9 articles
Scleroderma Renal Crisis (SRC) is a life-threatening complication of systemic sclerosis (SSc), traditionally associated with anti-RNA polymerase III antibodies, corticosteroid use, and diffuse skin involvement. However, the role of COVID-19 as a potential trigger for SRC remains poorly understood. This study explores the occurrence of COVID-19-associated SRC, focusing on its clinical presentation, underlying risk factors, and outcomes.
We present a case series of two unvaccinated patients with systemic sclerosis who developed SRC following COVID-19 infection, despite the absence of traditional risk factors. Clinical features, laboratory findings, renal histopathology, and disease progression were analyzed to assess potential mechanisms linking SARS-CoV-2 infection to SRC onset. Both patients developed abrupt-onset malignant hypertension and acute kidney injury after supporting the COVID-19. Neither patient had a history of corticosteroid use or known anti-RNA polymerase III positivity, suggesting an alternative mechanism of SRC activation. Notably, both cases had pre-existing renal anomalies (renal developmental abnormality and prior nephrectomy), which may have contributed to increased susceptibility. Despite aggressive management, both patients developed dialysis-dependent renal failure and succumbed to SRC-related complications.
Our findings highlight COVID-19 as a potential trigger for SRC, possibly through endothelial dysfunction, inflammatory cytokine storms, and renal microangiopathy. The presence of pre-existing kidney conditions may further predispose SSc patients to SRC following SARS-CoV-2 infection. Additionally, the lack of vaccination in these cases raises the question of whether COVID-19 immunization could reduce SRC risk. Further research is needed to elucidate the pathophysiology, risk stratification, and long-term outcomes of COVID-19-associated SRC, as well as the role of vaccination in prevention.
Chronic kidney disease (CKD) is a major and growing global public health problem, contributing to significant morbidity, mortality, and financial strain on healthcare systems. Despite available preventive measures, CKD often remains underdiagnosed and insufficiently addressed by health policies worldwide.
A literature review was conducted using the MEDLINE electronic database via PubMed, Scopus, and the HINARI (Research4Life) program, focusing on studies published since 2001. Search terms included “primary care”, “chronic kidney disease”, “chronic kidney disease public health”, and “chronic kidney disease costs”. Original articles, meta-analyses, and systematic reviews were included, with English-language articles prioritized. Bibliographic references of selected publications were also examined to identify additional relevant studies.
CKD affects approximately 700-850 million people globally, with rising prevalence and mortality rates, especially in low- and middle-income countries. The disease disproportionately burdens vulnerable populations and health systems due to high direct and indirect costs, particularly for advanced-stage care. While cost-effective prevention and early detection strategies are available, their implementation is uneven, and policy responses have historically lagged. Successful national initiatives demonstrate that early intervention and integrated care can reduce the incidence and economic impact of end-stage kidney disease.
CKD is a preventable, yet increasingly prevalent disease that requires urgent public health action. Prioritizing early detection, integrated care models, and policy reforms can significantly curb its global burden. Coordinated efforts at international, national, and local levels are essential to translate existing knowledge into effective practice and reduce the societal and financial costs of CKD.
The definition of metabolic syndrome is not yet consistent. However, many studies have been conducted in the latest decades about the effect of increased uric acid on metabolic syndrome development. Large epidemiological studies on the association between hyperuricemia and MS showed that increased concentration of serum urea is often observed in subjects with metabolic syndrome. The aim of the study was to characterize specific dysmetabolic changes and features of extraarticular evolution in patients with gout.
A descriptive study was conducted that included 501 patients with gout. The mean age of gout (423 men and 78 women) was 49.2 (36.9; 59.9). The diagnosis of gout was established according to the classification criteria for gout ACR/EULAR 2015. The raw data was processed in SPSS version 26.0.
According to our data, the highest severity of obesity and LDL-cholesterol was detected in those with tophaceous gout, which also caused an increase in the frequency of high blood pressure and type 2 diabetes, with age differences in the frequency of detection of metabolic syndrome and insulin resistance. Our data have noted that serum levels of uric acid correlated with the risk of developing both metabolic syndrome as well as its components - obesity, hypertension, and dyslipidemia, but inversely correlated with hyperglycemia.
Gout is associated with a severe lipid metabolism dysfunction, significantly increasing the rate of metabolic syndrome especially among patients with chronic tophaceous gout, than in the group of patients with gout under the age of 59 years. On the other hand, in patients with the onset of gout who are ≤59 years lipid metabolism disorders occur significantly earlier than in patients with the onset of gout at the age of ≥60 years.
The incidence and prevalence of gout have increased worldwide in recent decades. Scientists at the Rochester Epidemiology Project (MN, USA) have seen a two-fold increase in the incidence of primary gout (patients without diuretic exposure) over a 20-year period, which ended in 1996. The increase of incidence may be related due to the difficulty and often unsatisfactory treatment options. The aim of the study was to systematize the recommendations on dietary treatment, and medication for patients with gout.
An analytical, qualitative, and secondary study was performed in the form of a synthesis article. 115 sources were identified and analyzed; from this list, 44 sources were selected according to the impact score during the publication period and according to the level of recommendations.
44 articles were included. Most studies were small, retrospective analyses performed in single centers, with concerns for bias. Eleven studies (including five randomized controlled trials) reported improved patient outcomes following pharmacological interventions with known efficacy in gout, including allopurinol, prednisolone, NSAIDs and anakinra. Eight studies reported improved outcomes associated with non-pharmacological interventions: inpatient rheumatology consultation and a hospital gout management protocol. No studies to date have prospectively evaluated strategies designed to prevent re-admissions of patients hospitalized for gout flares.
Urate crystals is completely soluble when we can lower the serum level of uric acid to normal values, but this often requires long-term treatment. The early onset of rehabilitation of affected joints helps to reduce the articular inflammatory process, the pain syndrome and it delays the progression of the underlying pathology while improving the quality of life in patients with gout. Further research is needed to enable healthcare providers to individualize and optimize gout treatment strategies, ensuring that patients with gout receive effective, safe, and high-quality care.
Vitamin D plays an important role in maintaining musculoskeletal health. As the glomerular filtration rate decreases, vitamin D deficiency also occurs. The aim of this paper is to highlight the level of vitamin D depending on the stage of chronic kidney disease.
A structured search was performed in the PubMed, Scopus and HINARI databases, where the relevant articles have been taken into account, published in the last 20 years. The search terms used (in English) were: „vitamin D deficiency”, „pathogenesis of vitamin D”, ”the impact of vitamin D in chronic kidney disease”, „chronic kidney disease”.
Several studies have shown that the change in vitamin D levels is dependent to the decrease of glomerular filtration rate. The lowest serum vitamin D concentration was observed in stage 5 of chronic kidney disease. Vitamin D deficiency occurs due to a decrease in the number of nephrons and a decrease in the number of proximal tubular cells that absorb vitamin D (25 (OH) D) to be subsequently hydroxylated to its active form by 1α-hydroxylase.
Patients with vitamin D-deficient due to chronic kidney disease have an increased risk of decreased bone mineral density and multiple fractures.
Due to the heterogeneous nature of systemic sclerosis, it is difficult to predict disease progression and complications. Despite the discovery of novel autoantibodies associated with systemic sclerosis (SSc), there is an unmet need for biomarkers for diagnosis, disease progression, and response to treatment.
An analytical, qualitative study was performed with a narrative review of literature in the form of a synthesis article. Relevant primary sources published in 2020-2022 were identified and selected, using data extraction and analysis.
Anti-citrullinated protein/peptide antibody could be useful in identifying patients with a more prominent joint disease. Of most interest, the anti-carbamylated protein antibodies (anti-CarP) could be a relevant biomarker related to fibrotic skin and lung disease. Positive anti-RNA (Ribonucleic acid) polymerase III antibody and antinuclear antibodies (ANA) negativity were significantly associated with GAVE (gastral antral vascular ectasia). Autoantibodies against telomeres may help identify systemic sclerosis with lung disease. Osteopontin links myeloid activation and disease progression in systemic sclerosis. CTRP (C1q tumor necrosis factor-related proteins) 9 protein levels may be biomarker of lung disease severity. CD (cluster differentiation) 21-low B cells are linked to vascular damage. L-tyrosine, L-tryptophan, and 1-methyl-adenosine distinguished healthy controls from SSc patients. L-leucine, L-isoleucine, xanthosine, and adenosine monophosphate differentiated between progressing and stable SSc-ILD. CECs (circulating endothelial cells) are a direct indicator of systemic vascular damage. Levels of the protein, galectin-3, are associated with heart involvement in people with systemic sclerosis. Low levels of the galectin-10 protein (Gal-10) in scleroderma associate with inflammation and vascular changes in the lungs, leading to pulmonary arterial hypertension (PAH). High levels of the CD146 protein may be a potential biomarker in identifying people with systemic sclerosis. Blood levels of the protein endocan increased in scleroderma patients who are at risk for pulmonary arterial hypertension . FLCs (free light chain) could be employed as useful potential biomarker of early diagnosis and to follow disease activity.
Novel discovered biomarkers could predict disease development, activity, and severity of diverse organ involvement, predict risk of complications of systemic sclerosis.
Description of two clinical cases with gout and renal involvement, one male and one female, which were hospitalized in the „Timofei Mosneaga” Republican Clinical Hospital and Municipal Clinical Hospital „Saint Trinity” in 2021.
The male patient was hospitalized in a serious condition, being drowsy, disoriented and with bradyphrenia. Patient complained of dyspnea at mild exertion, severe fatigue, 5-day anuria and generalized edema. From the history collected from relatives, it was discovered that the patient has been diagnosed with gout a few years ago. The female patient has been hospitalized in the Nephrology department of the Republican Clinical Hospital „Timofei Moşneaga” for comprehensive evaluation. Her complaints: low back pain, dysuria, nocturia, moderate ankle edema, oliguria, marked asthenia, paresthesia.
In women, primary renal damage is more common until the onset of menopause. After the onset of menopause, there is primarily joint damage, then kidney damage, or this process develops simultaneously (kidney and joint damage). In males due to hyperuricemia, there is joint damage, which later is associated with gouty nephropathy or kidney and joint involvement evolve paralleled.
PsA are included in the group of HLA-B27-associated joint diseases, united in the group of seronegative spondylitis (SSA). At the same time, this disease differs from ankylosing spondylitis and other spondylitis with a particularly diverse clinical picture and the existence of only the syndromes inherent in it, for example, intermittent synovitis, palindromic rheumatism or mutilating arthritis.
Purpose of the study
Research of clinical heterogeneity of early psoriatic arthritis and the possibility of early diagnosis.
The current study included 104 patients with PsA who were admitted to the rheumatology and arthrology departments of the IMSP Republican Clinical Hospital „Timofei Moşneaga” from 2003 to October 2021.
The frequency of expression of individual clinico-anatomical variants of joint syndrome was different in patients with PsA-e and PsA-t (in PsA-e compared to PsA-t, the oligoarticular variant was significantly more likely to be observed (43.1% and 19%, respectively, p=0.01) and less often the variant of spondyloarthritis (7.8% and 19%, p=0.1), while the variant of polyarthritis (33.3% and 38%, p = 0,6) and distal interphalangeal (15,7% and 15%, p=0,9) were detected with the same frequency, as regards the mutilating variant, this was observed only in PsA-t.
The early stage of psoriatic arthritis is characterized by pronounced heterogeneity of manifestations of joint syndrome and damage to the tendon-ligament apparatus. In PsA-e oligoarthritis and polyarticular variants are the most common, less often - distal interphalangeal and spondyloarthritic. In the first 3 months after the onset of clinical manifestations of PsA, oligoarthritis was observed in 75.4% of patients and polyarthritis in 14% (p=0.0001), and after 6 months - 63% and 26.6% respectively (p=0.001). With a progression of the duration of the disease, the number of patients with arthritis increased, and by the end of the 2nd year was determined in 47.6% of patients, and oligoarthritis - in 28.6%.
To date, clinical manifestations, laboratory changes and the results of instrumental examinations of the joints and spine in axial seronegative spondyloarthritis (aSpA) caused by Chlamydia trachomatis have not been fully elucidated.
Purpose of the study: evaluation of clinical manifestations features, diagnosis, and evolution of seronegative spondyloarthritis associated with Chlamydia trachomatis infection.
Objectives of the study: To compare clinical manifestations, changes in laboratory parameters, results of instrumental examinations of the joints and spine in seronegative spondyloarthritis, the axial, peripheral, and mixed form. To appreciate the significance of Chlamydia trachomatis in the development of SpA by detecting the presence of DNA using the polymerase chain reaction (PCR) in real time and by isothermal amplification of NASBA-PCR (Nucleic acid sequence-based amplification).
During 2015-2021 were examined 138 patients with SpA hospitalized in the Republican Clinical Hospital „Timofei Moşneaga”. Chlamydia trachomatis in the form of monoinfection was detected in 87 (6.3%) patients, of which 52 (59.8%) were women and 35 (40.2%) men.
The results of the diagnosis of Chlamydia trachomatis infection in patients with arthritis: Chlamydia trachomatis infection was detected in 78 (89.7%) out of 87 patients examined by PCR, and in 9 (10.3%) cases by ELISA. The peripheral form begins mainly with inflammation of the joints of the lower extremities (81.8%), of which the knee joints are mainly involved in the pathological process (63.6%). SpA axial form associated with Chlamydia trachomatis infection occurs mainly in young men (85.7%). In more than half of the patients, large joints participate in the pathological process (58.8%), especially the lower extremities. The axial variant of the SpA can begin with an injury in any part of the spine.
SpA associated with Chlamydia trachomatis infection has more expressed clinical, laboratory and instrumental manifestations both in the onset and in the advanced stage of the disease.