High-frequency plasma exchange therapy for immunocompromised, type I crescentic glomerulonephritis complicated with IgA nephropathy: A case report and literature review.

RATIONALE: Anti-glomerular basement membrane (anti-GBM) disease has been reported to coexist with other immune-mediated glomerular disorders, including antineutrophil cytoplasmic autoantibody positive glomerulonephritis and membranous glomerulopathy. It is well known that anti-GBM disease often manifests as type I crescentic glomerulonephritis on renal biopsy. However, concurrent cases of both type I crescentic glomerulonephritis and IgA nephropathy are rare. PATIENT CONCERNS: We report the case of a 40-years-old woman with microscopic hematuria, mild proteinuria and an immunocompromised status. Laboratory data revealed serum creatinine showed progressive progress, suddenly rising from the normal range to 316.2µmol/L within 4 months. The CD4 lymphocyte count was 0.274 × 109/L (reference value 0.35-1.82 × 109/L). The anti-GBM antibody titer was 192.4 IU/mL (reference range: <20 RU/mL). DIAGNOSES: Renal biopsy was performed after admission. The pathological diagnosis was type I crescentic glomerulonephritis, IgA nephropathy, and clinical anti-GBM disease. INTERVENTIONS: The patient was seriously ill on admission and progressed rapidly. Combined with poor immune function, we immediately initiated high-frequency plasma exchange (PE). In addition, to avoid rebound of antibody levels, PE was performed for 5 times. Follow-up treatment was combined with standard-dose corticosteroids and cyclophosphamide. OUTCOMES: The patient was followed up for 1 year. On the last visit, her serum creatinine decreased to 103.5µmol/L, anti-GBM antibody remained negative, and proteinuria and hematuria disappeared. LESSONS: This case illustrates that when crescentic nephritis or anti-GBM disease is combined with other immune diseases, especially when the immune function is extremely low, if the application of high-dose steroid shocks may induce fatal infections, to some extent high frequency PE has certain advantages.

A Meta-Analysis and Cohort Study of Histopathologic and Clinical Outcomes in ANCA-Negative versus -Positive Vasculitis.

BACKGROUND: ANCA-negative pauci-immune glomerulonephritis (PIGN) represents a rare and often under-studied subgroup of the vasculitides. This study aims to investigate differences in the clinical phenotype, renal histological features, and clinical outcomes of patients with PIGN, with and without serum ANCA positivity. METHODS: A cohort of biopsy-proven PIGN with and without detectable circulating ANCA was constructed from a single center between 2006 and 2016. Primary outcomes compared clinical presentation and histopathological features according to ANCA status, with multivariate Cox regression to compare mortality and ESKD. A systematic review and meta-analysis of the published literature was undertaken. RESULTS: In our cohort of 146 patients, 22% (n=32) had ANCA-negative disease, with a comparatively younger mean age at diagnosis; 51.4 versus 65.6 years (P<0.001). In total, 14 studies, inclusive of our cohort, were eligible for meta-analysis, totaling 301 patients who were ANCA negative. Those with ANCA-negative disease tended to have fewer extrarenal symptoms and a higher frequency of renal-limited disease, but both failed to reach statistical significance (P=0.92 and P=0.07). The risk of ESKD was significantly higher in seronegative disease (RR, 2.28; 95% confidence interval, 1.42 to 3.65; P<0.001), reflecting our experience, with a fivefold increased risk of ESKD in ANCA-negative disease (P<0.001). No significant difference in the chronicity of histopathological findings was seen and the meta-analysis showed no difference in morality (RR, 1.22; 95% confidence interval, 0.63 to 2.38; P=0.55). CONCLUSION: Our findings demonstrate that ANCA-negative PIGN presents in younger patients, with fewer extrarenal manifestations and higher ESKD risk, despite a lack of difference in histopathology. This study provides the impetus for further research into the pathogenesis, treatment response, and duration of immunotherapy in ANCA-negative disease. We suggest that the absence of positive ANCA serology should not discourage treatment and for clinical trials to include patients who are ANCA negative.

New and old approaches to nutritional management of acute and chronic glomerulonephritis.

PURPOSE OF REVIEW: It has been well published that a low protein diet (0.6-0.8 g/kg/day) is optimal for nutritional management of chronic kidney disease and with care be used without inducing protein malnutrition. RECENT FINDINGS: Though care with this approach must be demonstrated in patients with end-stage renal disease and with prominent protein energy wasting, another category of renal patient exists for whom dietary recommendations need more exploration. The Kidney Disease Improving Global Outcomes consortium, actually identifies renal disease as those patients with reduced filtration and those with excessive proteinuria excretion. Proteinuria, indeed, has proven to be a serious marker predisposing renal patients to atherosclerotic heart disease, venous thromboembolism, cerebrovascular accidents, and overall mortality. We discuss what is known about nutritional strategies to curb proteinuria and control inflammation in the setting of glomerulonephritis. SUMMARY: While this area of management of a set of conditions maybe nascent, it has the potential to provide incredible breakthroughs in nutritional management of auto immune diseases of the kidney specifically and the body writ large.

Clinicopathological characteristics and outcome predictors of anti-glomerular basement membrane glomerulonephritis.

OBJECTIVE: To explore the clinicopathological features of anti-glomerular basement membrane (anti-GBM) glomerulonephritis (anti-GBM-GN) and the prognostic values of clinical and laboratory indicators at diagnosis on renal and patient survival. METHODS: A total of 76 patients (34 males and 42 females) with anti-GBM-GN who were hospitalized in the First Affiliated Hospital of Nanjing Medical University between January 2010 and June 2021 were included in this study. The baseline clinical features, histopathological data from renal biopsies, and predictors of renal and patient survival were retrospectively analyzed. RESULTS: Among the 76 patients, the median serum creatinine at diagnosis was 618.0 (350.98, 888.25) µmol/L and the median estimated glomerular filtration rate (eGFR) was 6.62 (4.39, 14.41) mL/min. Of these 76 patients, 55 (72.4%) received initial kidney replacement therapy (KRT) and 39 (51.3%) received plasma exchange or double-filtered plasmapheresis (DFPP). During a median follow-up duration of 28.5 (6.0, 71.8) months, 53 (69.7%) patients progressed to kidney failure with replacement therapy (KFRT) and received maintenance dialysis. Initial KRT (HR = 3.48, 95% CI = 1.22-9.97, p = 0.020) was a significant risk factor for renal survival. During the follow-up, 49 (64.5%) of 76 patients survived. Age (≥60 years, HR = 4.13, 95% CI = 1.65-10.38, p = 0.003) and initial KRT (HR = 2.87, 95% CI = 1.01-8.14, p = 0.047) were predictive of patient survival. CONCLUSIONS: Among patients with anti-GBM-GN, initial KRT at presentation was predictive of KFRT while older age and initial KRT were associated with higher all-cause mortality.

More difficult still: Treating severe rapidly progressive glomerulonephritis in the context of COVID-19 pneumonia.

We present the case of a male patient with severe SARS-CoV-2 pneumonia, with simultaneous onset of p-ANCA positive rapidly progressive glomerulonephritis. We discuss the different therapeutic possibilities, emphasising the appropriateness of their administration according to the time in the course of the infection.

Rapidly progressive glomerulonephritis in two Zambian children: a case report.

Rapidly progressive glomerulonephritis (RPGN) is a rare syndrome which is marked by a sudden rise in serum creatinine and the presence of crescents on renal biopsy. If appropriate and timely treatment is not instituted, as many as 90% of affected patients may develop End Stage Renal Disease (ESRD). There is only limited access to renal replacement therapy in many low resource countries, thus it is important that awareness of this entity is raised. We narrate the clinical course of two children who were admitted with rising serum creatinine, hypertension and haematuria and who were subsequently diagnosed with crescentic glomerulonephritis on biopsy. Despite having received immunosuppressive therapy, both children had a poor renal outcome, perhaps due to delays in institution of appropriate treatment. It is imperative that all clinicians who manage children are made aware of this clinical syndrome so that timely referrals to nephrology are done. This will help to improve renal outcomes.

The presentation, etiologies, pathophysiology, and treatment of pulmonary renal syndrome: A review of the literature.

Pulmonary renal syndrome (PRS) is a constellation of different disorders that cause both rapidly progressive glomerulonephritis and diffuse alveolar hemorrhage. While antineutrophil cytoplasmic antibody associated vasculitis and anti-glomerular basement membrane disease are the predominant causes of PRS, numerous other mechanisms have been shown to cause this syndrome, including thrombotic microangiopathies, drug exposures, and infections, among others. This syndrome has high morbidity and mortality, and early diagnosis and treatment is imperative to improve outcomes. Treatment generally involves glucocorticoids and immunosuppressive agents, but treatment targeted to the underlying disorder can improve outcomes and mitigate side effects. Familiarity with the wide range of possible causes of PRS can aid the clinician in workup, diagnosis and early initiation of treatment. This review provides a summary of the clinical presentation, etiologies, pathophysiology, and treatment of PRS.

Monoclonal Gammopathy-Related Kidney Diseases.

Monoclonal gammopathies occur secondary to a broad range of clonal B lymphocyte or plasma cell disorders, producing either whole or truncated monoclonal immunoglobulins. The kidneys are often affected by these monoclonal proteins, and, although not mutually exclusive, can involve the glomeruli, tubules, interstitium, and vasculature. The nephrotoxic potential of these monoclonal proteins is dependent on a variety of physicochemical characteristics that are responsible for the diverse clinicopathologic manifestations, including glomerular diseases with organized deposits, glomerular diseases with granular deposits, and other lesions, such as C3 glomerulopathy and thrombotic microangiopathy with unique pathophysiologic features. The diseases that involve primarily the tubulointerstitial and vascular compartments are light chain cast nephropathy, light chain proximal tubulopathy, crystal-storing histiocytosis, and crystalglobulin-induced nephropathy with distinct acute and chronic clinicopathologic features. The diagnosis of a monoclonal gammopathy-related kidney disease is established by identification of an underlying active or more commonly, low-grade hematologic malignancy, serologic evidence of a monoclonal gammopathy when detectable, and most importantly, monoclonal protein-induced pathologic lesions seen in a kidney biopsy, confirming the association with the monoclonal protein. Establishing a diagnosis may be challenging at times, particularly in the absence of an overt hematologic malignancy, with or without monoclonal gammopathy, such as proliferative glomerulonephritis with monoclonal immunoglobulin deposits. Overall, the treatment is directed against the underlying hematologic disorder and the potential source of the monoclonal protein.

Implantation of dedifferentiated fat cells ameliorated antineutrophil cytoplasmic antibody glomerulonephritis by immunosuppression and increases in tumor necrosis factor-stimulated gene-6.

INTRODUCTION: The implantation of dedifferentiated fat (DFAT) cells has been shown to exert immunosuppressive effects. To develop DFAT cell therapy for antineutrophil cytoplasmic antibody (ANCA) glomerulonephritis, the effects of the implantation of DFAT cells on ANCA glomerulonephritis were investigated in mice. METHODS: PKH26-labeled DFAT cells (105) were infused through the posterior orbital venous plexus to investigate delivery of DFAT cells in ICR mice. DFAT cells (105) were also implanted in SCG mice as a model for ANCA glomerulonephritis. Expression of tumor necrosis factor-stimulated gene-6 (TSG-6) mRNA and protein in kidney was evaluated, and the expression of microRNAs associated with TSG-6 in plasma, lung and kidney was analyzed. Expressions of CD44, prostaglandin (PG) E2, interleukin (IL)-10, IL-1ß, tumor necrosis factor (TNF)-α mRNAs, C-C motif chemokine ligand 17 (CCL-17) and monocyte chemoattractant protein (MCP)-1 proteins were measured in kidney from SCG mice implanted with DFAT cells. RESULTS: After their intravenous infusion, almost all DFAT cells were trapped in the lung and not delivered into the kidney. Implantation of DFAT cells in SCG mice suppressed glomerular crescent formation, decreased urinary protein excretions and increased expression of TSG-6 mRNA, protein and immunostaining in kidney from these mice. Increased expression of microRNA 23b-3p in plasma, kidney and lung; decreased expression of CD44 mRNA; and increased expression of PGE2 and IL-10 mRNAs were also observed in kidney from these mice. Implantation of DFAT cells also decreased the expression of TNF-α and MCP-1 proteins and increased that of CCL-17 protein in kidney from the SCG mice. Survival rates were higher in SCG mice implanted with DFAT cells than in SCG mice without implantation. CONCLUSION: Mechanisms underlying the effects of improvement of ANCA glomerulonephritis are associated with immunosuppressive effects by TSG-6 and the transition of M1-M2 macrophages, suggesting that implantation of DFAT cells may become a cell therapy for ANCA glomerulonephritis.

[The glomerulus in all its states]. / Le glomérule dans tous ses états.

Glomerulonephritis are the result of an inflammatory hit to the glomerulus. They are rare and heterogeneous renal diseases. Each glomerular compartment can be affected. The clinical manifestations present with hematuria, proteinuria and/or impaired renal function, either isolated or combined. Two main clinico-biological syndromes are described: nephrotic syndrome and nephritic syndrome. The latter can present in a more severe form i.e. rapidly progressive glomerulonephritis with the worst prognosis. These different clinical pictures are related to specific glomerular lesions. Thus, podocytic damage is mainly responsible for nephrotic syndromes, mesangial damage is responsible for proteinuria and hematuria and, finally, endothelial damage is responsible for nephritic syndrome and rapidly progressive glomerulonephritis. Therapeutic approaches include non-specific measures, combining both life-style and pharmacological interventions with the aim to reduce risk factors, and specific measures with the use of different immunosuppressive agents.

: Les glomérulonéphrites sont des atteintes inflammatoires du glomérule. Il s'agit de pathologies rénales rares et hétérogènes. Tous les compartiments glomérulaires peuvent être touchés. Les répercussions cliniques sont diverses. Elles se manifestent par une hématurie, une protéinurie et/ou une altération de la fonction rénale, présente chacune de manière isolée ou combinée. Deux principaux syndromes clinico-biologiques sont décrits : le syndrome néphrotique et le syndrome néphritique. Au sein de cette dernière entité, on distingue une forme plus sévère, les glomérulonéphrites rapidement progressives grevées du plus mauvais pronostic. Ces différents tableaux cliniques sont en lien avec des lésions glomérulaires spécifiques. Ainsi, les atteintes podocytaires sont principalement responsables des syndromes néphrotiques, les atteintes mésangiales sont responsables de protéinurie et d'hématurie et les atteintes endothéliales sont responsables de syndromes néphritiques et de glomérulonéphrites rapidement progressives. Les approches thérapeutiques comprennent des mesures non spécifiques, hygiéno-diététiques et pharmacologiques, visant à réduire les différents facteurs de risque, et des mesures spécifiques avec l'utilisation de divers médicaments immunosuppresseurs.

Sex and Gender in Glomerular Disease.

There is increasing understanding that a multifaceted interplay of sex-dependent genetic and immune dysregulation underpins the development of glomerular disorders. Regional and ethnic variations in glomerular disease incidence make delineating the effects of sex and gender on disease pathophysiology more complex, but there is a marked paucity of research in this area. This review article presents a summary of the current understanding of sex and gender in glomerular disease, highlighting the broader effects of sex and gender on autoimmunity, clinical presentations, and pathophysiology of individual glomerular diseases, as well as exploring sex, gender, and glomerular disease within a wider socioenvironmental context. It is important to specifically consider the effects of sex and gender when presenting and analyzing clinical and scientific studies on glomerular disease. Failure to do so risks promoting disparities within health care provision, neglecting opportunities to identify sex-specific biomarkers, and potentially hindering the development of sex-specific therapies.

Posterior reversible encephalopathy syndrome secondary to acute post-streptococcal glomerulonephritis in a child: a case report from the Tibetan plateau.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is a disorder of reversible vasogenic brain oedema with acute neurologic symptoms. It is a rare but serious disease that affects the central nervous system. PRES is a rare complication of acute post-streptococcal glomerulonephritis (APSGN). High altitude can accelerate vasogenic brain oedema by increasing cerebral blood flow (CBF), impairing cerebral autoregulation and promoting vascular inflammation. We report a case of PRES induced by acute post-streptococcal glomerulonephritis in a high-altitude environment. CASE PRESENTATION: A fourteen-year-old Tibetan girl presented with progressive headache with haematuria, facial swelling, dizziness and vomiting for 2 weeks as well as multiple episodes of tonic-clonic seizures for 14 h. She was diagnosed with APSGN based on laboratory tests and clinical symptoms. Brain magnetic resonance imaging (MRI) and computed tomography (CT) revealed bilateral frontal, parietal and occipital lesions that were compatible with the radiological diagnosis of PRES. The treatments included an antibiotic (penicillin), an antiepileptic drug, and hyperbaric oxygen (HBO) therapy. Follow-up MRI obtained 1 week after admission and CT obtained 4 weeks and 6 weeks after admission demonstrated complete resolution of the brain lesions. CONCLUSIONS: The case illustrates a rare occurrence of PRES following APSGN in a 14-year-old child in the Tibetan Plateau. The hypoxic conditions of a high-altitude setting might lower the cerebral autoregulation threshold and amplify the endothelial inflammatory reaction, thus inducing PRES in patients with APSGN. It is important to recognize the clinical and radiologic features of PRES, and adjuvant HBO therapy can promote rapid recovery from this condition in high-altitude areas.

Extracellular Vesicles Released from Stem Cells as a New Therapeutic Strategy for Primary and Secondary Glomerulonephritis.

Current treatment of primary and secondary glomerulopathies is hampered by many limits and a significant proportion of these disorders still evolves towards end-stage renal disease. A possible answer to this unmet challenge could be represented by therapies with stem cells, which include a variety of progenitor cell types derived from embryonic or adult tissues. Stem cell self-renewal and multi-lineage differentiation ability explain their potential to protect and regenerate injured cells, including kidney tubular cells, podocytes and endothelial cells. In addition, a broad spectrum of anti-inflammatory and immunomodulatory actions appears to interfere with the pathogenic mechanisms of glomerulonephritis. Of note, mesenchymal stromal cells have been particularly investigated as therapy for Lupus Nephritis and Diabetic Nephropathy, whereas initial evidence suggest their beneficial effects in primary glomerulopathies such as IgA nephritis. Extracellular vesicles mediate a complex intercellular communication network, shuttling proteins, nucleic acids and other bioactive molecules from origin to target cells to modulate their functions. Stem cell-derived extracellular vesicles recapitulate beneficial cytoprotective, reparative and immunomodulatory properties of parental cells and are increasingly recognized as a cell-free alternative to stem cell-based therapies for different diseases including glomerulonephritis, also considering the low risk for potential adverse effects such as maldifferentiation and tumorigenesis. We herein summarize the renoprotective potential of therapies with stem cells and extracellular vesicles derived from progenitor cells in glomerulonephritis, with a focus on their different mechanisms of actions. Technological progress and growing knowledge are paving the way for wider clinical application of regenerative medicine to primary and secondary glomerulonephritis: this multi-level, pleiotropic therapy may open new scenarios overcoming the limits and side effects of traditional treatments, although the promising results of experimental models need to be confirmed in the clinical setting.

The Critical Role of Therapeutic Plasma Exchange in the Treatment of MPO-ANCA Associated Crescentic IgA Nephropathy.

Crescentic IgA nephropathy (IgAN) with the positivity for antineutrophilic cytoplasmic antibody (ANCA) is a novel and uncommon entity. The optimal management of this condition is not well-defined. We report a 49-years-old woman with complaints of skin rash and swelling of lower limbs. She had hematuria, proteinuria and, progressive renal impairment with positive myeloperoxidase (MPO)-ANCA test. A renal biopsy revealed MPO-ANCA-associated crescentic IgAN. Induction therapy was intravenous methylprednisolone, cyclophosphamide and, therapeutic plasma exchange (TPE). An unexpected disease flare-up was observed during induction immunosuppressive therapy which regressed after long-term TPE. The patient experienced a full renal recovery after treatment with long-term TPE, cyclophosphamide, and corticosteroids.  DOI: 10.52547/ijkd.6490.

Proliferative glomerulonephritis with monoclonal immunoglobulin deposits triggered by COVID-19: a case report.

Acute kidney injury (AKI) frequently complicates corona virus disease 2019 (COVID-19) and is associated with significant mortality. Kidney disease in COVID-19 is usually due to acute tubular injury, but a variety of glomerular processes, especially collapsing glomerulopathy, have been increasingly described. Until recently, proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) had not been reported in the setting of COVID-19. We present a case of dialysis-dependent AKI developing soon after symptomatic COVID-19 which, on kidney biopsy, was found to be due to PGNMID with IgG3 kappa deposits. As is typical of PGNMID, a search for evidence of extra-renal monoclonal immunoglobulin or clonal lymphocyte population was negative. However, the patient had a favorable response to anti-plasma cell therapy and was ultimately able to stop hemodialysis. Though monoclonal gammopathy of renal significance (MGRS) is usually not associated with infection, other cases of post-viral MGRS, including PGNMID, have been previously reported. PGNMID has recently been linked specifically to COVID-19, with this representing one of only four cases reported thus far. Though causality between the preceding viral infection and the subsequent glomerulonephritis cannot be proven in these reports, nephrologists should be aware that not all kidney disease occurring in the aftermath of COVID-19 is due to tubular injury or collapsing glomerulopathy. As such, kidney biopsy should be routinely considered in the setting of COVID-19-associated glomerular disease as findings may change management. In the case of COVID-19-associated PGNMID data to guide treatment are limited, but our report suggests that anti-plasma cell therapy may be effective.

The survival nomograms for anti-neutrophil cytoplasmic antibody-associated glomerulonephritis patients with a follow-up of more than one year.

OBJECTIVES: Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis with kidney injury, manifested as ANCA-associated glomerulonephritis (AAGN), often portends a poor prognosis of renal function and life survival in long term. METHODS: A cohort of 339 AAGN patients were enrolled retrospectively. These patients survived and were followed up for at least 12 months after diagnosis in our centre. Multivariate Cox regression analysis and nomogram models were performed to determine the risk factors associated with renal survival and patient survival. RESULTS: The median follow-up time of all 339 patients was 65.2 (IQR 45.1, 91.3) months and the median age was 61(IQR 53, 69) years. In order to analyse the impact of the factors on renal survival, we divided the patients into 2 groups: non-dialysis group (204 patients without dialysis at the final visit) and dialysis group (135 patients with maintaining dialysis). The patients in dialysis group had lower haemoglobin level, lower eGFR level, lower platelets count, more daily urine protein, and higher Birmingham Vasculitis Activity Score (BVAS) at admission than those in non-dialysis group. Multivariate Cox regression revealed that low haemoglobin (HR=0.977, 95%CI 0.965-0.990, p<0.001), low eGFR (HR=0.957, 95%CI 0.941-0.973, p<0.001) and high proteinuria (HR=1.139, 95%CI 1.055-1.230, p=0.001) at admission were independent risk factors for developing maintaining dialysis. A nomogram was established based on the results of multivariate Cox analysis and the internal bootstrap resampling approach showed the C-index of the nomogram was 0.83. Then we divided all patients into death group (n=99) and survival group (n=240). The patients in death group had older age, more hypertension, more chronic lung disease, lower platelets count, lower serum albumin, higher BVAS and lower eGFR at admission than those in survival group. Multivariate Cox regression revealed that the status of maintaining dialysis (HR 3.51, 95% CI 1.91-6.47, p<0.001) and old age (HR 1.07, 95% CI 1.04-1.09, p<0.001) were independent risk factors for all-cause mortality. Again, a nomogram was established and the C-index was 0.74. CONCLUSIONS: We analysed the independent risk factors for maintaining dialysis and all-cause mortality in AAGN patients with a follow-up of more than 12 months. The two proposed nomograms were of predictive value.

Staphylococcus-induced proliferative glomerulonephritis and cerebral hemorrhage - fatal complications in a young female with postpartum cardiomyopathy and an implanted left ventricular assist device: a case report and review of the literature.

Background: The continuous-flow left ventricular assist device (CF-LVAD) is used to save the lives of patients in the final stage of congestive heart failure, replacing the pump function of the left ventricle. Although quality of life increases significantly, CF-LVAD-related complications might prove fatal, as in the case presented in this paper.Methods: A 20-year-old female, during her second pregnancy, presented with signs of heart failure. Emergency caesarean section was necessary to save the baby, but peripartum cardiomyopathy developed in the mother. The use of an implantable cardioverter-defibrillator (ICD) was necessary 5 years later. As the clinical progression was unfavorable under medical treatment, with the patient reaching INTERMACS (Interagency Registry for Mechanically Assisted Circulatory Support) Profile 1 (refractory cardiogenic shock), the treatment of choice was the implantation of a CF-LVAD.Results: After 3 years of follow-up (at the age of 28), the patient presented with a positive hemoculture for Staphylococcus aureus. Prolonged antibiotic therapy and attentive follow-up was prescribed. Although an effective antiplatelet and anticoagulant treatment was applied, and despite therapeutic values of prothrombin time and international normalized ratio (INR), the patient died as result of a fatal cerebral hemorrhage. The autopsy also revealed septic emboli, disseminated intravascular coagulation, and focal proliferative glomerulonephritis.Conclusions: Although the benefits of CF-LVAD are significant, bleeding episodes can be severe and LVAD-associated infection can trigger glomerular injury and increase mortality.

A massive natural disaster, the Great East Japan Earthquake, and the incidence of dialysis due to end-stage kidney disease.

BACKGROUND: Disaster-related stress can increase blood pressure and the incidence of cardiovascular diseases. However, the role of massive disasters in the development of end-stage kidney disease (ESKD) remains unknown. We investigated the incidence and different causes of dialysis initiation in patients with chronic kidney disease in a city affected by the Great East Japan Earthquake. METHODS: This was a single-center, retrospective observational study. All patients who initiated or were treated with dialysis at Kesennuma City Hospital between 2007 and 2020 were enrolled. The year of dialysis initiation was retrospectively determined based on the initiation date. The causative renal diseases that led to the need for dialysis initiation were divided into four groups: diabetic nephropathy, hypertensive renal disease, glomerulonephritis, and others. RESULTS: Age at dialysis initiation differed significantly among the four groups (p = 0.0262). There was a significant difference in the numbers of the four groups before and after the Great East Japan Earthquake (p = 0.0193). The age of hypertensive renal disease patients was significantly higher than those of patients with diabetic nephropathy (p = 0.0070) and glomerulonephritis (p = 0.0386) after the disaster. The increasing number of dialysis initiations after the Great East Japan Earthquake appeared to be associated with changes in hypertensive renal diseases; the number peaked after 10 years. CONCLUSIONS: There was an increase in the number of dialysis initiations, especially caused by hypertensive renal diseases, for up to 10 years after the Great East Japan Earthquake.