Chronic Kidney Disease, Gut Dysbiosis, and Constipation: A Burdensome Triplet.

Gut dysbiosis has been implicated in the progression of chronic kidney disease (CKD). Alterations in the gut environment induced by uremic toxins, the dietary restriction of fiber-rich foods, and multiple drugs may be involved in CKD-related gut dysbiosis. CKD-related gut dysbiosis is considered to be characterized by the expansion of bacterial species producing precursors of harmful uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, and the contraction of species generating beneficial short-chain fatty acids, such as butyrate.

Remission of membranoproliferative glomerulonephritis associated with a noncirrhotic portosystemic shunt after percutaneous transhepatic portal vein embolization.

We present a case of a 75-year-old man with nephrotic syndrome and renal insufficiency caused by immune complex-mediated secondary membranoproliferative glomerulonephritis. He developed hepatic encephalopathy. A congenital portosystemic shunt was identified, indicating a diagnosis of membranoproliferative glomerulonephritis with noncirrhotic portosystemic shunt.

[Relationship between serum calcium level and PTH concentration proved with sevelamer hydrochloride].

About a dialysis patient's calcium-phosphate (Ca.P) metabolism, in general good control is obtained by use of sevelamer hydrochloride. As for this, what is significantly depended on not only lower P concentration but also lower Ca concentration by the change to sevelamer hydrochloride from calcium carbonate.

[Treatment with phosphate binder (sevelamer hydrochloride, calcium carbonate) based on PTH].

When sevelamer hydrochloride is used as a phosphate binder instead of the more common calcium carbonate, the PTH rises. This has been observed in many cases and makes it more difficult for practical use. However, considering the calcium load, the excessive dosing of calcium carbonate must be avoided.