The Role of the Endocrine System in the Regulation of Acid–Base Balance by the Kidney and the Progression of Chronic Kidney Disease

Abstract

Systemic acid–base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate filtered by the kidney. In chronic kidney disease (CKD), acid retention may occur when dietary acid production is not balanced by bicarbonate generation by the diseased kidney. Hormones including aldosterone, angiotensin II, endothelin, PTH, glucocorticoids, insulin, thyroid hormone, and growth hormone can affect acid–base balance in different ways. The levels of some hormones such as aldosterone, angiotensin II and endothelin are increased with acid accumulation and contribute to an adaptive increase in renal acid excretion and bicarbonate generation. However, the persistent elevated levels of these hormones can damage the kidney and accelerate progression of CKD. Measures to slow the progression of CKD have included administration of medications which inhibit the production or action of deleterious hormones. However, since metabolic acidosis accompanying CKD stimulates the secretion of several of these hormones, treatment of CKD should also include administration of base to correct the metabolic acidosis.

Changes of Dissociative Properties of Hemoglobin in Patients with Chronic Kidney Disease

“…CKD is a disease correlating with the degree of interstitial fibrosis, renal tube destruction, the progression of numerous diseases, and kidney tissue hypoxia [ 23 ]. Typically, increased angiotensin II production is observed in CKD (ATII) [ 24 ]. It is formed as a result of a cascade of renin-dependent enzyme reactions and angiotensin-converting enzymes (ACE).…”