Contemporary Perspectives on Chronic Renal Disorders

Abstract

The prevalence of renal diseases and its associated burden on healthcare have tremendously risen in the past few years. From simple markers assessing kidney function, current renal research delves into understanding the diseases at the cellular and molecular levels and not just at treating, but at improving quality of life, arresting progression and providing personalized diagnostics and therapy. This narrative review highlights the improvements in diagnostic applications of kidney disease and briefly discusses a few notable biomarkers emphasizing the high throughput omics technologies, as well as contemporary perspectives on renal research. A thorough literature search was performed on PubMed, Scopus, Web of Science, and Medline. Suitable Mesh terms were included for the search strategy, and relevant evidence was documented. Language models and pharmacognosy, along with other omics strategies, impose a better understanding of the renal disease, and the remarkable discoveries of noninvasive biomarkers, urine 273-peptide classifier, and urine peptides-based fibrosis classifier have unraveled the associations between mechanistic studies and novel therapeutic drugs. Strides in biomarker research have been able to delineate stages and types with superior specificity and sensitivity, thereby providing a better diagnosis. Renal research reflects a powerful, dynamic, and multifaceted field that drives better advancements and discoveries in personalized medicine, drug interventions, and patient-centered outcomes. Understanding the tangled relationship of the etiology of kidney disease, these developments and future research hold promise for individuals affected by kidney diseases.

Keywords: SDG‐3: kidney disease progression; language models; omics; pharmacogenes; recent advances; renal research.

Figure 1

Chronic kidney disease (CKD)—risk factors and projected prevalence. This figure outlines the primary risk factors associated with CKD. The most significant among these are (a) diabetes and (b) hypertension, followed by (c) acute kidney injury, (d) genetic predisposition, (e) smoking, and (f) obesity. In the lower right section, a bar chart (g) illustrates the projected prevalence of CKD over time, featuring data points from 2013, 2016, and 2020, along with a forecast for 2040. The 2040 projection is based on forecasting models from Foreman et al. [13].

Figure 2

Consistent gene loci observed in European, Asian, and African populations.

Figure 3

Mitochondrial dysfunction is a notable consequence of chronic kidney disease (CKD). A decline in glomerular filtration rate (GFR), coupled with elevated levels of inflammation, contributes to this dysfunction by reducing the production of ATP and NADH, diminishing mitochondrial biogenesis, and increasing the generation of reactive oxygen species (ROS). The excessive release of ROS, including superoxide (•O²⁻) and hydroxyl ions (•OH), leads to oxidative stress, which further damages the kidneys. This detrimental process results in the release of mitochondrial DNA fragments into the bloodstream, which may serve as potential biomarkers.

Figure 4

Protein profiling in chronic kidney disease (CKD). The cycle represents a pathological cascade initiated by altered regulation of protein. Dysregulation of proteins/peptides leads to metabolic disturbances and pertinent inflammation. Thereby, the key extracellular matrix proteins are overexpressed, causing fibrosis. The flowchart on the right represents the development of the CKD 273 peptide classifier, a urinary proteomics tool that identifies urinary peptides of CKD, including collagen, inflammatory, and stress response markers. These peptides serve as biomarkers, allowing early stratification.

Figure 5

Crosstalk between gut microbiome and metabolites in chronic kidney disease (CKD). CKD is driven by dysregulated systemic metabolism. Changes in gut microbiota and hepatic metabolism produce uremic toxins and impair amino acid metabolism. These systemic changes impact renal injury and endothelial dysfunction, leading to exacerbated stress and inflammation within the kidney. This leads to epithelial‐mesenchymal transition (EMT) and CKD pathology. BCRP, breast cancer resistance protein; MATE, multidrug and toxin extrusion protein; MRP, multidrug resistance‐associated protein; OAT(P), organic anion transporter (protein); OCT, organic cation transporter.