Objective: to evaluate the effects of secondary hyperparathyroidism (HPT) in kidney transplantation (KT) candidates on recipients’ parathyroid gland function in the first postoperative year.Materials and methods. The retrospective cohort study included 210 patients (103 women, 107 men, age 45 ± 9 years) with stage 5 chronic kidney disease (stage 5 CKD, including dialysis-dependent patients), who had undergone cadaveric KT. Biochemical screening before kidney transplantation and in the postoperative period at 3 and 12 months determined serum levels of parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase activity, albumin and creatinine using standard methods. PTH levels of 130–595 pg/mL and ≤130 pg/mL were taken as the target level in the pre- and post-transplant periods, respectively.Results. Fifty-six KT candidates (group 1) had HPT and 154 (group 2) had the target PTH levels. PTH level was 897 (722; 1136) and 301 (229; 411) pg/mL, respectively, p < 0.001. PTH decreased in all recipients at 3 months after KT: by 595 (420; 812) in group 1 and 148 (77; 230) pg/ mL in group 2, p < 0.001, to 254 (180; 455) and 150 (118; 212) pg/mL, respectively, p < 0.001; the target level was detected in 10.7% and 42.2% of recipients, respectively, p < 0.001. At 12 months, blood PTH was 171 (94; 239) pg/mL in group 1 and 112 (90; 135) pg/mL in group 2, p = 0.004; target level was found in 48.2% and 73.4% of recipients, respectively, p < 0.001. Kidney graft function was identical in both recipient groups: acute tubular necrosis in 41.1% and 54.5%; at 3 months, median glomerular filtration rates (GFR) of 60 and 65 mL/min (n.d.); at 12 months, 56 and 54 mL/min (n.d.). Post-transplant PTH levels correlated directly with preoperative levels in both groups and inversely with renal graft function in group 2 recipients.Conclusion. HPT in kidney transplant candidates is a major, graft function-independent predictor of excess PTH secretion in recipients, increasing the risk of persistent HPT 1.9-fold, one year after KT.

Kidney injury in patients infected with the human immunodeficiency virus (HIV) has a diverse spectrum. Some antiretroviral therapy (ART) drugs have nephrotoxic effects. We present a clinical case of severe combined kidney injury — chronic kidney disease (CKD) and acute kidney disease (AKD) — in a patient with HIV infection. She was on long-term treatment with a fixed-dose combination of rilpivirine, tenofovir, and emtricitabine and had normal pre-treatment renal function (estimated glomerular filtration rate 69 mL/min/1.73m2 ). There was gradual increase in blood creatinine, but the patient did not visit a nephrologist and the ART was not changed. The patient was admitted to the nephrology department two years later because she had arterial hypertension and hyperazotemia (blood creatinine 718 μmol/l). Diagnosis: chronic tubulointerstitial nephritis, CKD G5 taking into account the gradual increase in blood creatinine during long-term ART. The patient was treated with peritoneal dialysis. There was persistent decrease and stabilization of blood creatinine (210-190 μmol/l was) which indicated in AKD. The presented observation demonstrates that ART in an HIVinfected patient can lead to the development of severe combined chronic and acute kidney injury. HIV-infected patients receiving ART require regular monitoring of renal function and follow-up by a nephrologist.

Patients with chronic kidney disease are susceptible to developing acute pancreatitis. We present a rare clinical case of acute pancreatitis with the formation of pancreatic necrosis in a patient on peritoneal dialysis (PD), debuted with PD–associated peritonitis. On hospitalization, there were no diagnostic criteria for acute pancreatitis; treatment for dialysis peritonitis was ineffective. Repeated ultrasound examination revealed signs of diffuse changes in the pancreas and multi-chamber formation of the small pelvis. Refractory peritonitis, inadequate ultrafiltration, and unclear nature of formation in the pelvic were the grounds for diagnostic laparoscopy and removal of the peritoneal catheter. Abdominal inspection revealed spots of stearin necrosis over the entire surface of the peritoneum and the greater omentum; in the pelvis there were adhesions between the uterus and the rectum. Development of pancreonecrosis was confirmed by abdominal CT scan. Treatment of acute pancreatitis was without effect, type 2 myocardial infarction developed, and with increasing symptoms of multiple organ failure, death occurred.

Cardiovascular disease is the leading cause of death in patients with a transplanted kidney and in graft loss. We present the first clinical case of successful surgical correction of ascending aortic dissection (DeBakey type I) in a young patient with a functioning kidney graft. The patient underwent the first cadaveric kidney transplantation (KTx), which was complicated by acute humoral rejection and suboptimal graft function. High blood pressure, anemia, elevated blood levels of triglycerides, phosphorus, parathyroid hormone, and uric acid were recorded. A repeat KTx was performed five years later; the patient’s condition and kidney function were satisfactory. Three years later,the patient started experiencing severe pain along the thoracic and lumbar spine; his blood creatinine level was 408 μmol/L. Computed tomography and echocardiography diagnosed DeBakey type I aortic dissection (AD) with critical narrowing of the true aortic lumen at certain levels, dissection of aortic branches. Aortic resection surgery with prosthetic replacement of the ascending aorta according to David procedure with reimplantation of coronary artery orifices according to Kouchoukos technique, prosthetic replacement of the aortic arch with debranching of brachiocephalic artery and left common carotid artery were successfully performed as planned under endotracheal anesthesia, cardiopulmonary bypass and selective pharmacological cold cardioplegia. The peculiarities of the course, possible causes and outcomes of surgical correction of thoracic AD in the patient are discussed.

Background . Non-alcoholic Wernicke’s encephalopathy occurs in various somatic conditions with thiamine deficiency, excessive excretion of thiamine, or impaired thiamine metabolism. Very few cases of this pathology have been described in chronic kidney disease (CKD). We present a unique case of non-alcoholic Wernicke’s encephalopathy in a patient with a kidney transplant is presented. Past medical history . The patient underwent kidney transplantation in 2008. Outpatient follow-up by a nephrologist was irregular. Renal graft function remained relatively stable: blood creatinine 200–240 μmol/L, estimated glomerular filtration rate 40–30 mL/min, tacrolimus plasma concentrations tended to increase (5.7–7.6–8.4–10.4 ng/mL); repeated graft biopsy (in 2015 and in 2017) determined the chronic toxicity of calcineurin inhibitors. The patient’s condition worsened in late January 2020: body temperature increased to 38°C, nausea, vomiting, loose, watery stools for up to 5 times per day, 8 kg weight loss, decreased diuresis. A few days later, double vision, shaky gait and then immobility appeared. Biochemical examination results: potassium 3.8 mmol/L, sodium 139 mmol/L, alpha-amylase 159 units/L (norm 0–100 units/L), creatinine 242 mmol/L, urea 13.2 mmol/L; ultrasound signs of pancreatitis. Magnetic resonance imaging (MRI) of the brain: bilateral diffuse lesions of the midbrain, thalamus, and cerebellum. Based on the clinical picture and on brain MRI results, Wernicke’s encephalopathy was diagnosed. Parenteral administration of thiamine had a good effect. Conclusion . Possible mechanisms of the development of Wernicke’s encephalopathy in a patient were discussed. Vigilance is required regarding this disease when metabolic disorders occur in patients with CKD.

Clinical observation of a young woman with chronic kidney disease IV stage and hyperparathyroidism is presented. Ultrasound and99mTc-sestamibi scintigraphy of the anterior surface of the neck visualized a tumor of the left upper parathyroid gland. In a histological examination of distant education was diagnosed a solid parathyroid adenoma. The difficulty of differential diagnosis between primary and secondary/tertiary hyperparathyroidism in chronic kidney disease is discussed.

Objective: to assess the prevalence of hyperparathyroidism (HPT) and the factors affecting its development in kidney transplant recipients. Materials and methods . The single-center observational cohort study included 97 kidney transplant recipients – 40 men, 57 women, age 50 ± 9 years. Inclusion criteria: more than 12 months of post-transplant period, 3 months of stable renal transplant function. Non-inclusion criterion: therapy with vitamin D, with its alternatives or with cinacalcet. Dialysis ranged from 0 to 132 months (median 18); 46% of patients had pre-operative secondary HPT. A comprehensive laboratory study included evaluation of serum concentrations of parathyroid hormone (PTH), 25-OH vitamin D, calcium, phosphorus, magnesium, total alkaline phosphatase (ALP) activity, albumin, creatinine and daily proteinuria. At the dialysis stage, the target PTH range of 130–585 pg/ ml was used, in the post-transplant period – ≤130 pg/ml. Glomerular filtration rate (eGFR) was calculated using the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) formula. Results. Patients were divided into two groups based on PTH threshold level (130 pg/ml): the first with HPT (PTH >130 pg/ml, median 203), the second without HPT (PTH ≤130 pg/ml, median 101). Both groups were comparable in terms of gender, age, primary renal disease, dialysis modality, post-transplant follow-up, and immunosuppressive therapy regimen. In group 1 and group 2 recipients, dialysis therapy, pre-transplant median PTH level, incidence of reoperation and incidence of immediate renal graft function were 30 (14; 50) and 14 (6; 28) months (p = 0.004), 681 (538; 858) and 310 (182; 556) pg/ml (p < 0.001), 17% and 2% (p = 0.028), 51% and 80% (p = 0.005), respectively. At the time of the study, 72% of group 1 recipients had eGFR <60 ml/min, versus 36% of group 2 (p >< 0.001). Among HPT biochemical parameters, there were differences for ionized serum calcium (1.32 ± 0.07 versus 1.29 ± 0.04 mmol/l, p = 0.017) and ALP activity (113 ± 61 versus 75 ± 19 u/l, p = 0.021). Serum vitamin D in both groups reduced in equal measures – 14 ± 4 and 15 ± 6 ng/ml. Conclusion. Persistent HPT in the long-term post-transplant period reaches 48.5%. Risk factors for its development included dialysis for more than 18 months, pre-operative secondary HPT, repeated kidney transplantation, delayed graft function, and eGFR <60 ml/min.

Vascular calcification is common in patients with chronic kidney disease and in kidney transplant recipients. It leads to increased arterial stiffness, left ventricular hypertrophy, complicates formation of arteriovenous fistula for hemodialysis, decreases coronary artery perfusion, and generally increases cardiovascular morbidity and mortality. Vascular calcification affects arteries of all sizes – starting from the intimal and medial layers of the arterial wall. In clinical practice, several non-invasive imaging techniques have been used to evaluate the location and severity of vascular calcification. There is a report positing a possibility of evaluating vascular calcification by dual-energy x-ray absorptiometry (DXA). This paper presents the experience of successful diagnosis of peripheral arterial calcification by DXA in kidney transplant recipients and end-stage renal disease patients.

The syndrome of mineral and bone disorders in patients with chronic kidney disease after kidney transplantation include hypophosphatemia, hypercalcemia, hypovitaminosis D, and decreased bone mineralization (secondary osteoporosis). The modern strategy of prevention and treatment of post-transplantation mineral and bone disorders is based on the principles of individual approach, taking into account the assessment of risk factors and minimizing the factors that caused these disorders. An attempt to compensate for phosphorus defi ciency is usually ineffective and even dangerous due to complications. This review analyzes different correction´s methods of symptomatic hypercalcemia and hypercalcemia after kidney transplantation secondary to hyperparathyroidism. Also in this review presented modern approaches to the prevention and treatment of posttransplant osteoporosis. Also it shows the effects and indications for use steroid sparing/withdrawal, vitamin D and vitamin D receptor activator, drug and surgical correction of hyperparathyroidism, bisphosphonates and other medications.

Bone disease is a serious and common condition in patients after kidney transplantation. The review analyzed the causes of bone disorders in the early and late postoperative period that are associated with renal transplantation: fibroblast growth factor 23, parathyroid hormone, vitamin D, immunosuppressive therapy and imbalance of mineral metabolism. It shows the most common clinical variant of the post-transplant bone disease – secondary osteoporosis, risk factors of its development and complications. It presents the diagnostic algorithm for dynamic monitoring and evaluating the effectiveness of the treatment of bone disorders

THE AIM of the study was to determine the prevalence and severity of mineral and bone metabolism in patients with chronic kidney disease (CKD) undergoing renal transplant. PATIENTS AND METHODS . The study included 77 patients (32 men, 45 women, mean age 44) with CKD who underwent transplantation of cadaveric kidneys from 2011 to 2015. Serum concentrations of electrolytes, the activity of total alkaline phosphatase (ALP), albumin, nitrogen metabolism parameters were determined by standard methods, blood concentrations of parathyroid hormone (PTH) and vitamin D (25-OH vitamin D) – by chemilumescent analysis on ARCHITECT-system. Serum calcium on serum albumin is reassessed, glomerular filtration rate (GFR) is calculated according to the formula CKD-EPI. RESULTS. Hypercalcemia, hypophosphatemia, hypomagnesemia and a high level of PTH respectively diagnosed in 15.6%, 16.9%, 16.9% and 87% patients. There was the high significant difference between blood PTH in patients with normal renal function and reduced renal graft function. The blood level of vitamin D ranged from 6 to 30 ng/ mL (median 14), only one patient was in a recommended range (≥30 ng/ml). There was the invert correlation of PTH with GFR (r=-0.543, p<0.001) and serum magnesium (r=-0.241, p=0.04), directl correlation with total ALP activity (r=0.280, p=0.015). The blood PTH is not associated with serum calcium and phosphorus. There was weak invert correlation between serum phosphorus and GFR (r=-0.232, p=0.04), between ALP activity and GFR (r =-0.267, p=0.02) and between serum magnesium and GFR (r=-0.230, p=0.05). CONCLUSION. Common manifestations of mineral and bone disorders in renal transplant recipients are pre- and post-transplantation hyperparathyroidism, which development/progression is associated with hypomagnesemia, deterioration of kidney function, as well as deficiency of vitamin D.

Successful kidney transplantation eliminates endocrine and metabolic disorders that predispose to the development of hyperparathyroidism, the complication typical for the chronic kidney disease; but the process of recovery from mineral and bone disorders is slowed down. The highest incidence of post-transplant hyperparathyroidism is recorded in the first postoperative year. The risk factors for its development or persistence include the high blood levels of parathyroid hormone, calcium, phosphorus, and/or alkaline phosphatase, a prolonged dialysis therapy, severe hyperparathyroidism in the preoperative period, vitamin D deficiency, a suboptimal transplanted kidney function, and also the recipient's previous history of subtotal or incomplete parathyroidectomy. The characteristic clinical and laboratory signs of posttransplant hyperparathyroidism are bone lesions, kidney graft abnormalities, hypercalcemia, and hypophosphatemia. The diagnostic algorithm includes monitoring the markers of mineral and bone metabolism, determining the bone mineral density, and imaging of thyroid glands. Correction of post-transplant hyperparathyroidism is performed surgically or pharmacologically. The article specifies the indications to, the extent and timing of parathyroidectomy, discusses the use of native vitamin D formulations, its analogues, and calcimimetics.

Беременные женщины, страдающие хронической болезнью почек (ХБП), имеют высокий риск развития ассоциированной с беременностью артериальной гипертензии (АГ) и преэклампсии, а их дети – высокий риск недоношенности или микросомии. У этих женщин высок риск и прогрессирования ХБП. Тем не менее, в настоящее время вероятность благополучного исхода беременности у женщин с ХБП II и даже III стадии довольно высока. Важное место в комплексной терапии и профилактике прогрессирования ХБП занимает организация лечебного питания – коррекция потребления белка и минералов, обмен которых тесно связан с функциональным состоянием почек – натрия, калия, кальция, фосфора. Рациональная организация питания с ограничением белка, применением комплекса незаменимых кето-/аминокислот, оптимальным потреблением жидкости и электролитов и с достаточной калорийностью рациона может способствовать успешному вынашиванию беременности и родоразрешению у женщин с ХБП.