Complication Of Nephrotic Syndrome Research Articles

Rivaroxaban for Thromboembolism Prophylaxis in Patients with Nephrotic Syndrome: A Single-Arm, Prospective Study

Introduction: Thromboembolism is a recognized complication of nephrotic syndrome (NS). Evidence supporting the use of rivaroxaban to prevent NS-related thrombosis is limited and controversial. This study aimed to explore the impact of NS on rivaroxaban pharmacokinetics and to collect observational data on the efficacy and safety of rivaroxaban as primary thromboprophylaxis in patients with NS. Methods: This prospective study analyzed 141 patients with NS who received rivaroxaban (10 mg/day) for thromboprophylaxis. High-performance liquid chromatography-tandem mass spectrometry was used to measure the trough and peak plasma concentrations (Ctrough and Cmax) of rivaroxaban. The influence of clinical and genetic factors on these concentrations was examined using multivariate logistic regression. Results: The median Cmax and Ctrough were 68.5 ng/mL (interquartile range [IQR], 31.7–105.5 ng/mL) and 4.4 ng/mL (IQR, 1.2–11.9 ng/mL), respectively. The incidence of thromboembolic events (TEs) was 12.8%, while that of bleeding events was 14.2%, although all were classified as minor. Albumin level was the most significant factor affecting Cmax (ρ = 0.55; p < 0.001) and was also significantly associated with TEs (0.81; 0.71–0.91 per 1.0 g/dL increase; p = 0.001) and bleeding risks (1.11; 1.03–1.19 per 1.0 g/dL increase; p = 0.008). Single nucleotide polymorphisms in the ABCB1 gene significantly influenced Ctrough but were not associated with clinical outcomes. Conclusion: Hypoalbuminemia significantly affects the pharmacokinetics of rivaroxaban in NS patients. A dose-adjustment strategy based on rivaroxaban concentrations, accounting for variable albumin levels, may improve the safety and efficacy of thromboprophylaxis in this population.

Endocrine Disorders in Nephrotic Syndrome-A Comprehensive Review.

Nephrotic syndrome is a clinical syndrome characterized by massive proteinuria, called nephrotic range proteinuria (over 3.5 g per day in adults or 40 mg/m2 per hour in children), hypoalbuminemia, oncotic edema, and hyperlipidemia, with an increasing incidence over several years. Nephrotic syndrome carries severe morbidity and mortality risk. The main pathophysiological event in nephrotic syndrome is increased glomerular permeability due to immunological, paraneoplastic, genetic, or infective triggers. Because of the marked increase in the glomerular permeability to macromolecules and the associated urinary loss of albumins and hormone-binding proteins, many metabolic and endocrine abnormalities are present. Some of them are well known, such as overt or subclinical hypothyroidism, growth hormone depletion, lack of testosterone, vitamin D, and calcium deficiency. The exact prevalence of these disorders is unknown because of the complexity of the human endocrine system and the differences in their prevalence. This review aims to comprehensively analyze all potential endocrine and hormonal complications of nephrotic syndrome and, vice versa, possible kidney complications of endocrine diseases that might remain unrecognized in everyday clinical practice.

Pattern of venous thromboembolism in childhood idiopathic nephrotic syndrome

ABSTRACT Introduction Nephrotic syndrome (NS) is one of the most common childhood kidney diseases. Thromboembolic (TE) events are among the most serious complications of NS in children, with a reported prevalence of 1.8–5%. Venous thromboembolism (VTE) is the predominant type. Most cases of TE are clinically symptomatic, but some may be subclinical, thus, their true incidence may be underestimated. Studies on TE in childhood onset NS are few and varied, this prompted us to conduct the present study. Objective To study the pattern of thromboembolism in childhood INS. Patients and Methods This descriptive retrospective study included 225 pediatric patients with idiopathic NS (11 with TE events and 214 with no TE events) regularly following up in Alexandria University Children’s Hospital, Egypt from 2013 to 2023. Diagnosis of thromboembolism was based on clinical diagnosis and appropriate diagnostic imaging. Results The frequency of TE among our cohort was 4.9%.The median age of onset of the first TE event was 5.5 years. Most of the TE events (63.6%) occurred during the 1st 6 months of NS diagnosis. The total number of TE events was 15 events, and the most common site was cerebral sino-venous thrombosis (CSVT). The triglyceride levels were significantly higher in the TE event group. The median urinary protein/creatinine ratio was slightly higher in the TE event group. In the TE event group, 4 patients (36.4%) were steroid-resistant and only one of the 11 patients died. Conclusion In conclusion, TE events are not uncommon among INS children and most of the events occurred early during the disease. There was no significant relationship between the degree of proteinuria, serum albumin level, and the occurrence of TE events, while the level of triglycerides was significantly higher in patients who developed TE events.

Association of elevated circulating monocyte-platelet aggregates with hypercoagulability in patients with nephrotic syndrome

BackgroundHypercoagulability emerges as a central pathological feature and clinical complication in nephrotic syndrome. Increased platelet activation and aggregability are closely related to hypercoagulability in nephrotic syndrome. Monocyte-platelet aggregates (MPAs) have been proposed to represent a robust biomarker of platelet activation. The aim of this study was to investigate levels of the circulating MPAs and MPAs with the different monocyte subsets to evaluate the association of MPAs with hypercoagulability in nephrotic syndrome.MethodsThirty-two patients with nephrotic syndrome were enrolled. In addition, thirty-two healthy age and sex matched adult volunteers served as healthy controls. MPAs were identified by CD14 monocytes positive for CD41a platelets. The classical (CD14 + + CD16-, CM), the intermediate (CD14 + + CD16+, IM) and the non-classical (CD14 + CD16++, NCM) monocytes, as well as subset specific MPAs, were measured by flow cytometry.ResultsPatients with nephrotic syndrome showed a higher percentage of circulating MPAs as compared with healthy controls (p < 0.001). The percentages of MPAs with CM, IM, and NCM were higher than those of healthy controls (p = 0.012, p < 0.001 and p < 0.001, respectively). Circulating MPAs showed correlations with hypoalbuminemia (r=-0.85; p < 0.001), hypercholesterolemia (r = 0.54; p < 0.001), fibrinogen (r = 0.70; p < 0.001) and D-dimer (r = 0.37; p = 0.003), but not with hypertriglyceridemia in nephrotic syndrome. The AUC for the prediction of hypercoagulability in nephrotic syndrome using MPAs was 0.79 (95% CI 0.68–0.90, p < 0.001). The sensitivity of MPAs in predicting hypercoagulability was 0.71, and the specificity was 0.78.ConclusionIncreased MPAs were correlated with hypercoagulability in nephrotic syndrome. MPAs may serve as a potential biomarker for thrombophilic or hypercoagulable state and provide novel insight into the mechanisms of anticoagulation in nephrotic syndrome.

#1246 The impact of severe nephrotic syndrome on thyroid function

Abstract Background and Aims Nephrotic syndrome (NS) is a clinical condition characterized by massive urinary loss of proteins, mostly albumin, but also hormones and their carrier proteins among others. The most frequently reported hormonal complication is thyroid dysfunction. The study aimed to assess the frequency of thyroid dysfunction in NS and its association with carrier protein levels and indicators of disease severity. Method A case-control study was conducted involving patients with newly diagnosed or relapsed severe NS, defined as proteinuria &amp;gt; 3.5 g/day and serum albumin ≤ 2.5 g/dL (NS group), and patients without proteinuria (control group). The evaluation included thyroid hormone profiles, serum levels of carrier proteins (prealbumin – PAB, and thyroid-binding globulin – TBG), and markers reflecting the course of NS. Results Forty-two nephrotic and 40 matched non-proteinuric patients were enrolled. The NS group comprised 67% males with a mean age of 49 years and an average proteinuria of 8.9 g/day (Table 1). The leading cause of NS was minimal change disease (22 patients), followed by membranous nephropathy (11 patients). The other causes included: amyloidosis (3 patients: AL – 2 cases, A – 1 case), focal segmental glomerulosclerosis (2 patients) and lupus nephritis (1 case). In 5 cases, no histological diagnosis was made. Thyroid dysfunction secondary to NS was observed in the majority of patients, occurring 18-times more frequently than in the control group (67% vs 10%, OR = 18, 95% CI: 5.3-60.7). Euthyroid sick syndrome was the most commonly seen in NS (15 cases, 36%), followed by overt (8 cases, 19%) and subclinical hypothyroidism (5 cases, 12%). According to the current guidelines, levothyroxine supplementation was required in 11 patients (26% of the NS group, 36% of those with thyroid dysfunction). Serum TSH correlated inversely with PAB (R = −0.63, p &amp;lt; 0.001), and positively with TBG (R = 0.39, p = 0.010), while no relationships were found between carrier proteins and free hormones (fT3 or fT4). The only indicator of NS severity related to thyroid function was serum albumin. It correlated, however, only with TSH (R = −0.41, p = 0.007), not with free hormones. Additionally, neither histological type, nor clinical course of NS distinguished between euthyroidism, euthyroid sick syndrome, or hypothyroidism (Table 2). Conclusion Thyroid dysfunction is a common complication of severe NS. Although euthyroid sick syndrome predominates, the proportion of patients with hypothyroidism who may potentially require levothyroxine replacement therapy remains substantial.

Nephrotic Syndrome: From Pathophysiology to Novel Therapeutic Approaches.

Nephrotic edema stands out as one of the most common complications of nephrotic syndrome. The effective management of hypervolemia is paramount in addressing this condition. Initially, "the underfill hypothesis" suggested that proteinuria and hypoalbuminemia led to fluid extravasation into the interstitial space, causing the intravascular hypovolemia and activation of neurohormonal compensatory mechanisms, which increased the retention of salt and water. Consequently, the recommended management involved diuretics and human-albumin infusion. However, recent findings from human and animal studies have unveiled a kidney-limited sodium-reabsorption mechanism, attributed to the presence of various serine proteases in the tubular lumen-activating ENaC channels, thereby causing sodium reabsorption. There is currently no standardized guideline for diuretic therapy. In clinical practice, loop diuretics continue to be the preferred initial choice. It is noteworthy that patients often exhibit diuretic resistance due to various factors such as high-sodium diets, poor drug compliance, changes in pharmacokinetics or pharmacodynamics, kidney dysfunction, decreased renal flow, nephron remodeling and proteasuria. Considering these challenges, combining diuretics may be a rational approach to overcoming diuretic resistance. Despite the limited data available on diuretic treatment in nephrotic syndrome complicated by hypervolemia, ENaC blockers emerge as a potential add-on treatment for nephrotic edema.

Septic arthritis following mumps in a case of steroid dependent nephrotic syndrome: a case report

Nephrotic syndrome is a common renal disorder with an incidence of 20 to 40 per million population in developed countries. Children with nephrotic syndrome are especially susceptible to infections such as cellulitis, spontaneous bacterial peritonitis, and bacteremia. However, septic arthritis is an extremely rare complication in nephrotic syndrome. A 6-year-old girl with steroid dependent nephrotic syndrome relapsed following mumps parotitis and developed swelling of the right knee with restricted movements. Ultrasonography (USG) and magnetic resonance imaging (MRI) were suggestive of septic arthritis. The child responded to intravenous Vancomycin and Ceftazidime. We present a rare complication of nephrotic syndrome as septic arthritis, previously reported only once.

Thromboembolic phenomena in patients with nephrotic syndrome: pathophysiology, risk factors, prophylaxis and treatment.

Thromboembolic events resulting from disturbances in the body's balance of thrombotic and antithrombotic abilities are among the most life-threatening complications of nephrotic syndrome. Certain causes of nephrotic syndrome leave the patient particularly susceptible to thromboembolism. The severity of proteinuria and degree of hypoalbuminaemia are other common predictors of risk. Timely initiation of prophylactic therapy can help prevent morbidity and mortality associated with this complication in patients with nephrotic syndrome. The duration of treatment and choice of therapeutic agent depends on several factors, including the degree of hypoalbuminaemia, risk factors for thrombosis and risk of bleeding. This article reviews current understanding of the pathophysiology and risk factors for thromboembolism associated with nephrotic syndrome, and summarises recommendations and strategies for preventing and treating thromboembolic events in patients with nephrotic syndrome.

How to Choose the Right Treatment for Membranous Nephropathy.

Membranous nephropathy is an autoimmune disease affecting the glomeruli and is one of the most common causes of nephrotic syndrome. In the absence of any therapy, 35% of patients develop end-stage renal disease. The discovery of autoantibodies such as phospholipase A2 receptor 1, antithrombospondin and neural epidermal growth factor-like 1 protein has greatly helped us to understand the pathogenesis and enable the diagnosis of this disease and to guide its treatment. Depending on the complications of nephrotic syndrome, patients with this disease receive supportive treatment with diuretics, ACE inhibitors or angiotensin-receptor blockers, lipid-lowering agents and anticoagulants. After assessing the risk of progression of end-stage renal disease, patients receive immunosuppressive therapy with various drugs such as cyclophosphamide, steroids, calcineurin inhibitors or rituximab. Since immunosuppressive drugs can cause life-threatening side effects and up to 30% of patients do not respond to therapy, new therapeutic approaches with drugs such as adrenocorticotropic hormone, belimumab, anti-plasma cell antibodies or complement-guided drugs are currently being tested. However, special attention needs to be paid to the choice of therapy in secondary forms or in specific clinical contexts such as membranous disease in children, pregnant women and patients undergoing kidney transplantation.

Edema and the Risk of Thromboembolic Complications in Nephrotic Syndrome: A Cohort Study

Edema and the Risk of Thromboembolic Complications in Nephrotic Syndrome: A Cohort Study

Longitudinal Analysis of Prophylactic Anticoagulation in Primary Nephrotic Syndrome: Low Incidence of Thromboembolic Complications

Introduction: Thromboembolic events (TEEs) are a serious and potentially fatal complication of nephrotic syndrome (NS). Despite this, there is a lack of evidence examining the benefits of prophylactic anticoagulation (PAC) in NS. It was our objective to review the risk factors, rates of TEEs, and patterns of PAC in patients with primary NS, with the aim to provide a pragmatic approach to PAC in primary NS. Methods: This is a retrospective longitudinal cohort study of adult patients with primary NS. Included were as follows: biopsy-proven minimal change disease and focal segmental glomerulosclerosis (described as a combined podocytopathy cohort) plus membranous nephropathy (MN) over an 8-year period from a single centre. Anticoagulation practice, TEEs, and longer term outcomes were recorded. Results: Fifty-four patients with MN and 48 patients with podocytopathies were included. Baseline demographics and severity of NS were comparable. Those with MN were more likely to develop TEE 12 (22%) versus 4 (8%) (p = 0.027) though this difference was predominantly seen at index diagnosis. Only 2 patients developed TEEs during active incident NS. Rates of PAC were similar when comparing MN (53%) and podocytopathies (58%). Those with a serum albumin <20 g/L and HAS-BLED score <3 were most likely to receive PAC (22/30, 73% in MN vs. 21/30, 70% in podocytopathy). Warfarin was the most common agent used in MN cohort 18/26 (69%) versus prophylactic dose low-molecular-weight heparin in the podocytopathy cohort 12/28 (43%). Discussion/Conclusion: PAC practices applied in this cohort of patients were pragmatic and effective, with low TEE rates during active NS.

Analysis of 6 pediatric nephrotic syndrome cases with complications of cerebral sinovenous thrombosis and literature review.

Cerebral venous sinus thrombosis (CVST) is a rare but serious complication of nephrotic syndrome (NS) in children. To investigate the clinical characteristics of CVST in children with NS in order to timely diagnose this complication and reduce poor outcome. Collect and analyze clinical data and magnetic resonance venography (MRV) results of children with NS complicated with CVST. Data of 6 patients with NS complicated with CVST were collected. 4 of the patients were steroid-sensitive nephrotic syndrome (SSNS) and 2 were steroid-resistant nephrotic syndrome (SRNS). The occurrence of CVST was observed within a time frame ranging from 12 days to 3 years following the diagnosis of NS. One patient had two episodes of thrombosis in three years, while the other five patients had only one episode of thrombosis. All patients had proteinuria at the time of episode of thrombosis. All patients presented with headache, and three of them had strabismus, seizures, and transient blindness, respectively. Neurological examination was negative. All patients were diagnosed with CVST by MRV within 3-16 days of the onset of headache. Two patients had TRPC6 gene mutation. All patients had resolution of neurological symptoms after anticoagulation treatment. CVST may occur in the early stages of NS. There is currently a lack of specific diagnostic indicators to reliably identify the presence of CVST in patients with NS. Children with NS who have neurological symptoms should be promptly evaluated with imaging studies. Whether TRPC6 gene mutation is also a risk factor for CVST remains to be further studied.

Nutritional Management of Idiopathic Nephrotic Syndrome in Pediatric Age.

Nephrotic syndrome (NS) is a common pediatric disease characterized by a dysfunction in the glomerular filtration barrier that leads to protein, fluid, and nutrient loss in urine. Corticosteroid therapy is the conventional treatment in children. Long-term complications of NS and prolonged exposure to steroids affect bones, growth, and the cardiovascular system. Diet can play an important role in preventing these complications, but there is a scarcity of scientific literature about nutritional recommendations for children with NS. They need individualized nutrition choices not only during the acute phase of the disease but also during remission to prevent the progression of kidney damage. The correct management of diet in these children requires a multidisciplinary approach that involves family pediatricians, pediatric nephrologists, dietitians, and parents.

#2827 RISK FACTORS FOR VENOUS AND ARTERIAL THROMBOEMBOLIC COMPLICATIONS IN NEPHROTIC SYNDROME: A COHORT STUDY

Abstract Background and Aims Venous thromboembolic events (VTE) and arterial thromboembolic events (ATE) are serious complications of nephrotic syndrome (NS). Studies are needed to identify patients at high risk for VTE and ATE. We aimed to describe patient-related risk factors for VTE and ATE in a mixed population of nephrotic patients. Method This multicentre cohort study included adult NS patients with plasma albumin &amp;lt;30 g/l and urine albumin-creatinine ratio (uACR) &amp;gt;2,200 mg/g, who were hospitalized or followed at an outpatient clinic in the Central Denmark Region between 2014-2018. Using computerized data extraction from medical files, patients were identified and followed until dialysis, transplantation, or end of study. We recorded comorbidities, family history, renal parameters and, histological diagnosis at index time as well as, renal parameters and medication at the time of VTE/ATE event. Categorical and continues data were compared using a risk difference and mean difference respectively. The incidence of event is presented as incidence rate. Results Among 531 included patients, 22 patients had their first VTE and 46 their first ATE within the first observation year (median time to event VTE 0.8 vs. ATE 0.9 years). Incidence rates were 11 per 1000 person-years (95% CI: 7-17) for VTE and 24 (95% CI: 18-32) for ATE. Plasma-albumin levels (27 g/l) were identical in the VTE and ATE group at event time, but eGFR was lower (Table 1), and uACR was higher in the ATE group (median uACR; VTE 1055 mg/g vs. ATE 2752 mg/g). Hypercholesterolemia was more prevalent among patients with VTE, and they were more often on corticosteroids than patients with ATE. Diabetes, hypertension, and heart failure was more prevalent at baseline in patients with ATE resulting in an increased CHADS-VASC score. Mortality was higher among patients with ATE (83%) than VTE patients (32%). Conclusion Patients with NS have a high risk of VTE and ATE. Corticosteroid use was more common among patients with VTE than ATE. ATE was associated with a higher uACR, higher CHADS2-VASC score, and increased mortality compared to patients with VTE.

#4949 COMBINED ORAL DIURETICS: A BETTER ALTERNATIVE FOR NEPHROTIC EDEMA THAN INTRAVENOUS FUROSEMIDE?

Abstract Background and Aims Edema is a serious complication of nephrotic syndrome and is the main reason why patients usually address to a doctor. There is no guideline on managing nephrotic edema. Besides non pharmacological interventions such as sodium and water restrictions, most doctors would choose high doses of intravenous furosemide as the first option, but still many patients fail to properly decrease their volume overload, as they become diuretic resistant. Amiloride, an ENaC mediated diuretic, is an optimistic management option, especially when used with other diuretics. The aim of the present study was to assess the non inferiority of the combined oral diuretics furosemide and the fixed combination of hydrochlorothiazide/amiloride diuretics with intravenous furosemide in diuretic resistant nephrotic edema. Method We conducted a prospective randomized trial in 22 patients with diuretic resistant nephrotic edema. Based on a computer-generated randomization we assigned patients to receive either intravenous furosemide (40 mg bolus and then continuous administration of 5 mg/h) or oral furosemide (40 mg/day) and hydrochlorothiazide/amiloride (50/5 mg/day). Clinical and laboratory measurements were performed daily, for five days (body weight, urinary output, blood pressure and hydration status by bioimpedance twice, creatinine, urea, albumin, hematocrit, Na, K, Ca, Mg, bicarbonate, pH). The primary outcome was weight and hydration status change from baseline to day 5. Secondary outcomes were safety outcomes (low blood pressure, severe dyselectrolytemia, acute kidney injury or aggravated hypervolemia). Results The patients were equally distributed between the two groups. Mean age was 47,77±15,97 (54,5% females and 45,5% males). Half of the patients had membranous nephropathy (45,5%), followed by minimal change disease (22,7%) and lupus nephritis (9,1%). 86,4% of patients had their first episode of nephrotic edema. The mean weight decrease was of significantly larger magnitude in the combined oral diuretics group compared with the intravenous furosemide group (-7,97±2,83 [SD] vs -4,5±2,6 [SD] kg; p = 0,018). Although the increase in 24-hour urine sodium excretion was higher in combined oral diuretics as compared to intravenous furosemide group, this increment was not statistically significant different (26,79±33,48 [SD] vs 16,04±42,81 mmol/24 h [SD]; p = 0,5). Mean values for changes in systolic and diastolic BP, 24-hour urine volume, hydration status measured by bioimpedance were not significantly different between the two groups. A total of 5 patients could not be followed through, 4 in the intravenous furosemide (two patients experienced low blood, one patient had no response to iv furosemide and one patient suffered from insomnia due to iv pump) and one patient in the oral combination of diuretics group had severe hyperkalemia (&amp;gt;6,5 mmol/l). Conclusion Combined oral diuretics with furosemide, amiloride and hydrochlorothiazide is more effective and safer than intravenous furosemide for the treatment of refractory nephrotic edema. These results make amiloride a promising diuretic and further trials with larger sample sizes and longer follow-up are needed in this regard.

Comparison of profile and short-term outcome of acute kidney injury between steroid sensitive and steroid resistant nephrotic syndrome

Background: Acute kidney injury (AKI), a severe complication of nephrotic syndrome (NS) is being more prevalent in recent times. Objectives were: 1) Determine incidence, etiology, short term outcome of AKI in children hospitalised with NS. 2) Compare above variables in steroid sensitive nephrotic syndrome (SSNS) versus steroid resistant nephrotic syndrome (SRNS). Methods: Prospective observational study over 18 months including all consecutive nephrotics hospitalized with AKI. AKI defined according to KDIGO criteria with baseline creatinine taken as lowest value in last 6 months/ nadir during stay. Secondary NS were excluded. Demographics, clinical features, labs, hospital course, treatment and follow up at 3 months were recorded. SSNS and SRNS were compared. Results: The incidence of AKI in hospitalised nephrotics (30/304) was 9.8%, 30 patients (16 boys) with mean age 4.08 years (± 4.04 SD). Common etiologies of AKI were infection (60%), nephrotoxic drugs, hypovolemia, and thrombosis in decreasing order. Nephrotics developing AKI had a longer hospital stay versus those without AKI (p&lt;0.001). The 2/30 patients died (6%), 10/30 (33.3%) required PICU, 7/30 (26%) needed RRT. Among discharged patients 4/28(14.28%) had persistent deranged renal functions at 3 months follow up, all of whom belonged to SRNS category. Comparison of 14 patients in SSNS with 16 in SRNS showed UTI (31.3%), drugs (25%), systemic infection (31.3%), thrombosis (12.5%) as etiologies in SRNS. Systemic infection (42.9%), drugs (21.4%), UTI (14.3%) and hypovolemia (21.4%) were causes in SSNS. Mortality rate, need for PICU (p=1.0), RRT (p=1.0) was similar (6%,37.5%, 25%) Vs (7%,28.5%, 21.4%). Conclusions: AKI is seen in up to a tenth of children with NS equally in SSNS and SRNS. While etiology and severity of AKI in the 2 groups is similar, short-term outcome in SRNS is more ominous.

Iliofemoral thrombosis in a patient with recurrent nephrotic syndrome

Nephrotic syndrome is one of the most common glomerulopathies in children, accompanied by a high risk of thrombosis due to hypoalbuminemia, hypovolemia, hyperlipidemia, hyperfibrinogenemia, and antithrombin III deficiency. The article describes a clinical case of iliofemoral thrombosis in a 16-year-old boy with recurrent nephrotic syndrome and primary thrombophilia (heterozygote F5 — Leiden mutation) was diagnosed. The presented clinical observation indicates the multifactorial origin of thrombotic complications in nephrotic syndrome, caused by a combination of an imbalance between the proand anticoagulant components of the blood coagulation system and individual risk factors (severity of proteinuria, hypoalbuminemia, comorbidity, hereditary thrombophilia), and therefore further study is needed to determine the tactics of prevention and treatment.

Posterior reversible encephalopathy syndrome: A conundrum of nephrotic syndrome complication

Nephrotic syndrome is a kidney disease with proteinuria, hypoalbuminemia, and edema. One rare, potentially life-threatening complication of nephrotic syndrome is posterior reversible encephalopathy syndrome (PRES). Sudden episodes of neurological symptoms such as headache, confusion, seizures, or focal neurological deficits with radiological findings of white matter abnormalities in the parietal and occipital lobes characterize it. Multiple factors predispose an individual with nephrotic syndrome to PRES, such as uncontrolled hypertension, reduced serum albumin levels, administration of drugs (cyclosporine, tacrolimus), anasarca, disturbed body fluid status and renal insufficiency. Here, we report a case of PRES in a seven-year-old girl with nephrotic syndrome who presented with high blood pressure while admitted to the ward. Her neurological symptom rapidly recovered after the control of hypertension. Recurrence of acute severe hypertension, nephrotic state (edema/ hypoalbuminemia), and renal insufficiency may lead to recurrent PRES. Thus, early treatment of trigger factors, especially of hypertension, is vital to reduce the episodes of PRES.

Research progress of nephrotic syndrome accompanied by thromboembolism.

Thromboembolism (TE) is a common and serious complication of nephrotic syndrome (NS). NS is associated with hypercoagulability, which may be induced by changes in coagulation, anticoagulant, and fibrinolytic factors. Moreover, accumulating evidence supports the hypothesis that the complex interactions between genetic and acquired risk factors in TE should be considered and that genetic susceptibility should not be ignored. Extracellular vesicles (EVs) also play unique roles. Further research on EVs may provide new insights into the discovery and treatment of TE associated with NS. The occurrence of NS accompanied by TE may be associated with various risk factors. Preventive anticoagulant therapy can not only reduce the risk of TE in patients but also aggravate the risk of bleeding. Heparin and vitamin K antagonists (VKAs), traditional anticoagulant drugs, have been extensively applied in the prevention and treatment of thromboembolic diseases, and emerging direct oral anticoagulants (DOACs) also provide an alternative choice. Owing to the particularity of NS, the safe application of DOACs still needs to be addressed. This review aimed to comprehensively describe the pathophysiology of TE in NS, as well as analyze the associated risk factors, the opportunity for preventive anticoagulation, and current anticoagulant information.

Случай острого инфаркта миокарда у молодого пациента с впервые выявленным нефротическим синдромом

Thromboembolic complications in nephrotic syndrome (NS) are frequently encountered in the practice of a nephrologist and in many cases determine the course and outcome of diseases. The article presents a clinical case of acute ST-segment elevation myocardial infarction with Q tooth of posterior basal, lateral localization in a 36-year-old patient with a newly diagnosed nephrotic syndrome. In the young patient without a history of cardiovascular risk factors, coronary angiography revealed signs of progressive atherosclerotic stenosis of the coronary arteries, and the cause of MI was thrombotic occlusion of the enveloping branch of the left coronary artery. This clinical case required a more detailed study; the examination revealed a set of factors that led to MI in this young patient.