PTRA is useful for renal artery angina by atherosclerotic plaque rupture with unilateral functioning kidney.

We report a case of acute ischemic nephropathy in a patient with severe renal artery stenosis and bradycardia due to sick sinus syndrome. An 83-year-old Japanese woman with a history of hypertension was diagnosed with sick sinus syndrome and scheduled for pacemaker implantation. Four days prior to admission for the procedure, she experienced sudden-onset severe right flank pain that persisted for 1 day. On the day of admission, her serum creatinine level increased from 1.35 mg/dL, measured 2 weeks earlier, to 7.04 mg/dL. Laboratory examinations showed elevated C-reactive protein and lactate dehydrogenase levels. A computed tomography scan showed a severely atrophied left kidney, suggesting that it was non-functioning. Doppler ultrasonography of the right renal artery showed an extended acceleration time, suggesting proximal stenosis. Magnetic resonance imaging showed no enhancement in the proximal portions of the right renal artery, consistent with severe stenosis or occlusion. The patient developed severe bradycardia with lightheadedness; as a result, pacemaker implantation was performed on post-admission day 7. On day 10, digital subtraction angiography revealed diffuse severe stenosis of the right renal artery; intravascular ultrasonography suggested plaque rupture. Percutaneous transluminal renal angioplasty (PTRA) was performed and a drug-eluting stent was placed. On day 11, hemodialysis was performed owing to deteriorating renal function. The patient's renal function dramatically improved shortly thereafter. This case highlights the importance of PTRA for select patients, as it can potentially save some patients from chronic dialysis, and outlines the possible implications of bradycardia in the pathogenesis of ischemic nephropathy.

Membranous nephropathy in a patient with pulmonary tuberculosis infection and lung adenocarcinoma: a case report.

We report a case of membranous nephropathy (MN) in a patient with tuberculosis infection and lung adenocarcinoma. A 50-year-old Filipino woman underwent a renal biopsy for the evaluation of proteinuria and hematuria. Immunofluorescence analysis revealed positive staining of IgG in the glomerular basement membrane and mesangial matrices, while electron microscopy demonstrated the presence of sub-epithelial deposits, suggesting MN. To screen for secondary causes of MN, we conducted a computed tomography (CT) scan of the chest and abdomen, which revealed a ground-glass opacity in the middle lobe of the right lung and an enlarged paraaortic lymph node. A T-SPOT test was positive, suggesting the possibility of a latent tuberculosis infection, as she was asymptomatic. A follow-up chest CT scan showed persistent presence of the ground-glass opacities, suggesting a non-infectious cause. Video-assisted thoracoscopic resection of the middle right lobe and partial resection of the lower right lobe were performed because the possibility of lung cancer could not be excluded. Notably, pathological analysis of the lung revealed adenocarcinoma in the middle lobe and epithelioid granuloma in the lower lobe, suggesting an active tuberculosis infection. One month after surgery, anti-tuberculosis treatment was initiated. Thereafter, her proteinuria, which had increased to 6 g/gCre preoperatively, began to decrease. Five months after surgery, the patient achieved complete remission. The speed of remission suggests that tuberculosis likely played a primary role in the etiology of MN. Our case underscores the importance of screening tests for infections and malignancies in patients with MN, even if suggestive symptoms are absent.

A Novel LMX1B Variant Identified in a Patient Presenting with Severe Renal Involvement and Thin Glomerular Basement Membrane.

We report a case of nail-patella syndrome (NPS) with unusual thinning of the glomerular basement membrane (GBM) associated with a novel heterozygous variant in the LMX1B gene. A 43-year-old female patient with a previous diagnosis of NPS, referred to our hospital for persistent proteinuria, underwent a renal biopsy, which revealed minor glomerular abnormalities. She underwent a second renal biopsy at the age of 56 owing to the presence of persistent proteinuria and decline in serum albumin, meeting the diagnostic criteria for nephrotic syndrome. Light microscopy demonstrated glomerulosclerosis and cystic dilatation of the renal tubules. Notably, electron microscopy revealed unusual thinning of the GBM, which is quite different from typical biopsy findings observed in patients with NPS, characterized by thick GBM with fibrillary material and electron-lucent structures. Comprehensive genetic screening for 168 known genes responsible for inherited kidney diseases using a next-generation sequencing panel identified a novel heterozygous in-frame deletion-insertion (c.723_729delinsCAAC: p.[Ser242_Lys243delinsAsn]) in exon 4 of the LMX1B gene, which may account for the disrupted GBM structure. Further studies are warranted to elucidate the complex genotype-phenotype relationship between LMX1B and proper GBM morphogenesis.

Immunotactoid glomerulonephritis in a patient with cold agglutinins: causal association or mere coincidence?

We report a case of immunotactoid glomerulonephritis (ITG) in a patient with cold agglutinins. An 86-year-old Japanese male with a history of hypertension, dyslipidemia, and gastric malignancy presented to our hospital for the evaluation of proteinuria and hematuria. He had an elevated blood pressure of 200/77 mmHg and edema of the lower extremities. Initial blood test results revealed an impaired renal function (creatinine, 1.37 mg/dL) and hypoalbuminemia (albumin, 2.6 g/dL). His estimated daily urinary protein was 5.89 g/g creatinine, meeting the diagnostic criteria for nephrotic syndrome. The selectivity index for proteinuria indicated low selectivity (0.329). We conducted a renal biopsy to identify the cause of nephrotic syndrome. Immunofluorescence microscopy demonstrated positive staining of IgM, C4, and C1q. Electron microscopy exhibited mesangial expansion with inflammatory cells and a lobular structure, suggesting membranoproliferative glomerulonephritis. Subendothelial deposits containing microtubular structures with a diameter of approximately 30-200 nm were found, concurrent with the criteria for the diagnosis of ITG. Screening for lymphoproliferative diseases and immunological abnormalities revealed a positive direct Coombs test result and the presence of cold agglutinins. Paraproteinemia was absent. The similarities between cold agglutinin disease and ITG, including the production of autoantibodies and involvement of complement pathways, raise the possibility that cold agglutinins played a role in the development of ITG; however, we were unable to prove it due to difficulties in detecting cold agglutinins on renal histology. We discuss the possible implications for pathogenesis considering prior reports on nephrotic syndrome being potentially associated with cold agglutinins.