Got this from another forum:
First thing to note is that "S. boulardii” is sometimes used as a probiotic with the purpose of introducing beneficial active cultures into the large and small intestines, as well as conferring protection against pathogenic microorganisms in the host"
https://en.wikipedia...myces_boulardii
Now, how does this related to kidney function? Well, it turns out that certain bacteria in the gut microbiome can produce uremic toxin, i.e. compounds that need to be metabolized and/or excreted by the kidneys and can cause (mainly cardiovascular) damage and inflammation if renal clearance is insufficient. To the extent that probiotics can alter the composition of the gut microbiome, they could reduce uremic toxin production.
“Probiotics are the focus of a thorough investigation as a natural biotreatment due to their various health-promoting effects and inherent ability to fight specific diseases including chronic kidney disease (CKD). Indeed, intestinal microbiota has recently emerged as an important player in the progression and complications of CKD. Because many of the multifactorial physiological functions of probiotics are highly strain specific, preselection of appropriate probiotic strains based on their expression of functional biomarkers is critical. The interest in developing new research initiatives on probiotics in CKD have increased over the last decade with the goal of fully exploring their therapeutic potentials. The efficacy of probiotics to decrease uremic toxin production and to improve renal function has been investigated in in vitro models and in various animal and human CKD studies. However to date, the quality of intervention trials investigating this novel CKD therapy is still lacking. This review outlines potential mechanisms of action and efficacy of probiotics as a new CKD management tool, with a particular emphasis on uremic toxin production and inflammation.”
https://www.kidney-i...1006-7/fulltext
In addition to altering the composition of the gut microbiome, S. boulardii also increases the immune response to certain toxins produced by bacteria, thereby further reducing uremic toxin levels.
In addition to its acting as an immune stimulant, S. boulardii also has an anti-inflammatory effect in the intestines. It's pretty complicated, see:
https://www.ncbi.nlm...les/PMC3296087/
With that in mind, let's look at the effect of S. boulardii on the specific case of IgA nepropathy, and autoimmune kidney disease. As Dante has posted, there could potentially be a beneficial effect of S. boulardii in this disease;
“Immunoglobulin A nephropathy (IgAN) is associated with mucosal IgA defect. Probiotics regulate specific and innate immunity. We evaluated the effect of Saccharomyces boulardii on experimental IgAN in mice. Four groups of BALB/c mice (eight for each) were formed. Group 1 was immunized by oral poliovirus vaccine (OPV) at 0, 14, and 28 days. Group 2 was also given S. boulardii in addition to OPV. Group 3 was given only S. boulardii, whereas group 4 received no treatment. At week 6, after urine and serum samples were obtained for urinalysis and serum creatinine and IgA measurements, all animals were sacrificed to get their kidneys for histopathological evaluation. Urinalysis and serum creatinine levels were normal in all groups. Serum IgA level was increased only in group 1. Whereas group 1 had mesangial proliferation, histology was normal in the other groups. Predominant IgA deposition was universal in group 1, whereas it was either not present or minimal in other groups. Three mice in group 1 also had C3 deposition, which was absent in other groups. Electron microscopy revealed mesangial proliferation, matrix expansion, focal glomerular basement membrane thickening and electron-dense deposits in group 1 only, whereas the other groups were normal. In conclusion, enteral S. boulardii prevented OPV-induced IgAN in mice.”
https://www.ncbi.nlm...pubmed/18446380
Thus, S. boulardii prevented the development of vaccine induced IgA nephropathy in mice. it's hard to say if this can be extrapolated to the case of non-vaccine induced IgA nephropathy in humans. But it's certainly worth a shot.
There is certainly good reason to suspect that S. boulardii could prevent flare ups of IgA nephropathy. Though the pathophysiology of the disease is poorly understood, it is becoming increasingly clear that the accumulation of aberrently glycosylated IgA1 (which leads to polymerization that fucks of the kidney's glomeruli) is "likely to be a consequence of abnormal systemic responses to mucosally encountered antigens"
https://www.ncbi.nlm...ubmed/17093066)
“In IgA nephropathy (IgAN), serum IgA1 with abnormal O-glycosylation deposits in the glomerular mesangium. The underlying mechanism of this IgA1 O-glycosylation abnormality is poorly understood, but recent evidence argues against a generic defect in B cell glycosyltransferases, suggesting that only a subpopulation of IgA1-committed B cells are affected. For investigation of whether the site of antigen encounter influences IgA1 O-glycosylation, the O-glycosylation of serum IgA1 antibodies against a systemic antigen, tetanus toxoid (TT), and a mucosal antigen, Helicobacter pylori (HP), was studied in patients with IgAN and control subjects. Serum IgA1 was purified from cohorts of patients with IgAN and control subjects with HP infection and after systemic TT immunization. The IgA1 samples were applied to HP- and TT-coated immunoplates to immobilize specific antibodies, and IgA1 O-glycosylation profiles were assessed by binding of the O-glycan-specific lectin Vicia villosa using a modified ELISA technique. Although total serum IgA1 had raised lectin binding in IgAN, the O-glycosylation of the specific IgA1 antibodies to TT and HP did not differ between patients and control subjects. In both groups, IgA1 anti-HP had higher lectin binding than IgA1 anti-TT. This study demonstrates that IgA1 O-glycosylation normally varies in different immune responses and that patients produce the full spectrum of IgA1 O-glycoforms. IgA1 with high lectin binding was produced in response to mucosal HP infection in all subjects. The raised circulating level of this type of IgA1 in IgAN is likely to be a consequence of abnormal systemic responses to mucosally encountered antigens rather than a fundamental defect in B cell O-glycosylation pathways.
https://www.ncbi.nlm...pubmed/17093066
S. boulardii could potentially remove some of the offending antigens (by removing producing bacteria from gut microbiome) from the gut and/or modulate the body's immune response in a way that reduces the production of the specific type of antibody that leads to kidney dysfunction.
