Chronic metabolic acidosis - are the clinical consequences underestimated?

Metabolic acidosis (MA) due to high protein intake, losses of bicarbonate ( renal-tubular or intestinal) as well as renal insufficiency may result in m ultiple disturbances. In the endocrine system alterations of the growth hor mone insulin-like growth factor I cascade, thyroid gland, insulin secretion and action, parathyroid hormone and plasma catecholamines were reported. C onsequences of MA are growth retardation, protein catabolism, muscle wastin g and negative nitrogen balance following stimulation of the ATP-dependent ubiquitin proteasom pathway and an enhanced oxidation of the branched chain amino acids. In bone demineralization (loss of CaCO3, Na and K) as well as stimulation of the activities of osteoclasts and inhibition of osteoblasts were reported. In the absence of renal insufficiency, hypercalciuria may d evelop and contribute to negative calcium balance and bone demineralization . Renal effects of MA include hypertrophy of the tubuli (due to increased a mmoniogenesis), nephrocalcinosis and urolithiasis (due to hypercalciuria an d hypocitraturia) as well as increased incidence of renal cysts. Whether co rrection of MA can retard the progression of renal failure is unknown as ye t. Prior correction of MA hyperphosphatemia should be treated to prevent th e risk of precipitation of calcium phospate in soft tissues, cardiac valves and kidney.