IgA nephropathy (IgAN), first described in 1968, is the most common primary glomerulonephritis worldwide. The prevalence of the disease is highest in Asia compared with Europe and North America, with the possible underdiagnosis in regions such as Africa.

Typically, debuting in young patients, IgAN is one of the major causes of the development of end-stage chronic kidney disease, which requires the use of renal replacement therapy. However, recent studies have shown a rising incidence among older individuals, often with more severe outcomes.

The time course and prognosis of IgAN remain difficult to predict due to the pronounced polymorphism of clinical manifestations and morphological features, apparently reflecting a wide range of possible etiopathogenesis mechanisms. This literature review discusses current approaches to evaluating clinical symptoms and biomarkers in relation to pathomorphological features and disease prognosis. Traditionally, severe proteinuria has been regarded as the only reliable predictor of poor outcomes and the main indication for active treatment. However, recently evidence highlights the prognostic significance of proteinuria of any level, including persistent microhematuria, suggesting the need to reconsider current therapeutic paradigm. Two long-standing debates over the prognostic role of macrohematuria also remain unresolves. In addition, the review addresses the prognostic value of nephrotic syndrome depending on specific histological patterns, such as IgAN with minimal change disease or endocapillary proliferation. Based on published data, clinical variants of IgAN and their associations with disease outcomes are analyzed. The first results of cluster analysis, which have identified distinct disease phenotypes with differing risks of progression and treatment response, are also presented.

Background: in patients with chronic kidney disease (CKD), particularly in advanced stages, pregnancy carries a high risk of complications and adverse outcomes. To date, no direct comparison has been made of pregnancy complications, obstetric, and nephrological outcomes in women with stage 3-5 CKD due to diabetic nephropathy (DN) versus chronic glomerulonephritis (CGN).

Objective: to compare the course of pregnancy, gestational complications, pregnancy outcomes, and postnatal renal survival in women with advanced CKD due to type 1 diabetes mellitus with DN and those with CGN.

Patients and methods: the retrospective study included 53 pregnant women with CKD stage 3-5: 23 women with type 1 diabetes and DN, who had (25 pregnancies; main group), and 30 women with CGN (30 pregnancies; comparison group). Each pregnancy was assessed as a separate clinical case. The groups did not differ in the age, CKD duration, or CKD of stages. Obstetrics complications, perinatal outcomes, and renal survival after delivery were evaluated studied in both groups.

Results: favorable pregnancy outcomes were observed in 92% of pregnancies in the DN group and in 93.3% in the CGN group. Compared with the CGN group, women in the DN group had a significantly higher incidence of pre-existing chronic pyelonephritis (72% vs. 10%, p<0.001), episodes of pyelonephritis during gestation (44.0% vs. 16.7%, p=0.038), the need for multicomponent antihypertensive therapy (84.2% vs. 52.2%, p=0.048), preterm delivery before 37 weeks (79.2% vs. 50%, p=0.046), cesarean section (91.7% vs. 66.7%, p=0.046), and neonatal intensive care admission (70.8% vs. 36.7%, p=0.016). In both groups, preterm birth was significantly associated with gestational hypertension and preeclampsia, but not with proteinuria 3 g/day and above. Renal survival after delivery did not differ between the groups (Log Rank – p = 0.973).

Conclusion: women with type 1 diabetes and CKD stage 3-5 experience higher rates of gestational complications and preterm delivery compared to those with CGN. Preconception counselling and multidisciplinary monitoring are essential to improve both obstetric and nephrological outcomes in this high-risk population.

Objective: to analyze the frequency and risk factors for the development or progression of chronic kidney disease (CKD) during the year following acute decompensated heart failure (ADHF), to assess the role of kidney damage patterns identified during hospitalization in the development of composite renal and cardiovascular outcomes.

Materials and methods: patients with ADHF and documented serum creatinine levels within the 3 months preceding hospitalization were included. Patients with CKD stage 4, 5 or advanced heart failure (HF) who were unable to undergo outpatient follow-up were included. Composite renal outcome: rapid progression, de novo development or stage progression of CKD. Composite cardiovascular outcome: all-cause mortality or rehospitalizations for ADHF. Physical, laboratory, and instrumental examinations were performed.

Results: A total of 108 patients were enrolled. Of these, 60% were men; mean age 71 (61-75) years, left ventricle ejection fraction was 45% (35-53%). The prevalence of comorbities was: arterial hypertension (AH) 92%, diabetes mellitus (DM) 35%, and CKD 26%. During hospitalization 47% had an estimated GFR < 60 ml/min/1.73 m².

The incidence of composite renal outcomes was 42%. Specifically, stage progression of CKD in 29% (n=13), de novo CKD in 46% (n=21), rapid progression in 49% (n=22), and isolated rapid progression (decline in GFR within the CKD stage) in 25% (n=11).

Logistic regression identified the following independent risk factors for adverse renal outcomes: prior history of CKD (HR– 8.7, 95% CI 2.2 – 35, p=0.002), venous congestion discharge (VExUS) (HR 5.5, 95% CI 1.5 – 20, p=0.008), loop diuretic dose >40 mg/day at discharge (HR – 4.2, 95% CI 1.3 – 13, p=0.012), elevated NT-proBNP at discharge (HR 4.2, 95% CI 1.2 – 15, p=0.025), serum uric acid >360 mmol/l on admission (HR – 4.1, 95% CI 1.4 – 12, p=0.009), loop diuretic dose >80 mg/day on admission (HR 3.7, 95% CI 1.2 – 11, p=0.019), acute kidney disease (AKD) during hospitalization (HR – 3.6, 95% CI 1.3 – 10, p=0.017), serum urea >8.3 mmol/l on admission (HR – 3.1, 95% CI 1 – 9, p=0.037), and higher median of age (HR 1.1, 95% CI 1 – 1.1, p=0.017).

The incidence of composite cardiovascular outcomes was 38%. Kaplan-Meyer curves demonstrated poorer cardiovascular outcomes in the AKI/AKD group compared with groups with patients with stable CKD or no kidney pathology (log-rank p=0.02).

Conclusion: composite renal outcome events occurred in 42% of participants. The most significant risk factors were a history of CKD and HF-related congestion. Cardiovascular outcomes were more frequent in patients with AKI/AKD than in those with stable CKD or no kidney disease.

Introduction. Women with chronic kidney disease (CKD) are at high risk of developing placenta-associated complications.

Aim. To investigate the prevalence of placenta-associated complications and characterize maternal hemostasis in pregnant women with CKD.

Patients and methods. This prospective observational study included 150 women with CKD stages G1-G3 in the second trimester of pregnancy: CKD G1 – 58, CKD G2 – 45, CKD G3 – 47 patients. The CKD stage was determined according to KDIGO criteria for estimated glomerular filtration rate (eGFR) in women with known before pregnancy serum creatinine and endogenous creatinine clearance at study entry. Between 28 and 39.5 weeks of gestation, 55 patients developed preeclampsia combined with fetoplacental insufficiency, and 19 had preeclampsia with fetoplacental insufficiency and acute kidney injury (AKI). A comparison group included 20 healthy women with uncomplicated pregnancies. Observation lasted 13-27 weeks before delivery, and maternal. The study and analysis of the maternal hemostasis parameters were analyzed in the third trimester.

Results. The overall frequency of placenta-associated complications in pregnant women with CKD G1-G3 was 50.7%, compared to 0% in women without CKD (HR 10.1 95% CI 1.5; 68.9). Among CKD stages, the complication rates were 34,9% in G1-G2, and 80,9 % in G3 (HR 2.3, 95% CI 1.7; 3,1), similar across glomerular and non-glomerular pathologies. Women with placenta-associated complications showed increased in platelet counts with thrombocrit, elevated homocysteine, fibrinogen, and D-dimer levels, and decreased activated partial thromboplastin time compared with healthy women with uncomplicated pregnancies. The addition of AKI was associated with a trend toward lower platelet counts and serum homocysteine and D-dimer levels. Serum creatinine negatively correlated with platelet count (p=0.046), thrombocyte (p=0.007), and mean platelet volume (p=0.001), and positively correlated with fibrin level (p=0.048). Daily proteinuria correlated directly with fibrinogen (p=0.005) and D-dimer (p=0.007) the levels.

Conclusion. Pregnant women with CKD are at high risk for developing placenta-associated complications and exhibit complex maternal hemostasis disturbances, leading of a hypercoagulable state.

Introduction. Bioimpedance is a promising method for assessing hydration status in hemodialysis patients. However, the optimal algorithm for "dry" weight correction and its effectiveness – particularly with respect to hard outcomes – remains to be clarified.

Patients and methods. In a single-center, open-label randomized trial involving 98 patients, we evaluated both the short-term (weight dynamics, peridialysis blood pressure, and intradialysis complications) and long-term outcomes (five-year survival from study initiation) of dry weight correction guided by clinical and instrumental data compared with correction based solely on clinical indicators. Weight correction was performed according to a newly developed algorithm incorporatinh multi-frequency bioimpedance spectroscopy and vector bioimpedance analysis for six months, followed by a five-year observation period.

Results. 51 patients were assigned to study group (SG), and 47 to the control group (CG). Baseline clinical and laboratory parameters did no differ between the groups. In the SG, target weight increased in 13 patients by 1.3±0.9 kg, decreased in 26 patients (-1.1±0.4 kg), and remained unchanged in 12. In the CG, during the three-month follow-up period, target weight increased in 19 patients (1.3±0.9 kg), decreased in 26 (-1.2±0.8 kg), and remained unchanged in 2. The SG demonstrated a significant reduction in the number of complications per month (32 vs. 52, p=0.033), primary due to a reduction in intradialysis hypertension (15 vs. 34, p=0.009). A greater intradialytic blood pressure decrease was achieved in the SG; an effect size of 5.3 mmHg compared to CG (p=0.04). Moreover, 65% of SG patients did not require a second adjustment of target weight. Five-year survival rate was significantly higher in the in SG (χ²=4.096; p=0.043). Active dehydration was not associated with reduced survival compared with maintaining or increasing target weight (χ²=2.454, p=0.117).

Conclusions. A comprehensive algorithm for "dry" weight correction – incorporating a calculated hyperhydration coefficient, bioimpedance spectroscopy with vector analysis, and clinical signs of impaired hydration – can reduce the complications rates and the hypertension severity, improve hemodynamic stability during dialysis, and enhance patient survival.

Primary hyperoxaluria is a severe autosomal recessive disorder that leads to chronic kidney disease and often necessitates renal replacement therapy in childhood. Some patients with primary hyperoxaluria type 1 respond to pyridoxine therapy, whereas patients with types 2 and 3 receive only citrate therapy. In recent years, a targeted drug – lumasiran – has become available for treating 1 type primary hyperoxaluria. Its mechanism is based on reducing glioxylate production and, consequently, oxalate formation. To date, no published data exist on the efficacy of lumasiran in Russian patients.

Materials: Since 2014, 14 children with primary hyperoxaluria have been followed in the Nephrology Department of the National Research Center for Children’s Health: 12 with 1 type and 2 with type 3. Among the 12 children type 1 patients, 5 received pathogenetic therapy with lumasiran. The duration of treatment ranged from 9 months to 3 years, with a mean 26 months (SD 13 months).

Results: After 12 months of therapy, no patients showed worsening of nephrocalcinosis or decline in kidney function. Four patients achieved marked reduction in urinary oxalate excretion (90%, 88%, 89% and 74%). One child had been on treatment for less than one year.

Conclusions: Early treatment initiation of treatment for primary hyperoxaluria – particularly type 1 – significantly improve not only renal but also overall survival.

Objective of the study: to evaluate the clinical efficacy and safety of a new method for implanting a tunneled central venous catheter (tCVC) at the confluence of the transverse cervical vein and the external jugular vein in patients undergoing programmed hemodialysis (PHD), compared with the traditional approach of placing the tCVC in the internal jugular vein.

Materials and methods: the study included 164 patients who underwent tCVC implantation for PHD in City Clinical Hospital No. 52 of the Moscow Health Department between August 2022 and December 2024. Group 1 (study group, n=82) comprised patients with occlusion of the internal jugular vein who received tCVC placement at the transverse-external jugular vein confluence. Group 2 (control group, n=82) comprised patients who underwent standard tCVC placement in the internal jugular vein. In both groups, catheter function, incidence and types of complications in the early and late postoperative period, and the feasibility of creating long-term vascular access (AVF) on the side of the previously implanted tCVC were assessed.

Results: Hemodialysis efficiency in patients with tCVC placed with the new technique was comparable to that in the control group. The flow rate (Me [IQR]) through tCVC was 300 [290; 300] ml/min. Blood collection and blood return pressures were 140 [140; 150] mmHg and -140 [-140; -130] mmHg, respectivelyю The Kt/V index was 1.60 [1.40; 1.60] (p=0.329) in the main and control groups. The frequency and types of complications, intraoperative and postoperative, did not differ between groups. AVFs were formed with similar frequency (54.9% in the main group and 53.7% in the control group (p=0.875)), and in most patients the possibility of AVF formation on the same side as the tCVC was preserved.

Conclusion: The proposed alternative method of tCVC placement can be effectively used in patients with limited vascular access for hemodialysis, such as those with the internal jugular vein occlusion. It avoids the need for catheter placement in the subclavian or femoral vein, while maintaining adequate hemodialysis efficiency and safety compared to the standard tCVC technique.

Background: neurofibromatosis type 2 (NF2) is a rare autosomal dominant disorder characterized by the formation of multiple tumors in the central and peripheral nervous system. Kidney involvement in NF2, including the formation of renal sclerosing peritubular nodules (RSPN), is uncommon and typically subclinical. Most of previous descriptions of this renal changes are based on the results of autopsy studies of patients who died from NF2.

Case presentation: we report a 21-year-old patient with a confirmed diagnosis of NF2 treated with bevacizumab who developed combined kidney injury. Renal involvement was detected during a routine follow-up 14 months after initiating bevacizumab therapy and manifested as persistent proteinuria (1.0-3.6 g/day) and significant hematuria. Kidney biopsy revealed a combined lesion consisting of RSPN and IgA nephropathy with focal proliferative and sclerosing features. Morphological interpretation required evaluating the contribution of each lesion to disease progression and determining whether the glomerulonephritis was primary or secondary to the underlying disorder or therapy. Despite the potential association of renal pathology with ongoing bevacizumab therapy, treatment could not be discontinued due to the worsening clinical manifestations of NF2.

Over time, renal function gradually declines (serum creatinine 128-303 mmol/L). Second kidney biopsy demonstrated increased glomerulosclerosis and interstitial fibrosis.

Conclusion: this case illustrates previously unreported combined kidney damage – renal sclerosing peritubular nodules and IgA nephropathy – in a patient with NF2 undergoing bevacizumab therapy.

Patient A. with end-stage chronic renal failure secondary to urolithiasis and chronic tubulointerstitial nephritis has been undergoing programmed hemodialysis since 2021. Her medical history includes multiple surgeries for permanent vascular access: arteriovenous fistulas (AVF) in both upper limbs, arteriovenous grafts (AVG, synthetic prosthesis) in the left shoulder, and four tunnel central venous catheter (tCVC). She was admitted with AVF thrombosis on the left shoulder. Ultrasound examination revealed occlusions in both internal jugular veins, stenosis of the external jugular veins to 2 mm, and patients subclavian veins. A tCVC was implanted at the confluence of the transverse vein and the external jugular. The postoperative period was uneventful, and the catheter function was satisfactorily. After 14 days, an AVG was implanted in the right forearm with shoulder anastomoses, using a "forearm loop" configuration. In the postoperative period, an edema of the right upper limb appeared. After 21 days, the tCVC was removed, and fistulography revealed subocclusion of the right brachiocephalic trunk, with no stenosis or occlusion at the tCVC implantation site. Balloon angioplasty of the right brachiocephalic trunk was performed, resulting in regression of swelling in the right upper limb and chest. Over a 60 day follow-up period, the patient's condition remained, and hemodialysis was succesfuuly performed via the AVG.

One of the complications of autogenous arteriovenous fistula (AVF) used for hemodialysis is the development of a true arteriovenous vein (VA) aneurysm. The consequences of aneurysm formation – including infection – skin changes at the aneurysm site, bleeding, rupture, thrombosis, and impaired blood flow – can result in inadequate hemodialysis. Among these complications, the most critical indication requiring urgent intervention is life-threatening bleeding. The standard treatment for a massive AVF aneurysm often involves ligation or resection with prosthetic interposition. Whenever possible, the first surgical intervention should aim to preserve natural access ideally without prosthetic grafting, creation of new vascular anastomoses or fistula ligation. Partial aneurysmectomy with or without reductive venoplasty, has been proposed as a method of managing this complication while maintaining fully autogenic access. The article describes a simple surgical technique for correcting a double aneurysmally altered AVF in a patient 7 years after the creation of an AVF mid-forearm. The procedure did not require postoperative central catheter implantation. Given the risk of partial fistula thrombosis, suppuration, and potentially fatal hemorrhage due to rupture, reconstructive surgery was performed. The operation consisted of partial excision of of the diseased venous segments (aneurysmorrhaphy), while preserving AVF function. The advantages of aneurysmorraphy include technical simplicity, safety under local anesthesia, effective removal of diseased tissues; and preservation of AVF function. This approach maintains inherent benefits of an autogenous AVF, while conserving vascular access site for future use. Aneurysmorraphy – also referred as reductive aneurysmoplasty, partial aneurysmectomy, or restoration/recalibration – represents a valuable surgical option, particularly for megaphystules. It emphasized preservation of native access while allowing flexibility in surgical technique tailoring individual case.