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The production of concentrated urine inevitably leads to the precipitation of poorly soluble waste salts in the renal tubular fluid. These crystallization processes are physiologic and without consequences as long as all crystals are excreted with the urine. The retention of crystals in the renal tubules, however, may lead to tubular nephrocalcinosis. Here, we present a brief survey of the possible mechanisms involved in this process, which seems to depend predominantly on the presence of regenerating/(re)differentiating cells in the renal tubules. Crystal binding to the surface of these cells can be mediated by a number of luminal membrane molecules, including acidic fragment of nucleolin-related protein, annexin-II, osteopontin, and hyaluronan.Kidney International (2007) 72, 13–18; doi:10.1038/sj.ki.5002272; published online 11 April 2007 [ABSTRACT FROM AUTHOR]

Oxalate or calcium oxalate crystal-induced tissue damage could be conducive to renal stone disease. We studied the response of renal proximal (LLC-PK1 and MDCK-II) and collecting (RCCD1 and MDCK-I) tubule cell lines to oxalate ions as well as to calcium oxalate monohydrate (COM) crystals. Cells grown on tissue culture plastic or permeable growth substrates were exposed to high (1 mM) and extremely high (5 and 10 mM) oxalate concentrations, or to a relatively large quantity of crystals (146 µg), after which cell morphology, prostaglandin E2 (PGE2) secretion, [3H]thymidine incorporation, total cell numbers and various forms of cell death were studied. Morphological alterations, increased PGE2 secretion, elevated levels of DNA synthesis and necrotic cell death were induced by extremely high, but not by high oxalate. Crystals were rapidly internalized by proximal tubular cells, which stimulated PGE2 secretion and DNA synthesis and the release of crystal-containing necrotic cells from the monolayer. Crystals did not bind to, were not taken up by, and did not cause marked responses in collecting tubule cells. These results show that free oxalate is toxic only at supraphysiological concentrations and that calcium oxalate is toxic only to renal tubular cells that usually do not encounter crystals. Based on these results, it is unlikely that oxalate anions or calcium oxalate crystals are responsible for the tissue damage that may precede renal stone formation. [ABSTRACT FROM AUTHOR]

Taylor and Curhan report that consumption of fructose is independently associated with an increased risk of incident kidney stones. What could be the mechanisms underlying the relation between fructose intake and stone risk? And how should we incorporate this finding into the dietary advice that we give to our patients to prevent kidney stone formation?Kidney International (2008) 73, 139–140; doi:10.1038/sj.ki.5002700 [ABSTRACT FROM AUTHOR]

Background: Glucosamine (GlcN) used by patients with osteoarthritis was demonstrated to reduce pain, but the working mechanism is still not clear. Viscosupplementation with hyaluronic acid (HA) is also described to reduce pain in osteoarthritis. The synthesis of HA requires GlcN as one of its main building blocks. We therefore hypothesized that addition of GlcN might increase HA production by synovium tissue. Methods: Human osteoarthritic synovium explants were obtained at total knee surgery and pre-cultured for 1 day. The experimental conditions consisted of a 2 days continuation of the culture with addition of N-Acetyl-glucosamine (GlcN-Ac; 5 mM), glucosamine-hydrochloride (GlcN-HCl; 0.5 and 5 mM), glucose (Gluc; 0.5 and 5 mM). Hereafter HA production was measured in culture medium supernatant using an enzyme-linked binding protein assay. Real time RT-PCR was performed for hyaluronic acid synthase (HAS) 1, 2 and 3 on RNA isolated from the explants. Results: 0.5 mM and 5 mM GlcN-HCl significantly increased HA production compared to control (approximately 2 - 4-fold), whereas GlcN-Ac had no significant effect. Addition of 5 mM Gluc also increased HA production (approximately 2-fold), but 0.5 mM Gluc did not. Gene expression of the HA forming enzymes HAS 1, 2 and 3 was not altered by the addition of GlcN or Gluc. Conclusion: Our data suggest that exogenous GlcN can increase HA production by synovium tissue and is more effective at lower concentrations than Gluc. This might indicate that GlcN exerts its potential analgesic properties through stimulation of synovial HA production. [ABSTRACT FROM AUTHOR]

Background: Glucosamine (GlcN) used by patients with osteoarthritis was demonstrated to reduce pain, but the working mechanism is still not clear. Viscosupplementation with hyaluronic acid (HA) is also described to reduce pain in osteoarthritis. The synthesis of HA requires GlcN as one of its main building blocks. We therefore hypothesized that addition of GlcN might increase HA production by synovium tissue.Methods: Human osteoarthritic synovium explants were obtained at total knee surgery and pre-cultured for 1 day. The experimental conditions consisted of a 2 days continuation of the culture with addition of N-Acetyl-glucosamine (GlcN-Ac; 5 mM), glucosamine-hydrochloride (GlcN-HCl; 0.5 and 5 mM), glucose (Gluc; 0.5 and 5 mM). Hereafter HA production was measured in culture medium supernatant using an enzyme-linked binding protein assay. Real time RT-PCR was performed for hyaluronic acid synthase (HAS) 1, 2 and 3 on RNA isolated from the explants.Results: 0.5 mM and 5 mM GlcN-HCl significantly increased HA production compared to control (approximately 2 - 4-fold), whereas GlcN-Ac had no significant effect. Addition of 5 mM Gluc also increased HA production (approximately 2-fold), but 0.5 mM Gluc did not. Gene expression of the HA forming enzymes HAS 1, 2 and 3 was not altered by the addition of GlcN or Gluc.Conclusion: Our data suggest that exogenous GlcN can increase HA production by synovium tissue and is more effective at lower concentrations than Gluc. This might indicate that GlcN exerts its potential analgesic properties through stimulation of synovial HA production. [ABSTRACT FROM AUTHOR]