The current kidney care model-focused on late-stage disease and in-center hemodialysis – is unsustainable, due to costs, environmental burden, poor outcomes, and reduced quality of life. The 78^th World Health Assembly’s recognition of kidney disease as a serious health threat presents a critical opportunity to reshape kidney care. Aligned with this, the 2026 World Kidney Day theme, Kidney Health for All: Caring for People, Protecting the Planet, calls for a systematic change. A sustainable model must prioritize early detection and prevention, reducing the need for kidney replacement therapy (KRT). Transplantation and home dialysis benefit people with kidney failure, environment and society. Dialysis itself must become more eco-friendly without compromising care quality, recognizing that planetary perturbations in turn affect kidney health. Conservative care should also be considered, particularly for elderly and frail patients, if the quality of life benefits outweigh the perspectives offered by dialysis. Achieving this shift requires coordinated action across all stakeholders; education and engagement of public, policymakers and health professionals to raise awareness about the threat of kidney disease; and an urgent move toward patient-centered care.

Translated into Russian by E.V. Parshina, edited by E.V. Zakharova

Translation into Russian initiated by Russian Dialysis Society, and approved by World Kidney Day Steering Committee

The prevalence of chronic kidney disease (CKD) has not decreased over the past 50 years and is now comparable to that of major conditions as hypertension and diabetes mellitus. It is now well established that CKD may develop as a consequence of acute kidney injury (AKI). Recent studies indicate that AKI is among the most common complications following emergency abdominal surgery. However, this problem remains insufficiently represented in general surgical literature, partly due to limited scientific interaction between surgeons and nephrologists.

In general surgical hospitals, the diagnosis of AKI is currently based mainly increases in serum creatinine and/or decreases in urine output. However, serum creatinine, as a marker of glomerular filtration rate, is relatively insensitive to acute changes in renal function. This limitation may contribute to delayed clinical diagnosis and underestimation of the severity tubular and glomerular injury.

Circulatory collapse is a prominent clinical sign of the early stage of AKI, but in some cases it is so transient that it remains unnoticed. A detailed understanding of the dynamics of morphological and functional changes at the level of the renal microcirculation, renal corpuscles, and parenchymal microcirculation during endotoxicosis is essential, as these processes form the pathogenetic basis of AKI and the subsequent development of CKD even after apparent recovery. Without such knowledge, meaningful improvements in pathogenetically targeted therapy for complications of urgent abdominal surgical diseases and in the prevention of dependence on renal replacement therapy, both in the early and late postoperative periods, are unlikely.

One objective criterion for assessing the severity of AKI and the effectiveness of its prevention and treatment in abdominal surgical diseases of the is the time factor. Its significance should be validated experimentally through models of acute strangulatory small intestinal obstruction and through the study of associated morphological and functional changes in the renal corpuscles.

Objective. The present study aimed to compare key demographic and clinical parameters with morphological features defined by the Oxford MEST-C classification, supplemented by additional quantitative assessment, in order to identify the principal clinico-morphological phenotypes of IgA nephropathy (IgAN).

Materials and Methods. This retrospective study included 2,679 patients with biopsy-proven IgAN. The mean age was 35.3±13 years. Clinical and laboratory variables (degree of hematuria, 24-hour proteinuria, and serum creatinine) were assessed at the time of biopsy. Morphological evaluation comprised Oxford MESTC scoring, quantitative assessment of of interstitial fibrosis/tubular atrophy (IFTA), global and segmental glomerulosclerosis, cellular/fibrocellular and fibrous crescents.

Results. At the time of biopsy, median proteinuria was 2.1 g/day (IQR: 0.75-3.0), estimated glomerular filtration rate (eGFR) was 60.4 mL/min (IQR: 33.3-84.16). Hematuria was detected in 88% of patients. The distribution of Oxford MEST-C lesions was as follows: M1, 37%; E1, 21%; S, 73%; T1, 37%; T2, 16%; C1, 16.5%; C2, 2.5%. The severity of proteinuria correlated with E and C lesions, as well as the extent of IFTA and both global and segmental glomerulosclerosis. Correlation coefficients were higher when lesions C and S were quantified (% involvement): 0.17 vs 0.24 and 0.07 vs 0.23, respectively. Decline in eGFR were associated with the degree of IFTA and the presence of crescents.

Based on clinicopathological correlations and morphological profiling, three distinct phenotypes of IgAN, likely reflecting different dominant mechanisms of disease progression, were identified:

Phenotype 1: (Typical): Defined by mesangial proliferation and segmental glomerulosclerosis. Clinically characterized by persistent microhematuria, gradually increasing proteinuria, and arterial hypertension.

Phenotype 2: (Aggressive): Defined by endocapillary hypercellularity with or without crescents. Clinically associated with acute nephritic syndrome, marked proteinuria – often at nephrotic range – and hematuria.

Phenotype 3: (Macrohematuric): Defined by focal necrosis of capillary loops and crescent formation in the absence of endocapillary hypercellularity. Clinically manifests with episodes of macroscopic hematuria; during remission, urinary abnormalities are typically absent and renal function remains preserved.

Conclusion. Identification of clinicopathological phenotypes in IgAN represents a promising strategy for personalizing therapy and refining prognostic assessment, thereby improving risk stratification for disease progression.

Background. Chronic kidney disease (CKD) is associated with disturbances in calcium-phosphate homeostasis and vitamin D metabolism, leading in mineral and bone disorders (CKD-MBD). However, the pathogenetic features of these alterations at predialysis CKD stages and the effects of high-dose cholecalciferol therapy remain insufficiently characterized.

Objective. To compare vitamin D metabolites and calcium-phosphate metabolism parameters in patients with predialysis CKD and individuals without impaired kidney function, and to assess their dynamics after a single bolus dose of 150,000 IU of cholecalciferol.

Materials and Methods. The study included 58 participants: 23 patients with CKD stage C3, 14 with CKD stages C4-5, and 21 controls. Parameters of calcium-phosphate metabolism and vitamin D metabolites were assessed at baseline and 7 days after a single oral dose of aqueous cholecalciferol (150,000 IU). Vitamin D metabolites were measured using LC–MS/MS.

Results. Data are presented as follows: control group, CKD C3, CKD C4-5. At baseline, CKD patients had higher parathyroid hormone (PTH) levels (51.3 [40.6; 62.7] vs 70.9 [49.0; 105.9] vs 101.0 [91.7; 120.1] pg/mL), lower calcitriol concentrations (40.9 [34.3; 59.4] vs 25.0 [19.8; 29.1] vs 26.4 [13.8; 30.6] pg/mL), a trend toward higher fibroblast growth factor 23 (FGF-23) levels (0.73 [0.43; 1.07] vs 1.08 [0.61; 2.52] vs 3.22 [1.78; 4.51] pmol/L), and a reduced 24,25 (OH)₂D₃/25(OH)D₃ ratio (0.06 [0.04; 0.08] vs 0.03 [0.01; 0.04] vs 0.03 [0.02; 0.04]), indicating impaired 24-hydroxylase activity. Total and free 25(OH)D levels and vitamin D-binding protein (VDBP) were comparable between groups.

Seven days after cholecalciferol administration, a similar increase in total 25(OH)D₃, 3-epi-25(OH)D₃, and 24,25(OH)₂D₃ was observed in all groups. However, the increase in free 25(OH)D was significantly smaller in CKD C3 and C4-5 compared with controls (p=0.036 and p=0.028). PTH decreased in CKD C3 (p=0.039), whereas FGF-23 increased in CKD C4-5 (p=0.042). Serum calcium, phosphorus, calcitriol, and VDBP remained unchanged.

Conclusion. Alterations in calcium-phosphate and vitamin D metabolism at predialysis CKD stages show a sequential pattern. Reduced vitamin D activation and inactivation, increased FGF-23 levels, and a blunted free 25(OH)D response to bolus cholecalciferol indicate specific regulatory features and limit the applicability of standard vitamin D correction regimens in this population.

Introduction. Hypocalcaemia, including hungry bone syndrome (HBS) after parathyroidectomy (PTE), is associated with adverse outcomes, yet its prevention is often inadequate. We evaluated whether preoperative cinacalcet therapy reduces the risk severe postoperative hypocalcemia.

Methods. A retrospective, single-center study (2011-2019) included 713 patients. The primary endpoint was of hypocalcemia, defined as an ionized calcium (Ca²⁺) level below 0.9 mmol/L on day 2 or 3 after PTE. Secondary endpoints included the need for intravenous calcium supplementation and length of hospital stay (<7 days vs. ≥7 days).

Results. Preoperative median parathyroid hormone (PTH) was 1.247 pg/L [910-1.871], mean total serum calcium was 2.47 mmol/L (±0.22), ionized calcium was 1.23 mmol/l (±0.13), and alkaline phosphatase was IU/L 188 [128-491]. HBS was detected in 68.4% [95% CI 64.6-71.9] of patients. The median minimum Ca²⁺ level on postoperative days 2-3 was 0.73 mmol [0.64-0.82] in patients with HBS versus 1.02 mmol [0.95-1.1] in those without HBS (p<0.001). ROC analysis using total calcium to detect HBS showed a sensitivity of 85.7% [95CI 80%-88%] and specificity of 97.6 [93-99%] at a cutoff of <1.78 mmol, with an AUC of 0.96 [95%CI 093-0.99]. Cinacalcet was used preoperatively in 32% of patients at doses of 30 mg/day (n=101), 60 mg/d (n=66), 90 mg (n=22) or more (n=2). In a multivariable logistic analysis, HBS development was not associated with cinacalcet use but it was associated with baseline PTH (24% higher HBS risk of per 100 pg/ml increase) and with Ca²⁺ (43% lower risk per 0.1 mmol/l increase). In the multivariable regression, cinacalcet use was independently associated with shorter hospital stay (36% risk reduction). Patients receiving ≥60 mg/day of cinacalcet were more likely to require intravenous more than 10 grams of intravenous calcium (p=0.005).

Conclusion: Preoperative cinacalcet therapy was not associated with the frequency of biochemical HBS, as defined by the minimum Ca2+ level. However, prior cinacalcet risk use was associated with shorter hospital stay, which may serve as a surrogate marker of lower HBS severity.

Background: the catabolism of aromatic amino acids is closely linked to the immune response. Their metabolites act as molecular messengers, facilitating communication between the microbiome and the immune system. Selected studies suggested that the pathogenesis of immunoglobulin A nephropathy (IgAN) may be associated with alterations in tryptophan (Trp) metabolic pathways.

Aim: to test the hypothesis about probable changes in Trp metabolism in IgAN using untargeted and targeted metabolomics analyses.

Materials and methods: the cohort study included 113 patients with a clinical and morphological diagnosis of primary IgAN, comprised two subgroups: with an active/progressive process who did not receive treatment (IgAN-A, n=85); with inactive IgAN/remission (IgAN-R, n=28). Control groups included healthy volunteers without kidney disease (K1, n=31) and patients with non-inflammatory glomerulopathies (K2, n=33). Untargeted and targeted metabolomics studies of serum were performed using high-resolution high-performance liquid chromatography with mass spectrometric detection (HPLC-MS) in positive and negative ionisation mode. Intergroup differences in Trp metabolites were assessed, and their associations with clinical parameters were analysed.

Results: untargeted analysis of mass spectrometric data revealed that tryptophan synthesis and metabolism were enriched among other metabolic pathways in patients with IgAN. Significant differences were found in kynurenic acid (KynA), kynurenine (Kyn), 5-hydroxytryptophan (HTrp), 3-hydroxyanthranilic acid, tryptamine, and indole-3-lactic acid (ILA), suggesting alterations in the serotonin, kynurenine, and indole metabolic pathways. Targeted analyses showed that Trp and its metabolites’ levels differed significantly in patients with IgAN (overall group, n=113) compared to healthy controls. Compared with the IgA-R subgroup, subjects with IgAN-A had higher levels of KynA:Kyn, Kyn:Trp, KynA:Trp, and HTrp:Trp ratios, alongside decreased tryptophan and indoxyacetic acid (IAA). In the IgAN-A group, diverse associations of Trp and its metabolites with clinical parameters were revealed. Except for Trp and indole acetate, metabolites of the Trp pathway were negatively correlated with estimated glomerular filtration rate (eGFR), blood pressure, and age. Tryptophan and indole acetate had negative associations with proteinuria and positive associations with serum albumin levels. Tryptophan and IAA concentrations were inversely associated with proteinuria and directly with serum albumin levels; the associations of these clinical indicators and the ratios of HTrp, Kyn, KynA, NA and ILA to tryptophan were opposite.

Conclusions: In IgAN patients, apparent alterations in tryptophan metabolic pathways are associated with clinical parameters and may contribute to the pathogenesis of the disease.

Dent disease and Lowe syndrome are hereditary tubulopathies characterized by low-molecular-weight proteinuria, hypercalciuria, and nephrocalcinosis. Proteinuria may reach high levels, necessitating differential diagnosis with steroid-resistant nephrotic syndrome.

Materials and Methods: from 2010 to 2025, 41 children with Dent disease or Lowe syndrome were followed at the Nephrology Department of the National Medical Research Center for Children's Health. Dent disease type 1 was confirmed in 29 children (71%), type 2 in 3 children (7%), and type 3 in 3 children (7%). Lowe syndrome was diagnosed in 6 children (15%).

Results: all children exhibited low-molecular-weight proteinuria, ranging from 139 to 3,653 mg/m²/day, with a median of 1,590 (952; 2248) mg/m²/day. Ultrasound signs of nephrocalcinosis were observed in 61% of patients, and hypercalciuria was detected in 66%.

Molecular genetic testing identified causative variants in the CLCN5 and OCRL genes in all but three children. Nearly all detected pathogenic variants were unique; only one variant, CLCN5 c.2320C>T was found in two unrelated children.

At the time of analysis (mean age 9 years 8 months, SD 5 years 1 months), decreased renal function was present in 41% of patients. Renal replacement therapy was required in only one child (2%). No correlations were found between decreased estimated GFR and maximum proteinuria level, presence of nephrocalcinosis, or growth retardation. However, a significant correlation was observed between growth Z-score and the daily proteinuria level (ϱ=-0.451, p<0.01).

Conclusions: Dent disease and Lowe syndrome can be clinically based on laboratory and instrumental findings, with molecular genetic testing confirming the diagnosis.

Given the wide variety of variants identified in the CLCN5 and OCRL genes, establishing genotype-phenotypic correlations is challenging and requires further investigation in larger cohorts.

Relevance. Pregnant women with chronic glomerulonephritis (CGN) are at high risk of placenta-associated and perinatal complications. We present a clinical case of successful pregancy outcome in a patient with CGN and nephrotic syndrome (NS), diagnosed in the first trimester, achieved through long-term maintenance combination therapy with heparin and acetylsalicylic acid.

Clinical observation. A 24-year-old woman experienced two episodes of macrohematuria within one and a half years prior pregnancy, but was not evaluated at that time. A tendency towards the development of nephrotic syndrome (NS) was identified in the first trimester of pregnancy; secondary causes of kidney disease was excluded. Primary CGN was diagnosed. Although termination of pregnancy was recommended, the patient declined. Dipyridamole and low-molecular-weight heparin were prescribed until 13 weeks gestation; from 13 week onward, dipyridamole was replaced with aspirin, and thrombodynamic parameters were monitored. The patient's condition remained stable and satisfactory throughout pregnancy: no edema, blood pressure up to 120/80 mm Hg, without antihypertensive therapy, daily proteinuria 1.5-1.7 g/L, erythrocyturia 10-20 per high-power field, blood creatinine 67-72 μmol/L, total protein 55-59 g/L, albumin 30-32 g/L. Markers of preeclampsia within the reference range. At 39 weeks of gestation, operative delivery was performed. A full-term female infant was born with Apgar scores of 8/9. In the postpartum period, NS recurred, and a kidney biopsy was performed revealing focal global and segmental glomerulosclerosis. Cyclosporine therapy was administered for one and a half years, resulting in complete remission of NS. Currently, there patient remains in stable remission of the NS and receives nephroprotective therapy with losartan 50 mg/day.

Conclusion. Close multidisciplinary monitoring and therapy with heparin and acetylsalicylic acid may increase the likelihood of a favorable pregnancy outcome in patients with CGN.