Keyword: Hemodialysis
10 results found.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A38, https://doi.org/10.63946/cajn/19542
ABSTRACT:
Background: Intradialytic hypotension (IDH) is one of the most common complications of hemodialysis and may manifest as weakness, dizziness, syncope, and poor tolerance of treatment. The risk is increased in elderly patients and those with diabetes mellitus or cardiovascular disease. A key mechanism is an imbalance between ultrafiltration rate and plasma refilling of the intravascular compartment. We present a case of recurrent IDH in a high-risk patient with stage 5 chronic kidney disease (CKD), type 2 diabetes mellitus, and hypertensive heart and kidney disease.Case Presentation
A female patient, born in 1952, had stage 5 CKD (N18.5), extracorporeal dialysis (Z49.1), anemia in chronic disease (D63.8), type 2 diabetes mellitus (E11), and hypertensive heart and kidney disease (I13). Diabetes mellitus had been diagnosed in 2010, with longstanding arterial hypertension.
On December 15, 2022, following a fall and osteosynthesis of the right femur, serum creatinine was 481 μmol/L and blood urea 29.1 mmol/L. Repeat testing showed creatinine 505 μmol/L and urea 32 mmol/L. A double-lumen catheter was placed and renal replacement therapy initiated. On February 27, 2023, an arteriovenous fistula was created. The patient subsequently continued maintenance hemodialysis at Fresenius Medical Care Kazakhstan LLP, Talgar.
Baseline blood pressure was 160/90 mmHg. During every hemodialysis session, approximately 30 minutes after initiation, blood pressure decreased to 80/50 mmHg without adjustment of dialysis parameters.
Management included individualized dialysis prescription. Dry weight was assessed by bioimpedance spectroscopy (BCM), with adjustment of ultrafiltration volume and rate. Dialysate temperature was reduced to 35.5–36.5°C. Dialysate sodium, potassium, and calcium concentrations were 138, 3, and 1.5 mmol/L, respectively. Ultrafiltration profiling was used when fluid overload exceeded 3% of body weight. During hypotensive episodes, the patient was placed in the Trendelenburg position with elevated lower extremities, and ultrafiltration and dialysis parameters were adjusted. AF81 dialysate was used.
Following optimization, intradialytic blood pressure remained approximately 100/60–120/70 mmHg without significant hypotensive episodes. Post-dialysis blood pressure was 130/80 mmHg. Treatment tolerance improved, with clinical observations indicating improved quality of life.
Conclusion: Individualized hemodialysis prescription, including accurate dry-weight assessment, optimized ultrafiltration, reduced dialysate temperature, appropriate dialysate composition, ultrafiltration profiling, timely Trendelenburg positioning, and regular blood pressure monitoring, contributed to improved hemodynamic stability and reduced IDH severity in this high-risk patient.
A female patient, born in 1952, had stage 5 CKD (N18.5), extracorporeal dialysis (Z49.1), anemia in chronic disease (D63.8), type 2 diabetes mellitus (E11), and hypertensive heart and kidney disease (I13). Diabetes mellitus had been diagnosed in 2010, with longstanding arterial hypertension.
On December 15, 2022, following a fall and osteosynthesis of the right femur, serum creatinine was 481 μmol/L and blood urea 29.1 mmol/L. Repeat testing showed creatinine 505 μmol/L and urea 32 mmol/L. A double-lumen catheter was placed and renal replacement therapy initiated. On February 27, 2023, an arteriovenous fistula was created. The patient subsequently continued maintenance hemodialysis at Fresenius Medical Care Kazakhstan LLP, Talgar.
Baseline blood pressure was 160/90 mmHg. During every hemodialysis session, approximately 30 minutes after initiation, blood pressure decreased to 80/50 mmHg without adjustment of dialysis parameters.
Management included individualized dialysis prescription. Dry weight was assessed by bioimpedance spectroscopy (BCM), with adjustment of ultrafiltration volume and rate. Dialysate temperature was reduced to 35.5–36.5°C. Dialysate sodium, potassium, and calcium concentrations were 138, 3, and 1.5 mmol/L, respectively. Ultrafiltration profiling was used when fluid overload exceeded 3% of body weight. During hypotensive episodes, the patient was placed in the Trendelenburg position with elevated lower extremities, and ultrafiltration and dialysis parameters were adjusted. AF81 dialysate was used.
Following optimization, intradialytic blood pressure remained approximately 100/60–120/70 mmHg without significant hypotensive episodes. Post-dialysis blood pressure was 130/80 mmHg. Treatment tolerance improved, with clinical observations indicating improved quality of life.
Conclusion: Individualized hemodialysis prescription, including accurate dry-weight assessment, optimized ultrafiltration, reduced dialysate temperature, appropriate dialysate composition, ultrafiltration profiling, timely Trendelenburg positioning, and regular blood pressure monitoring, contributed to improved hemodynamic stability and reduced IDH severity in this high-risk patient.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A34, https://doi.org/10.63946/cajn/19540
ABSTRACT:
Background: Renal involvement may be the first and only manifestation of systemic autoimmune disease, including ANCA-associated vasculitis (AAV) and systemic lupus erythematosus (SLE). In some cases the diagnosis is established only at stage 5 chronic kidney disease (CKD), once renal replacement therapy (RRT) becomes unavoidable, substantially worsening prognosis. Early recognition of autoimmune etiology is particularly important in patients urgently starting maintenance hemodialysis, since timely immunosuppressive therapy may, in selected cases, restore renal function and allow RRT discontinuation. This study aimed to characterize detection of autoimmune etiology of renal injury among patients with newly diagnosed stage 5 CKD urgently initiating maintenance hemodialysis.
Methods: We conducted a retrospective observational study of patients admitted to BBNURA LLP (Astana, Kazakhstan) with newly diagnosed stage 5 CKD requiring urgent hemodialysis initiation. Urgent admissions accounted for 98 of 330 patients in 2023, 89 of 363 in 2024, 70 of 424 in 2025, and 85 from January through September 2026 (342 total). From this cohort, 70 patients with clinical evidence of multisystem involvement (≥2 extrarenal systems affected, or unexplained systemic symptoms at admission) were selected for diagnostic work-up, assessing the ENT organs, lungs, skin, nervous system, eyes, gastrointestinal tract, musculoskeletal system, and cardiovascular system. Immunological markers (ANCA, anti-dsDNA antibodies, complement components) were evaluated, and diagnoses were confirmed using clinical, laboratory, and, where indicated, histopathological data.
Results: Systemic autoimmune markers were identified in 17 of 342 patients (5.0%) overall, and in 17 of 70 (24.3%) among those selected for screening (10 women, 7 men). AAV was diagnosed in 11 patients, confirmed by renal biopsy in 2 cases. SLE with renal, cutaneous, articular, and vascular involvement was diagnosed in 6 patients. Within the first 3 months, 3 patients died from complications of autoimmune disease, and 14 remained on maintenance hemodialysis. One patient with biopsy-confirmed AAV achieved complete remission, with recovery of kidney function and discontinuation of hemodialysis, following immunosuppressive therapy.
Conclusion: Autoimmune etiology of renal injury is clinically significant among patients with newly diagnosed stage 5 CKD urgently initiating hemodialysis, and targeted clinical screening substantially increased detection yield (5.0% overall vs. 24.3% among selected patients), predominantly identifying AAV and SLE. These findings support active screening for systemic autoimmune disease in newly diagnosed end-stage renal disease and warrant prospective, unselected screening to determine true population prevalence. Timely diagnosis and early therapy may restore renal function, reduce reliance on long-term RRT, and decrease mortality associated with disease complications.
Methods: We conducted a retrospective observational study of patients admitted to BBNURA LLP (Astana, Kazakhstan) with newly diagnosed stage 5 CKD requiring urgent hemodialysis initiation. Urgent admissions accounted for 98 of 330 patients in 2023, 89 of 363 in 2024, 70 of 424 in 2025, and 85 from January through September 2026 (342 total). From this cohort, 70 patients with clinical evidence of multisystem involvement (≥2 extrarenal systems affected, or unexplained systemic symptoms at admission) were selected for diagnostic work-up, assessing the ENT organs, lungs, skin, nervous system, eyes, gastrointestinal tract, musculoskeletal system, and cardiovascular system. Immunological markers (ANCA, anti-dsDNA antibodies, complement components) were evaluated, and diagnoses were confirmed using clinical, laboratory, and, where indicated, histopathological data.
Results: Systemic autoimmune markers were identified in 17 of 342 patients (5.0%) overall, and in 17 of 70 (24.3%) among those selected for screening (10 women, 7 men). AAV was diagnosed in 11 patients, confirmed by renal biopsy in 2 cases. SLE with renal, cutaneous, articular, and vascular involvement was diagnosed in 6 patients. Within the first 3 months, 3 patients died from complications of autoimmune disease, and 14 remained on maintenance hemodialysis. One patient with biopsy-confirmed AAV achieved complete remission, with recovery of kidney function and discontinuation of hemodialysis, following immunosuppressive therapy.
Conclusion: Autoimmune etiology of renal injury is clinically significant among patients with newly diagnosed stage 5 CKD urgently initiating hemodialysis, and targeted clinical screening substantially increased detection yield (5.0% overall vs. 24.3% among selected patients), predominantly identifying AAV and SLE. These findings support active screening for systemic autoimmune disease in newly diagnosed end-stage renal disease and warrant prospective, unselected screening to determine true population prevalence. Timely diagnosis and early therapy may restore renal function, reduce reliance on long-term RRT, and decrease mortality associated with disease complications.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A8, https://doi.org/10.63946/cajn/19526
ABSTRACT:
Introduction: Diabetic kidney disease is a major cause of end-stage kidney disease and is frequently accompanied by cardiovascular and metabolic complications. Patients receiving maintenance hemodialysis remain at high risk of life-threatening complications, particularly when multiple comorbidities are present. We present a case of severe metabolic decompensation in a patient with end-stage diabetic kidney disease receiving maintenance hemodialysis.
Aim: To describe the clinical presentation, laboratory abnormalities, emergency management, and short-term clinical response in a patient with end-stage diabetic kidney disease and multiple comorbidities receiving maintenance hemodialysis.
Methods: A clinical case was analyzed based on the patient's medical records, including clinical presentation, laboratory investigations, comorbid conditions, treatment, and clinical course during hospitalization.
Results: A 59-year-old woman with type 2 diabetes mellitus complicated by diabetic kidney disease and end-stage chronic kidney disease (CKD stage 5) had been receiving maintenance hemodialysis three times weekly since March 2026. Her comorbidities included rheumatoid arthritis, congestive heart failure, diabetic polyneuropathy, anemia of chronic disease, bilateral secondary gonarthrosis, cholelithiasis without cholecystitis, hemorrhoids, and a stage III pressure ulcer. She was admitted in a severe condition with marked weakness, poor appetite, nausea, vomiting, and impaired consciousness. Laboratory evaluation demonstrated severe azotemia, with a creatinine level of approximately 1154 µmol/L and urea of 47.7 mmol/L, accompanied by hyperkalemia (6.3 mmol/L). The clinical picture was consistent with severe uremic and metabolic decompensation in the setting of end-stage kidney disease. Emergency hemodialysis and comprehensive supportive treatment were performed. Following treatment, serum creatinine, urea, and potassium levels decreased, accompanied by clinical stabilization.
Conclusion: This case highlights the high risk of severe metabolic complications in patients with end-stage diabetic kidney disease receiving maintenance hemodialysis, particularly in the presence of substantial cardiovascular and systemic comorbidity. Early recognition of uremic and electrolyte disturbances and timely initiation of hemodialysis are essential for preventing life-threatening complications and achieving clinical stabilization.
Aim: To describe the clinical presentation, laboratory abnormalities, emergency management, and short-term clinical response in a patient with end-stage diabetic kidney disease and multiple comorbidities receiving maintenance hemodialysis.
Methods: A clinical case was analyzed based on the patient's medical records, including clinical presentation, laboratory investigations, comorbid conditions, treatment, and clinical course during hospitalization.
Results: A 59-year-old woman with type 2 diabetes mellitus complicated by diabetic kidney disease and end-stage chronic kidney disease (CKD stage 5) had been receiving maintenance hemodialysis three times weekly since March 2026. Her comorbidities included rheumatoid arthritis, congestive heart failure, diabetic polyneuropathy, anemia of chronic disease, bilateral secondary gonarthrosis, cholelithiasis without cholecystitis, hemorrhoids, and a stage III pressure ulcer. She was admitted in a severe condition with marked weakness, poor appetite, nausea, vomiting, and impaired consciousness. Laboratory evaluation demonstrated severe azotemia, with a creatinine level of approximately 1154 µmol/L and urea of 47.7 mmol/L, accompanied by hyperkalemia (6.3 mmol/L). The clinical picture was consistent with severe uremic and metabolic decompensation in the setting of end-stage kidney disease. Emergency hemodialysis and comprehensive supportive treatment were performed. Following treatment, serum creatinine, urea, and potassium levels decreased, accompanied by clinical stabilization.
Conclusion: This case highlights the high risk of severe metabolic complications in patients with end-stage diabetic kidney disease receiving maintenance hemodialysis, particularly in the presence of substantial cardiovascular and systemic comorbidity. Early recognition of uremic and electrolyte disturbances and timely initiation of hemodialysis are essential for preventing life-threatening complications and achieving clinical stabilization.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A3, https://doi.org/10.63946/cajn/19524
ABSTRACT:
Background: Patients with end-stage chronic kidney disease have an increased risk of recurrent gastrointestinal bleeding due to a combination of uremic thrombocytopathy, anemia, nutritional deficiency, microcirculatory disorders, and regular anticoagulation during hemodialysis. However, the prognostic value of ulcer morphology and the intensity of acid-suppressive therapy in this population has not been adequately studied.
Aim: To determine endoscopic, laboratory, and therapeutic factors associated with ulcer recurrence in patients with end-stage chronic kidney disease receiving programmatic hemodialysis. Materials and Methods. A prospective observational analysis included 84 patients on program hemodialysis who experienced non-variceal ulcer bleeding. Recurrence was recorded in 22 patients, while no recurrence was observed in 62. The location and size of the ulcer defect, endoscopic stigmata of bleeding according to the Forrest classification, hemoglobin and total protein levels, mineral metabolism parameters, and proton pump inhibitor therapy regimen were assessed. Associations were assessed by calculating odds ratios with 95% confidence intervals.
Results: The most significant association with recurrence was found for ulcer defect size. Ulcers larger than 20 mm were detected in 36.4% of patients with recurrence and in 11.3% of patients without a recurrence; their presence increased the odds of recurrence by 4.49 times (OR = 4.49; 95% CI 1.39–14.49; p < 0.05). In contrast, ulcer defects smaller than 10 mm occurred in 18.2% and 53.2% of cases, respectively, and were associated with a lower likelihood of recurrence (OR = 0.20; 95% CI 0.06–0.66; p < 0.01).
Attached Forrest IIb thrombus was more often detected in patients with recurrence—54.5% versus 32.3% (OR = 2.52; 95% CI 0.93–6.81), while pigmented Forrest IIc spots were more often detected in patients with a favorable course—35.5% versus 13.6% (OR = 0.29; 95% CI 0.08–1.09). However, the confidence intervals for these features included unity, which does not allow them to be considered statistically confirmed independent predictors. Relapse was accompanied by more severe anemia: the median hemoglobin was 9.9 g/dL versus 12.0 g/dL in patients without relapse (p<0.01). A decrease in total protein was also observed: 4.8 g/dL versus 5.7 g/dL (p<0.05). Serum iron, calcium, phosphorus, cholesterol, and intact parathyroid hormone levels did not differ significantly.
In univariate analysis, the use of high-dose proton pump inhibitors was associated with a reduced odds of relapse (OR=0.31; 95% CI 0.11–0.85; p<0.05), while low-dose therapy was associated with an increased odds (OR=3.18; 95% CI 1.16–8.75; p<0.05). The initial treatment groups were comparable in terms of clinical and demographic characteristics, ulcer size and location, Forrest stigmata, comorbidities, and concomitant pharmacotherapy.
Conclusion: Ulcer recurrence in patients on scheduled hemodialysis is determined by the interaction of local morphological and systemic metabolic factors. The most compelling endoscopic predictor is ulcer size greater than 20 mm, while anemia and hypoproteinemia reflect a decrease in systemic reparative reserve. High-dose PPI therapy is associated with a lower risk of recurrence; however, the lack of multifactorial adjustment precludes the independent assessment of this effect. These results support a risk-adapted strategy combining intensive acid suppression in high-risk patients with mandatory correction of anemia and nutritional deficiencies.
Aim: To determine endoscopic, laboratory, and therapeutic factors associated with ulcer recurrence in patients with end-stage chronic kidney disease receiving programmatic hemodialysis. Materials and Methods. A prospective observational analysis included 84 patients on program hemodialysis who experienced non-variceal ulcer bleeding. Recurrence was recorded in 22 patients, while no recurrence was observed in 62. The location and size of the ulcer defect, endoscopic stigmata of bleeding according to the Forrest classification, hemoglobin and total protein levels, mineral metabolism parameters, and proton pump inhibitor therapy regimen were assessed. Associations were assessed by calculating odds ratios with 95% confidence intervals.
Results: The most significant association with recurrence was found for ulcer defect size. Ulcers larger than 20 mm were detected in 36.4% of patients with recurrence and in 11.3% of patients without a recurrence; their presence increased the odds of recurrence by 4.49 times (OR = 4.49; 95% CI 1.39–14.49; p < 0.05). In contrast, ulcer defects smaller than 10 mm occurred in 18.2% and 53.2% of cases, respectively, and were associated with a lower likelihood of recurrence (OR = 0.20; 95% CI 0.06–0.66; p < 0.01).
Attached Forrest IIb thrombus was more often detected in patients with recurrence—54.5% versus 32.3% (OR = 2.52; 95% CI 0.93–6.81), while pigmented Forrest IIc spots were more often detected in patients with a favorable course—35.5% versus 13.6% (OR = 0.29; 95% CI 0.08–1.09). However, the confidence intervals for these features included unity, which does not allow them to be considered statistically confirmed independent predictors. Relapse was accompanied by more severe anemia: the median hemoglobin was 9.9 g/dL versus 12.0 g/dL in patients without relapse (p<0.01). A decrease in total protein was also observed: 4.8 g/dL versus 5.7 g/dL (p<0.05). Serum iron, calcium, phosphorus, cholesterol, and intact parathyroid hormone levels did not differ significantly.
In univariate analysis, the use of high-dose proton pump inhibitors was associated with a reduced odds of relapse (OR=0.31; 95% CI 0.11–0.85; p<0.05), while low-dose therapy was associated with an increased odds (OR=3.18; 95% CI 1.16–8.75; p<0.05). The initial treatment groups were comparable in terms of clinical and demographic characteristics, ulcer size and location, Forrest stigmata, comorbidities, and concomitant pharmacotherapy.
Conclusion: Ulcer recurrence in patients on scheduled hemodialysis is determined by the interaction of local morphological and systemic metabolic factors. The most compelling endoscopic predictor is ulcer size greater than 20 mm, while anemia and hypoproteinemia reflect a decrease in systemic reparative reserve. High-dose PPI therapy is associated with a lower risk of recurrence; however, the lack of multifactorial adjustment precludes the independent assessment of this effect. These results support a risk-adapted strategy combining intensive acid suppression in high-risk patients with mandatory correction of anemia and nutritional deficiencies.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A2, https://doi.org/10.63946/cajn/19523
ABSTRACT:
Background: Gastroduodenal lesions in patients with end-stage chronic kidney disease often present with nonspecific clinical manifestations. Standard esophagogastroduodenoscopy allows for the detection of macroscopic changes in the gastric mucosa; however, its ability to reflect the severity of chronic inflammation and structural changes in the stomach in hemodialysis patients has been poorly studied.
Aim of the study: To evaluate the correlation between clinical manifestations, endoscopic findings, and morphological changes in the gastric mucosa in patients with end-stage chronic kidney disease receiving programmatic hemodialysis.
Materials and Methods: This prospective comparative study included 92 patients with stage V chronic kidney disease who had been receiving hemodialysis for at least 6 months and had dyspeptic symptoms, as well as 60 patients with preserved renal function who were examined for dyspepsia. The groups were matched for gender and age. All participants underwent esophagogastroduodenoscopy with biopsy of the antral and corpus mucosa. Histological examination assessed chronic inflammation, disease activity, atrophy, and the presence of Helicobacter pylori.
Results: The clinical presentation in hemodialysis patients was dominated by episodic epigastric pain (61.9%), bloating (58.7%), and nausea (46.7%). Persistent epigastric pain and vomiting were significantly more common than in patients with preserved renal function (p=0.041 and p=0.008, respectively). However, the pattern of complaints remained nonspecific and did not allow us to determine the nature of the structural damage to the mucosa.
Endoscopically, gastritis was detected in 51.1% of patients on program hemodialysis and in 58.3% of patients in the comparison group; no statistically significant difference was found between the groups. Thus, the visual endoscopic picture did not reflect the more severe nature of mucosal damage in end-stage renal failure.
Fundamental differences were revealed by morphological examination. Atrophy of the gastric body mucosa was diagnosed in 34.8% of hemodialysis patients, significantly exceeding the rate in the comparison group (p=0.009). In patients with preserved renal function, active superficial inflammation without significant structural changes in the mucosa predominated. Atrophic changes in dialysis patients were associated with a longer duration of renal replacement therapy (p<0.001) and more pronounced acid-base imbalances (p=0.013). The detection rate of H. pylori in the corpus and antrum of the stomach was 48.9% and 57.6%, respectively, and did not differ significantly from the comparison group. Therefore, the observed morphological dissociation could not be explained solely by differences in the prevalence of infection.
Conclusion: In patients on program hemodialysis, the severity of morphological damage to the gastric mucosa does not correspond to the severity of dyspeptic symptoms and the standard endoscopic picture. A comparable frequency of endoscopically diagnosed gastritis with a significantly higher prevalence of atrophy indicates a systematic underestimation of uremic gastropathy when using visual EGDS alone. Biopsy of the corpus and antrum of the stomach should be considered a mandatory component of the evaluation of patients with a long history of dialysis, regardless of the severity of complaints and the macroscopic picture.
Aim of the study: To evaluate the correlation between clinical manifestations, endoscopic findings, and morphological changes in the gastric mucosa in patients with end-stage chronic kidney disease receiving programmatic hemodialysis.
Materials and Methods: This prospective comparative study included 92 patients with stage V chronic kidney disease who had been receiving hemodialysis for at least 6 months and had dyspeptic symptoms, as well as 60 patients with preserved renal function who were examined for dyspepsia. The groups were matched for gender and age. All participants underwent esophagogastroduodenoscopy with biopsy of the antral and corpus mucosa. Histological examination assessed chronic inflammation, disease activity, atrophy, and the presence of Helicobacter pylori.
Results: The clinical presentation in hemodialysis patients was dominated by episodic epigastric pain (61.9%), bloating (58.7%), and nausea (46.7%). Persistent epigastric pain and vomiting were significantly more common than in patients with preserved renal function (p=0.041 and p=0.008, respectively). However, the pattern of complaints remained nonspecific and did not allow us to determine the nature of the structural damage to the mucosa.
Endoscopically, gastritis was detected in 51.1% of patients on program hemodialysis and in 58.3% of patients in the comparison group; no statistically significant difference was found between the groups. Thus, the visual endoscopic picture did not reflect the more severe nature of mucosal damage in end-stage renal failure.
Fundamental differences were revealed by morphological examination. Atrophy of the gastric body mucosa was diagnosed in 34.8% of hemodialysis patients, significantly exceeding the rate in the comparison group (p=0.009). In patients with preserved renal function, active superficial inflammation without significant structural changes in the mucosa predominated. Atrophic changes in dialysis patients were associated with a longer duration of renal replacement therapy (p<0.001) and more pronounced acid-base imbalances (p=0.013). The detection rate of H. pylori in the corpus and antrum of the stomach was 48.9% and 57.6%, respectively, and did not differ significantly from the comparison group. Therefore, the observed morphological dissociation could not be explained solely by differences in the prevalence of infection.
Conclusion: In patients on program hemodialysis, the severity of morphological damage to the gastric mucosa does not correspond to the severity of dyspeptic symptoms and the standard endoscopic picture. A comparable frequency of endoscopically diagnosed gastritis with a significantly higher prevalence of atrophy indicates a systematic underestimation of uremic gastropathy when using visual EGDS alone. Biopsy of the corpus and antrum of the stomach should be considered a mandatory component of the evaluation of patients with a long history of dialysis, regardless of the severity of complaints and the macroscopic picture.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A26, https://doi.org/10.63946/cajn/19515
ABSTRACT:
Background: Treatment of rheumatoid arthritis (RA) in patients with end-stage chronic kidney disease (CKD stage 5D) on maintenance hemodialysis is challenging because of limited therapeutic options and increased drug toxicity. Stevens–Johnson syndrome (SJS) is a rare, life-threatening drug reaction that may cause severe systemic complications. This case is noteworthy for severe SJS complicated by sepsis and progressive coagulation abnormalities in a patient with seropositive RA, secondary renal amyloidosis, and CKD stage 5D.
Case Presentation: A 61-year-old woman with seropositive RA (anti-CCP+, RF+), late-stage disease, high activity (DAS28 5.3), secondary renal amyloidosis, and CKD stage 5D had received maintenance hemodialysis since December 2025. From January 21 to February 2, 2026, she was hospitalized due to RA exacerbation. Before therapy, hemoglobin was 106 g/L, erythrocytes 3.64 × 10¹²/L, leukocytes 21.57 × 10⁹/L, hematocrit 32.4%, neutrophils 17.99 × 10⁹/L, ESR 30 mm/h. Creatinine was 405 μmol/L, urea 14.1 mmol/L, total protein 63 g/L, potassium 4.05 mmol/L, glucose 6.77 mmol/L, ALT 18 U/L, AST 16 U/L. Hemostasis lab tests: PTI 79%, INR 1.24, fibrinogen 684 mg/dL, aPTT 26.0 s. Therapy included methotrexate 15 mg, colchicine 1.0 mg, infliximab 200 mg, denosumab 60 mg, and prednisolone 10 mg. Subsequently, severe stomatitis and generalized skin eruptions developed. On March 24, she was hospitalized; on March 25, was diagnosed drug-induced SJS. On March 27, she was transferred to the intensive care unit. At admission, hemoglobin was 67 g/L, leukocytes 1.68 × 10⁹/L, platelets 88 × 10⁹/L, creatinine 605.3 μmol/L, urea 21.99 mmol/L, and total protein 53.6 g/L. By March 29, platelets decreased to 12 × 10⁹/L, total protein to 36.3 g/L, and albumin to 17.6 g/L. Hemostasis lab tests deteriorated: PTI 79%-74%-59%, INR 1.24-1.31-1.60, and aPTT 26.0-26.9-77.3 s (January 21, March 24, and March 29, respectively). Sepsis developed, requiring antibacterial and antifungal therapy, platelet concentrates, fresh frozen plasma, and maintenance hemodialysis. Despite intensive treatment, her condition progressively deteriorated. Treatment was stopped at her family's request.
Conclusion: This case highlights the high risk of severe drug-related complications in patients with RA and CKD stage 5D on hemodialysis. Individualized antirheumatic therapy, careful assessment of drug toxicity and renal status, early recognition of severe mucocutaneous reactions, and prompt multidisciplinary management of SJS, sepsis, and coagulation abnormalities are essential to improve outcomes. Early withdrawal of suspected offending agents and close monitoring of hematological and hemostatic parameters are critical to prevent progression.
Case Presentation: A 61-year-old woman with seropositive RA (anti-CCP+, RF+), late-stage disease, high activity (DAS28 5.3), secondary renal amyloidosis, and CKD stage 5D had received maintenance hemodialysis since December 2025. From January 21 to February 2, 2026, she was hospitalized due to RA exacerbation. Before therapy, hemoglobin was 106 g/L, erythrocytes 3.64 × 10¹²/L, leukocytes 21.57 × 10⁹/L, hematocrit 32.4%, neutrophils 17.99 × 10⁹/L, ESR 30 mm/h. Creatinine was 405 μmol/L, urea 14.1 mmol/L, total protein 63 g/L, potassium 4.05 mmol/L, glucose 6.77 mmol/L, ALT 18 U/L, AST 16 U/L. Hemostasis lab tests: PTI 79%, INR 1.24, fibrinogen 684 mg/dL, aPTT 26.0 s. Therapy included methotrexate 15 mg, colchicine 1.0 mg, infliximab 200 mg, denosumab 60 mg, and prednisolone 10 mg. Subsequently, severe stomatitis and generalized skin eruptions developed. On March 24, she was hospitalized; on March 25, was diagnosed drug-induced SJS. On March 27, she was transferred to the intensive care unit. At admission, hemoglobin was 67 g/L, leukocytes 1.68 × 10⁹/L, platelets 88 × 10⁹/L, creatinine 605.3 μmol/L, urea 21.99 mmol/L, and total protein 53.6 g/L. By March 29, platelets decreased to 12 × 10⁹/L, total protein to 36.3 g/L, and albumin to 17.6 g/L. Hemostasis lab tests deteriorated: PTI 79%-74%-59%, INR 1.24-1.31-1.60, and aPTT 26.0-26.9-77.3 s (January 21, March 24, and March 29, respectively). Sepsis developed, requiring antibacterial and antifungal therapy, platelet concentrates, fresh frozen plasma, and maintenance hemodialysis. Despite intensive treatment, her condition progressively deteriorated. Treatment was stopped at her family's request.
Conclusion: This case highlights the high risk of severe drug-related complications in patients with RA and CKD stage 5D on hemodialysis. Individualized antirheumatic therapy, careful assessment of drug toxicity and renal status, early recognition of severe mucocutaneous reactions, and prompt multidisciplinary management of SJS, sepsis, and coagulation abnormalities are essential to improve outcomes. Early withdrawal of suspected offending agents and close monitoring of hematological and hemostatic parameters are critical to prevent progression.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A24, https://doi.org/10.63946/cajn/19514
ABSTRACT:
Background: Patients with type 2 diabetes mellitus (T2DM) on maintenance hemodialysis represent one of the highest-risk populations in nephrology practice. End-stage kidney disease (ESKD) and T2DM create a state of profound immunosuppression that predisposes patients to life-threatening infections.
Central venous catheters (CVCs), frequently required for hemodialysis access, are a well-recognized gateway for bacteremia. When bacteremia is complicated by coagulopathy, the clinical course can rapidly evolve toward disseminated intravascular coagulation (DIC).
Case Presentation: A 58-year-old woman was admitted with a 3-day history of nausea, vomiting, and body pain. Examination revealed anasarca, lower-extremity purpura, and petechial rash, with concern for coagulopathy. T2DM diagnosed in 2007 and ESKD on maintenance hemodialysis since October 2025 (three 4-hour sessions weekly). Vascular access was a right internal jugular CVC.
On admission, hemoglobin 62 g/L, RBC 2.02 ×10¹²/L, platelets 93 ×10⁹/L, WBC 11.18 ×10⁹/L, glucose 24.28 mmol/L, total protein 63 g/L, D-dimer 2,680 ng/mL, procalcitonin (PCT) 14.8 ng/mL, creatinine 405 μmol/L, urea 13.9 mmol/L, INR 1.46, Prothrombin Index 66%, fibrinogen 4.0 g/L, APTT 28.2 sec. Antibiotics had been started at home without improvement. In hospital, broad-spectrum therapy was escalated to a carbapenem plus a fluoroquinolone, with packed red blood cell and fresh frozen plasma transfusions. Hemoglobin increased to 87 g/L, PCT decreased to 1.78 ng/mL, and D-dimer to 1,178 ng/mL; thrombocytopenia persisted. After treatment, creatinine 592 μmol/L, urea 20.7 mmol/L, glucose 16.55 mmol/L, albumin 26 g/L, total protein 53 g/L, INR 1.39, Prothrombin Index 69%, fibrinogen 7.55 g/L, APTT 25.4 sec.
On days 5–6, livedo reticularis, worsening dyspnea, and persistent coagulopathy prompted chest MSCT. It revealed bilateral peribronchial foci with formed cavities, consistent with abscessing (necrotizing) pneumonia. The bilateral cavitary pattern suggested hematogenous dissemination, likely from the indwelling CVC. Patient transferred to the ICU with sepsis-associated DIC.
Linezolid 600 mg IV twice a day was added to provide coverage for possible methicillin-resistant Staphylococcus aureus and other gram-positive organisms. Following treatment escalation, hemoglobin reached 118 g/L, PCT decreased to 0.9 ng/mL, INR normalized to 0.92, and Prothrombin Index increased to 117%.
Conclusion: CVC-related bacteremia should be considered early in hemodialysis patients with unexplained coagulopathy or bilateral pulmonary infiltrates. Purpura followed by livedo reticularis may indicate DIC progression and should prompt urgent reassessment. Cavitation despite antibiotics signals treatment failure and need to reassess pathogen coverage, including biofilm-forming gram-positive organisms. T2DM and ESKD create a multiplicative immunocompromised state, requiring multimodal management and glycemic control.
Central venous catheters (CVCs), frequently required for hemodialysis access, are a well-recognized gateway for bacteremia. When bacteremia is complicated by coagulopathy, the clinical course can rapidly evolve toward disseminated intravascular coagulation (DIC).
Case Presentation: A 58-year-old woman was admitted with a 3-day history of nausea, vomiting, and body pain. Examination revealed anasarca, lower-extremity purpura, and petechial rash, with concern for coagulopathy. T2DM diagnosed in 2007 and ESKD on maintenance hemodialysis since October 2025 (three 4-hour sessions weekly). Vascular access was a right internal jugular CVC.
On admission, hemoglobin 62 g/L, RBC 2.02 ×10¹²/L, platelets 93 ×10⁹/L, WBC 11.18 ×10⁹/L, glucose 24.28 mmol/L, total protein 63 g/L, D-dimer 2,680 ng/mL, procalcitonin (PCT) 14.8 ng/mL, creatinine 405 μmol/L, urea 13.9 mmol/L, INR 1.46, Prothrombin Index 66%, fibrinogen 4.0 g/L, APTT 28.2 sec. Antibiotics had been started at home without improvement. In hospital, broad-spectrum therapy was escalated to a carbapenem plus a fluoroquinolone, with packed red blood cell and fresh frozen plasma transfusions. Hemoglobin increased to 87 g/L, PCT decreased to 1.78 ng/mL, and D-dimer to 1,178 ng/mL; thrombocytopenia persisted. After treatment, creatinine 592 μmol/L, urea 20.7 mmol/L, glucose 16.55 mmol/L, albumin 26 g/L, total protein 53 g/L, INR 1.39, Prothrombin Index 69%, fibrinogen 7.55 g/L, APTT 25.4 sec.
On days 5–6, livedo reticularis, worsening dyspnea, and persistent coagulopathy prompted chest MSCT. It revealed bilateral peribronchial foci with formed cavities, consistent with abscessing (necrotizing) pneumonia. The bilateral cavitary pattern suggested hematogenous dissemination, likely from the indwelling CVC. Patient transferred to the ICU with sepsis-associated DIC.
Linezolid 600 mg IV twice a day was added to provide coverage for possible methicillin-resistant Staphylococcus aureus and other gram-positive organisms. Following treatment escalation, hemoglobin reached 118 g/L, PCT decreased to 0.9 ng/mL, INR normalized to 0.92, and Prothrombin Index increased to 117%.
Conclusion: CVC-related bacteremia should be considered early in hemodialysis patients with unexplained coagulopathy or bilateral pulmonary infiltrates. Purpura followed by livedo reticularis may indicate DIC progression and should prompt urgent reassessment. Cavitation despite antibiotics signals treatment failure and need to reassess pathogen coverage, including biofilm-forming gram-positive organisms. T2DM and ESKD create a multiplicative immunocompromised state, requiring multimodal management and glycemic control.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A22, https://doi.org/10.63946/cajn/19513
ABSTRACT:
Objective: To assess dietary practices and challenges in managing hyperphosphatemia in CKD patients from nephrology specialists’ perspective.
Methods: An online survey of 68 nephrologists, hemodialysis physicians, and nurses at the Republican Specialized Medical Center of Nephrology and Kidney Transplantation (Tashkent, Uzbekistan) evaluated dietary habits, phosphorus awareness, and adherence difficulties. Descriptive statistics were applied.
Results: 64.7% reported increased consumption of ready-to-eat foods, 70.6%—phosphate-containing products, and 82.4% noted higher patient awareness. Adherence challenges were greatest among hemodialysis patients (51–75%). Most specialists (76.5%) emphasized equal importance of protein intake and phosphorus restriction.
Conclusion: Despite improved awareness, dietary adherence remains difficult. Increased processed and phosphate-rich food consumption complicates hyperphosphatemia management, highlighting the need for enhanced dietetic support.
Methods: An online survey of 68 nephrologists, hemodialysis physicians, and nurses at the Republican Specialized Medical Center of Nephrology and Kidney Transplantation (Tashkent, Uzbekistan) evaluated dietary habits, phosphorus awareness, and adherence difficulties. Descriptive statistics were applied.
Results: 64.7% reported increased consumption of ready-to-eat foods, 70.6%—phosphate-containing products, and 82.4% noted higher patient awareness. Adherence challenges were greatest among hemodialysis patients (51–75%). Most specialists (76.5%) emphasized equal importance of protein intake and phosphorus restriction.
Conclusion: Despite improved awareness, dietary adherence remains difficult. Increased processed and phosphate-rich food consumption complicates hyperphosphatemia management, highlighting the need for enhanced dietetic support.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A7, https://doi.org/10.63946/cajn/19507
ABSTRACT:
Patient T., 43 years old. End-stage chronic kidney disease (CKD) was diagnosed in 2013, and emergency kidney replacement therapy with maintenance hemodialysis was initiated. Prior to this, the patient had not been followed by a nephrologist. Throughout the course of hemodialysis treatment, the patient failed to comply with medical recommendations regarding regular laboratory monitoring of mineral metabolism.
In 2024, a markedly elevated parathyroid hormone (PTH) level (>1,935 pg/mL; October 2024) was detected for the first time. The patient had not received any specific medical therapy. Clinical manifestations included generalized weakness, bone and joint pain, impaired mobility (waddling gait), and skeletal deformities involving the sternum and tibial bones.
Scintigraphy performed on December 13, 2024, demonstrated increased functional activity of all four parathyroid glands (Figure 1). Despite prolonged combined medical therapy with cinacalcet 90 mg/day and paricalcitol 15 μg three times weekly, laboratory markers of calcium-phosphate metabolism continued to deteriorate, with the PTH level rising to 2,338 pg/mL. Bone mineral density assessment by dual-energy X-ray absorptiometry (DXA) revealed a Z-score of −5, consistent with severe secondary osteoporosis (Figure 2).
In December 2024, the patient underwent cervical exploration with removal of the hyperplastic left superior, left inferior, and right inferior parathyroid glands at Poytaxt Medical Clinic. In the postoperative period, a significant reduction in serum PTH was observed, decreasing to 492 pg/mL (December 27, 2024) compared with the preoperative level of 2,338 pg/mL.
During the one-year follow-up after parathyroidectomy, the patient's condition remained stable, with no recurrence of hyperparathyroidism. As replacement therapy, the patient has been receiving long-term calcium supplementation and alfacalcidol.
Biochemical blood tests performed in August–September 2025 demonstrated total serum calcium levels ranging from 1.79 to 2.71 mmol/L (reference range: 2.1–2.6 mmol/L) and serum phosphorus levels of 1.0–1.15 mmol/L (reference range: 0.81–1.45 mmol/L).
In November 2025, dysfunction of the patient's arteriovenous fistula (AVF) resulted in complete loss of vascular access. The exact etiology could not be established because of insufficient diagnostic evaluation; however, vascular wall calcification was considered a possible contributing factor. A temporary central venous catheter was inserted for hemodialysis, followed by successful creation of a new arteriovenous fistula.
According to the most recent laboratory evaluation performed on January 7, 2026, the PTH level remained within the target range (200 pg/mL), serum phosphorus was 0.98 mmol/L, and alkaline phosphatase was 410.5 U/L.
Conclusion: This clinical case illustrates the consequences of delayed diagnosis and inadequate management of secondary hyperparathyroidism, resulting from both poor patient adherence to treatment and systemic healthcare limitations, including insufficient long-term follow-up, limited access to regular laboratory monitoring, and shortcomings in the standard management of maintenance hemodialysis patients.
Although parathyroidectomy is effective in improving quality of life and reducing cardiovascular mortality, it is associated with postoperative complications and is generally performed only in advanced stages of the disease, when irreversible disorders of mineral and bone metabolism have already developed.
Therefore, early diagnosis and timely initiation of long-term medical therapy remain the cornerstone of secondary hyperparathyroidism management, allowing better disease control and reducing the need for surgical intervention.
In 2024, a markedly elevated parathyroid hormone (PTH) level (>1,935 pg/mL; October 2024) was detected for the first time. The patient had not received any specific medical therapy. Clinical manifestations included generalized weakness, bone and joint pain, impaired mobility (waddling gait), and skeletal deformities involving the sternum and tibial bones.
Scintigraphy performed on December 13, 2024, demonstrated increased functional activity of all four parathyroid glands (Figure 1). Despite prolonged combined medical therapy with cinacalcet 90 mg/day and paricalcitol 15 μg three times weekly, laboratory markers of calcium-phosphate metabolism continued to deteriorate, with the PTH level rising to 2,338 pg/mL. Bone mineral density assessment by dual-energy X-ray absorptiometry (DXA) revealed a Z-score of −5, consistent with severe secondary osteoporosis (Figure 2).
In December 2024, the patient underwent cervical exploration with removal of the hyperplastic left superior, left inferior, and right inferior parathyroid glands at Poytaxt Medical Clinic. In the postoperative period, a significant reduction in serum PTH was observed, decreasing to 492 pg/mL (December 27, 2024) compared with the preoperative level of 2,338 pg/mL.
During the one-year follow-up after parathyroidectomy, the patient's condition remained stable, with no recurrence of hyperparathyroidism. As replacement therapy, the patient has been receiving long-term calcium supplementation and alfacalcidol.
Biochemical blood tests performed in August–September 2025 demonstrated total serum calcium levels ranging from 1.79 to 2.71 mmol/L (reference range: 2.1–2.6 mmol/L) and serum phosphorus levels of 1.0–1.15 mmol/L (reference range: 0.81–1.45 mmol/L).
In November 2025, dysfunction of the patient's arteriovenous fistula (AVF) resulted in complete loss of vascular access. The exact etiology could not be established because of insufficient diagnostic evaluation; however, vascular wall calcification was considered a possible contributing factor. A temporary central venous catheter was inserted for hemodialysis, followed by successful creation of a new arteriovenous fistula.
According to the most recent laboratory evaluation performed on January 7, 2026, the PTH level remained within the target range (200 pg/mL), serum phosphorus was 0.98 mmol/L, and alkaline phosphatase was 410.5 U/L.
Conclusion: This clinical case illustrates the consequences of delayed diagnosis and inadequate management of secondary hyperparathyroidism, resulting from both poor patient adherence to treatment and systemic healthcare limitations, including insufficient long-term follow-up, limited access to regular laboratory monitoring, and shortcomings in the standard management of maintenance hemodialysis patients.
Although parathyroidectomy is effective in improving quality of life and reducing cardiovascular mortality, it is associated with postoperative complications and is generally performed only in advanced stages of the disease, when irreversible disorders of mineral and bone metabolism have already developed.
Therefore, early diagnosis and timely initiation of long-term medical therapy remain the cornerstone of secondary hyperparathyroidism management, allowing better disease control and reducing the need for surgical intervention.
Original Article
Central Asian Journal of Nephrology, 1(1), 2025, cajn001, https://doi.org/10.63946/cajn/16627
ABSTRACT:
Background: Despite the fact that the prevalence of CKD and its effects on health have been studied mainly in economically developed countries, the burden of this disease is even greater in developing countries. It has been established that more than 50% of deaths in patients with ESRD are due to cardiovascular causes. The objective of our study is to comparatively study the structure of cardiovascular diseases in dialysis patients at different levels of health care in Uzbekistan.
Methods: 165 dialysis patients (90 men and 75 women) were studied. The main initial diseases were chronic glomerulonephritis (n=76), diabetes mellitus (n=44), urolithiasis (n=14), chronic pyelonephritis (n=10), etc. Patients were included from 3 clinics of different administrative levels - republican (n=32), urban (n=72) and rural (n=61).
Results: CVDs were identified in 69% of the urban, 44% of the regional and 47% of the republican population. In the structure of CVD, AH, IHD and CHF prevailed in all groups. Also, in the groups of the republican and city level, CVD was more common in a combined form, while dialysis patients at the regional level had more isolated CVD pathology.
Conclusion: Patients of the urban population on dialysis more often suffer from CVD than patients receiving HD at the republican and regional levels of health care. The combined lesion of the CVS occupies a leading place in the structure of CVD in dialysis patients at both urban and national levels.
Methods: 165 dialysis patients (90 men and 75 women) were studied. The main initial diseases were chronic glomerulonephritis (n=76), diabetes mellitus (n=44), urolithiasis (n=14), chronic pyelonephritis (n=10), etc. Patients were included from 3 clinics of different administrative levels - republican (n=32), urban (n=72) and rural (n=61).
Results: CVDs were identified in 69% of the urban, 44% of the regional and 47% of the republican population. In the structure of CVD, AH, IHD and CHF prevailed in all groups. Also, in the groups of the republican and city level, CVD was more common in a combined form, while dialysis patients at the regional level had more isolated CVD pathology.
Conclusion: Patients of the urban population on dialysis more often suffer from CVD than patients receiving HD at the republican and regional levels of health care. The combined lesion of the CVS occupies a leading place in the structure of CVD in dialysis patients at both urban and national levels.