Fanconi's syndrome is a set of pathological effects, including hypophosphatemia and proteinuria and electrolyte abnormalities and urinary amino acid loss, that result from proximal tubule dysfunction or, more generally, renal tubular acidosis and that can be caused by drugs or any number of other factors. Although the authors of many articles state that Fanconi's syndrome is rare and typically only occurs in people who have multiple myeloma, it is possible that primary Epstein-Barr Virus (EBV) infection could cause Fanconi's syndrome or pathological effects akin to Fanconi's syndrome. EBV infects proximal tubule epithelial cells (http://scholar.google.com/scholar?hl=en&q=%22Epstein-Barr%22+%22proximal+tubule%22+interstitial), and researchers have suggested that the inflammatory immune response to EBV-infected proximal tubule cells could account for cases of EBV-induced interstitial nephritis. A large amount of evidence has implicated late, primary EBV infection as being an important factor that may contribute to the development of lupus in some people (http://scholar.google.com/scholar?hl=en&q=%22Epstein-Barr%22+lupus), and the autoimmune hemolytic anemia that is characteristic of infectious mono (http://scholar.google.com/scholar?hl=en&q=%22Epstein-Barr%22+hemolytic+anemia) could contribute to proximal tubule dysfunction and acidosis, etc. EBV infection has caused outright renal failure, also [Federman and Hammer, 1996; Davies et al., 1980: (http://scholar.google.com/scholar?hl=en&q=%22Epstein-Barr%22+%22renal+failure%22)]. The infection of epithelial cells of the biliary tree by EBV could also contribute to renal tubular acidosis and conceivably produce Fanconi's syndrome, given that liver dysfunction tends to lead to kidney disease of one kind or another. Although the authors of many articles tend to say that EBV does not infect biliary epithelial cells, other authors accept that EBV almost certainly infects biliary epithelial cells and epithelial cells in many other organs, etc. If it doesn't infect any cells in the liver, why are there massive numbers of reports of hepatitis following EBV-induced (as opposed to the more rare, CMV-induced) mononucleosis (http://scholar.google.com/scholar?hl=en&q=%22Epstein-Barr%22+mononucleosis+hepatitis+OR+hepatic+OR+hepatocellular)? Come on. (Of course, there's often an obligatory statement, in each of those countless articles, stating that the complication is "rare.") Also, IgG light-chain nephropathy can cause Fanconi's syndrome [Messian et al., 2000: (http://www.ncbi.nlm.nih.gov/pubmed/10844934)], such as in people who have hematological malignancies, and primary EBV infection is essentially a self-limiting lymphoproliferative condition, a self-limiting B-cell lymphoma.
It's interesting that hypophosphatemia, which is a major effect of Fanconi's syndrome, has been treated with oral phosphate and relatively high doses of vitamin D3 for many years [a bad example, and I'm talking about people who have hypophosphatemia that is not caused by the genetic disorder of vitamin D-resistant rickets: Berkelhammer and Bear, 1984: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1875686&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/6418367)]. Haglin (2004) [Haglin, 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15236787)] suggested that phosphate depletion could contribute to the development of multiple sclerosis, and there is a large amount of evidence that EBV infection may interact with other factors to contribute to the development of MS, etc. It's possible that the osmoregulatory disturbances and hypophosphatemia that can result from proximal tubule dysfunction, such as might result from and persist in response to primary EBV infection, could contribute to the development of MS. Vitamin D is widely known to reduce urinary phosphate loss, by reducing parathyroid hormone levels and by other mechanisms, and that could be one mechanism underlying the supposed protective effects of UVB-induced elevations in serum 25-hydroxyvitamin D, in the context of the etiology of MS.
Hypophosphatemia can produce outright hypoxic brain injuries (by depleting 2,3-bisphosphoglycerate/2,3-diphosphoglycerate) and not just cerebral ischemia [Jacob, 1975: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1129800&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/1136448)], and bicarbonate administration can be disastrous in people with hypophosphatemia (Jacob, 1975). I generally think ATP disodium would be more effective and potentially safer than sodium phosphate for the correction of hypophosphatemia, in some cases, but that's just my opinion. I say that because phosphate depletion causes ATP depletion, and phosphate, by itself, would be expected to not-especially-effectively restore, in my opinion, the adenosine nucleotide pools that have been lost as a result of chronic hypophosphatemia or cellular phosphate depletion. One should discuss any of these things with one's doctor, and oral phosphate supplementation can be very problematic and dangerous, especially in people in any disease state of any kind. But a key point that I discussed in a past posting is that ATP depletion can result from phosphate depletion and not produce any significant decrease in serum phosphate levels, for example. In many of the instances in which researchers have stated that phosphate depletion is rare or that Fanconi's syndrome is rare, the statements have presumably been made on the basis of serum phosphate levels or on some sort of measurement of urinary phosphate excretion, in response to phosphate ingestion or another stimulus. But it's not possible to rule out phosphate depletion by looking at those indications, in my opinion. Thus, any statement that phosphate depletion is a rare cause of such-and-such a condition is unlikely to be a defensible statement, from a logical or rational standpoint. I don't think that phosphate depletion is necessarily all that common, but the point is that, as noted by Jacob (1975), phosphate depletion may go undetected and contribute to encephalopathies in people with alcoholism and diabetes, etc. Phosphate depletion can also cause immunosuppression, and, paradoxically, immunosuppression is thought to be able to contribute to the development of lupus and other autoimmune diseases (to the extent that immunological factors contribute in primary ways to the progression of MS), such as by reducing the levels of circulating anti-idiotypic antibodies (naturally-occurring, circulating anti-IgG IgG's that prevent the binding of autoantibodies to proteins and other targets), etc. [see Berchtold et al., 1989: (http://bloodjournal.hematologylibrary.org/cgi/content/abstract/74/7/2414)]. That's not the only mechanism underlying that paradoxical phenomenon, in any case.
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