureterohydronephrosis from 2 sides. On day 9 posttransplant, her creatinine level decreased from 0.40 to 0.066 mmol/L. Doppler ultrasonogram showed normal size and echogenicity of the graft, as well as adequate blood flow in the renal and iliac vessels. The patient was discharged on day 10 posttransplant in a satisfactory condition. In about 50% of cases, the cause of chronic renal failure in children is congenital anomalies of the urinary tract. The most common causes of hydronephrosis in newborns and children are vesicourethral reflux, which leads to the expansion of the urinary tract collecting system and the development of chronic renal failure. Early and accurate diagnosis and timely treatment of urinary tract abnormalities can reduce the incidence of end-stage chronic kidney disease in children.

Efficacy and safety of Corbrin Capsule on malnutrition, inflammation, and atherosclerosis syndrome in patients with uremia: systematic review and meta-analysis.

Uremia is a clinical syndrome caused by the development of chronic renal failure to the end-stage. Corbrin Capsule has the effect of tonifying the lungs and kidneys and improving the essence and qi, which can improve the metabolic disorders of the body. However, there is currently no systematic evaluation of the efficacy of Corbrin Capsule in the treatment of uremia malnutrition, inflammation, and atherosclerosis (MIA) syndrome. This paper aiming to provide a reference for improving the prognosis of uremic MIA patients. According to the PICOS principle, the literature inclusion and exclusion criteria were formulated. The databases such as PubMed, Web of Science, Embase, and Cochrane Library were searched by computer using "Corbrin Capsule", "uremia", "MIA syndrome", and "kidney function" as search items. The outcome indicators were body mass index (BMI), C-reactive protein (CRP), blood urea nitrogen (BUN), and serum creatinine (sCr). Subsequently, the Cochrane Reviewer's Handbook 4.2.5 was adopted to assess the literature quality. The conventional treatment combined with Corbrin Capsule was defined as MIA/treatment group, and the conventional treatment was defined as the control group. The Review Manager (RevMan) 5.3 software was used to conduct a meta-analysis of the experimental data. A total of 6 suitable included articles were selected, including 894 patients. The included literature was analyzed and found that there was no obvious publication bias. According to the results of meta-analysis, the total BMI score was mean difference (MD) [95% confidence interval (CI)]: -0.10 (-3.44to3.24) with Z=0.06 and P=0.95. The CRP total score was MD (95% CI): 1.40 (0.34to2.46) with Z=2.58 and P=0.010. The BUN index was MD (95% CI): -1.15 (-3.05to0.75) with Z=1.18, P=0.24. Analysis result of sCr index data was MD (95% CI): -72.82 (-202.16to56.52) with Z=1.10 and P=0.27. Corbrin Capsule can effectively improve the relevant physiological indicators of patients with uremic MIA syndrome. However, the outcome indicators included in this study were insufficient, and it is necessary to further expand the sample size and outcome indicators in the future.

Disability in systemic lupus erythematosus

Systemic lupus erythematosus is one of the most severe systemic diseases with autoimmune damage to the connective tissue, microvasculature vessels and a number of internal organs. In the clinical picture of the disease, lesions of the skin (pathognomonic feature is the appearance of an erythematous rash in the form of a butterfly on the bridge of the nose and cheeks), the occurrence of Raynaud's syndrome, involvement of the joints in the pathological process, proceeding as arthritis, damage to the lungs and kidneys are in the first place. Most often, the onset of disease is noted at the age of 15-25 years; mainly women are affected. The disease onset is not very specific: a temperature reaction and asthenic syndrome are noted; skin rashes or a microcirculatory reaction may appear in response to exposure to cold or stressful situations. The danger of systemic lupus erythematosus is the polysyndromic nature of the disease, which consists in the involvement of many organs and systems in the pathological process. The kidneys are most often and severely affected with the development of lupus nephritis, which can cause the rapid development of chronic renal failure. The manifestation of a convulsive syndrome with the subsequent development of mental disorders is not uncommon. Disability in systemic lupus erythematosus is given in case of the development of chronic renal failure of stage 2A and above, with complete atrioventricular block with the need to install a pacemaker, with damage to the vision organ and the nervous system with impaired functional activity. Systemic lupus erythematosus requires lifelong use of glucocorticoid drugs and, in some cases, the use of extracorporeal detoxification methods to remove metabolic products and circulating immune complexes.

POSTPARTUM RENAL THROMBOTIC MICROANGIOPATHY: A TURN-BASED DIFFERENTIAL DIAGNOSIS

Pregnancy-associated renal thrombotic microangiopathy is a rare condition with poor maternal outcome. Pregnancy may trigger atypical hemolytic uremic syndrome or thrombotic thrombocytopenic purpura. The article describes the clinical case of a 37-year-old woman who developed acute renal failure following complicated delivery. A turn-based differential diagnosis of atypical hemolytic uremic syndrome was performed. Unwarranted discontinuation of the targeted therapy with Eculisumab led to the development of chronic renal failure. Pregnancy-associated atypical hemolytic uremic syndrome is a life-threatening condition rarely seen in pregnancy making its early recognition difficult. As thrombotic microangiopathies require urgent treatment, plasmapheresis should be started as soon as they are suspected, followed by Eculisumab after the confirmation of the diagnosis of atypical hemolytic uremic syndrome. This may contribute to reducing maternal morbidity and mortality rates.

Роль нефропатій генетичного генезу у формуванні хронічної ниркової недостатності у дітей (клінічне спостереження дитини з акроренальним синдромом)

У статті автори аналізують дані літератури, а також результати власного багаторічного досвіду діагностики генетично детермінованих захворювань нирок, що супроводжувалися розвитком хронічної ниркової недостатності. Викладено основні причини захворювань, принципи їх діагностики та лікування. Наведено клінічне спостереження за пацієнтом з акроренальним синдромом, ускладненим розвитком хронічної ниркової недостатності.

Особливості порушень функціонування нирок у дітей із системним червоним вовчаком та ювенільним ідіопатичним артритом

Актуальність. При системних захворюваннях сполучної тканини автоімунної природи ураження нирок в одних випадках є синдромом захворювання, а в інших — наслідком основного процесу. Мета роботи — встановити частоту та характер порушень функціонування нирок у дітей та підлітків, хворих на ювенільний ідіопатичний артрит (ЮІА) та системний червоний вовчак (СЧВ), залежно від тривалості та активності цих захворювань. Матеріали та методи. Обстежені 113 дітей у віці від 7 до 18 років, із них хворих на ЮІА — 70, 43 дитини — з СЧВ. Розподіл на групи проведений залежно від тривалості та активності захворювання. Стан функції нирок оцінювали за допомогою геморенальних проб (рівень креатиніну сироватки крові), визначення швидкості клубочкової фільтрації. Установлювали рівень протеїнурії в добовій сечі, а також вивчали концентраційну функцію нирок за допомогою аналізу сечі за Зимницьким. Статистична обробка проводилася за допомогою пакета статистичних програм Statgrafics 16.0. Результати. Так, у дітей з ЮІА при тривалості хвороби більше ніж 3 роки відбувалися зміни функції нирок, що виражалися протеїнурією, порушенням швидкості клубочкової фільтрації та зниженням концентраційної функції нирок. При вивченні частоти порушень залежно від активності патологічного процесу встановлено що у групі з 0 ст. було зниження як швидкості клубочкової фільтрації (25,0 %), так і концентраційної функції нирок (12,5 %). У групі з I ст. активності виявлені мікропротеїнурія (4,4 %), порушення швидкості клубочкової фільтрації (12,3 %) та зниження концентраційної функції нирок (6,6 %). У групі з II ст. також виявлені мікропротеїнурія (14,2 %) та певне зниження швидкості клубочкової фільтрації (14,2 %), а в групі з III ст. майже у всіх хворих зареєстровані мікропротеїнурія (66,6 %) та зниження концентраційної функції нирок (33,3 %). При вивченні функції нирок залежно від активності патологічного процесу привертали увагу приріст рівня мікропротеїнурії (р < 0,01) та зниження клубочкової фільтрації в групі з III ступенем активності (р < 0,01). Також установлено зростання рівня протеїнурії в групі з тривалістю захворювання понад 3 роки. Таким чином, установлено, що ураження нирок супроводжується значним зниженням клубочкової фільтрації та протеїнурією, тобто порушенням функції клубочкового апарату нирок. У хворих на СЧВ дітей із тривалістю захворювання від 1 до 3 років в 68,1 % випадків зареєстровані наявність протеїнурії та в поодиноких випадках — зміни швидкості клубочкової фільтрації. У групі дітей із тривалістю патологічного процесу понад 3 роки виявлено більш глибокі зміни функції нирок. Так, майже в усіх хворих установлена протеїнурія (90,4 %), частота зниження швидкості клубочкової фільтрації збільшилась до 19,0 %, у 14,2 % випадків встановлено зниження концентраційної функції нирок. При аналізі частоти порушень функції нирок залежно від активності СЧВ привертали увагу зростання рівня протеїнурії (р < 0,05) та зниження швидкості клубочкової фільтрації (р < 0,02) саме у хворих із II ступенем активності захворювання. При вивченні показників функції нирок залежно від тривалості захворювання на СЧВ установлено, що в групі з тривалістю хвороби понад 3 роки відбувається зниження швидкості клубочкової фільтрації (р < 0,03), зростання рівня мікроальбумінурії (р < 0,03) та зниження максимальної щільності сечі (р < 0,03). При дослідженні показників функції нирок залежно від активності патологічного процесу виявлено зростання рівня мікроальбумінурії при II ступені активності (р < 0,01). Таким чином, майже у третини дітей із СЧВ із тривалістю захворювання понад 3 роки та збереженням активності патологічного процесу відбувається формування ознак ураження нирок із порушенням функції як клубочкового, так і канальцевого апарату нирок, що надалі буде сприяти розвитку хронічної ниркової недостатності. Висновки. У дітей, хворих на ЮІА та на СЧВ, із тривалістю захворювання понад 3 роки при збереженні активності патологічного процесу формуються порушення функції нирок. Ознаками ураження нирок є наявність протеїнурії, зниження клубочкової фільтрації, зниження концентраційної здатності нирок.

Гостре та хронічне ушкодження нирок внаслідок дії опіоїдів. Огляд літератури

Acute kidney injury is the cause of death for about 2 million people a year worldwide and often leads to the development of chronic renal failure. Use of opioids is one of the reasons of acute and chronic kidney injuries. Most drugs or their metabolites are excreted by the kidneys and lead to the changes of the structure and functions of this organ. Drug abuse is a social problem in the modern world and the use of opioids in treatment of chronic pain syndrome is common in medical practice, because of this, knowledge of the mechanisms of kidney injury under the influence of opioids is important in medical practice. Compliance of morphological changes in kidneys to the severity of clinical syndrome of decreased glomerular filtration rate and the level of biochemical markers due to acute kidney injury and chronic renal disease remains relevant. Causes of acute kidney injury while using opioids may be renal ischemia as a result of decreased glomerular filtration rate, hypotension, dehydration and also rhabdomyolysis and acute urinary retention. It is shown that one of the causes of renal ischemia while using the opioids is increased influence of parasympathetic nervous system and decreased influence of sympathetic nervous system. Usage of opioids indirectly inhibits renin-angiotensin-aldosterone system through the changes of catecholamines. The influence of opioids on synthesis of antidiuretic hormone was established, namely – usage of opioids leads to the decreased secretion of antidiuretic hormone, and as a result – to increased diuresis. Presented review of literature was used for analysis of pathogenic factors, biochemical changes and morphological forms of kidney ingury due to the usage of opioids. Sources which were used include studies of morphofunctional changes of kidneys of those who had drug addiction and those who used opioids for a long time because of medical reasons. The results of experimental studies of the structure and function of the kidneys under the opioid influence are also presented. The morphological forms of kidney injury under the action of the most commonly used opioids, in particular morphine, cocaine, heroin, were analyzed. The data of investigation of pathogenetic links of acute and chronic kidney injuries and biochemical deviations that are common for disturbance of functions of kidneys under the influence of opioids are presented. This review can be used for experimental works related to the study of the mechanisms of kidney damage under the influence of opioids, as well as in the treatment of kidney pathology of drug addicts and people who used opioids for a long time due to medical reasons

Yoğun Bakımda Akut Böbrek Hasarı Takibinde NGAL, Kreatinin ve Renal Kan Akımının Monitörizasyonu

Objectıve: Acute Kidney Injury (AKI) and subsequent renal failure are the leading causes of morbidity and mortality in the intensive care unit (ICU). In this study, it was planned to compare Neutrophil Gelatinase-associated Lipocalin (NGAL) and creatinine values in patients diagnosed with AKI and to determine the effect of renal dose dopamine use on renal blood flow, development of chronic renal failure (CRF) and mortality. Materıals and methods: This prospective study was planned with 35 patients developed AKI in the ICU of Bakırköy Dr. Sadi Konuk Training and Research Hospital. The patients were randomized into 2 groups as 18 patients who received dopamine treatment with the recommendation of the cardiology clinic and 17 patients who did not receive dopamine treatment. Urea, creatinine and NGAL plasma levels were compared between groups. Results: There was no difference between the groups in terms of age, gender and AKI stage. The 0th, 24th hour results and 24-hour changes of urea, creatinine and NGAL values of dopamine patient, who took dopamine, were found to be similar to those of patients who did not take dopamine. A significant positive correlation was found between the 24-hour change in creatinine value and the 24-hour change in NGAL (r=0.374; p<0.05). There was no significant change in the diameter and flow of renal arteries between measurements in patients who received dopamine. The rates of patients who regain normal kidney functions, develop CRF or develop mortality between the two groups were found to be similar. Conclusıon: Treatment results of AKI developing in ICU are not satisfactory. Low-dose dopamine treatment has no effect on patient outcomes in these patients. NGAL is a biomarker that has the ability to show renal damage at an early stage. Serial measurement of NGAL concentration during ICU stay may benefit the clinician in early diagnosis and follow-up of AKI.

Serum lncRNA HAND2-AS1 is downregulated in diabetic patients with chronic renal failure and ameliorates cell apoptosis

BackgroundLncRNA HAND2-AS1 has been reported to be a tumor suppressor in several types of malignancy, while its involvement in other human diseases is unclear. Our preliminary RNA-seq analysis revealed the downregulation of lncRNA HAND2-AS1 in diabetic patients with chronic renal failure, indicating the involvement of lncRNA HAND2-AS1 in this disease. This study was therefore carried out to explore the role of lncRNA HAND2-AS1 in the development of chronic renal failure in diabetic patients.MethodsMouse podocyte cells and plasma samples of diabetic patients (46 diabetic patients with chronic renal failure, 38 diabetic patients without obvious complications and 42 healthy volunteers) were used in this study. Cell apoptosis assay and PCR were performed.ResultsLncRNA HAND2-AS1 was downregulated in diabetic patients with chronic renal failure but not in diabetic patients without obvious complications. Downregulation of lncRNA HAND2-AS1 distinguished diabetic patients with chronic renal failure from diabetic patients and healthy controls. High glucose environment did not affect the expression of lncRNA HAND2-AS1 in mouse podocyte cells. Overexpression of lncRNA HAND2-AS1 inhibited the apoptosis of mouse podocyte cells under high glucose treatment.ConclusionsWe therefore conclude that lncRNA HAND2-AS1 may participate in the development of chronic renal failure in diabetic patients by regulating cell apoptosis.

APOL1 renal risk alleles in patients on chronic hemodialysis in Northwest of Iran

Introduction: Apolipoprotein L1 (APOL1) gene’s risk variants located on chromosome 22 are newly discovered factors for the development of chronic renal failure among African-American. These risk alleles were developed on the African continent as an evolutionary defense against sleep sickness due to Trypanosoma brucei rhodesiense and then spread with human migrations. Objectives: In the present study, we sought to examine these risk variants in a group of hemodialysis patients of Northwest of Iran. Patients and Methods: Two hundred patients receiving hemodialysis in different centers of the city (Tabriz in Northwest of Iran) were allocated randomly from a total number of 825 patients. The assessment of APOL1 polymorphisms (rs73885319, rs60910145, and rs71785313) was conducted using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method. Patients’ demographic data, history, and their biochemical parameters were recorded based on their last measurement. Results: No proposed renal risk variants of APOL1 gene in our hemodialysis population were found. All the participants had a wild genotype. Conclusion: The results of our study match with reports from Europe and Asia. In the paleoanthropological point of view, our results do not support African human migration hypothesis.

ANALGESIC NEPHROPATHY. A MODERN VIEW ON THE PROBLEM

Aim. To review Russian and foreign literature on modern methods of diagnosis and treatment of patients with analgesic nephropathy.Materials and methods. Russian and foreign literature sources published in recent years on the aforementioned problem were analyzed.Results. This article presents the concept of analgesic nephropathy (AN) and discusses causes and mechanisms of its development. The pathogenic effect of non-steroidal antiinfl ammatory drugs on renal tissue is indicated. Key stages of the disease and its clinical features are determined. An algorithm of diagnosis is proposed. The importance of a patient’s detailed medical history is emphasized, including the duration, multiplicity and reasons for taking analgesics. A particular attention is paid to questions of AN therapy and its prevention. Provided timely diagnosis and analgesics withdrawal, the possibility of reverting tubulointerstitial infl ammation is shown.Conclusion. It is shown that optimal solutions with regard to AN diagnosis and its treatment are yet to be found. A timely diagnosis inhibits the development of chronic renal failure, which early detection provides for a higher treatment effi ciency and improved prognosis.