Quinapyramine Got You Straight Down? We Already Have The Remedy

In the study assessing the effect of a single dose of FCM in fatigued women, Favrat et al. [28] have indeed found that 86% of patients had a phosphate level Neratinib manufacturer fatigue persistence, and hypophosphatemia development were reported. Iron-induced hypophosphatemia could play a role given that the results of some cognitive function tests do not improve after treatment. In patients with chronic kidney disease (CKD) and IDA, Macdougall et al. [40] have also found that the mean serum phosphate level decreased by 0.18?mmol/L at week 4 from baseline value but returned to normal value at week 52. In 2010, Mani et al. [10] has reported a case of profound hypophosphatemia after FCM injection in a stable renal transplant recipient. Some case reports have been published since then [9�C11] and we have recently published Quinapyramine the case of a patient with severe hypophosphatemia due to phosphate diabetes secondary to FCM injection [8]. In our study, 22% of patients developed hypophosphatemia after FS treatment but none of them developed severe hypophosphatemia. This frequency is high but hypophosphatemia was always moderate. We found only two case reports of hypophosphatemia after iron sucrose injection [41, 42]. Phosphate plays a key Selleck S3I 201 role in various biological processes. In recent years, new insights into the regulation of the phosphate metabolism have been obtained, including growing evidence suggesting that factors other than the PTH and vitamin D are involved in maintaining the phosphate balance. A new class of phosphate-regulating factors, the so-called ��phosphatonins,�� has also been shown to play a role in phosphate-wasting diseases [43]. Among them, FGF23 is involved in various diseases, including autosomal dominant hypophosphatemic rickets/osteomalacia (ADHR) or tumor-induced osteomalacia [44]. True hypophosphatemia can be induced by a decrease in intestinal absorption, increase in urinary phosphate excretion, or acute movement of extracellular phosphate into the cells. Then, the normal renal response to phosphate depletion is to increase phosphate reabsorption, leading to the virtual abolition of urinary phosphate excretion. Most of the filtered phosphate is reabsorbed in the proximal tubule by the sodium-phosphate cotransporter in the luminal membrane [45]. A phosphate plasma level