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We have found that nanobacteria, recently discovered Gram-negative atypical bacteria, can cause local calciphylaxis on the mitral valve in a setting of high-calcium X phosphorous product in the blood. We present the case of a 33-year-old man with diabetic renal failure on continuous ambulatory peritoneal dialysis who died as a result of multiple brain infarcts due to embolizations from mitral valve vegetations. Systemic calciphylaxis was not present. Spectrometric analysis of the mitral valve vegetations showed that they were composed of calcium phosphate, carbonate apatite form, and fibrin. The electron microscopy of the thrombotic vegetation demonstrated nanobacterium as a nidus for carbonate apatite formation. Investigation for the presence of nanobacteria in the multiple organs involved in systemic calciphylaxis may be of help in elucidating the pathogenesis of this frequently fatal disorder.

Background: Painless myocardial ischemia (PMI) is associated with poor outcomes in the general population. We hypothesized that the presence of PMI is inversely related to the level of kidney function and is associated with impaired survival in chronic kidney disease (CKD). Methods: A total of 356 patients who underwent percutaneous coronary intervention were assessed for PMI, which was defined as the absence of chest pain in response to balloon dilation of the affected vessel. Cox proportional hazards analysis was used to calculate 10-year all-cause mortality. Results: There was an increase in PMI occurrence by strata of estimated glomerular filtration rate (eGFR), whereby PMI was present in only 20.6% of individuals with eGFR ≥90 ml/min/1.73 m², but was found in 50.0% of individuals with eGFR <30 ml/min/1.73m² (p = 0.004 for trend). Classification of individuals as having either CKD or PMI showed significant differences in adjusted mortality between groups (p < 0.001 for trend), with individuals having both CKD and PMI demonstrating the highest 10-year mortality. Compared to individuals with neither CKD nor PMI, individuals with CKD and no PMI had a hazard ratio (HR) for mortality of 1.64 (95% CI: 1.03-2.63, p = 0.038), while individuals with both PMI and CKD had an HR of 2.08 (1.30-3.33, p = 0.002). Conclusion: PMI is common in the CKD population, is inversely related to the level of eGFR, and confers a substantially increased risk in CKD. These findings may partially explain the high mortality traditionally attributed to cardiovascular disease in CKD patients.

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