Effects of Acute Acid Loading on the Risk of Calcium Phosphate and Calcium Oxalate Crystallization in Urine

The aim of this study was to examine the risk of calcium phosphate and calcium oxalate crystallization during acute acid loading under controlled conditions. The effects of acute acid loading on rates of renal excretion of calcium, magnesium, phosphate, citrate, oxalate and urine pH were studied in healthy subjects. The risk of calcium phosphate and calcium oxalate crystallization were evaluated by estimates of the ion activity products of calcium phosphate [AP(CaP)-index] and calcium oxalate [AP(CaOx)-index] according to Tiselius. In addition, the risk of brushite [AP(Bru)-index] crystallization was estimated. An acute acid load administered as ammonium chloride (NH4Cl) produced increased urinary excretion of calcium, phosphate and oxalate, decreased urinary excretion of citrate, and a decrease in urine pH. Consequently, calcium-citrate-ratio in urine increased markedly in response to acid loading. AP(CaP)-index decreased markedly due to a fall in urine pH. AP(Bru)-index decreased slightly and remained low throughout the study. AP(CaOx)-index increased significantly, and acid loading is suggested as a risk factor for calcium oxalate stone formation

Whole body acid-base modeling revisited

The textbook account of whole-body acid-base balance in terms of endogenous acid production, renal net acid excretion and gastrointestinal alkali absorption which is the only comprehensive model around, has never been applied in clinical practice or been formally validated. In order to improve understanding of acid-base modeling, we managed to write up this conventional model as an expression solely on urine chemistry. Renal net acid excretion and endogenous acid production was already formulated in terms of urine chemistry, and we could from the literature also see gastrointestinal alkali absorption in terms of urine excretions. With few assumptions it was possible to see that this expression of net acid balance was arithmetically identical to minus urine charge, whereby under the development of acidosis, urine was predicted to acquire a net negative charge. The literature already mentions unexplained negative urine charges so we scrutinized a series of seminal papers and confirmed empirically the theoretical prediction that observed urine charge did acquire negative charge as acidosis developed. Hence we can conclude that the conventional model is problematic since it predicts what is physiologically impossible. Therefore, we need a new model for whole-body acid-base balance, which doesn't have impossible implications. Furthermore, new experimental studies are needed to account for charge imbalance in urine under development of acidosis.</p