Advances in Diagnostics of Chronic Kidney Disease

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Pathology and Molecular Diagnostics".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 8706

Special Issue Editors


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Guest Editor
Wroclaw Medical University, Department of Nephrology and Transplantation Medicine, Wrocław, Poland
Interests: nephrology; chronic kidney disease; hemodialysis; vascular access
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Guest Editor
Wroclaw Medical University, Department of Nephrology and Transplantation Medicine, Wrocław, Poland
Interests: nephrology; primary glomerulonephritis; systemic vasculitis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of Diagnostics will be devoted to the latest advances in chronic kidney disease (CKD) diagnostics.

CKD in different stages affects approximately 12% of the world's population. Nowadays, diabetes and hypertension are among the leading causes of CKD.

Due to the constant increase in the total number of diabetic patients, the incidence of CKD caused by diabetic nephropathy and subsequently the number of patients with end-stage renal disease (ESRD) is expected to rise. Early diagnosis and treatment of diabetic nephropathy may have a crucial impact on disease progression.

Glomerulonephritis (GN) is, next to hypertension and diabetes, one of the leading causes of CKD. Both nephrotic and nephritic syndromes are clinical conditions, requiring extensive diagnostic workup, including laboratory tests, imaging studies and eventually renal biopsy, with additional tests and specialized stains. In many GN patients, electron microscopy and genotyping might be crucial to achieve final diagnosis. Innovative IT tools are increasingly used in clinical settings. For example, artificial intelligence (AI) may help with precise diagnosis due to its ability to combine multiple clinical and laboratory data.

Acute kidney injury (AKI) is frequently observed in elderly patients, following surgical and radiological procedures, involving the administration of radiocontrast, with potential progression to CKD. Urinary biochemical markers may be helpful in predicting the development and severity of AKI. Point of care testing methods are increasingly used in nephrology patients with unstable clinical conditions, but also to assess CKD complications including electrolyte and acid–base disorders.

Hemodialysis (HD) is a one of the main forms of renal replacement therapy (RTT) in ESRD. Anemia, electrolyte disturbances, metabolic bone disease and both dialysis fistula and catheter dysfunction are the basic HD complications requiring appropriate diagnostic tools. More and more uremic toxins are being discovered in patients with ESRD, which influence the prognosis of dialysis patients.

We invite scientists to submit articles presenting new achievements in chronic kidney disease. We look forward to your submission.

Dr. Tomasz Gołębiowski
Dr. Andrzej Konieczny
Guest Editors

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Keywords

  • chronic kidney disease
  • diabetic nephropathy
  • glomerulonephritis
  • acid–base disorders
  • uremic toxin
  • artificial intelligence
  • metabolic bone disease
  • vascular access
  • arteriovenous fistula
  • catheter
  • hemodialysis

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Published Papers (5 papers)

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Research

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15 pages, 825 KB  
Article
Changes of Dissociative Properties of Hemoglobin in Patients with Chronic Kidney Disease
by Justyna Korus, Maria Wydro, Maciej Gołębiowski, Kornelia Krakowska, Paweł Poznański, Kinga Musiał, Andrzej Konieczny, Hanna Augustyniak-Bartosik, Jakub Stojanowski, Mariusz Andrzej Kusztal and Tomasz Gołębiowski
Diagnostics 2024, 14(12), 1219; https://doi.org/10.3390/diagnostics14121219 - 8 Jun 2024
Cited by 1 | Viewed by 3326
Abstract
Background: The ability of hemoglobin to bind and dissociate oxygen is crucial in delivering oxygen to tissues and is influenced by a range of physiological states, compensatory mechanisms, and pathological conditions. This may be illustrated by the oxyhemoglobin dissociation curve (ODC). The [...] Read more.
Background: The ability of hemoglobin to bind and dissociate oxygen is crucial in delivering oxygen to tissues and is influenced by a range of physiological states, compensatory mechanisms, and pathological conditions. This may be illustrated by the oxyhemoglobin dissociation curve (ODC). The key parameter for evaluating the oxygen affinity to hemoglobin is p50. The aim of this study was to evaluate the impact of hemodialysis on p50 in a group of patients with chronic kidney disease (CKD). An additional goal was to assess the correlation between p50 and the parameters of erythropoiesis, point-of-care testing (POCT), and other laboratory parameters. Methods: One hundred and eighty patients (106 male, 74 female), mean age 62.5 ± 17 years, with CKD stage G4 and G5 were enrolled in this cross-sectional study. Patients were divided into two groups, including 65 hemodialysis (HD) patients and 115 patients not receiving dialysis (non-HD). During the standard procedure of arteriovenous fistula creation, blood samples from the artery (A) and the vein (V) were taken for POCT. The causes of CKD, as well as demographic and comorbidity data, were obtained from medical records and direct interviews. Results: The weekly dose of erythropoietin was higher in HD patients than in non-HD patients (4914 ± 2253 UI vs. 403 ± 798 UI, p < 0.01), but hemoglobin levels did not differ between these groups. In the group of non-HD patients, more advanced metabolic acidosis (MA) was found, compared to the group with HD. In arterial and venosus blood samples, the non-HD group had significantly lower pH, pCO2 and HCO3. This group had a higher proportion of individuals with MA with HCO3 < 22 mmol/L (42% vs. 24%, p < 0.01). The absolute difference of p50 in arterial and venous blood was determined using the formula Δp50 = (p50-A) − (p50-V). Δp50 was significantly higher in the HD group in comparison to non-HD (0.08 ± 2.05 mmHg vs. −0.66 ± 1.93 mmHg, p = 0,02). There was a negative correlation between pH and the p50 value in arterial (pH-A vs. p50-A, r = −0.56, p < 0.01) and venous blood (pH-V vs. p50-V, r = −0.45, p < 0.01). In non-HD patients, hemoglobin levels correlated negatively with p50 (r = −0.29, p < 0.01), whereas no significant relation was found in HD patients. Conclusions: The ODC in pre-dialysis CKD (non-HD) patients is shifted to the right due to MA, and this is an additional factor influencing erythropoiesis. Hemodialysis restores the natural differences in hemoglobin’s dissociation characteristics in the arterial and venous circulation. Full article
(This article belongs to the Special Issue Advances in Diagnostics of Chronic Kidney Disease)
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18 pages, 7376 KB  
Article
Downregulation of Glycine N-Acyltransferase in Kidney Renal Clear Cell Carcinoma: A Bioinformatic-Based Screening
by Juan P. Muñoz and Gloria M. Calaf
Diagnostics 2023, 13(23), 3505; https://doi.org/10.3390/diagnostics13233505 - 22 Nov 2023
Cited by 5 | Viewed by 2073
Abstract
Clear cell renal cell carcinoma (KIRC) is the most common subtype of renal cell carcinoma (RCC). This form of cancer is characterized by resistance to traditional therapies and an increased likelihood of metastasis. A major factor contributing to the pathogenesis of KIRC is [...] Read more.
Clear cell renal cell carcinoma (KIRC) is the most common subtype of renal cell carcinoma (RCC). This form of cancer is characterized by resistance to traditional therapies and an increased likelihood of metastasis. A major factor contributing to the pathogenesis of KIRC is the alteration of metabolic pathways. As kidney cancer is increasingly considered a metabolic disease, there is a growing need to understand the enzymes involved in the regulation of metabolism in tumorigenic cells. In this context, our research focused on glycine N-acyltransferase (GLYAT), an enzyme known to play a role in various metabolic diseases and cancer. Here, through a bioinformatic analysis of public databases, we performed a characterization of GLYAT expression levels in KIRC cases. Our goal is to evaluate whether GLYAT could serve as a compelling candidate for an in-depth study, given its pivotal role in metabolic regulation and previously established links to other malignancies. The analysis showed a marked decrease in GLYAT expression in all stages and grades of KIRC, regardless of mutation rates, suggesting an alternative mechanism of regulation along the tumor development. Additionally, we observed a hypomethylation in the GLYAT promoter region and a negative correlation between the expression of the GLYAT and the levels of cancer-associated fibroblasts. Finally, the data show a correlation between higher levels of GLYAT expression and better patient prognosis. In conclusion, this article underscores the potential of GLYAT as a diagnostic and prognostic marker in KIRC. Full article
(This article belongs to the Special Issue Advances in Diagnostics of Chronic Kidney Disease)
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Review

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44 pages, 3699 KB  
Review
IgA Nephropathy: Mechanisms, Risk Stratification, and Precision Therapy
by Sami Alobaidi
Diagnostics 2026, 16(9), 1259; https://doi.org/10.3390/diagnostics16091259 - 22 Apr 2026
Viewed by 486
Abstract
IgA nephropathy is the most common primary glomerulonephritis worldwide and a leading cause of chronic kidney disease and kidney failure, with geographic and ancestral variation and a course ranging from asymptomatic urinary abnormalities to progressive loss of kidney function. This narrative review links [...] Read more.
IgA nephropathy is the most common primary glomerulonephritis worldwide and a leading cause of chronic kidney disease and kidney failure, with geographic and ancestral variation and a course ranging from asymptomatic urinary abnormalities to progressive loss of kidney function. This narrative review links the multi-hit model to risk stratification, biomarkers, current management, and emerging therapies, and highlights implementation gaps. Risk assessment is longitudinal, prioritizing proteinuria and estimated glomerular filtration rate trajectories and integrating Oxford MEST-C, prediction tools, and biomarker and multi-omics approaches, while recognizing limitations in histologic reproducibility and model calibration. Current management is anchored in optimized supportive care aimed at sustained proteinuria reduction and kidney protection, including intensive blood pressure control with maximal tolerated renin–angiotensin system blockade, dietary sodium restriction and lifestyle measures, and sodium–glucose co-transporter 2 inhibitors for eligible patients. For selected higher-risk patients with persistent proteinuria despite optimized supportive care, immunomodulatory strategies are discussed, including systemic corticosteroids and targeted-release budesonide (Nefecon), emphasizing structured toxicity risk mitigation and cautioning against assuming interchangeability among alternative oral budesonide formulations. Emerging therapies are organized around mechanism-aligned targets across the BAFF/APRIL axis, complement pathways, and endothelin-based approaches, with growing interest in sequencing and combination regimens layered on supportive care. Key gaps include reliance on surrogate endpoints, limited long-term durability and safety data, and uneven evidence for special populations. Full article
(This article belongs to the Special Issue Advances in Diagnostics of Chronic Kidney Disease)
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17 pages, 852 KB  
Review
Unravelling Sarcopenia in Chronic Kidney Disease: From Pathogenesis to Diagnosis and Therapeutics
by Natalia G. Vallianou, Apostolos A. Evangelopoulos, Gerasimos Socrates Christodoulatos, Ioanna Tantsi, Nikos Mantouvalos, Dimitrios Chatzis, Theodora Stratigou, Eleni V. Geladari, Kyriaki Constantinou, Alexandros Tousis and Dimitris C. Kounatidis
Diagnostics 2026, 16(7), 1063; https://doi.org/10.3390/diagnostics16071063 - 1 Apr 2026
Viewed by 1734
Abstract
Chronic kidney disease (CKD) is on the rise, with sarcopenia accompanying CKD in an estimated 25% of patients, featuring as a potentially debilitating issue that should not be overlooked. Sarcopenia, characterized by a loss of skeletal muscle mass and strength, is multifactorial. The [...] Read more.
Chronic kidney disease (CKD) is on the rise, with sarcopenia accompanying CKD in an estimated 25% of patients, featuring as a potentially debilitating issue that should not be overlooked. Sarcopenia, characterized by a loss of skeletal muscle mass and strength, is multifactorial. The aging process, uremic toxins, systemic inflammation, oxidative stress, gut dysbiosis, hormonal dysregulation, dietary deficits, and even air pollution are among the major parameters being implicated in sarcopenia among patients with CKD. Additionally, the existence of various comorbidities, such as type 2 diabetes mellitus (T2DM), depression, and cardiovascular diseases (CVD), also contribute to the chronic low-grade inflammation associated with skeletal muscle inflammation and atrophy. The purpose of this review is to delve into the complex interplay of multiple factors being involved in the pathogenesis of sarcopenia in patients with CKD. Moreover, we aim to shed light upon nutritional aspects that could delay the development and progression of sarcopenia among patients with CKD. To address vitamin D deficiency, micronutrients and macronutrients together with physical activity remain the cornerstone of delaying the progression of sarcopenia in this sub-population. Additionally, experimental drugs exhibiting therapeutic potential are also being discussed. As sarcopenia and quality of life are interconnected, the timely recognition of sarcopenia, together with nutritional and therapeutic interventions, is of the utmost importance in our crusade for a better quality of life (QoL) in patients with CKD. Full article
(This article belongs to the Special Issue Advances in Diagnostics of Chronic Kidney Disease)
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Other

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10 pages, 57532 KB  
Case Report
Autosomal Dominant Tubulointerstitial Kidney Disease—UMOD: Case Report and Disease Update
by Mario Bonomini, Valeria Vezzani, Michele Rossini, Lorenzo Di Liberato, Liborio Stuppia and Valentina Gatta
Diagnostics 2026, 16(10), 1467; https://doi.org/10.3390/diagnostics16101467 - 12 May 2026
Abstract
Background and Clinical Significance: Autosomal dominant tubulointerstitial kidney disease caused by a mutation in the uromodulin gene (ADTKD-UMOD) is a rare kidney disorder characterized by progressive tubulointerstitial damage and a slowly progressive loss of renal function. ADTKD is often under-recognized in the [...] Read more.
Background and Clinical Significance: Autosomal dominant tubulointerstitial kidney disease caused by a mutation in the uromodulin gene (ADTKD-UMOD) is a rare kidney disorder characterized by progressive tubulointerstitial damage and a slowly progressive loss of renal function. ADTKD is often under-recognized in the clinical setting. Diagnosis of ADTKD-UMOD can be challenging due to its nonspecific symptoms and is confirmed by genetic testing alone. Case presentation: We report the case of a 42-year-old male patient referred for evaluation of renal dysfunction, which was accidentally discovered during routine laboratory checks. He had no significant medical history and no known family history of kidney disease or gout. Physical examination was unremarkable. Renal dysfunction was confirmed, with serum creatinine at 1.44 mg/dL and eGFR at 59.5 mL/min/1.73 m2. Urinalysis was within physiological limits, proteinuria being 75 mg/day. Uric acid was mildly elevated (7.5 mg/dL) without a history of gout. Other laboratory findings, including autoantibodies, were in the normal range. The patient underwent a kidney biopsy, though it was not diagnostic, showing mild focal tubular atrophy and interstitial fibrosis without glomerular involvement. Immunofluorescence staining was negative for complement and immunoglobulins. Given the above nonspecific findings, the patient was suspected of having possible ADTKD. Genetic investigation using a clinical exome next-generation sequencing approach identified a novel heterozygous missense variant in the UMOD gene (c.409T>C; p.Cysteine137Arginine (p.Cys137Arg)) that is likely pathogenic. The patient is under regular clinical-laboratory monitoring. After one year, his overall health is good, renal function is stable with no proteinuria, and uric acid is mildly increased without gout attacks. Conclusions: Increased clinical awareness is crucial for detecting ADTKD-UMOD. Genetic testing can help to resolve clinical diagnostic challenges in patients with unexplained decreased kidney function. Full article
(This article belongs to the Special Issue Advances in Diagnostics of Chronic Kidney Disease)
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