1.
Challenges in management of diabetic ketoacidosis in hemodialysis patients, case presentation and review of literature.
Seddik, AA, Bashier, A, Alhadari, AK, AlAlawi, F, Alnour, HH, Bin Hussain, AA, Frankel, A, Railey, MJ
Diabetes & metabolic syndrome. 2019;(4):2481-2487
Abstract
Chronic kidney disease is associated with accumulation of uremic toxins that increases insulin resistance which will lead to blunted ability to suppress hepatic gluconeogenesis and reduce peripheral utilization of insulin. CKD patients fail to increase insulin secretion in response to insulin resistance because of acidosis, 1,25 vitamin D deficiency, and secondary hyperparathyroidism. Hemodialysis causes further fluctuations in glycemic control due to alterations in insulin secretion, clearance and resistance. DKA is uncommon in hemodialysis patients because of the absence of glycosuria and osmotic diuresis which accounts for most of the fluid and electrolyte losses seen in DKA, anuric patients may be somewhat protected from dehydration and shock, although still subject to hyperkalemia and metabolic acidosis. However, substantial volume loss can still occur due to a prolonged decrease in oral intake or increased insensible water losses related to tachypnoea and fever. There is no current guidelines for the management of diabetic ketoacidosis in anuric hemodialysis patients considering their differences than general population. In this review article we reviewed the literature and came with specific recommendations for management of Ketoacidosis in patients with CKD treated by hemodialysis.
2.
SGLT2 inhibitors-induced electrolyte abnormalities: An analysis of the associated mechanisms.
Filippatos, TD, Tsimihodimos, V, Liamis, G, Elisaf, MS
Diabetes & metabolic syndrome. 2018;(1):59-63
Abstract
AIMS: Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs that affect serum electrolytes levels. The aim of this review is the detailed presentation of the associated mechanisms of the SGLT2 inhibitors-induced electrolyte abnormalities. MATERIALS AND METHODS Eligible trials and relevant articles published in PubMed (last search in July 2017) are included in the review. RESULTS SGLT2 inhibitors induce small increases in serum concentrations of magnesium, potassium and phosphate. The small increase in serum phosphate concentration may result in reduced bone density and increased risk of bone fractures, mainly seen with canagliflozin, but recent meta-analyses did not show increased risk of bone fractures with SGLT2 inhibitors. CONCLUSION The increases in serum electrolytes levels may play a role in the cardiovascular protection that has been recently reported with empagliflozin and canagliflozin.
3.
Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome.
Davidson, MB, Thakkar, S, Hix, JK, Bhandarkar, ND, Wong, A, Schreiber, MJ
The American journal of medicine. 2004;(8):546-54
Abstract
Tumor lysis syndrome is an oncologic emergency that is characterized by severe electrolyte abnormalities and, frequently, by acute renal failure. The syndrome typically occurs in patients with lymphoproliferative malignancies, most often after initiation of treatment. The pathophysiology involves massive tumor cell lysis resulting in the release of large amounts of potassium, phosphate, and uric acid. Deposition of uric acid and calcium phosphate crystals in the renal tubules may lead to acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. The kidney normally excretes these products, and consequently preexisting renal failure exacerbates the metabolic derangements of tumor lysis syndrome. Standard treatment aims to clear high plasma levels of potassium, uric acid, and phosphorus; correct acidosis; and prevent acute renal failure by way of aggressive intravenous hydration; lowering serum potassium levels; use of allopurinol; urinary alkalinization; or renal replacement therapy (if necessary). Allopurinol is the standard of care for treating hyperuricemia of malignancy, but is associated with drawbacks. Recombinant urate oxidase (rasburicase), which recently became available in the United States, provides a safe and effective alternative to allopurinol for lowering uric acid levels and preventing uric acid nephropathy.