Recent advances in LncRNAs and chronic kidney disease / 药学学报

Long non-coding RNAs (LncRNAs), defined as transcripts which are hundreds of nucleotides with little or non-protein coding potential. Recently, LncRNAs have caught much more attentions, instead of considering as noises of genome transcripts, and indeed they have been found to play important roles associated with some biological processes, such as tumorigenesis, immunology dysfunction, metabolism adjustment, and so on. The incidence of chronic kidney disease (CKD) in different regions of the world is about 10% to 15%, with high growth rate and high unawareness, including the diabetic nephropathy, membranous nephropathy, etc. Previous publications also suggest that LncRNAs have a close relationship with the kidneys, and it may become new therapeutic targets or new biomarkers to diagnose diseases. In this review, we will summarize LncRNAs' functions with chronic kidney diseases, and discuss the prospects of the clinical applications of LncRNAs in the treatment of CKD treatment.

Placental site tumour associated with IgA nephropathy as paraneoplastic manifestation: case report / Tumor del lecho placentario asociado a nefropatía por IgA como manifestación paraneoplásica: reporte de caso

ABSTRACT Objective: To report the case of a placental site tumour which presented clinically in the form of a nephrotic syndrome secondary to IgA nephropathy. Case presentation: A 24-year-old woman, primigravida, referred to a Level IV complexity institution in Bogotá (Colombia), where she was diagnosed with IgA nephropathy as a paraneoplastic manifestation of a placental site trophoblastic tumour. After total hysterectomy as treatment, the patient evolved well, with oedema resolution and a drop in proteinuria. The patient completed one year of medical follow-up, with no evidence of disease. Discussion: Placental site trophoblastic tumour is rare, is part of the differential diagnosis for gestational trophoblastic disease and may present as a renal paraneoplastic manifestation which usually resolves once the tumour is treated. IgA nephropathy may be secondary to chronic inflammatory diseases and neoplastic diseases, as in this case.

RESUMEN Objetivo: reportar un caso de tumor del lecho placentario, cuya manifestación clínica fue síndrome nefrótico secundario a nefropatía IgA. Presentación del caso: se describe el caso de una paciente de 24 años, primigestante, quien fue remitida a una institución de cuarto nivel de complejidad localizada en Bogotá (Colombia), en donde se le hizo diagnóstico de nefropatía por IgA como manifestación paraneoplásica de un tumor trofoblástico del lecho placentario. Se realizó histerectomía total como tratamiento, con evolución satisfactoria, con resolución de los edemas y descenso de proteinuria; completó un año en seguimiento médico, sin evidencia de enfermedad. Discusión: el tumor trofoblástico del lecho placentario es infrecuente, hace parte del diagnóstico diferencial de la enfermedad trofoblástica gestacional (ETG), y puede manifestarse con fenómenos paraneoplásicos a nivel renal, que generalmente se resuelven con el tratamiento del tumor. La nefropatía por IgA puede ser secundaria a enfermedades inflamatorias crónicas y a patologías neoplásicas, como en este caso.

IgA nephropathy in a patient with ankylosing spondylitis well controlled with etanercept / 고신대학교의과대학학술지

Ankylosing spondylitis (AS) can involve the eye, gastrointestinal system, cardiopulmonary system, skin, kidneys, and spinal and peripheral joints. It is rarely accompanied by immunoglobulin A (IgA) nephropathy. Although IgA is involved in both AS and IgA nephropathy, the relationship between these diseases remains unclear. We detected hematuria and proteinuria in a 32-year-old male patient with ankylosing spondylitis that remained stable for 4 years through treatment with etanercept, a tumor necrosis factor-α (TNF-α) inhibitor, and diagnosed IgA nephropathy through a renal biopsy. IgA nephropathy seems to be less commonly associated with AS disease activity or specific treatment such as TNF-α inhibitor use.

A Patient with IgA Nephropathy: 5 Years after Complete Remission of Minimal Change Nephrotic Syndrome / 이화의대지

A 37-year-old male patient was admitted with generalized edema as the main symptom. A blood test confirmed hypoalbuminemia and hyperlipidemia, and a urine test confirmed severe albuminuria. A renal biopsy was conducted, which revealed a diagnosis of minimal change disease. Although the patient experienced complete remission of minimal change nephrotic syndrome after oral prednisolone and cyclophosphamide treatment, he is readmitted due to bilateral leg edema 5 years later since minimal change nephrotic syndrome was completely cured. The patient is diagnosed with IgA nephropathy. Although the exact mechanisms of IgA nephropathy in this patient remain unclear, this case represents an extremely rare development, and is separate from the remission of minimal change nephrotic syndrome.

Impact of gene polymorphisms of interleukin-18, transforming growth factor-beta, and vascular endothelial growth factor on development of IgA nephropathy and thin glomerular basement membrane disease

BACKGROUND: We investigated the effects of gene polymorphisms on the development of IgA nephropathy and thin glomerular basement membrane (GBM) disease by analyzing polymorphisms in the interleukin (IL)-18, transforming growth factor (TGF)-beta, and vascular endothelial growth factor (VEGF) genes in Korean patients. METHODS: This study included 146 normal individuals and 69 biopsy-proven IgA nephropathy and 44 thin GBM disease patients. The gene polymorphisms -607A/C and -137G/C in IL-18, -509C/T and T869C in TGF-beta, and -2578C/A and 405C/G in VEGF were investigated in DNA extracted from peripheral blood. RESULTS: The frequencies of the IL-18 -607CC genotype (43.5% vs. 21.2%, P=0.002, P corrected=0.012) and the VEGF 405GG genotype (37.7% vs. 21.2%, P=0.002, P corrected=0.012) were significantly increased in the IgA nephropathy group compared with the control group, whereas no significant differences in genotype frequency were observed between the thin GBM disease and control groups. However, there were no significant differences in genotype and allele frequencies between the IgA nephropathy and thin GBM disease groups. CONCLUSION: This study did not show any statistically significant differences of six selected gene polymorphisms of the IL-18, TGF-beta, and VEGF genes between IgA nephropathy and thin GBM disease. Additional extensive studies are required to clarify the potential role of gene polymorphism to discriminate IgA nephropathy and thin GBM disease without renal biopsy.

Nefropatia por IgA em portadores de espondiloartrites acompanhados no Serviço de Reumatologia do Hospital das Clínicas da UFMG / IgA nephropathy in patients with spondyloarthritis followed-up at the Rheumatology Service of Hospital das Clínicas/UFMG

OBJETIVO: Determinar a frequência das glomerulonefrites nos pacientes espondiloartríticos acompanhados em Serviço de Reumatologia Brasileiro e avaliar variáveis clínicas correlacionadas. PACIENTES E MÉTODOS: Os pacientes foram avaliados quanto às características sociodemográfi cas, tipo de espondiloartrite, tempo e atividade da doença, uso de anti-infl amatórios não esteroides, presença do HLA-B27, níveis de creatinina e ureia séricas, presença de comorbidades e presença de hematúria e/ou proteinúria. Os pacientes com hematúria foram submetidos à pesquisa de dismorfi smo eritrocitário, e aqueles com proteinúria submeteram-se à quantifi cação da proteína na urina de 24 horas. Biópsia renal foi indicada para aqueles com hematúria de origem glomerular e/ou proteinúria maior que 3,5 g. RESULTADOS: Foram avaliados 76 pacientes. A alteração mais frequente no exame de urina de rotina foi a hematúria microscópica (44,7 por cento), geralmente intermitente e em amostra isolada de urina durante o seguimento do paciente. Em oito (10,5 por cento) dos pacientes a hematúria sugeriu origem glomerular. A biópsia renal foi realizada em cinco deles, e mostrou nefropatia por IgA em quatro (5,3 por cento) e doença da membrana fi na em um paciente. CONCLUSÕES: Notou-se alta frequência de alterações no exame de urina desse subgrupo de pacientes, assim como alta prevalência de nefropatia por IgA. Apesar de mais estudos sobre o assunto serem necessários para melhor esclarecimento desses resultados, a realização periódica de exames de urina deveria ser recomendável.

OBJECTIVE: To determine the frequency of glomerulonephritis in patients with spondyloarthritis followed-up at a Brazilian Rheumatology Service, and to evaluate the clinical variables associated. PATIENTS AND METHODS: Patients were assessed for sociodemographic characteristics, type of spondyloarthritis, time since diagnosis and disease activity, non-steroidal anti-infl ammatory drug use, HLA-B27 positivity, creatinine and urea serum levels, major comorbidities, hematuria and proteinuria. Patients with hematuria were subsequently assessed for the presence of dysmorphic red blood cells in urine, and those with proteinuria underwent 24-hour urine protein measurement. Renal biopsy was performed in patients with glomerular hematuria and/or proteinuria over 3.5 g/24-hour. RESULTS: Seventy-six patients were assessed. Microscopic hematuria was the most frequently found abnormality in urinalysis (44.7 percent), usually intermittent and in spot urine samples during patients' follow-up. In eight patients (10.5 percent), glomerular hematuria was suspected. Renal biopsy was performed in fi ve of them, showing IgA nephropathy in four (5.3 percent) and thin membrane disease in one patient. CONCLUSIONS: A high frequency of urinalysis alterations was observed in that subgroup of patients, as well as a high prevalence of IgA nephropathy. Although further studies on this subject are needed to better clarify these results, periodic urinalysis of patients with spondyloarthritis should be recommended.

Nefropatia por IgA nas espondiloartrites / IgA nephropathy in spondyloarthritis

Pacientes com espondiloartrites poderiam ser mais acometidos pela nefropatia por IgA do que a população geral, havendo, possivelmente, um mecanismo etiopatogênico comum. O seguinte artigo relaciona quatro casos que exemplificam essa possível associação.

Spondyloarthritis patients can be more frequently affected by IgA nephropathy than the general population, and a common etiopathogenic mechanism can be involved. We report four cases that may exemplify that association.

A Case of IgA Nephropathy Associated with Thin Basement Membrane Disease / 대한신장학회지

IgA nephropathy and thin basement membrane disease are common glomerular diseases in persistent microscopic hematuria with or without proteinuria. However, these two conditions cannot be easily distinguished on the biochemical or urinary findings alone. Therefore, renal biopsy is required for correct identification of the two conditions in most cases. Recently, it has been reported that thinning of glomerular basement membrane is accompanied with precipitation of electron dense deposits in some patients with IgA nephropathy. We report a case of IgA nephropathy associated with thin basement membrane disease in a 19-year-old male with microscopic hematuria and mild proteinuria. After 2 years' treatment with angiotensin II receptor blocker, the patient exhibited persistent microscopic hematuria but decreased proteinuria. Our finding concurs with the previous reports indicating that patients with both IgA nephropathy and thin basement membrane disease do not have different clinical features compared to those with IgA nephropathy alone. In addition, clinical outcome does not appear to be affected by thin basement membrane disease when these two conditions are combined.