Cause Of Chronic Kidney Disease Research Articles

POS-003 THE ETIOPTHALOGY OF ACUTE KIDNEY DISEASE AND DISORDERS IN PATIENTS FROM CKDu ENDEMIC REGIONS OF SRI LANKA

The uncertain/unknown etiology (CKDu) is the common cause of chronic kidney diseases in the North Central Region (NCR) of Sri Lanka. Recently, an acute phenotype of CKDu has been described in the same region, histologically consistent with acute interstitial nephritis (AIN). It was defined by serum creatinine elevation above the normal laboratory range, associated renal damage markers, acute symptoms, and exclusion of known causes (Badurdeen et al., 2016). The clinical profiles of these patients are compatible with the diagnosis of acute kidney disease and disorders (AKD) definition (Levey et al., 2020).

POS-355 IMMUNE REGULATION OF HMGN1 BY TARGETING TLR4 SIGNAL PATHWAY IN DIABETIC NEPHROPATHY

Diabetic nephropathy (DKD) is one of the most important complications in diabetic patients, and also the primary cause of end stage nephropathy (ESRD). About 40% of diabetics develop DKD.DKD has become the primary cause of chronic kidney disease (CKD) in China, and the

POS-671 PATIENTS WITH POLYCYSTIC KIDNEY DISEASE ON PERITONEAL DIALYSIS: A SINGLE CENTRE TERTIARY CARE RENAL UNIT EXPERIENCE FROM UNITED KINGDOM

Autosomal dominant polycystic kidney disease is the commonest hereditary cause of chronic kidney disease. The reduction of intra-abdominal volume for peritoneal dialysis (PD) due to the enlarging polycystic kidneys and other cystic organs, and the higher risk of complications such as abdominal and inguinal hernias, pericatheter leaks, intestinal perforations, hydrothorax due to pleuro-peritoneal communication, diverticular disease and gastrointestinal reflux raise the concerns about PD catheter insertions, survival, and outcome.

POS-407 COMPLEMENT RECEPTOR 1 IS A POTENTIAL THERAPEUTIC TARGET OF INTERSTITIAL LESION IN IgA NEPHROPATHY

IgA nephropathy is one of leading causes of chronic kidney disease. Interstitial lesion in IgA nephropathy is correlated with unfavorable prognosis. Sensitive biomarkers are important for early detection and intervention targets of the disease. This study aims to identify Complement Receptor 1 (CR1) as a potential therapeutic target in IgA nephropathy patients with interstitial lesion. Renal tissue proteomics data is accessed from a local IgA nephropathy cohort with 59 IgA nephropathy patients and 19 healthy controls. CD21/35+B cells are separated with fluorescence activated cell sorting from mice spleen. Adaptive transfer is operated with a single injection from the renal vein immediately after urethral obstruction. Renal pathology is evaluated on pictures captured by a visual microscope. CR1 is identified as the most significantly downregulated complement component in IgA nephropathy patients. Clinical information characterization of IgA nephropathy patients is assessed with Pearson R correlation test to confirm their linear independence. Of the 28 complement components recognized, 24 protein expression is increased in IgA nephropathy patients and 4 is decreased compared to healthy control. CR1 is identified as the most significantly decreased complement component in IgA nephropathy patients. CR1 protein expression is inversely correlated with IgA nephropathy interstitial lesion but not with renal function progress. Further correlation analysis of clinical information reveals that CR1 protein expression is inversely correlated with IgA nephropathy interstitial lesion, as represented as Oxford Classification T score. However, CR1 is not significantly correlated with serum creatine level or renal function loss progress (calculated as average eGFR decline per month). CD21/35+ cells are increased in the experimental renal interstitial injury mice. To test the hypothesis CR1 may be associated with interstitial lesion, we study the CD21/35 (CD21/35 is the mouse homolog of CR1 molecule) expression in unilateral urethral obstruction mice. We find that CD45+bone marrow derived cells significantly infiltrated the obstructed kidney at day 12, of which the CD5+ CD21/35+cells significantly increased compared to control. Adaptive transfer of CD21/35+B cells protects the cortex structure in experimental renal interstitial injury. To test whether the CD21/35 molecule on immune cells are protective against interstitial lesion, we sorted CD21/35+B cells and CD21/35-B cells and test their respective protective potential through adaptive transfer into UUO mice. We find that the renal cortex width is significantly increased in CD21/35+group than that in CD21/35-group at day 12 after UUO. CR1 is inversely correlated with renal interstitial lesion in IgA nephropathy patients and is potentially protective in experimental renal interstitial injury.

POS-445 CONTRIBUTION OF RENAL SYMPATHETIC NERVES TO THE DEVELOPMENT OF IgA NEPHROPATHY IN MICE

Renal sympathetic overactivity has been associated with the progression of various chronic kidney diseases. It not only contributes to the development of hypertension, but also impairs the kidney via pressure-independent mechanisms. IgA nephropathy (IgAN) is a leading cause of chronic kidney disease in China. However, whether and how renal sympathetic nerves play a role in IgA nephropathy remain obscure.

POS-787 LONG-TERM OUTCOMES OF KIDNEY TRANSPLANTATION IN CHILDREN WITH CAKUT VERSUS NON-CAKUT CAUSES OF CHRONIC KIDNEY DISEASE

Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common cause of end stage renal disease in children. Little is known about long-term outcomes after kidney transplantation in this group. The aim of this study is to evaluate the clinical characteristics of pediatric kidney transplantation (KTx) in CAKUT children and its outcomes. We conducted a retrospective study, from December 2007 to December 2020, including living donor kidney transplant recipients ≤17 years transplanted in our center. Patients were divided into those with CAKUT and those with non-CAKUT as the cause of chronic kidney disease (CKD). Our aim was to compare delayed graft function (DGF) rate, acute rejection, complication’s rates, and graft loss between groups. A total of 259 living donor kidney transplants were done till 2019. 38 (15%) were ≤17 years, The cause of CKD was CAKUT in 13 patients (34,2%) and non-CAKUT in 25 patients. Of the latter, 15 (60%) had glomerular disease. The most common CAKUT-related cause of CKD was primary vesicoureteral reflux (84,6%). There was no difference in age between the groups, with a mean age of 13,4 +/- 2,9 years in the CAKUT group and 12,7 +/- 3,4 years in the non-CAKUT group (p=0,542). Recipients with CAKUT showed female preponderance, and were more likely to be seropositive for both CMV and EBV (all p<0,05). A nephrectomy is most often performed in patients with CAKUT (53,8%) versus 4,3% in the non CAKUT patients (p=0,001). For both groups, there was no difference in cytotoxic PRA (15,4 % vs 16%, p=0,331) or mean number of compatibilities (3,53 vs 2,92, p=0,314). The post transplant hypertension was significantly higher in non CAKUT recipients than in those with CAKUT (p=0,049). . Compared to non CAKUT-group, CAKUT patients had more urinary tract infection (p=0,043). There was no difference in DGF (7,7% vs 8%, p=0,734), Acute rejection (7,7% vs 20%, p=0,141) or graft loss (7,7% vs 8%, p=0,784). Graft survival of the transplant in children with CAKUT is favourable. However, they have an increased risk of urinary tract infections.

More dissimilarities than affinities between DNAJB11-PKD and ADPKD.

ABSTRACTBackgroundPolycystic kidney diseases (PKD) are an important cause of chronic kidney disease (CKD). Autosomal dominant polycystic kidney disease (ADPKD) due to PKD1 or PKD2 mutations is the most common form, but other genes can be responsible for ADPKD and its phenocopies. Among them, a form of atypical ADPKD caused by DNAJB11 mutations (DNAJB11-PKD) has been recently described.MethodsWe retrospectively recruited a cohort of 27 patients from six different families sharing common ancestries and harboring the same DNAJB11 mutation (c.100C>T, p.Arg34*) and we compared it with a cohort of 42 typical ADPKD patients.ResultsDNAJB11-PKD patients show small/normal-sized kidneys, with significantly smaller cysts and a slower progression to end-stage kidney disease (ESKD) than ADPKD patients. In the DNAJB11-PKD cohort, the cystic phenotype could not be detected by ultrasound in about half of the patients, but all cases with available computed tomography/magnetic resonance scans displayed cysts. Clinically, DNAJB11-PKD patients displayed proteinuria (mostly albuminuria). Compared with ADPKD, DNAJB11-PKD patients were older and had a higher prevalence of type 2 diabetes mellitus (19% versus 0%; P = 0.007) and nephrolithiasis (62% versus 29%; P = 0.01), whereas the prevalence of cardiac valvular defects was lower (4% versus 51%; P < 0.001).ConclusionsOverall, clinical features of DNAJB11-PKD were more subtle compared with those of ADPKD. DNAJB11-PKD shows a unique renal and extrarenal phenotype, clinical presentation and natural history. Therefore our data support that this genetic disease is classified separately from ADPKD.

The effects of the renin-angiotensin-aldosterone system blockers on serum ischemia-modified albumin levels in autosomal dominant polycystic kidney disease.

Among one of the common hereditary causes of chronic kidney disease is autosomal-dominant polycystic kidney disease (ADPKD), and its incidence rate is reported as one between 500 and 1.000 individuals. The most common complications of ADPKD are hypertension (HT) and end-stage renal disease (ESRD). HT occurring in the early stage of ADPKD leads to deteriorations in renal function. It was aimed to investigate the ischemia-modified albumin (IMA) levels and the effect of renin-angiotensin-aldosterone system (RAAS) blockers on serum IMA levels in patients with ADPKD. One hundred and fifteen patients were included as ADPKD (n = 50), HT (n = 35), and healthy control (HC) groups (n = 30). Patients with ADPKD and HT were divided into two subgroups as RAAS blocker-users and non-users. Serum IMA levels were detected as 0.42 (0.17-0.80) in ADPKD and 0.28 (0.04-0.51) in HT and 0.36 (0.22-0.56) in HC groups as absorbance units (ABSU), and the highest serum IMA level was seen in Group ADPKD. Serum IMA levels were 0.33 ± 0.14 in RAAS blocker-users and 0.41 ± 0.11 ABSU in non-users with ADPKD. Serum IMA levels were witnessed to be significantly lower in RAAS blocker-users in Groups ADPKD (p = 0.038) and HT (p = 0.004), compared to non-users. Given basal and 6-month values of those with ADPKD, the levels of serum IMA within 6months were significantly lower (p = 0.002). We consider that serum IM levels should be assessed in oxidative stress (OS)-related conditions, such as ADPKD, and RAAS blockers may be effective in reducing serum IMA levels in ADPKD and HT patients.

Xanthine oxidoreductase activity in platelet-poor and rich plasma as a oxidative stress indicator in patients required renal replacement therapy

BackgroundXanthine oxidoreductase (XOR) is a hydroxylase enzyme involved in the metabolism of purines. XOR activity can vary: the homodimer protein can be converted into two different isoforms XD (antioxidant) and XO (prooxidant). Oxidative stress and inflammation that accompanying chronic kidney disease (CKD), dialysis, and kidney transplantation, resulted in platelet activation. Present study aimed to determine the influence of applied renal replacement therapy on xanthine oxidoreductase and its isoforms activity.Materials and MethodsThe study group consisted of 117 patients, divided into 4 groups: hemodialysis - 30 patients, peritoneal dialysis - 30 patients, kidney transplant patients - 27 and conservative treatment - 30 patients. The control group consisted of 30 healthy volunteers.ResultsSignificant differences were found in XOR activity in platelet-poor plasma (PPP) within the groups studied (p = 0.001). There was a relationship between the type of renal replacement therapy of all oxidoreductase isoforms in PPP (p < 0.001 all isoforms) and XD (p = 0.008), XO (p < 0.001) in platelet rich-plasma (PRP). A relationship was observed between the activity of all oxidoreductase isoforms in PPP and PRP, and the type of renal replacement therapy and the duration of dialysis and the age of patients. The cause of chronic kidney disease was also reflected differences in XD and XO activity in PPP.ConclusionsThe type of renal replacement therapy used in CKD patients, age of patients, duration of dialysis, CKD causes, and stage of progression significantly affect the activity of XOR and its isoforms.

Renal biopsy in diabetic patients: Histopathological and clinical correlations

Introduction: Diabetes is the leading cause of chronic kidney disease and end-stage kidney disease worldwide. A kidney biopsy in a diabetic patient must be considered when non-diabetic renal disease is suspected, such as in the presence of a rapid decline in renal function or severe unexplained proteinuria. However, the timing and criteria of a biopsy remain controversial in these patients. We aimed to identify clinical and histological markers that could help differentiate diabetic and non-diabetic renal disease and decide if this invasive approach is needed or not. Subjects and Methods: We reviewed 30 years of biopsies from diabetic patients performed at a tertiary hospital. We collected patient demographic data, biopsy indications, histological findings, and clinical and analytical data both at the moment of the biopsy and extensive followup. Based on kidney biopsy findings, patients were categorized as isolated diabetic nephropathy, non-diabetic kidney disease, or non-diabetic kidney disease superimposed on diabetic nephropathy (diabetic kidney disease). Results and Discussion: We enrolled 92 patients, mostly with type 2 diabetes, with a mean age of 62.9 ± 13.2 years. Nearly half of them had isolated diabetic nephropathy (53.3%), and 15.2% had diabetic nephropathy superimposed on non-diabetic kidney disease, comprising a total of 63 patients (68.5%) with diabetic kidney disease. Twenty-nine patients (31.5%) were considered to have non-diabetic kidney disease. These last patients were significantly less likely to need insulin therapy (p=0.002), had more frequently an acute deterioration of renal function (p=0.01), lower albumin levels (p=0.03), and a higher prevalence of microhematuria (p=0.001). We found the latter to be an independent predictor of non-diabetic kidney disease. Further, patients with the primary diagnosis of diabetic nephropathy had higher survival than those who had nondiabetic kidney disease, contradicting published data. Conclusions: The criteria for performing a biopsy in diabetic patients still lack consensus, although the priority to identify non-diabetic kidney disease prevails. We believe the non-diabetic kidney disease predictors we describe may prove helpful for determining the need for a histological assessment in diabetic patients.

A Deep Neural Network for Early Detection and Prediction of Chronic Kidney Disease.

Diabetes and high blood pressure are the primary causes of Chronic Kidney Disease (CKD). Glomerular Filtration Rate (GFR) and kidney damage markers are used by researchers around the world to identify CKD as a condition that leads to reduced renal function over time. A person with CKD has a higher chance of dying young. Doctors face a difficult task in diagnosing the different diseases linked to CKD at an early stage in order to prevent the disease. This research presents a novel deep learning model for the early detection and prediction of CKD. This research objectives to create a deep neural network and compare its performance to that of other contemporary machine learning techniques. In tests, the average of the associated features was used to replace all missing values in the database. After that, the neural network’s optimum parameters were fixed by establishing the parameters and running multiple trials. The foremost important features were selected by Recursive Feature Elimination (RFE). Hemoglobin, Specific Gravity, Serum Creatinine, Red Blood Cell Count, Albumin, Packed Cell Volume, and Hypertension were found as key features in the RFE. Selected features were passed to machine learning models for classification purposes. The proposed Deep neural model outperformed the other four classifiers (Support Vector Machine (SVM), K-Nearest Neighbor (KNN), Logistic regression, Random Forest, and Naive Bayes classifier) by achieving 100% accuracy. The proposed approach could be a useful tool for nephrologists in detecting CKD.

Dijabetesna nefropatija - klinička slika, tok i savremene mogućnosti lečenja

Diabetic kidney disease (DBD) is one of the major complications of diabetes (DM) and the leading cause of chronic kidney disease (CKD) worldwide. About 10% of patients with DBD progress to terminal HBB, and the rest die mostly due to cardiovascular disorders and infection even before they need treatment for kidney replacement. The main strategies to prevent the development and alleviate the progression of DBB in recent decades have been intensive glycemic con trol and blockade of the renin-angiotensin-aldosterone system. However, this approach did not achieve optimal results. Taking into account the increase in patients with DBB, high spending from the health care budget and the development of new therapeutic possibilities with significant kidney protection, the International Society of Nephrology issued in 2020. (Kidney Disease: Improving Global Outcomes (KDIGO) Guideline) is the first guide to treating patients with DBB. This review paper aims to point out phenotypic variability and present recent advances in the treatment of DBB.

TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases.

Glomerulonephritis is a common cause of chronic kidney disease, which has emerged as a major cause of end-stage renal disease. Autoimmune diseases, such as Systemic Lupus Erythematosus (SLE) and ANCA-associated vasculitis (AAV) are often associated with proliferative glomerulonephritis. Transforming growth factor-β1 (TGF-β1) is a cytokine with pleiotropic effects in chronic renal diseases, based on in vivo and in vitro studies. The Smad-dependent signalling pathway plays an important role in the regulation of renal fibrosis (excessive production of extracellular matrix [ECM]) and inflammation. However, clinical trials targeting TGF-β1 have presented disappointing results, suggesting that the downstream signalling is quite complex. The diversity of the effects may associate with the interactions between TGF-β1 signalling and other downstream signalling, as well as the different cellular responses, which TGF-β1 promotes. Recently, macrophage chemoattract and epigenetic effects have also been identified as new mechanisms, wherefore TGF-β1/Smad signalling mediates renal injury. This review provides an overview of the role of TGF-β1/Smad signalling pathway from in vivo and in vitro studies in the pathogenesis of glomerulonephritis and particularly in proliferative glomerulonephritis, which is associated with autoimmune diseases.

Left Ventricular Global Longitudinal Strain Predicts Adverse Cardiovascular Outcomes in Patients With Comorbid Chronic Kidney Disease and Diabetes Mellitus

Diabetes mellitus (DM) is a leading cause of chronic kidney disease (CKD) with patients with diabetic nephropathy having a disproportionately higher risk of cardiovascular (CV) disease compared to those with DM alone. Left ventricular (LV) global longitudinal strain (GLS) has been used to identify early LV dysfunction in DM. We sought to evaluate the prognostic value of LV-GLS in the diabetic population with concurrent CKD. Patients without prior cardiovascular disease with concurrent DM and CKD were prospectively recruited from outpatient Nephrology clinics across two tertiary institutions. All patients underwent clinical assessment and transthoracic echocardiogram with LV-GLS assessment at index recruitment. Patients were followed for up to five years for the primary outcome of CV death or development of major adverse cardiovascular outcomes (MACE). A total of 121 pts (67.17±10.98 yrs, 64% male) with DM and CKD were included. The mean eGFR was 36.2±13.4, with 68% having Stage 3 and 32% having Stage 4 disease. The primary outcome occurred in 33 (27%) patients over a mean follow-up period of 29.2±13.7 months. Log rank tests showed increased indexed LV mass (p<0.01), elevated E/e’ (p=0.04), larger indexed left atrial volume (p<0.01) and reduced LV-GLS (p<0.01) to be associated with the distribution to time to adverse outcomes. Nested multi-variable Cox regression analysis showed LV-GLS to be an independent predictor of CV death and MACE (p<0.01). In diabetic patients with CKD, LV-GLS was associated with cardiovascular death and MACE. This marker may be useful in risk stratification of this population.

Clinico-Epidemiological Profile of Dialysis Services in Karnataka, India - A Multicentric Exploratory Study.

Introduction:New challenges in dialysis care delivery confront caregivers with the rise in dialysis numbers. There are significant lacunae in the knowledge and efficient application of dialysis therapy in the absence of a dialysis registry. This multicentric study was conducted by the Nephrology Association of Karnataka to systematically study patient demographics and dialysis characteristics in Karnataka state, India, as a basis for a statewide dialysis registry.Material and Methods:Data were collected from the consenting dialysis centers after institutional ethics board clearances. Residents of Karnataka state, who were confirmed prevalent patients with end-stage renal disease, on either maintenance hemodialysis (HD) or peritoneal dialysis were included. Demographic data of patients and details of dialysis as well as dialysis facilities were collected on an online platform. Statistical analysis was done using SPSS software Version 16.Results:Thirty-two centers contributed to the data of 2,050 patients (males 70.3%, mean age 53.49 ± 14.09 years). Most patients were on HD (95.3%). Diabetes was the commonest cause of chronic kidney disease. About 72% of patients had temporary venous catheters as initial vascular access. In all, 1,156 patients (59.9%) were on thrice weekly HD. Around 65% of the centers were in private hospitals. The majority (90%) of the centers reused dialyzers, 56% reprocessed dialyzers mechanically, and 66% tested viral serology quarterly.Conclusions:This study was one of the initial attempts to capture dialysis data across Karnataka, and it offers useful insight into the existing dialysis demographics and care delivery. Participation of more centers and continued effort to form a dialysis registry for deriving meaningful clinico-epidemiological insight are desirable.

Serum and urine periostin and cytokeratin-18 in children with congenital obstructive nephropathy.

Congenital obstructive nephropathy (CON) is one of the most common causes of chronic kidney disease in children. The aim of the study was to investigate serum and urine periostin and cytokeratin-18 (CK-18) in children with CON in relation to CON etiology, treatment, and kidney injury. We evaluated 81 children with CON secondary to ureteropelvic junction obstruction (UPJO), ureterovesical junction obstruction (UVJO), posterior urethral valves (PUV) and 60 controls. Neither biomarker demonstrated any relation to CON etiology. However, all patients showed significantly higher urine periostin (uPeriostin) and uPeriostin/Cr levels than the controls. Also, UVJO patients showed higher sCK-18 and uCK-18/Cr levels, and PUV patients showed higher uCK-18/Cr levels than the controls. Neither biomarker was found to have any relation to CON treatment. However, conservatively treated children and those before and after surgery showed significantly higher uPeriostin and uPeriostin/Cr levels than the controls. uPeriostin strongly correlated with differential renal function (DRF) < 40%. The ROC analysis demonstrated the best area under the curve (AUC) for uPeriostin (0.831) and uPeriostin/Cr (0.768), and low for sPeriostin (0.656) and uCK-18 (0.615) for detecting renal injury. In conclusion, although serum and urine periostin and CK-18 did not display any relation to etiology or the type of CON treatment, uPeriostin seems to be a useful tool for detecting renal injury in children with CON, especially due to its strong negative correlation with DRF < 40%.

Does serum kidney injury molecule-1 predict early diabetic nephropathy: A comparative study with microalbuminuria.

Introduction:Diabetic nephropathy (DN) is a multifactorial disease, one of the most common complications of diabetes and a major cause of chronic kidney disease. Kidney injury molecule-1 (KIM-1) is a sensitive and specific marker of kidney injury as well as a predictor of prognosis.Objective:The present study aimed to investigate the usefulness of serum KIM-1 as an early marker of DN.Patients and Methods:The present study included total 75 participants, among whom 25 nondiabetic participants were chosen as controls. The 50 diabetic participants were divided into two groups according to urine protein/creatinine ratio (UPCR) as participants with normoalbuminuria (T2DM patients without nephropathy) and microalbuminuria (T2DM patients with nephropathy). The complete blood count, blood glucose, HbA1c, serum electrolytes, and creatinine levels were measured using standard laboratory techniques, and serum KIM-1 levels were measured by sandwich enzyme-linked immunosorbent assay.Results:There was a significant difference in the mean serum KIM-1 between the control and diabetics without microalbuminuria (P = 0.0001). Patients with longer duration of diabetes had a higher serum KIM-1 values (P = 0.05 in DM without microalbuminuria; P = 0.007 for DM with microalbuminuria). Serum KIM-1 did not correlate with UPCR in controls (P = ‒0.167), in diabetics with microalbuminuria (P = 0.487). However, there was a significant correlation observed between UPCR and serum KIM-1 in diabetics without microalbuminuria (P = 0.04).Conclusion:The present study observed significantly increased levels of serum KIM-1 in both the diabetic groups compared to controls. Moreover, serum KIM-1 positively correlated with the duration of diabetes. Therefore, serum KIM-1 may be used as an early diagnostic marker to predict nephropathy among diabetes in our population.

Circulating miRNAs in Type 2 Diabetic Patients with and without Albuminuria in Malaysia

Introduction: Diabetic kidney disease (DKD) remains the leading cause of chronic kidney disease. Dysregulation of circulating miRNAs has been reported, suggesting their pathological roles in DKD. This study aimed to investigate differentially expressed miRNAs in the sera of type 2 diabetes mellitus (T2DM) patients with and without albuminuria in a selected Malaysian population. Method: Forty-one T2DM patients on follow-up at a community clinic were divided into normo-(NA), micro-(MIC), and macroalbuminuria (MAC) groups. Differential levels of miRNAs in 12 samples were determined using the pathway-focused (human fibrosis) miScript miRNA qPCR array and was validated in 33 samples, using the miScript custom qPCR array (CMIHS02742) (Qiagen GmbH, Hilden, Germany). Results: Trends of upregulation of 3 miRNAs in the serum, namely, miR-874-3p, miR-101-3p, and miR-145-5p of T2DM patients with MAC compared to those with NA. Statistically significant upregulation of miR-874-3p (p = 0.04) and miR-101-3p (p = 0.01) was seen in validation cohort. Significant negative correlations between the estimated glomerular filtration rate (eGFR) and miR-874-3p (p = 0.05), miR-101-3p (p = 0.03), and miR-145-5p (p = 0.05) as well as positive correlation between miR-874-3p and age (p = 0.03) were shown by Pearson’s correlation coefficient analysis. Conclusion: Upregulation of previously known miRNA, namely, miR-145-5p, and possibly novel ones, namely, miR-874-3p and miR-101-3p in the serum of T2DM patients, was found in this study. There was a significant correlation between the eGFR and these miRNAs. The findings of this study have provided encouraging evidence to further investigate the putative roles of these differentially expressed miRNAs in DKD.

Weight Change Alters the Small RNA Profile of Urinary Extracellular Vesicles in Obesity

Introduction: Various kidney diseases reportedly show different urinary extracellular vesicle (EV) RNA profiles. Although obesity is one of the main causes of chronic kidney disease, the expression pattern of urinary EV RNA in obesity is uncertain. Our aim was to sequence the small RNA profiles of urinary EVs in obese patients before and after weight reduction and compare them to those of healthy volunteers (HVs). Methods: We recruited age-sex-matched obese patients and HVs. The small RNA profiles of urinary EVs were analyzed using RNA sequencing. To evaluate the effect of weight reduction, small RNA profiles of urinary EVs 6 months after bariatric surgery were also analyzed. Results: The proportion of urinary EVs transfer RNA and microRNA of obese patients differed from that of HVs. Obese patients showed differential expression of 1,343 small RNAs in urinary EVs compared to HVs (fold change ≥2 and p value <0.05). Among those, 61 small RNAs were upregulated in obese patients and downregulated after weight reduction, whereas 167 small RNAs were downregulated in obese patients and upregulated after weight reduction. RNA sequencing revealed the correlation between the specific urinary EV small RNAs and clinical parameters including body weight, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol, serum glucose, estimated glomerular filtration rate, and albuminuria. Conclusion: Obese patients showed distinct urinary EV small RNA profiles compared to HVs. Weight reduction altered urinary EV small-RNA profiles in obese patients.

Histopathological Pattern of Primary Glomerulonephritis - A Single Center Experience

lomerulonephritis is the most common cause of chronic kidney disease in our country like in other developing countries. The incidence and histological pattern of primary GN in our countare is inadequately described. This cross-sectional prospective study was conducted at the nephrology unit in Holy Family Red Crescent Medical College Hospital, a tertiary care teaching hospital in Dhaka, Bangladesh starting from January 2019 - December 2019 including all patients with suspected primary GN who underwent kidney biopsies. Total 35 biopsies were performed. M: F 1.3:1 .Mean age was 33.71+_12.2 yrs. Membranoproliferative GN (34.28%) was the most common cause followed by mesangioproliferative (22.85%), IgA nephropathy (17.14%), membranous (11.42%), FSGS ( 11.42%) and minimal change disease (2.8%). Among 35 cases, 20 had proliferative verity. In immunofluroscence study, 19 had mild to marked deposits of immunoglubulin. 5.71% had post-biopsy complication which was not significant enough. As the sample size was small so needs more studies in large to get the specific epidemiological patterns of primary GN.