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Kevin Tandarto
Medhub Academy

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Correlation between Gut Microbiome and the Development of Diabetic Kidney Disease Belinda Mufidah; Muthia Ara Agusti Ayu; Muhammad Al Qarni; Laila Fitria Djaimi; Khairina Azlina; Kevin Tandarto
Indonesian Journal of Global Health Research Vol. 8 No. 3 (2026): Indonesian Journal of Global Health Research
Publisher : GLOBAL HEALTH SCIENCE GROUP

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37287/ijghr.v8i3.729

Abstract

Diabetic kidney disease (DKD) is a major complication of diabetes mellitus characterized by progressive renal damage driven by metabolic, hemodynamic, and inflammatory mechanisms. Recent studies highlight the gut–kidney axis as a crucial pathway linking intestinal dysbiosis to DKD progression. Therefore, this study aims to investigate the association between gut microbiome alterations and the progression of DKD, as well as to explore potential mechanistic pathways linking microbial dysregulation to renal injury. A comprehensive literature review was conducted using PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar up to August 2025. Eligible studies included English-language human and experimental research evaluating the relationship between gut microbiota composition and DKD pathogenesis. From 241 retrieved articles, 22 studies met inclusion criteria. Most demonstrated significant gut dysbiosis in DKD, with decreased Faecalibacterium prausnitzii, Akkermansia muciniphila, and Butyricicoccus, and increased Escherichia-Shigella, Hungatella, and Enterococcus. Reduced short-chain fatty acid (SCFA) production and accumulation of uremic toxins—such as indoxyl sulfate, p-cresyl sulfate, and phenyl sulfate—were strongly associated with inflammation, fibrosis, and renal decline. The analysis was conducted through qualitative synthesis of study methodologies, microbial profiles, and biochemical markers to identify consistent patterns linking gut dysbiosis to DKD progression. These findings suggest that microbial imbalance and altered metabolite profiles play pivotal roles in DKD development. Interventions targeting the gut microbiota, including probiotics, prebiotics, and dietary fiber, may offer renoprotective benefits through restoration of SCFA-producing bacteria and reduction of uremic toxins. Gut dysbiosis in diabetic kidney disease (DKD) disrupts metabolic and immune balance by reducing beneficial short-chain fatty acid–producing bacteria and increasing pathogenic species, leading to inflammation, proteinuria, and progressive renal decline.
Diabetes Mellitus Type 5 (Malnutrition-Related Diabetes): Pathophysiology, Clinical Characteristics, and Therapeutic Challenges Eunike Alicia Valentina; Aryo Hanun Harjanto; Afifah Sekarkusuma; Bernita Nur Cahyani; Maudita Sri Lestari; Kevin Tandarto
Indonesian Journal of Global Health Research Vol. 8 No. 4 (2026): Indonesian Journal of Global Health Research
Publisher : GLOBAL HEALTH SCIENCE GROUP

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37287/ijghr.v8i4.1836

Abstract

Type 5 diabetes mellitus (T5DM), historically referred to as malnutrition-related diabetes mellitus (MRDM), represents an emerging and underrecognized subtype of diabetes that predominantly affects individuals in low- and middle-income countries (LMICs). Unlike type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM), T5DM is characterized by severe insulin deficiency in the absence of autoimmune destruction or significant insulin resistance, reflecting a distinct pathophysiological mechanism linked to chronic undernutrition and impaired pancreatic development. Despite increasing recognition, variability in terminology, diagnostic criteria, and clinical characterization has limited its identification and management in both clinical practice and research settings. This narrative literature review aims to synthesize current evidence on the epidemiology, pathophysiology, clinical features, and therapeutic approaches of T5DM, as well as to evaluate its distinction from classical diabetes subtypes and its implications for global health. A structured literature search was conducted across major electronic databases, including PubMed, Scopus, EMBASE, and Google Scholar, covering publications from January 2020 to March 2026. Relevant studies were selected based on predefined inclusion criteria encompassing epidemiological data, mechanistic insights, clinical characteristics, and treatment outcomes. Due to heterogeneity in study design, populations, and reported outcomes, findings were synthesized descriptively. The available evidence indicates that T5DM typically presents in young, underweight individuals with preserved insulin sensitivity, detectable but reduced C-peptide levels, and minimal risk of ketosis despite significant hyperglycemia. Pathophysiological mechanisms involve early-life nutritional deprivation leading to reduced β-cell mass, epigenetic modifications, and impaired insulin secretion. Therapeutically, patients often require lower insulin doses and may respond to selected oral antidiabetic agents, although evidence remains limited. Significant diagnostic challenges persist, particularly in resource-limited settings, where misclassification as T1DM or T2DM is common.  
Targeting Aldosterone in Chronic Kidney Disease: from Mineralocorticoid Receptor Antagonism to Synthase Inhibition Jeremiah Suwandi; Afifah Sekarkusuma; Fatah Jati Pamungkas; Anzalia Arzak; Chatrine Evania Palangan Sangka; Kevin Tandarto
Indonesian Journal of Global Health Research Vol. 8 No. 6 (2026): Indonesian Journal of Global Health Research: December 2026
Publisher : GLOBAL HEALTH SCIENCE GROUP

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37287/ijghr.v8i6.2680

Abstract

Chronic kidney disease (CKD) remains a major cause of morbidity and mortality despite advances in renin–angiotensin system blockade and sodium–glucose cotransporter-2 inhibitors. Persistent aldosterone production and mineralocorticoid receptor (MR) overactivation may contribute to residual cardiorenal risk through sodium retention, hypertension, oxidative stress, inflammation, endothelial dysfunction, and fibrosis. This narrative review summarizes the biological rationale and clinical evidence for aldosterone-targeted therapies in CKD, including steroidal MR antagonists, finerenone, and emerging aldosterone synthase inhibitors (ASIs). Steroidal MR antagonists reduce albuminuria but are limited by hyperkalemia and endocrine adverse effects. Finerenone has the most mature outcome evidence among nonsteroidal MR antagonists, reducing kidney and cardiovascular events in CKD with type 2 diabetes. Recent trials also support greater albuminuria reduction when finerenone is combined with empagliflozin and extend anti-albuminuric evidence to type 1 diabetes. Selective ASIs, including vicadrostat, baxdrostat, and lorundrostat, directly suppress aldosterone synthesis and have shown promising effects on albuminuria or blood pressure. However, hyperkalemia, adrenal safety, and the absence of definitive long-term kidney and cardiovascular outcome data remain important limitations. Current evidence supports a layered approach to CKD therapy, while ASIs remain investigational pending larger outcome trials. The objective of this narrative review is to critically summarize the role of aldosterone and mineralocorticoid receptor activation in CKD progression, compare steroidal and nonsteroidal mineralocorticoid receptor antagonists, and evaluate the emerging efficacy, safety, and clinical positioning of aldosterone synthase inhibitors within contemporary layered CKD therapy.
Co-Authors Afifah Sekarkusuma Afifah Sekarkusuma Anzalia Arzak Aryo Hanun Harjanto Belinda Mufidah Bernita Nur Cahyani Chatrine Evania Palangan Sangka Eunike Alicia Valentina Fatah Jati Pamungkas Jeremiah Suwandi Khairina Azlina Laila Fitria Djaimi Maudita Sri Lestari Muhammad Al Qarni Muthia Ara Agusti Ayu