Obesity and chronic kidney disease (CKD) are converging global epidemics with a complex, bidirectional relationship. Obesity directly drives de novo CKD and accelerates its progression via hemodynamic, metabolic, inflammatory, and neuroendocrine pathways culminating in obesity-related glomerulopathy. While advanced and dialysis-dependent CKD exhibit an "obesity paradox, " where higher BMI correlates with survival, this is largely driven by reverse causality, survival bias, and BMI's failure to capture true body composition. Emerging metrics like the Body Roundness Index (BRI) demonstrate that central adiposity remains harmful in dialysis populations, with no paradox found in early CKD or kidney transplantation, adding a second, under-recognised dimension to this dual burden. Beyond progression, obesity significantly increases technical risks for core procedures: kidney biopsies, vascular access creation, peritoneal catheter insertion, and kidney transplantation. This review translates these procedural risks into practical optimization strategies, establishes that intentional, structured weight loss in obese CKD individuals is not associated with the excess mortality attributed to unintentional weight loss in CKD. An expanded overview of body composition assessment methods, contemporary and emerging pharmacotherapy including dual incretin agonists, and bariatric and metabolic surgery, including its role and timing relative to kidney transplantation, is presented, alongside a research agenda emphasising precision obesity management and artificial intelligence-assisted risk prediction.

This narrative review summarized the latest findings on halitosis in patients living with chronic kidney disease (CKD), including its epidemiology, etiology, classification, contributing compounds, diagnosis and treatment. Halitosis is present in 30-57% of patients living CKD in most reports. Accumulated metabolites in the blood circulation and multiple oral changes secondary to CKD are its main causes. It consists of intra-oral halitosis and extra-oral halitosis according to etiology. Ammonia, dimethylamine, trimethylamine, hydrogen sulfide, methyl mercaptan and dimethyl sulfide are its main contributing compounds. A combination of the subjective organoleptic test and the objective OralChroma breath test is essential for its diagnosis. Also, it is recommended that the organoleptic test and OralChroma breath test be performed for both mouth and nose breath. By comparing these two sets of results, clinicians can identify which subtype of halitosis is predominant in an individual patient. Kidney replacement therapies and antibiotics appear to be effective to treat this condition through reducing accumulated metabolites in the blood circulation.

AA amyloidosis is driven by persistently elevated serum amyloid A (SAA) in chronic inflammation. Severe obesity has emerged as a potential inflammatory driver of renal AA amyloidosis. We report a 47-year-old man with prior sleeve gastrectomy who developed progressive kidney dysfunction and proteinuria after substantial weight regain. At presentation, he weighed 126 kg (body mass index, 45.2 kg/m2); serum creatinine was 4.3 mg/dL (estimated glomerular filtration rate, 15 mL/min/1.73 m2) and urine albumin-to-creatinine ratio (UACR) was 3.4 g/g. Kidney biopsy confirmed AA amyloidosis, while extensive evaluation for autoimmune, infectious, hereditary, malignant, and monoclonal causes was unrevealing. SAA was 80 mg/L with persistently elevated inflammatory markers. Semaglutide was initiated as part of a weight-management strategy. Following a 47-kg weight loss, creatinine decreased to 2.34 mg/dL, estimated glomerular filtration rate increased to 32 mL/min/1.73 m2, UACR declined to 1.0 g/g, and SAA fell to <10 mg/L, with improvement in C-reactive protein, erythrocyte sedimentation rate, and HbA1c. In the absence of another identifiable cause, the parallel improvement in SAA, systemic inflammation, proteinuria, and kidney function supports severe obesity as a potential inflammatory contributor to renal AA amyloidosis, although causality cannot be inferred from a single case.