Search Results (173)

Background: Olmesartan-induced enteropathy is a rare complication of a widely used angiotensin II receptor blocker. Patients usually present with chronic diarrhea and weight loss. Histologically, villous atrophy and intraepithelial lymphocyte infiltrates within the duodenum confirm the diagnosis. The prognosis is usually good after withdrawal of the offending drug. Case presentation: Here, we report the case of a 76-year-old woman who developed a severe form of Olmesartan-induced enteropathy complicated by acute kidney injury and acute recurrence after drug rechallenge. After definite cessation of the drug, the patient did not experience any gastrointestinal (GI) symptom recurrence after 6 months of follow-up. However, she experienced chronic kidney disease stage G3b. Histological analysis did not show any villous atrophy or intraepithelial lymphocyte infiltrates within the duodenum or the colon biopsy. Discussion and conclusion: This case highlights the broad spectrum of clinical manifestations and histological findings in Olmesartan-induced enteropathy. It also highlights the importance of rapid diagnosis in order to limit organ damage such as chronic kidney disease. Full article

Background: Several recent studies have documented an increased cardiovascular risk in patients with primary hyperparathyroidism (PHPT), thereby stimulating interest in the association with uric acid (UA), a metabolite linked to cardiovascular disease and chronic kidney disease (CKD) progression, whose role in these conditions is still the subject of study. The aim of this review is to summarize the underlying pathophysiological mechanisms of the PHPT-UA relation and discuss their potential clinical implications. Methods: We conducted a comprehensive literature review, with a focus on the physiological and clinical aspects of the relationship between PHPT and UA. Results: The evidence in the literature supports the association between PHPT and elevated UA levels, although the underlying mechanisms still need to be elucidated. Key mechanisms seem to involve tubular and intestinal transporters, particularly the ABCG2 transporter, as well as indirect effects mediated by hypercalcemia and inflammatory processes. Conclusions: The association between PHPT and UA, though recognized for years, highlights the existence of linked pathophysiological mechanisms between mineral and purine metabolism. However, the current knowledge does not clarify whether uric acid plays an active role in the development of complications related to hyperparathyroidism or if it just represents an indirect marker of metabolic dysfunction. In the absence of specific guidelines, measuring UA levels to screen for hyperuricemia, especially in patients with additional risk factors, should be considered to prevent related complications. Future studies could clarify the role of UA in PHPT, improving our understanding of the disease and potentially leading to new therapeutic strategies to prevent cardiovascular, renal and joint manifestations. Full article

Background\Objectives: Chronic kidney disease (CKD) is defined as a clinical syndrome secondary to a permanent change in kidney function or structure, making it irreversible. Most patients at the onset of the disease are asymptomatic or present nonspecific symptoms, including signs and symptoms at the oral level. These manifestations, such as hyposalivation, increased calculus index, enamel defects, or changes in saliva composition, contribute to the diagnosis of this pathology and can also significantly affect the patient’s quality of life. The aim is to systematically assess the presence and relevance of oral manifestations in patients with CKD, and to identify correlations between these symptoms and clinical parameters such as glomerular filtration rate or concomitant conditions of the patient. Materials and Methods: A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A search was carried out in the PubMed, Scopus, Scielo, and The Cochrane Library databases on 7 April 2025, using terms related to “chronic kidney disease” and “oral manifestations”. Inclusion criteria referred to observational studies published in the last ten years that reported oral symptoms in patients with CKD. The quality of cohort and case-control studies was assessed using the Newcastle–Ottawa Scale (NOS), while for cross-sectional studies, the Joanna Briggs Institute (JBI) critical appraisal checklist was used. Results: A total of 27 studies met the inclusion criteria, primarily cross-sectional in design. The most frequently reported oral manifestations included hyposalivation, increased calculus and plaque indices, enamel defects, periodontal disease, and oral candidiasis. Significant associations were identified between the duration of dialysis and severity of periodontal disease, as well as between CKD stage and taste dysfunction. Findings varied by age group and CKD stage, with children showing distinct salivary profiles and adults presenting more pronounced periodontal and mucosal conditions. Conclusions: This review highlights a clear relationship between CKD and various oral health disturbances, although more studies are needed to better understand oral–systemic interactions in CKD. What is necessary is the establishment of multidisciplinary care approaches. Full article

Renal anemia (RA) is a common complication of chronic kidney disease (CKD). Patients with prolonged RA may present with nonspecific systemic manifestations, including cold intolerance, fatigue, drowsiness, anorexia, muscle weakness, reduced physical activity, impaired memory and cognitive function, and difficulty concentrating. Although previous studies have identified risk factors for anemia development in CKD, challenges remain in early diagnosis and therapeutic intervention. Therefore, we analyzed a dataset of CKD patients with RA from the MIMIC database and used machine learning models to predict whether RA will occur in CKD patients. In addition, an optimized model was designed, and is explained in the article, that tunes the hyperparameters of FT-Transformer (FTT) with the Bayesian optimization (BO) algorithm. The proposed BO–FTT model achieved an accuracy of 91.81%, outperforming the untuned FTT as well as TabNet, Multilayer Perceptron (MLP), and Kolmogorov–Arnold Networks (KAN) that were optimized by the BO algorithm. Full article

Arsenic, in the form of inorganic arsenite, is toxic to the kidney and can cause acute kidney injury, manifesting as destruction of proximal tubule cells. Nephron repair is possible through the proliferation of resident tubular progenitor cells expressing CD133 and CD24 surface markers. We simulated regenerative repair in the continued presence of i-As (III) using a cell culture model of a renal progenitor cell line expressing CD133 (PROM1) and CD24. Continued exposure and subculturing of progenitor cells to i-As (III) led to a reduction in the expression of PROM1 and CD24, as well as a decrease in the ability to differentiate into tubule-like structures. Cessation of i-As (III) and recovery for up to three passages resulted in continued repression of PROM1 and reduced ability to differentiate. Chronically exposed cells exhibited an ability to form colonies in soft agar, suggesting neoplastic transformation. Chronically exposed cells also exhibited an induction of CD44, a cell surface marker commonly found in renal cell carcinoma, as well as in tubular repair in chronic renal injury such as chronic kidney disease. These results demonstrate potential adverse outcomes of renal progenitor cells chronically exposed to a nephrotoxicant, as well as in environmental exposure to arsenic. Full article

Background: According to a study conducted among a relatively healthy population of Mongolia (2017), the prevalence of hepatitis C virus (HCV) infection is 8.5%, which is considered a high prevalence of this infection. In addition to inflammation of the liver, other organ systems are affected by HCV infection, according to research. Our study aimed to evaluate renal dysfunction in patients with HCV infection. Methods: In the study, 111 people with chronic hepatitis C virus infection were included in the study group, and 111 relatively healthy people were included in the control group. Laboratory parameters were analyzed. Liver fibrosis score was assessed and evaluated by renal function. Results: There were 22.9% (51) men and 77.1% (171) women among the 222 participants, and the average age was 40.7 ± 11.1 years. The glomerular filtration rate was 105.3 ± 24.5 in the chronic hepatitis C virus-infected group and 118.7 ± 18.5 in the control group, or the statistically significant difference in the case group compared to the control group was p < 0.01. The liver fibrosis score was higher in the case group than in the control group. According to logistic regression analysis, patients with hepatitis C virus infection are 25 times more likely to have a decrease in glomerular filtration rate than those without viral infection (OR 24.91, 95% CI 3.13–198.38, p = 0.002). Conclusions: Our study showed that HCV infection leads to kidney function loss. In addition, older age, obesity, and severe liver fibrosis contribute to kidney function decline. Full article

Background: Systemic sclerosis (SSc) is a rare connective tissue disease characterized by vasculopathy, autoimmunity, and fibrosis. Due to its low prevalence and heterogeneous clinical presentation, early diagnosis remains challenging, often delaying appropriate treatment. The disease progresses from microvascular dysfunction, manifesting as Raynaud’s phenomenon, to systemic fibrosis affecting multiple organs, including the lungs, gastrointestinal tract, heart, and kidneys. There have been considerable advancements in understanding the pathophysiology of the disease during the last few years and this has already resulted in the improvement of the therapeutic approaches used to control organ-specific manifestations. However, the underlying cause of the disease still remains incompletely elucidated. Methods: Here, we summarize the current knowledge on the SSc pathogenesis. Results: The pathophysiology involves an interplay of chronic inflammation, impaired vascular function, and excessive extracellular matrix deposition, leading to progressive organ damage. Endothelial dysfunction in SSc is driven by immune-mediated injury, oxidative stress, and the imbalance of vasoconstrictors and vasodilators, leading to capillary loss and chronic hypoxia. Autoantibodies against endothelial cells or other toxic factors induce apoptosis and impair angiogenesis, further exacerbating vascular damage. Despite increased angiogenic factor levels, capillary repair mechanisms are defective, resulting in progressive ischemic damage. Dysregulated immune responses involving Th2 cytokines, B cells, and macrophages contribute to fibroblast activation and excessive collagen deposition. Transforming growth factor-beta (TGF-β) plays a central role in fibrotic progression, while fibroblasts resist apoptosis, perpetuating tissue scarring. The extracellular matrix in SSc is abnormally stiff, reinforcing fibroblast activation and creating a self-perpetuating fibrotic cycle. Conclusions: Advances in molecular and cellular understanding have facilitated targeted therapies, yet effective disease-modifying treatments remain limited. Future research should focus on precision medicine approaches, integrating biomarkers and novel therapeutics to improve patient outcomes. Full article

Hepatitis E virus (HEV), the causative agent of hepatitis E, is the leading cause of acute viral hepatitis worldwide; under immunosuppression, infection can lead to chronic liver disease. Furthermore, extrahepatic manifestations, particularly renal manifestations, are frequently associated with infection. This is important considering the global burden of chronic kidney disease (CKD). However, the study of chronic hepatitis E has been limited to liver disease, and its definition with respect to renal disease is still incomplete. Recently, through a protocol aimed at identifying HEV seroprevalence in a cohort of patients on hemodialysis, we incidentally identified HEV RNA in a patient with a history of alcoholism, diabetes mellitus, and essential systemic hypertension. In this study, we aimed to follow up this case to characterize hepatitis E in the context of CKD. Notably, we identified the development of chronic HEV genotype 3 infection without seroconversion or evidence of liver damage. Moreover, apparent immunocompetence was identified in the patient. Considering that HEV is still neglected in numerous countries and that it is not included in the differential diagnosis of kidney disease, our findings support the need to consider HEV infection in patients with renal disease, even in the absence of liver deterioration. Full article

Melioidosis, caused by Burkholderia pseudomallei, is a potentially fatal infection, particularly affecting individuals with chronic conditions such as diabetes or kidney or liver diseases. This review examines melioidosis in India over the past two decades, focusing on its prevalence, risk factors and clinical manifestations. A PubMed search (2000–2024) identified a rise in melioidosis publications, with most from Southern India, followed by Eastern India, and an increase post-2019. Eight studies from 2010–2022 identified fever (86%), cough (26%) and joint pain (23%) as the most common symptoms, while diabetes (75%), alcohol abuse (19%) and cancer (6%) were primary predisposing factors. Severe clinical manifestations were also observed, including bacteremia (50%), pneumonia (37%) and splenic abscess (18%). Although environmental exposure risks were not significantly high, individuals with diabetes or chronic kidney disease, particularly those working in high-risk environments, were more likely to contract melioidosis. Cryptic environmental factors that might bridge known epidemiological risk factors are also addressed. The review emphasizes the increasing awareness and research in clinical epidemiology and also highlights a gap in studies on antimicrobial treatments, vaccines and environmental surveillance. Targeted interventions in diabetes and poverty hotspots could help control the disease more effectively. Full article

Background: The most common cause of chronic liver disease is now known to be non-alcoholic fatty liver disease (NAFLD), recently redefined as metabolic-associated fatty liver disease (MAFLD). This review aims to synthesize current evidence on the pathophysiology and clinical implications of nephrological, pulmonary, and dermatological manifestations among NAFLD/MAFLD patients. In order to find safe and efficient treatments, NAFLD/MAFLD has emerged as a primary concern for hepatologists worldwide. Methods: We conducted a comprehensive review of the literature from major databases, focusing on studies that evaluated the extrahepatic manifestations of NAFLD/MAFLD. Emphasis was placed on identifying pathophysiological mechanisms and assessing their clinical impact on renal, pulmonary, and dermatological systems. Results: Recent developments in the management of chronic viral hepatitis have lowered the mortality rate associated with chronic liver disease. However, the prevalence of NAFLD/MAFLD continues to rise, making chronic liver disease a significant health concern for the future. An increasing percentage of patients on liver transplant waiting lists now have cirrhosis and hepatocellular carcinoma due to non-alcoholic liver disease. Furthermore, the incidence and prevalence of chronic kidney disease have surged, linking NAFLD/MAFLD to higher morbidity, mortality, and healthcare costs. Conclusions: NAFLD/MAFLD is underdiagnosed and underappreciated, yet its incidence is rapidly increasing, raising concerns about a potential global epidemic. Given its multisystemic impact—extending to renal, pulmonary, and dermatological complications—it is crucial to develop interdisciplinary strategies for early detection and effective management of the disease. Full article

Pathogenic variants in the Wilms’ tumor suppressor gene 1 (WT1 gene) can lead to serious disorders within the kidney and urogenital system, including chronic kidney disease. There is still much uncertainty regarding the optimal management of diseases caused by WT1 dysfunction, posing a challenge for physicians caring for these patients. The aim of our study is to present experiences related to the course and treatment of patients with confirmed WT1 pathogenic variants. Data from seven patients (five girls, two boys), who were at the age of 4.8 ± 5.1 years (0.3–14 years) at their first admission and were treated between 1997–2022, were analyzed. The analysis included each patient’s age at the day of diagnosis, anthropometric measurements, comorbidities, and laboratory and genetic test results, as well as their treatment, oncological procedures, and performed surgeries. Wilms’ tumor was the first manifestation of the disease in three patients. Arterial hypertension was diagnosed in three patients, and anemia in four. Treatment of patients with nephrotic syndrome included glucocorticosteroid therapy (GCS), calcineurin inhibitors (CNIs), and mycophenolate mofetil (MMF). Nephrectomy was performed in five children, while kidney transplantation was carried out in two patients. An interdisciplinary approach to WT1 gene pathogenic variants, including early diagnosis, individualization, regular monitoring of treatment, and oncological vigilance, is crucial for improving prognosis and ensuring proper care for patients with nephrological manifestations of WT1 gene region disorders. Furthermore, for a comprehensive understanding of the scope of this disease and the development of effective therapy methods, continued research on the clinical manifestations of WT1 pathogenic variants is essential. Full article

Background: Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease predominantly affecting young individuals; however, its late-onset manifestation poses distinct clinical and diagnostic challenges. Methods: This report describes the case of a 93-year-old patient who presented in the Emergency Department with exertional dyspnea, lower limb edema, fatiguability, diffuse abdominal pain, predominantly in the hypogastric region, and loss of appetite. Results: Based on the clinical examination, laboratory tests, and imagistic investigations, we excluded the most common etiologies of edema (decompensated chronic heart failure, glomerular nephropathy/chronic kidney disease, decompensated vascular cirrhosis, hypothyroidism, and hypoproteinemia). Further diagnostic evaluation revealed elevated levels of anti-nuclear antibodies and anti-dsDNA antibodies, along with reduced complement levels, indicating active SLE as the underlying cause of the patient’s edema. During hospitalization, the patient received corticosteroid therapy and, after discharge, was referred to the Rheumatology Department for further treatment. Conclusions: In elderly patients, late-onset SLE exhibits distinct clinical manifestations compared to its early-onset counterpart, likely due to age-related alterations in immune system function. Full article

Atrial fibrillation (AF) is the most common chronic arrhythmia and is a leading cause of stroke, with well-documented differences in pathophysiology, clinical manifestations, and prognosis according to the sex of the patient. This review provides an overview of known or hypothesized sex differences in physiology and stroke risk for patients with AF. Women are reported to have more extensive fibrosis of the left atrium, different functional properties of the atria, and higher sensitivity to prothrombotic stimuli, especially after menopause. Variations in stroke risk with AF are linked to age, hypertension, diabetes, and chronic kidney disease; overall, women have worse outcomes. The widely clinically implemented CHA₂DS₂-VASc score no longer considers sex as a variable, and its propriety for women is still debated. However, women are usually under prescribed anticoagulation despite having a higher long-term risk of stroke compared to men, suggesting a lack of equity of treatment for certain patient groups. New AI-based risk stratification models and precision medicine approaches are potentially useful in reducing these gaps. Future work should also aim to improve sex-based predictive models, considering different gender categories, and understanding the part played by hormonal alterations, atrial structural alterations, and thromboembolic risk in the treatment of AF. Full article

Background and Objectives: Pathogenic variants in the PAX2 gene have been associated with a spectrum of eye and kidney disorders, ranging from papillorenal syndrome (known as renal coloboma syndrome) to isolated nephrosis without kidney morphological anomalies (focal segmental glomerulosclerosis), inherited in an autosomal dominant manner. However, due to the growing number of reports of pathogenic variants in the PAX2 gene, it is observed that genotype–phenotype correlation is not always consistent. We present patients from two unrelated families with PAX2 pathogenic variants c.685C>T and c.250G>A, highlighting the diverse phenotypic expression of PAX2-related disorders. Materials and Methods: We analyzed clinical and genetic data from two families who were tested for genomic abnormalities using targeted next-generation sequencing and Sanger sequencing for segregation analysis. Results: In Family A, a 27-year-old male presented with chronic kidney disease stage 3, proteinuria, and multicystic kidney dysplasia diagnosed at 11 years old. An ophthalmologic examination revealed bilateral optic nerve dysplasia. In Family B, a 6-year-old female and her 4-year-old sister were clinically diagnosed with renal hypoplasia, while their 36-year-old father presented with chronic kidney disease stage 3, focal segmental glomerulosclerosis, and optic disc pits. Genetic analysis identified a heterozygous PAX2 pathogenic variant c.685C>T, p.(Arg229*), in Family A and a heterozygous PAX2 pathogenic variant c.250G>A, p.(Gly84Ser) in Family B. Conclusions: The literature and our data further support that the same PAX2 variants may cause diverse kidney and ocular phenotypes among unrelated families and within the same family. Due to variable expressivity, a wide range of clinical manifestations of rare hereditary kidney diseases are still underdiagnosed, and a multidisciplinary approach is required to detect extrarenal signs of PAX2-related disorder. Full article

Background and Objectives: Peripheral arterial disease (PAD) is a severe manifestation of atherosclerosis that disproportionately affects patients with chronic kidney disease (CKD) stages 3–5, resulting in a higher prevalence in this group. Currently, it is challenging to detect early PAD in this patient population. This study investigated the association between serum endocan levels and PAD based on the ankle–brachial index (ABI) in non-dialysis patients with CKD stages 3–5. Materials and Methods: Specimens of blood and baseline demographic characteristics were gathered from a total of 164 patients presenting with stages 3–5 CKD, who were not receiving dialysis. We used a commercially available oscillometric technique to ascertain ABI values for our participants, and used a common and well-established threshold for defining low ABI, known to be associated with PAD: ABI values < 0.9. Endocan levels in patients’ serum samples were measured by using enzyme-linked immunosorbent assays. Results: A total of 24 out of 164 people (14.6%) showed lower-than-normal ABIs. Compared to the group with normal ABIs, the individuals with low ABIs had more of the following conditions: diabetes mellitus (DM, p = 0.030), urine protein-to-creatinine ratio (p = 0.031), serum C-reactive protein concentrations (p = 0.037), and serum endocan levels (p < 0.001). After adjusting for variables significantly correlated with PAD by multivariate logistic regression analysis, age (odds ratio [OR]: 1.097, 95% confidence interval [CI]: 1.038–1.159, p = 0.001), DM (OR: 3.437, 95% CI: 1.053–11.225, p = 0.041), and serum endocan concentration (OR: 1.098, 95% CI: 1.042–1.157, p = 0.001) were identified as independent predictors of PAD in patients with CKD stages 3–5. Conclusions: Elevated serum endocan levels were found to be independent correlates of PAD in non-dialysis patients with CKD stages 3 through 5. Full article