Introduction: Chronic inflammation plays a significant role in cardiovascular disease (CVD)–related mortality among patients with chronic kidney disease (CKD). The neutrophil‑to‑albumin percentage ratio (NPAR) has emerged as an indicator of an individual’s inflammatory status. This study aimed to investigate the association between elevated NPAR and the risk of CVD mortality in patients with CKD. Materials and Methods: The study was conducted in accordance with the PRISMA reporting guidelines. Comprehensive searches were performed across the Cochrane Library, Scopus, Web of Science, Embase, and PubMed databases, as well as the Google Scholar search engine, up to 30 January 2026. All statistical analyses were carried out using STATA version 14. Results: Compared with lower NPAR values, elevated NPAR was associated with a higher risk of cardiovascular mortality (OR = 1.54; 95% CI: 1.33–1.78) and all‑cause mortality (OR = 1.62; 95% CI: 1.40–1.89) in patients with CKD. In addition, higher NPAR increased the risk of CVD‑related death among patients undergoing hemodialysis (OR = 1.66; 95% CI: 1.29–2.15) and peritoneal dialysis (OR = 1.56; 95% CI: 1.25–1.94). Furthermore, the third quartile of NPAR (OR = 1.44; 95% CI: 1.16–1.78), the fourth quartile (OR = 1.92; 95% CI: 1.61–2.30), the second tertile (OR = 1.38; 95% CI: 1.07–1.80), and the third tertile (OR = 1.97; 95% CI: 1.61–2.41) were all associated with increased CVD mortality compared with the lowest category. Elevated NPAR also increased the risk of CVD‑related mortality in both men (OR = 1.23; 95% CI: 1.04–1.45) and women (OR = 1.16; 95% CI: 1.08–1.24) with CKD. Conclusion: Higher NPAR levels were associated with an increased likelihood of cardiovascular and all‑cause mortality among individuals with CKD. As NPAR values rose, the risk of CVD‑related death increased correspondingly when compared with lower levels. In addition, cardiovascular mortality risk was greater in men than in women, and higher among patients receiving hemodialysis than those undergoing peritoneal dialysis. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO (ID: CRD420261304086) and Research Registry (UIN: reviewregistry2082) websites.
Dental implant therapy in dialysis-dependent chronic kidney disease (CKD) patients presents significant osseointegration challenges due to systemic metabolic disturbances inherent to end-stage renal disease. Renal osteodystrophy, characterized by abnormal bone turnover, mineralization defects, and secondary hyperparathyroidism, critically compromises alveolar bone quality and remodeling capacity essential for implant stability. Elevated parathyroid hormone levels induce excessive bone resorption, while hyperphosphatemia and hypocalcemia disrupt hydroxyapatite crystallization, impairing the bone-implant interface formation. Uremic toxins accumulate despite dialysis, inducing chronic inflammation and oxidative stress that suppress osteoblast activity and angiogenesis while promoting osteoclastogenesis. Additionally, frequent comorbidities, including diabetes, hypertension, and anemia further compromise microcirculation and tissue healing. Anticoagulant use during hemodialysis increases perioperative bleeding risks, potentially disrupting early clot formation and cellular migration at the surgical site. Although dental implants remain a viable rehabilitation option for edentulous CKD patients, success rates are generally lower compared to healthy populations, with higher incidences of marginal bone loss and late failures. Careful patient selection, optimized dialysis timing around surgery, stringent control of calcium-phosphate products and parathyroid hormone levels, and also extended healing periods are recommended clinical strategies. Limited long-term prospective studies specifically addressing implant outcomes in this population highlight an evidence gap requiring further investigation. Multidisciplinary coordination between nephrologists and implantologists is essential to mitigate risks. Though not an absolute contraindication, implant placement in dialysis-dependent patients demands thorough preoperative assessment of bone metabolism markers, individualized surgical protocols, and realistic patient counseling regarding potentially prolonged osseointegration timelines and guarded long-term prognosis compared to non-renal compromised individuals.
Artificial intelligence (AI) is rapidly transforming the field of nephrology by enhancing the diagnosis, prognosis, and management of kidney diseases through advanced data-driven techniques. AI-driven medical image analysis using deep learning and radiomics enables early detection of structural abnormalities in chronic kidney disease (CKD) and diabetic kidney disease (DKD), improving diagnostic accuracy and enabling standardized interpretation of ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI). Machine learning (ML)models that integrate clinical, laboratory, and genetic data surpass traditional risk equations in predicting CKD progression, dialysis initiation, and mortality, facilitating personalized monitoring and intervention. In renal pathology, AI-powered digital pathology tools automate lesion detection, quantification, and classification from biopsy specimens, offering objective metrics that correlate with clinical outcomes. Within kidney transplantation, AI refines donor–recipient matching, predicts acute rejection and graft survival, and augments biopsy interpretation to optimize use of scarce donor organs. AI-enabled decision support systems and real-time monitoring algorithms in dialysis and continuous kidney replacement therapy personalize treatment parameters, enhance symptom control, and predict complications. Despite these advances, challenges related to data bias, model interpretability, ethical considerations, and clinical integration must be addressed. Prospects include the integration of multi-omics data, federated learning to protect patient privacy, explainable AI models for transparent decision-making, and telemedicine applications to extend nephrology expertise globally. Continued interdisciplinary collaboration and rigorous clinical validation will be essential to fully harness AI’s potential and usher in an era of precision nephrology.
Brain metastasis (BM) from renal cell carcinoma (RCC) represent a significant clinical challenge, associated with high morbidity and poor prognosis. The advent of targeted therapies and immune checkpoint inhibitors (ICIs) has transformed the management of metastatic RCC (mRCC), yet patients with brain metastasis remain underrepresented in clinical trials, and optimal management strategies are still evolving. The findings indicated that brain metastasis occur in approximately 5–15% of patients with mRCC, with clear cell histology and the presence of extracranial metastases as key risk factors. The pathophysiology involves complex molecular mechanisms, including hematogenous dissemination and genetic alterations. Clinical presentation is often symptomatic, with headaches, focal deficits, and seizures, but a substantial proportion of cases are detected incidentally. Magnetic resonance imaging (MRI) remains the gold standard for diagnosis, though screening is typically reserved for symptomatic or high-risk patients. Treatment is multimodal: surgery and stereotactic radiosurgery (SRS) are mainstays for local control, while systemic therapies, particularly cabozantinib and ICI-based regimens, have shown promising intracranial activity. Prognosis remains guarded, with median survival after BM diagnosis ranging from 10 to 18 months, but outcomes have improved in the ICI era. In conclusion, the management of RCC brain metastases requires a multidisciplinary, individualized approach. Advances in systemic and local therapies have improved survival, but significant challenges remain, including the risk of intracranial hemorrhage and the need for better screening and surveillance strategies. Ongoing research into molecular mechanisms and novel therapeutics holds promise for further progress in this high-risk population.
Malignancy-associated hypercalcemia represents a severe metabolic complication frequently observed in advanced renal cell carcinoma (RCC), often precipitating acute kidney injury (AKT) and limiting therapeutic options. Though systemic volume depletion and renal vasoconstriction contribute to renal disturbance, direct tubular toxicity mediated by intrinsic mitochondrial dysfunction remains underexplored. This review discusses on mechanistic framework linking excessive extracellular calcium load to renal tubular epithelial failure. Hypercalcemia induces profound intracellular calcium overload within proximal tubular cells, triggering mitochondrial calcium uniporter activation. Consequently, mitochondrial membrane potential collapses due to permeability transition pore opening, effectively uncoupling oxidative phosphorylation. This bioenergetic crisis generates excessive reactive oxygen species (ROS), promoting lipid peroxidation, protein oxidation and DNA damage. Simultaneously, cytochrome c release initiates apoptotic cascades, whereas severe ATP depletion triggers necrotic cell death. The resulting tubular obstruction, cast formation, and inflammation exacerbate glomerular filtration rate loss. Furthermore, tumor-derived factors like parathyroid hormone-related protein (PTHrP) may sensitize mitochondria to calcium-induced stress, amplifying injury. Dysregulated mitochondrial dynamics, including fission and fusion imbalance, further compromise cellular resilience against calcium stress. Identification this pathway highlights mitochondria as critical therapeutic targets beyond standard hydration and bisphosphonates. Interventions stabilizing mitochondrial integrity, modulating calcium handling, or scavenging ROS could mitigate tubular injury. Eventually, deciphering these molecular events offers novel strategies to preserve renal function in patients with advanced renal cancer suffering from hypercalcemic crises. Such approaches may significantly improve survival outcomes and enable continued systemic therapy, addressing a critical unmet need in oncology nephrology where renal preservation dictates treatment eligibility and quality of life during palliative care.
Introduction: Kidney cancer is a common tumor of the urinary system, and existing data on the relationship between sodium–glucose cotransporter 2 (SGLT2) inhibitors use and kidney cancer are inconsistent. Therefore, this study aimed to investigate the association between SGLT2 inhibitor use and the risk of developing kidney cancer. Materials and Methods: This study was designed as a systematic review and meta-analysis following the PRISMA guidelines. Accordingly, a comprehensive search was conducted in the Cochrane, Scopus, Web of Science, Embase, and PubMed databases, as well as the Google Scholar search engine, up to January 5, 2026. Data analysis was performed using STATA version 14. Results: The results showed that the association between the use of SGLT2 inhibitors (OR: 1.14, 95% CI: 0.86–1.52), dapagliflozin (OR: 1.67, 95% CI: 0.47–5.93), canagliflozin (OR: 1.59, 95% CI: 0.61–4.15), and empagliflozin (OR: 1.31, 95% CI: 0.52–3.27) with the risk of kidney cancer was not statistically significant. However, SGLT2 inhibitor use was associated with a reduced risk of renal cell carcinoma (RCC) (OR: 0.69, 95% CI: 0.63–0.76). In contrast, compared with dipeptidyl peptidase‑4 (DPP‑4) inhibitors, SGLT2 inhibitor use was linked to an increased risk of kidney cancer (OR: 1.64, 95% CI: 1.11–2.43). Conclusion: In conclusion, the use of SGLT2 inhibitors did not affect the incidence of kidney cancer, but it was associated with a 31% reduction in the risk of RCC. In contrast, compared with DPP‑4 inhibitors, SGLT2 inhibitor use increased the risk of kidney cancer by 64%. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO (ID: CRD420261293668) and Research Registry (UIN; reviewregistry2078) websites.
Preeclampsia-associated nephropathy represents a distinct form of pregnancy-induced kidney injury characterized by proteinuria, hypertension, and endothelial dysfunction, posing significant risks to both maternal and fetal health. Historically defined by the hallmark lesion of glomerular endotheliosis, contemporary histopathological analyses have expanded this paradigm to reveal widespread podocyte effacement, mesangial expansion, and subtle tubulointerstitial alterations that correlate with disease severity and postpartum renal recovery trajectories. At the molecular level, recent insights emphasize a profound angiogenic imbalance driven by excessive placental release of anti-angiogenic factors, particularly soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin, which disrupt glomerular capillary integrity and impair endothelial nitric oxide signaling. Concurrently, oxidative stress, complement activation, and dysregulated inflammatory cascades amplify endothelial injury, while emerging evidence highlights mitochondrial dysfunction and epigenetic modifications as critical contributors to sustained podocyte damage and maladaptive repair. Integrative multi-omics approaches have further identified dysregulated lipid metabolism, extracellular matrix remodeling, and autophagy impairment as pivotal pathways linking systemic vascular stress to localized nephropathy. Despite these advances, the precise temporal sequence of molecular events and their translation into targeted therapeutics remain unresolved. Current research is increasingly focused on biomarker validation, noninvasive imaging correlates, and repurposing angiogenic or complement-modulating agents to mitigate renal injury. Translational efforts are now prioritizing interventions that restore vascular homeostasis and preserve podocyte architecture, alongside longitudinal cohorts designed to delineate long-term renal sequelae. Finally, a deeper mechanistic understanding of preeclampsia-associated nephropathy refines risk stratification, informs postpartum monitoring, and illuminates broader paradigms of endothelial-driven kidney disease across the lifespan.
Introduction: Chronic kidney disease often progresses to end-stage renal disease (ESRD), necessitating renal replacement therapies such as peritoneal dialysis (PD). Long-term PD is frequently associated with inflammation, which can affect dialysis efficacy and patient outcomes. Genetic polymorphisms in genes involved in the inflammation and vascular function, including integrin subunit alpha V (ITGAV) and vascular endothelial growth factor A (VEGFA), may influence PD outcomes. Objectives: This study aims to elucidate the correlation between ITGAV (rs39111238, rs3738919, rs3768777) and VEGFA (rs699947, rs3025039, rs833061) polymorphisms, and their influence on renal-peritoneal Kt/V and PD outcomes. Patients and Methods: In this cross-sectional study, 46 ESRD patients undergoing chronic PD at Shahid Modarres hospital in Tehran (2020–2021) were enrolled. Demographic and clinical data were collected, and peritoneal membrane transport was assessed using the peritoneal equilibration test (PET). Patients were categorized as high (HT) or low (LT) transporters. Genotyping for ITGAV (rs39111238, rs3738919, rs3768777) and VEGFA (rs699947, rs3025039, rs833061) polymorphisms was conducted using sequencing methods. Associations between genotypes and dialysis adequacy were considered. Results: Among 46 participants, 21 were high transporters and 25 were low transporters. A significant association was observed between VEGFA rs3025039 and PET classification, while no patients carrying the CC genotype among high transporters. In addition, VEGFA rs833061 TT genotype was positively associated with renal Kt/V (B = 0.93; 95% CI: 0.11–1.75). Moreover, no significant associations were found for ITGAV polymorphisms. Conclusion: VEGFA polymorphisms, particularly rs3025039 and rs833061, may influence peritoneal membrane transport and dialysis adequacy in PD patients. Further studies with larger cohorts and broader genetic screening are warranted to validate these findings.
Introduction: Diabetic nephropathy is a main cause of chronic kidney disease (CKD) throughout the world, which requiring early detection and management. Anti-diabetic medications, like sodium-glucose cotransporter-2 (SGLT2) inhibitors, metformin, dipeptidyl peptidase-4 (DPP-4) inhibitors, and sulfonylurea compounds have determined various kidney protective efficacies; nevertheless, their effects on renal biomarkers remained disputing. Objectives: This study intended to assess renal function biomarkers, regarding anti-diabetic consumption, providing insights into their usefulness for risk categorization and management decision-making in diabetic nephropathy. Patients and Methods: This cross-sectional investigation, conducted in Basra Governorate, Iraq (October 2024–January 2025) with ethical approval from Basra University’s College of Pharmacy, enrolled participants to evaluate renal function biomarkers across antidiabetic medication regimens. Demographic and clinical data, including age, body mass index, gender, diabetes duration, hypertension status, and treatment regimen like metformin, sulfonylurea, DPP-4 inhibitors and SGLT-2 inhibitors, or combination therapies were gathered by interviews and clinical document reviews. In this study, fasting blood samples were analyzed for kidney function biomarkers, comprising serum creatinine, urea, blood urea nitrogen (BUN), and estimated glomerular filtration rate (eGFR). The study outcomes comprised comparing renal function biomarkers among antidiabetic medication regimens. Results: The study population comprised of 250 diabetes mellitus individuals (50.8% female) with a mean age of 55.67 ± 8.58 years. The findings showed considerable alterations of BUN, creatinine, urea and eGFR among the five groups. The individuals who received DPP-4 inhibitors had significantly higher BUN and urea levels than individuals treated with metformin or sulfonylurea monotherapy and higher serum creatinine concentration compared to metformin monotherapy, sulfonylurea monotherapy and combination therapy. Regarding eGFR, the DPP-4 inhibitor users had considerably lower value compared to all the other groups, both in metformin monotherapy, sulfonylurea monotherapy, and SGLT-2 inhibitor groups and also in patients under combination therapy. Conclusion: We found that the consequences of the antidiabetic drug therapy on kidney function are not the same. This study showed that DPP-4 cases had early indications of diminished kidney function than the individuals receiving metformin, sulfonylurea, SGLT-2, or a combination of them. This finding focuses on the importance of considering the potential impact on renal health in cases of selecting diabetes treatments.
Tubulointerstitial nephritis and uveitis (TINU) syndrome is a rare immune-mediated disorder usually affecting young individuals. Corticosteroids are considered the mainstay of therapy, although alternative immunosuppressive strategies may be required when contraindications exist. We report a 71-year-old woman with no prior kidney disease who presented with bilateral anterior uveitis and acute renal failure. Laboratory tests showed hematoproteinuria and positive antinuclear and anti-centromere antibodies. Renal biopsy revealed acute interstitial nephritis with inflammatory infiltrates and nephroangiosclerosis. Clinical and serological findings met EULAR criteria for systemic sclerosis. To avoid the risk of scleroderma renal crisis associated with corticosteroid therapy, mycophenolate mofetil (MMF) was initiated as monotherapy. Progressive renal recovery was observed, with serum creatinine (sCr) decreasing from 4.4 mg/dL to 1.3 mg/dL after six months, and stabilization at 1.1 mg/dL following MMF withdrawal. This case explains the diagnostic challenges of TINU in an elderly patient with systemic sclerosis and reports, to our knowledge, the first successful use of MMF monotherapy. MMF may represent a valuable alternative in corticosteroid-contraindicated cases, warranting further evaluation in future studies.
Introduction: Pregnancy induces substantial physiological adjustments that extend to renal function, driven by changes in blood volume, hormonal activity, and metabolic demands that alter the normal behavior of key biochemical markers. Understanding how these renal parameters evolve across gestation is essential for distinguishing healthy physiological adaptation from early signs of renal impairment. Objectives: This study aimed to examine trimester‑specific changes in renal function within a prospective cohort of pregnant women to clarify the expected trajectory of renal biomarkers during normal pregnancy. Materials and Methods: The study employed a prospective cohort design conducted at a maternity teaching hospital in Nasiriyah, Iraq, enrolling 49 first‑trimester singleton pregnant women who were followed from January 2024 to January 2025 to assess longitudinal renal changes. Eligible participants were singleton pregnant women who provided informed written consent. Demographic and obstetric data were collected at enrollment, and venous blood samples were obtained at the end of each trimester to measure blood urea and serum creatinine using standardized biochemical procedures. Renal biomarkers were compared across trimesters to evaluate alterations in kidney function during pregnancy. Results: The study included 49 pregnant women with a mean age of 30.22 ± 8.25 years. The results demonstrated progressive alterations in renal biomarkers across pregnancy, with both blood urea and creatinine levels indicating a steady and statistically significant rise from the first to the third trimester (P<0.05). Conclusion: Pregnancy is associated with a steady and significant increase in renal biomarkers across trimesters. These findings highlight the importance of considering trimester‑specific changes when evaluating maternal renal function.
Congestive heart failure (CHF) is a major cause of morbidity and mortality in patients with end-stage kidney disease (ESKD), where fluid overload often necessitates kidney replacement therapy. While both hemodialysis (HD) and peritoneal dialysis (PD) are viable options, PD has been suggested to offer hemodynamic advantages due to its gradual ultrafiltration process. This review examines the comparative effects of PD and HD in ESKD patients with CHF undergoing maintenance dialysis, focusing on hospitalization rates, cardiac function, survival outcomes, and volume management. Several studies suggest that PD is associated with reduced hospitalization rates, particularly in diuretic-resistant CHF patients, and improved left ventricular ejection fraction (LVEF), especially in those with heart failure with reduced ejection fraction (HFrEF). Additionally, PD’s continuous ultrafiltration may lower the risk of intradialytic hypotension (IDH) compared to HD. However, survival outcomes remain inconsistent, with some studies reporting higher mortality in PD patients, likely due to selection bias, as PD is often used in hemodynamically unstable CHF patients. Despite these findings, there is no definitive consensus on whether PD offers a survival advantage over HD in CHF patients. Given the limitations of existing studies, further large-scale, prospective research is required to determine the optimal dialysis modality for CHF patients with ESKD and to clarify its impact on long-term clinical outcomes.
Patients with systemic lupus erythematosus (SLE) exhibit a distinct cancer risk profile characterized by increased susceptibility to hematologic malignancies such as non-Hodgkin lymphoma (NHL), as well as certain solid tumors like lung, thyroid, and hepatobiliary cancers. Conversely, they also demonstrate a reduced risk for some cancers including breast, melanoma, and prostate cancer. This unique pattern is influenced by a combination of disease-related immune dysregulation and treatment-related factors. Additionally, immunosuppressive therapy administered in SLE management, including agents like cyclophosphamide, is known to contribute to an elevated risk of malignancies such as cervical dysplasia and certain hematologic cancers. However, specific immunosuppressants like calcineurin inhibitors have shown no significant increase in cancer incidence in some cohorts, suggesting that cancer risk is multifactorial and may depend on the type and duration of immunosuppression. However, in SLE patients, screening practices for cancers like cervical cancer are suboptimal despite their increased risk. However, some studies have found lower cervical cancer screening rates in women with SLE compared to control subjects, which influenced by factors like age, income, and comorbidities. Improved screening uptake is crucial for early cancer detection and better outcomes in this vulnerable population. Moreover, lupus nephritis enhances cancer risk and progression through complex interplay of chronic inflammation, immune dysregulation, treatment effects, and molecular pathway alterations. Inflammation-induced oxidative stress and impaired autophagy, combined with immunosuppressive therapies, provide a background for malignant transformation and decreased tumor immune surveillance.
Antiphospholipid antibody (aPL) nephropathy in pregnancy is a critical and complex medical condition that poses significant risks to both maternal renal health and fetal development. This autoimmune disorder is characterized by the presence of aPLs, which target phospholipid-binding proteins, leading to a procoagulant state. In the context of pregnancy, this predisposition to thrombosis can manifest as thrombotic microangiopathy (TMA) within the renal vasculature, directly impacting kidney function. The resulting renal microvascular injury contributes to a decline in maternal renal health, potentially leading to proteinuria, hypertension, and even acute kidney injury, exacerbating the already delicate physiological changes of pregnancy. The intricate interplay between autoimmune-mediated thrombosis and placental dysfunction is central to the high-risk nature of this condition. aPLs can cause thrombosis in the placental vasculature, leading to placental insufficiency, intrauterine growth restriction, preeclampsia, and recurrent pregnancy loss. This compromise in placental blood flow not only jeopardizes fetal development but also indirectly strains maternal renal function. The systemic inflammation and endothelial dysfunction associated with aPLs further complicate the clinical picture, making accurate diagnosis and timely intervention paramount for managing these multifaceted challenges. Effective management of aPL nephropathy in pregnancy necessitates a highly individualized and multidisciplinary approach, focusing on meticulous monitoring of both maternal and fetal well-being. This includes close surveillance of renal function, blood pressure, and proteinuria, alongside regular assessments of fetal growth and placental health. Therapeutic strategies often involve anticoagulation with heparin, sometimes combined with low-dose aspirin, to mitigate the thrombotic risk. Such precise monitoring and tailored interventions are crucial for optimizing outcomes, aiming to preserve maternal renal health while supporting successful fetal development in this challenging clinical scenario.
Introduction: Crescentic glomerulonephritis is an essential kind of glomerulonephritis. According to its rapid progression and aggressiveness, recognizing its risk factors helps to manage a better treatment and outcome. Objectives: This study was designed to compare demographic, laboratory, and renal biopsy findings of patients with crescentic glomerulonephritis among males and females. Patients and Methods: This cross-sectional study compared age, gender, types of crescentic glomerulonephritis, serum creatinine, 24-hour proteinuria, the number of crescents, and percentage of fibrosis. Results: Of 169 patients with crescentic glomerulonephritis, 54.4% were males, and 45.6% were females. The mean age, serum creatinine level, and 24-hour proteinuria were 37.73±15.32 years, 2.06±1.35 mg/d, and 2084.82±1170.98 mg/d, respectively. Serum creatinine level and 24-hour proteinuria were not significantly different by gender. In addition, the number of crescents had no relationship with age and 24-hour proteinuria; however, it had a significant direct relationship with serum creatinine. Conclusion: According to our study, lupus nephritis affected women more than men, while other forms of crescentic glomerulonephritis were more common in males. Depending on the population, a significant relationship between the number of crescent and serum creatinine was detected. The mean age of females with crescentic glomerulonephritis was significantly lower than males.
Introduction: Chronic kidney disease (CKD) is a progressive condition marked by declining glomerular filtration and disturbances in biochemical and electrolyte profiles; identifying stage‑specific changes in demographics and serum markers may improve early detection and guide stage‑appropriate management. Objectives: This study compared demographic characteristics and serum biochemical parameters across stages 1–3 in patients with CKD to identify stage‑related differences associated with disease progression. Patients and Methods: This cross‑sectional study enrolled 75 patients with early CKD (stage 1: n=24, stage 2: n=25, stage 3: n=26) attending specialist clinics at Al‑Fayhaa teaching hospital, Basra, Iraq (Feb–May 2025). Demographic data (age, sex) and fasting venous blood samples were collected for routine renal tests (creatinine, urea, estimated glomerular filtration rate [eGFR]), uric acid, total protein, albumin, total cholesterol, electrolytes (sodium [Na], potassium [K], chloride [Cl], magnesium [Mg], phosphate), and biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL) and Cathepsin D. Group comparisons across CKD stages plus correlation analyses were performed to assess associations with disease progression. Results: The results indicated that CKD progression was associated with male gender and older age, across with changes in serum electrolytes, kidney function tests, and biochemical parameters, including increasing creatinine, urea, uric acid, sodium, K, cholesterol, NGAL, and cathepsin D. The CKD progression also decreased eGFR, Mg, and total protein (P < 0.05), with no significant impact on albumin, phosphate, and Cl (P > 0.05). Conclusion: CKD progression is associated with male gender, older age, and biochemical changes, including increased renal markers, lipids, sodium, K, NGAL, and cathepsin D, as well as decreased eGFR, Mg, and total protein. Albumin, phosphate, and Cl remained stable, demonstrating the complexity of CKD and the potential of new biomarkers.
Introduction: The kidney disease index (KDI), a novel index combining estimated glomerular filtration rate (eGFR) and urinary albumin/creatinine ratio (UACR), has been proposed as a potential clinical tool for accurately assessing kidney function. This may aid in the better prediction of cardiovascular events in type 2 diabetes mellitus (DM) patients. Objectives: This study aims to investigate the mean value of the KDI and to evaluate the association between KDI, clinical, and paraclinical factors, and the 10-year cardiovascular risk in type 2 diabetes patients. Patients and Methods: A cross-sectional descriptive study was conducted on 87 individuals (42 males and 45 females) diagnosed with type 2 DM. Fasting blood samples were taken to measure fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), blood lipid profile, creatinine, and cystatin C levels. Spot urine samples were collected to assess urinary albumin, creatinine, and UACR. The eGFR values were calculated using the 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) Creatinine-Cystatin C equation. KDI was calculated as the geometric mean of 1/eGFR and the natural logarithmic transformation of (100×UACR). Traditional cardiovascular disease risk factors were included in calculating the 10-year cardiovascular risk, based on the Framingham risk score. Results: The results show that the mean value of KDI was 0.54±0.28. Independently associated factors with KDI were age (P=0.044), duration of DM (P< 0.001), high-density lipoprotein cholesterol (HDL-c) (P=0.008), and HbA1c (P= 0.001). The correlation between the 10-year cardiovascular disease risk, as determined by the Framingham risk score, and KDI (r = 0.294, P=0.024) was stronger than that of eGFR (r = -0.257, P=0.049) but not UACR (r = 0.182, P=0.168). Conclusion: Adhering to recommendations for screening kidney function and injury in type 2 DM patients who are of advanced age, have a long duration of DM, have low plasma HDL-c levels, and high HbA1c levels is crucial. The potential inclusion of KDI in the prognostic models for adverse events, particularly cardiovascular disease and mortality, may provide additional insight alongside routine tests such as eGFR and UACR.
IgA nephropathy (IgAN) is the most frequent primary glomerulonephritis throughout world and a leading cause of chronic renal failure across with end-stage kidney failure. Proteinuria, as a hallmark of IgAN, is a key driver of disease progression and a strong predictor of poor renal outcome. Despite current standard therapies, including RAAS (renin-angiotensin-aldosterone system) blockade with ACEIs (angiotensin-converting enzyme inhibitors) or ARBs (angiotensin II receptor blockers), many patients continue to experience persistent proteinuria and progressive kidney function decline. This condition emphasizes the need for more effective and targeted treatment strategies. The endothelin pathway, particularly endothelin-1 signaling promotes vasoconstriction, inflammation, and fibrosis, contributing to podocyte dysfunction and renal damage. Endothelin A receptor antagonists demonstrate renoprotective properties through various mechanisms in IgAN. By selectively blocking endothelin A receptors, these agents can improve glomerular hemodynamics by reducing intraglomerular pressure, thereby alleviating the damage caused by excessive pressure and promoting an improved renal environment. This blockade leads to decreased proteinuria, as a crucial factor in the progression of the disease. Furthermore, endothelin A receptor antagonists can also mitigate inflammatory pathways that are activated in response to endothelin-1, reducing renal inflammation and subsequent fibrosis. The efficacy of endothelin A receptor antagonists in the treatment of IgAN has been substantiated by numerous clinical trials. In particular, atrasentan, a specific endothelin-A receptor antagonist, has shown significant promise in reducing proteinuria compared to placebo.
Introduction: Pre-eclampsia represents a potentially life-threatening condition during pregnancy that significantly contributes to maternal and neonatal morbidity and mortality. Numerous studies within the fields of obstetrics and gynecology have documented elevated concentrations of interleukin-6 (IL-6) in women diagnosed with preeclampsia, suggesting that this cytokine may play a critical role in the pathophysiological mechanisms underlying the hypertension associated with this condition. Objectives: The aim of this investigation was to conduct a case-control study aimed at comparing the levels of IL-6 between pregnant women diagnosed with preeclampsia and those with normal pregnancies, in order to ascertain the presence of elevated IL-6 levels among the former group. Patients and Methods: This case-control study comprised 384 pregnant women at a gestational age exceeding 20 weeks, who were already diagnosed as preeclamptic and designated as cases, alongside a control group of 384 women devoid of any signs of hypertension or proteinuria during their pregnancies, matched for maternal age, body mass index (BMI), and gestational age. For all participants, IL-6 levels were quantified using an enzyme-linked immunosorbent assay (ELISA) that employs the Sandwich-ELISA methodology for the in vitro determination of human IL-6 concentrations in serum. Additionally, hemoglobin concentration, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), white blood cell (WBC) count, and platelets count were assessed utilizing a hematology analyzer based on the Coulter Principle. Furthermore, age, body mass index, gestational age, systolic blood pressure, and diastolic blood pressure were meticulously recorded. Results: Our findings revealed a statistically significant elevation in the levels of IL-6 among pregnant women with preeclampsia compared to those with normal pregnancy (P<0.001). Moreover, IL-6 exhibited a positive correlation with diastolic blood pressure (P=0.001). Conclusion: Our study indicates that IL-6 levels are markedly elevated during pregnancy in women diagnosed with preeclampsia.
Systemic amyloidosis is a collection of diseases caused by the deposition of protein fibrils in organ tissues, leading to significant morbidity. Cardiac amyloidosis, a rare and debilitating condition, can affect any organ in the body. The two primary types of cardiac amyloidosis are systemic light chain (AL) amyloidosis, which is more common and related to light chain overproduction in the bone marrow, and wild-type transthyretin cardiac amyloidosis (ATTRwt). This case report describes a unique and uncommon case of cardiac amyloidosis observed in a patient following kidney transplant, which was effectively managed using a novel therapeutic regimen.
