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LAM KID

OCTOBER 04, 2013

[A simple method to detect urate crystals in formalin-fixed tissue]

BÉLY Miklós, KRUTSAY Miklós

[In our previous study we refuted the thesis that sodium urate crystals are not, or only rarely detectable in formalin-fixed histological samples because they dissolve in the aqueous formalin solution. Our observations indicate that dissolution of urate crystals is primarily caused by haematoxylineosin staining. Undeniably, however, urate crystals are partially dissolved in the aqueous solution of formaldehyde, and thus a small amount of urate deposits may totally dissolve from tissue samples. The aim of the present study was to identify those steps of the staining procedure that are responsible for the dissolution of urate crystals. We found that the dissolution of urate crystals during the course of staining was caused by the combined effects of haematoxylin staining, treatment with 1% aqueous lithium carbonate solution and dehydration with acetone. As the simplest histological method for the detection of urate crystals, we recommend examining unstained sections (mounted with Canada balsam) of formalin-fixed, paraffin-embedded tissue samples in polarised light. According to our previous study, about two thirds of urate crystals remain detectable on unstaied sections, whereas haematoxylin-eosin stained sections of the same tissue samples (derived from patients with gout) did not contain urate crystals. In the samples where urate crystals could be detected in haematoxylin- eosin stained sections using polarised light, the unstained sections contained much more crystals, which shows that dissolution is greatly decreased on unstained sections.]

Lege Artis Medicinae

JUNE 20, 2013

[A simple method to demonstrate urate crystals in formalin fixed tissue]

BÉLY Miklós, KRUTSAY Miklós

[In our previous study we refuted the thesis that sodium urate crystals are not, or only rarely detectable in formalin-fixed histological samples because they dissolve in the aqueous formalin solution. Our observations indicate that dissolution of urate crystals is primarily caused by haematoxylineosin staining. Undeniably, however, urate crystals are partially dissolved in the aqueous solution of formaldehyde, and thus a small amount of urate deposits may totally dissolve from tissue samples. The aim of the present study was to identify those steps of the staining procedure that are responsible for the dissolution of urate crystals. We found that the dissolution of urate crystals during the course of staining was caused by the combined effects of haematoxylin staining, treatment with 1% aqueous lithium carbonate solution and dehydration with acetone. As the simplest histological method for the detection of urate crystals, we recommend examining unstained sections (mounted with Canada balsam) of formalin-fixed, paraffin-embedded tissue samples in polarised light. According to our previous study, about two thirds of urate crystals remain detectable on unstaied sections, whereas haematoxylin-eosin stained sections of the same tissue samples (derived from patients with gout) did not contain urate crystals. In the samples where urate crystals could be detected in haematoxylin- eosin stained sections using polarised light, the unstained sections contained much more crystals, which shows that dissolution is greatly decreased on unstained sections.]

Hypertension and nephrology

JUNE 20, 2010

[Sevelamer: an old-new phosphate binder in chronic kidney disease]

BERECZKI Csaba, TÚRI Sándor

[Sevelamer HCl is a non-metal and non-calcium based phosphate binder, ion exchange resin, which not selectively binds the phosphate ions in the gastrointestinal tract. In Hungary since 2005, on the basis of strict professional guidelines, sevelamer is available therapy for chronic kidney disease patients with severe hyperphosphatemia on dialysis. On the basis of 17 prospective and retrospective studies, sevelamer HCl is an at least as effective phosphate binder as other calcium based binders, in reducing the serum phosphate level. The advantage of sevelamer compared to the other widely used calcium based phosphate binders is the significantly lower serum calcium level and less hypercalcemic episodes. Sevelamer therapy in chronic kidney disease patients reduces the progression of cardiovascular calcification and it has also a positive effect on cholesterol and LDL-cholesterol levels. The side effects of sevelamer therapy may be acidosis, and gastrointestinal complaints. This year the improved form, sevelamer carbonate, becomes available in Hungary. Sevelamer carbonate has similar phosphate and cholesterol binding capacity as that of sevelamer HCl, but it has several advantages: it has a positive effect on acid-base parameters, and may be administered in powder form, which is beneficial for children and for patients with swallowing disorders. The primary analysis of the DCOR study has not revealed any significant difference in the survival and cardiovascular mortality between patient groups treated with calcium based binder or sevelamer. The RIND trial data showed improved survival of new dialysis patients, who were initially treated with sevelamer. Further clinical studies are needed to kaverify the benefits of sevelamer therapy (mortality, cardiovascular calcification) in chronic kidney disease patients. The management of hyperphosphatemia in chronic renal failure is a major challenge even in the first decade of the 21th century. This is the fact, despite that recently three different groups of phosphate binders are available in the clinical practice: the calcium based binders (calcium carbonate, calcium acetate), sevelamer and lanthanum. Which is the best binder? A calcium based or a non-calcium based one? Over the past decade, these issues are in the mainstream of clinical research of nephrology.]