Congenital Kidney Research Articles

Kegiatan Pengabdian Masyarakat dalam Rangka Edukasi Masyarakat Terhadap Hipertensi serta Deteksi Dini Penyakit Gagal Ginjal Sebagai Komplikasi dari Hipertensi

Hypertension and kidney failure are two types of diseases related to kidney health. Hypertension or high blood pressure can cause damage to the kidneys, while kidney failure is a condition in which the kidneys cannot function properly to build up metabolic waste and fluids from the body. Hypertension can cause damage to the small blood vessels in the kidneys, so that the kidneys cannot excrete waste properly. As a result, harmful substances can accumulate in the body and cause organ damage. If hypertension cannot be controlled properly, it can cause kidney damage and eventually lead to kidney failure. Failure is a kidney condition in which the kidneys cannot function properly to remove metabolic wastes and fluids from the body. Kidney failure can occur for a variety of reasons, including untreated hypertension, diabetes, congenital kidney disease, and use of certain medications. If left untreated, kidney failure can lead to accumulation of waste in the body and serious complications such as anemia, osteoporosis, heart disease and even death. Treatment of hypertension and kidney failure usually involves medication and lifestyle changes. Treatment includes the use of drugs prescribed by a doctor and the management of complications that may occur. Lifestyle changes include managing a healthy diet, reducing salt and fat consumption, exercising regularly, avoiding smoking, and managing stress. Early detection is very important in the management of hypertension and kidney failure. Regular blood pressure checks, urine tests to detect protein in the urine, and blood tests to detect levels of creatinine, blood glucose, and cholesterol in the blood can help detect risks and early symptoms of kidney disease.
 

Amniotic fluid content in children with kidney and urinary tract anomalies determines pre- and postnatal development

BackgroundRenal oligohydramnios (ROH) describes an abnormally low volume of amniotic fluid (AF) during pregnancy. ROH is mostly caused by congenital fetal kidney anomalies. The ROH diagnosis frequently implies an increased risk of peri- and postnatal fetal mortality and morbidity. The present study aimed to evaluate the impact of ROH on pre-and postnatal development in children with congenital kidney anomalies.MethodsThis retrospective study included 168 fetuses with anomalies in the kidney and urinary tract. Based on the amount of AF measured by ultrasound, patients were divided into three groups: normal amniotic fluid (NAF), amniotic fluid in the lower normal range (LAF), and ROH. These groups were compared with respect to prenatal sonographic parameters, perinatal outcomes, and postnatal outcomes.ResultsAmong the 168 patients with congenital kidney anomalies, 26 (15%) had ROH, 132 (79%) had NAF, and 10 (6%) had LAF. Of the 26 families affected by ROH, 14 (54%) decided to terminate pregnancy. Of 10 live-born children in the ROH group, 6 (60%) survived the observation time; of these, 5/6 presented with chronic kidney disease, stages I–III, at their last examination. The main differences in postnatal development between the ROH group and the NAF and LAF groups were: restricted height and weight gain, respiratory issues, complicated feeding, and the presence of extrarenal malformations.ConclusionsROH is not a mandatory indicator of severe postnatal kidney function impairment. However, children with ROH have complicated peri-and postnatal periods, due to the presence of concomitant malformations, which must be considered in prenatal care.Graphical abstractA higher resolution version of the Graphical abstract is available as Supplementary information

An infant girl with bilateral multicystic dysplastic kidney: a case report

Multicystic dysplastic kidney (MCDK) is a congenital kidney abnormality with an overall incidence rate of 1/4300 live births that is more prevalent in males than females. Here, we describe a rare case of bilateral MCDK complicated by hypertension, severe vesicoureteral reflux (VUR), and urinary tract infection (UTI), who stabilized during hospitalization with prospective kidney transplantation due to poor prognosis. Since bilateral MCDK is a rare disease with numerous complications and a poor prognosis, patient symptom management and treatment may be more challenging.

Subclinical C1q Nephropathy Combined with Possible Donor-Derived IgA Deposition in a 1-Year Kidney Allograft Biopsy: A Case Report

Few previous studies have reported immune-complex nephropathy that has not been classified as a specific phenotype in kidney allografts. We report a case of a de novo subclinical "full-house" pattern of deposition in a pediatric transplantation recipient with possible donor-derived IgA deposition. A five-year-old boy underwent living kidney transplantation due to congenital kidney and urinary tract anomalies. A one-hour implantation biopsy revealed IgA deposition. A four-month protocol biopsy finding showed less intense IgA deposition, in contrast with the one-hour biopsy, and trace para-mesangial deposits. A one-year protocol biopsy demonstrated a full-house deposition pattern and massive electron-dense deposits with minor glomerular changes. At the time of the one-year biopsy, kidney function was stable, with no urinalysis abnormalities. No evidence of systemic lupus erythematosus was observed in clinical and serologic examinations. Mesangial IgG, IgM, C3, and C1q deposition was codominant, and IgA deposition was weaker. We diagnosed this case as C1q nephropathy combined with remaining donor-derived IgA deposition. Few studies have reported C1q nephropathy in kidney allograft; further accumulation of cases is required. To distinguish between donor-derived and de novo glomerular lesions, it is important to assess the serial histologic findings of immunofluorescence and electron microscopy. Here, we report a rare case of subclinical C1q nephropathy with possible donor-derived IgA nephropathy.

Rapid identification of chronic kidney disease in electronic health record database using computable phenotype combining a common data model.

Rapid identification of chronic kidney disease in electronic health record database using computable phenotype combining a common data model.

PD37-01 THE CADHERIN-CATENIN COMPLEX IS CRUCIAL FOR THE INITIAL STEP OF NEPHRON FORMATION

You have accessJournal of UrologyCME1 Apr 2023PD37-01 THE CADHERIN-CATENIN COMPLEX IS CRUCIAL FOR THE INITIAL STEP OF NEPHRON FORMATION Balint Der, Helena Bugacov, Muskaan Singh, and Andrew P. McMahon Balint DerBalint Der More articles by this author , Helena BugacovHelena Bugacov More articles by this author , Muskaan SinghMuskaan Singh More articles by this author , and Andrew P. McMahonAndrew P. McMahon More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003335.01AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Congenital anomalies of the kidney and urinary tract contribute to a significant share of pre- and neonatal developmental abnormalities. In nephron formation, canonical Wnt-signaling induces mesenchymal nephron progenitor cells (NPCs) to aggregate and epithelialize forming the renal vesicle (RV), the nephron precursor. β-catenin is essential for the inductive process though the mechanism of morphological transition is not well understood (Park et al., 2007). We hypothesized that ß-catenin also directs RV formation through its critical role in cadherin mediated cell adhesion, the potential redundancy amongst cadherin members confounding earlier genetic studies (Dahl et al., 2002). METHODS: Using a chemically defined culture medium replicating in vivo NPC signaling, we examined the requirement for multiple cadherin adhesion complex components in the canonical Wnt signaling induced aggregation of induced NPCs in vitro. RESULTS: Removal of extracellular calcium, an essential ion in cadherin complexes, resulted in reversible loss of cell-cell contacts, consistent with a role for cadherin adhesion in the aggregation process. In vitro knockout of β-catenin inhibited the induction and aggregation of NPCs replicating the findings of the in vivo loss-of-function mouse experiments. Interestingly, the deletion of α-catenin phenocopied the results of β-catenin knockout experiments blocking cell aggregation providing further evidence for the role of the cadherin-catenin complex in the aggregation. To identify the cadherin members of the adhesion complex, we screened in vitro bulk RNA-seq. dataset and validated the presence of four cadherin proteins by immunofluorescent staining. The quadruple removal of in vitro expressed cadherins replicated the previously characterized phenomenon of inhibited aggregation of the NPCs. CONCLUSIONS: The aggregation of NPCs in vitro is exclusively mediated via the cadherin-catenin complex which models the initial step of nephrogenesis in vivo. A mechanistic insight into NPC aggregation fits within the larger framework of how a healthy kidney is formed and might explain the genetic background of certain congenital kidney anomalies. Source of Funding: National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK054364 Cell Interaction in Development of the Mammalian Kidney) © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e986 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Balint Der More articles by this author Helena Bugacov More articles by this author Muskaan Singh More articles by this author Andrew P. McMahon More articles by this author Expand All Advertisement PDF downloadLoading ...

Congenital renal hypoplasia and contralateral kidney failure in a giant otter (Pteronura brasiliensis) ex situ in Southeastern Brazil

Renal hypoplasia is incomplete development of the kidneys, in which fewer than normal numbers of nephrons are present at birth. This report is the first of these conditions in mustelids. A female adult giant otter (Pteronura brasiliensis), ex situ, presented clinically an unusual behavior with prostration, anorexia, hiding in the shelter, ataxia, paraparesis, and death in a clinical course of one day. At the postmortem exam, the left kidney was markedly enlarged and pale and the right kidney was severely reduced and had mild to moderate capsular thickening. Histologically, the left kidney had mineralization, proliferation of fibrous connective tissue and a mild neutrophilic infiltrate. The right kidney presented a reduced number of glomeruli, tubular atrophy and an increase in fibrous connective tissue, which were findings compatible with congenital kidney hypoplasia. Due the clinical condition of the animal, gross and microscopic findings, the cause of death was established as kidney failure induced by renal hypoplasia.

Spotlight on Genetic Kidney Diseases: A Call for Drug Delivery and Nanomedicine Solutions.

Nanoparticles as drug delivery carriers have benefited diseases, including cancer, since the 1990s, and more recently, their promise to quickly and efficiently be mobilized to fight against global diseases such as in the COVID-19 pandemic have been proven. Despite these success stories, there are limited nanomedicine efforts for chronic kidney diseases (CKDs), which affect 844 million people worldwide and can be linked to a variety of genetic kidney diseases. In this Perspective, we provide a brief overview of the clinical status of genetic kidney diseases, background on kidney physiology and a summary of nanoparticle design that enable kidney access and targeting, and emerging technological strategies that can be applied for genetic kidney diseases, including rare and congenital kidney diseases. Finally, we conclude by discussing gaps in knowledge remaining in both genetic kidney diseases and kidney nanomedicine and collective efforts that are needed to bring together stakeholders from diverse expertise and industries to enable the development of the most relevant drug delivery strategies that can make an impact in the clinic.

Fetal and Perinatal Nephrology: Small but Mighty.

Fetal and Perinatal Nephrology: Small but Mighty.

Role of hypertension in progression of pediatric CKD.

Hypertension is frequent in children with chronic kidney disease (CKD). Its prevalence varies according to CKD stage and cause. It is relatively uncommon in children with congenital kidney disease, while acquired kidney disease is associated with a higher prevalence of hypertension. Studies in children with CKD utilizing ambulatory blood pressure monitoring also showed a high prevalence of masked hypertension. Uncontrolled and longstanding hypertension in children is associated with progression of CKD. Aggressive treatment of high blood pressure should be an essential part of care to delay CKD progression in children.

Primary cilia-associated protein IFT172 in ciliopathies.

Cilium is a highly conserved antenna-like structure protruding from the surface of the cell membrane, which is widely distributed on most mammalian cells. Two types of cilia have been described so far which include motile cilia and immotile cilia and the latter are also known as primary cilia. Dysfunctional primary cilia are commonly associated with a variety of congenital diseases called ciliopathies with multifaceted presentations such as retinopathy, congenital kidney disease, intellectual disability, cancer, polycystic kidney, obesity, Bardet Biedl syndrome (BBS), etc. Intraflagellar transport (IFT) is a bi-directional transportation process that helps maintain a balanced flow of proteins or signaling molecules essential for the communication between cilia and cytoplasm. Disrupted IFT contributes to the abnormal structure or function of cilia and frequently promotes the occurrence of ciliopathies. Intraflagellar transport 172 (IFT172) is a newly identified member of IFT proteins closely involved in some rare ciliopathies such as Mainzer-Saldino syndrome (MZSDS) and BBS, though the underpinning causal mechanisms remain largely elusive. In this review, we summarize the key findings on the genetic and protein characteristic of IFT172, as well as its function in intraflagellar transport, to provide comprehensive insights to understand IFT172-related ciliopathies.

Prevalence and Clinical Significance of Urinary Tract Infection among Neonates Presenting with Unexplained Hyperbilirubinemia in Lebanon: A Retrospective Study.

Neonatal jaundice is commonly seen in term and preterm newly born babies. It could be either physiologic or secondary to multiple underlying pathologies like urinary tract infection (UTI). Our main objective was to confirm the relationship between neonatal jaundice without apparent cause like hemolysis and the presence of UTI. We, retrospectively over a period extended from 2017 to 2020, included 496 babies admitted for elevated indirect hyperbilirubinemia for whom demographic, clinical, laboratory, and therapeutic data were collected through a detailed questionnaire. Our study included 496 neonates and showed a prevalence of UTI in 8.9% of neonates. The two most common microorganisms in urine culture were Escherichia coli (65.9%) and Klebsiella pneumoniae (25.0%). A multivariate logistic analysis showed that UTI was associated with male neonates (odds ratio [OR] = 2.366, 95% confidence interval [CI]: 1.173 - 4.774; P = 0.016), history of prenatal UTI (OR = 5.378, 95% CI: 2.369 - 12.209; P <0.001), poor feeding (OR = 3.687, 95% CI: 1.570 - 8.661; P = 0.003), and positive urine culture in catheter (OR = 2.704, 95% CI: 1.255 - 5.826; P = 0.011). The mean length of stay was higher in patients with positive UTI (Median = 216 hours) compared to patients with negative UTI (Median = 48 hours) (P <0.001). Neonatal sreening for UTI should be recommended whenever there is unexplaind early or prolonged hyperbilirubinemia with no evidence of alloimmune hemolysis or blood group incompatibility and to prevent the morbidity of urosepsis and congenital kidneys malformations.

The developing murine kidney actively negotiates geometric packing conflicts to avoid defects.

The physiological functions of several organs rely on branched epithelial tubule networks bearing specialized structures for secretion, gas exchange, or filtration. Little is known about conflicts in development between building enough tubules for adequate function and geometric constraints imposed by organ size. We show that the mouse embryonic kidney epithelium negotiates a physical packing conflict between increasing tubule tip numbers through branching and limited organ surface area. Through imaging of whole kidney explants, combined with computational and soft material modeling of tubule families, we identify six possible geometric packing phases, including two defective ones. Experiments in explants show that a radially oriented tension on tubule families is necessary and sufficient for them to switch to a vertical packing arrangement that increases surface tip density while avoiding defects. These results reveal developmental contingencies in response to physical limitations and create a framework for classifying congenital kidney defects.

Hnf1b renal expression directed by a distal enhancer responsive to Pax8

Xenopus provides a simple and efficient model system to study nephrogenesis and explore the mechanisms causing renal developmental defects in human. Hnf1b (hepatocyte nuclear factor 1 homeobox b), a gene whose mutations are the most commonly identified genetic cause of developmental kidney disease, is required for the acquisition of a proximo-intermediate nephron segment in Xenopus as well as in mouse. Genetic networks involved in Hnf1b expression during kidney development remain poorly understood. We decided to explore the transcriptional regulation of Hnf1b in the developing Xenopus pronephros and mammalian renal cells. Using phylogenetic footprinting, we identified an evolutionary conserved sequence (CNS1) located several kilobases (kb) upstream the Hnf1b transcription start and harboring epigenomic marks characteristics of a distal enhancer in embryonic and adult renal cells in mammals. By means of functional expression assays in Xenopus and mammalian renal cell lines we showed that CNS1 displays enhancer activity in renal tissue. Using CRISPR/cas9 editing in Xenopus tropicalis, we demonstrated the in vivo functional relevance of CNS1 in driving hnf1b expression in the pronephros. We further showed the importance of Pax8-CNS1 interaction for CNS1 enhancer activity allowing us to conclude that Hnf1b is a direct target of Pax8. Our work identified for the first time a Hnf1b renal specific enhancer and may open important perspectives into the diagnosis for congenital kidney anomalies in human, as well as modeling HNF1B-related diseases.

Atypical segmental multicystic dysplastic kidney with severe reflux in a newborn

Segmental cases of multicystic dysplastic kidney (SMCDK) are rare and hard to diagnose, imaging characteristics are not evident. SMCDK can be presented with duplex collecting system, vesicoureteral reflux (VUR), pyeloureteric junction obstruction and orthotopic ureterocele. Typical cases are localized to the upper pole of a duplex collecting system. Atypical cases are rarely reported. We present an unique atypical SMCDK case, with unconventional disease manifestation to bring attention to the variable presentation of this rare disorder and to draw attention to differential diagnostic challenges of cystic kidney malformations. In our patient newborn screening abdominal ultrasound detected severe hydronephrosis and hydroureter of the lower pole of the right kidney. Dynamic renal scintigraphy and sonocystography confirmed duplication of both collecting systems and severe VUR in the right lower pole. Heminephrectomy was performed. The suspected diagnosis of atypical SMCDK was confirmed by histopathology. The patient recovered uneventfully. This unusual case of atypical SMCDK highlights the importance of considering the possibility of SMCDK in patients with partial kidney malformation or unusual appearance of congenital kidney disease.

Evaluation of urinary acidification in children: Clinical utility.

The kidney plays a fundamental role in acid-base homeostasis by reabsorbing the filtered bicarbonate and by generating new bicarbonate, to replace that consumed in the buffering of non-volatile acids, a process that leads to the acidification of urine and the excretion of ammonium (NH4 +). Therefore, urine pH (UpH) and urinary NH4 + (UNH4 +) are valuable parameters to assess urinary acidification. The adaptation of automated plasma NH4 + quantification methods to measure UNH4 + has proven to be an accurate and feasible technique, with diverse potential indications in clinical practice. Recently, reference values for spot urine NH4 +/creatinine ratio in children have been published. UpH and UNH4 +, aside from their classical application in the study of metabolic acidosis, have shown to be useful in the identification of incomplete distal renal tubular acidosis (dRTA), an acidification disorder, without overt metabolic acidosis, extensively described in adults, and barely known in children, in whom it has been found to be associated to hypocitraturia, congenital kidney abnormalities and growth impairment. In addition, a low UNH4 + in chronic kidney disease (CKD) is a risk factor for glomerular filtration decay and mortality in adults, even in the absence of overt metabolic acidosis. We here emphasize on the need of measuring UpH and UNH4 + in pediatric population, establishing reference values, as well as exploring their application in metabolic acidosis, CKD and disorders associated with incomplete dRTA, including growth retardation of unknown cause.

Kidney replacement therapy in neonates: utilization trends and outcomes.

We aimed to assess prevalence and clinical characteristics of newborns receiving kidney replacement therapy (KRT). We used the National Inpatient Sample (NIS) dataset for the years 2000-2017. Newborns treated with peritoneal dialysis (PD), hemodialysis (HD), and continuous KRT (CKRT) were included. Trend analysis using the Cochran-Armitage test was used to assess prevalence over the years. A total of 64,532,552 hospitalized newborns were included. Among the 4281 infants treated with KRT, 2501 (58.4%) were treated with PD, 997 (23.3%) had HD, and 783 (18.3%) used CKRT. Associated diagnoses included congenital kidney anomalies (37.4% vs. 15% vs. 9.5%), urinary tract anomalies (35% vs. 12.5% vs. 6.3%), and congenital heart disease (68% vs. 25.7% vs. 72.3%). Median length of stay was longest in PD patients (39days vs. 18days vs. 26days), respectively. However, cost of hospitalization was greatest in CKRT patients (US $490,916 vs. US $218,514 vs. US $621,554), respectively. In the entire cohort, 54,424 newborns had acute kidney injury (AKI); of them 16,999 (31%) died. KRT was used in 2,688 (4.9%) of infants with AKI. Over the study period, trends for utilization of PD (from 0.042 to 0.06%) and CKRT (from 0.03 to 0.21%) increased whereas the hemodialysis trend decreased (from 0.021 to 0.013%). Congenital heart disease(CHD) and congenital anomalies of the kidneys and urinary tract (CAKUT) are the major diagnoses in newborns receiving KRT. Utilization of PD was greater than HD and CKRT. Trends of PD and CKRT utilization increased over time. Less than 5% of infants diagnosed with AKI received KRT.

Combined Preimplantation Genetic Testing for Genetic Kidney Disease: Genetic Risk Identification, Assisted Reproductive Cycle, and Pregnancy Outcome Analysis.

BackgroundGenetic kidney disease is a major cause of morbidity and mortality in neonates and end-stage renal disease (ESRD) in children and adolescents. Genetic diagnosis provides key information for early identification of congenital kidney disease and reproductive risk counseling. Preimplantation genetic testing for monogenic disease (PGT-M) as a reproductive technology helps prospective parents to prevent passing on disease-causing mutations to their offspring.Materials and MethodsA retrospective cohort of couples counseled on PGT who had a risk to given birth to a child with genetic kidney disease or had a history of prenatal fetal kidney and urinary system development abnormalities from 2011 to 2021. Through a combination of simultaneously screening for aneuploidy and monogenic kidney disease, we achieved reproductive genetic intervention.ResultsA total of 64 couples counseled on PGT for monogenic kidney disease in a single reproductive center during the past 10 years, of whom 38 different genetic kidney diseases were identified. The most frequent indications for referral were autosomal recessive disease (54.7%), then autosomal dominant disease (29.7%), and X-linked disease (15.6%). Polycystic kidney disease was the most common diseases counted for 34.4%. After oocyte-retrieval in all of 64 females, a total of 339 embryos were diagnosed and 63 embryos were transferred in succession. Among 61 cycles of frozen-embryo transfer (FET), ongoing pregnancy/live birth rate (OP/LBR) reached 57.38%. The cumulative OP/LBR in our cohort for the 64 couples was 54.69%. In addition, we have carried out expanded carrier screening (ECS) in all the in vitro fertilization (IVF) couples performed PGT covering 7,311 individuals. The carrier frequency of the candidate genes for monogenic kidney diseases accounted for 12.19%.ConclusionOverall, the customization PGT-M plan in our IVF center is pivotal to decreasing the morbidity and implementing reproductive genetic intervention of genetic kidney disease.

Exosomal proteomics in kidney disease: From technical approaches to clinical applications

Exosomes are small extracellular vesicles (sEVs) secreted from cells and have a general diameter ranging from 30~150 nm. It was reported that exosomes have essential roles in intercellular communication and can be targeted as biomarkers of disease or as therapeutic agents. Among the different techniques used for exosome investigation, the mass spectrometry-based proteomics approach has accelerated the unraveling of the molecular composition of exosomes and has contributed to improved knowledge of molecular processes in various diseases. In this review, we focused on proteomics-based studies of exosomes and clinical applications in kidney diseases. A general introduction of exosomes, isolation and characterization techniques, and proteomics-based study workflows are included in this article. We also categorized applications in acute kidney injury, chronic kidney disease, renal transplantation, congenital kidney disease, and malignant kidney disorder to show the important findings from proteomics-based exosomal investigations.

MO668: An Increase of Free Fatty Acids on Patients Starting Peritoneal Dialysis Suggests an Increased Cardiovascular Risk Beyond Classical Dyslipidemia Biomarkers

Abstract BACKGROUND AND AIMS Chronic kidney disease (CKD) produces profound changes in lipid metabolism, and these associated lipid disorders, in turn, contribute to the progression of CKD and its cardiovascular complications. Patients on peritoneal dialysis have a more atherogenic lipid profile than non-dialysis-dependent CKD patients or on HD. In the general population, the reduction of total cholesterol and LDL levels is associated with improved clinical outcomes in terms of morbidity and mortality; however, several studies have failed to obtain these same results in patients on dialysis. The use of lipidomics to detect a broader panel of lipid species can improve the prediction of the different alterations that influence cardiovascular mortality. METHOD This is a single-center prospective observational study of a cohort of CKD patients who start renal replacement therapy with continuous ambulatory peritoneal dialysis (CAPD). Data from 39 patients were examined. All samples for routine laboratories and lipidomics studies were obtained the day before starting CAPD (T0) and 6 months after (T1). Samples were analysed on an Ultra-Performance Liquid Chromatography system. The differences in the lipid profile analytical variables between baseline and 6 months after the start of CAPD were analysed. For the lipidomic analysis, each compound was grouped with its possible adducts and compound class based on the International Lipid Classification. RESULTS Thirty-nine patients were enrolled the study. Their mean age was 57.9 ± 16.3 years. The underlying renal diseases were glomerular disease (15 patients), diabetic kidney disease (10), congenital kidney disease (4), hypertensive kidney disease (2), interstitial nephropathy (2) and others (6). Hypertension was present in 96.3% of the patients, diabetes mellitus in 30.8% and 30 of the 39 patients had dyslipidemia (76.9%). Of the group of patients with dyslipidemia, only one of them was not on statin treatment. Table 1 shows the results of the analytical variables of lipid profile, serum glucose and renal function before and 6 months after initiating CAPD. The levels of CT and LDL were lower 6 months after CAPD initiation, but these were not statistically significant. Using the plasma lipid profile, with a mass spectrometry approach, a significant increase (P &amp;lt; 0.05) in total free fatty acids (FFA) was observed from T0 to T1. FFA (16:1) and FFA (18:0) were the FFAs with the highest peak response (Fig. 1). CONCLUSION Our LC-QTOF/MS-based lipidomics approach to study the effect of starting renal replacement therapy with CAPD in patients with CKD shows that total FFAs increased after 6 months on this technique. Within this group of lipids, FA 16:1 (palmitoleic acid) and FA 18:0 (stearic acid) were the ones that increased the most. An earlier study demonstrated that FFA levels are increased in the plasma of CKD patients; moreover, they have reported that higher levels of saturated fatty acids in serum correlate with sudden cardiac death in patients starting HD. Likewise, monounsaturated fatty acids are the products of stearoyl-CoA desaturase (SCD) catalyzed reactions and act as substrates to synthesize phospholipids and triglycerides. The activity of SCD is very high in patients with cardiovascular disease, hypertension and diabetes.