Ca2+-Mg2+-dependent ATP-ase activity in hemodialyzed children. Effect of a hemodialysis session

In the course of chronic kidney disease (CKD) the intracellular erythrocyte calcium (Cai2+) level increases along with the progression of the disease. The decreased activity of Ca2+-Mg2+-dependent ATP-ase (PMCA) and its endogenous modulators calmodulin (CALM), calpain (CANP), and calpastatin (CAST) are all responsible for disturbed calcium metabolism. The aim of the study was to analyze the activity of PMCA, CALM, and the CANP-CAST system in the red blood cells (RBCs) of hemodialyzed (HD) children and to estimate the impact of a single HD session on the aforementioned disturbances. Eighteen patients on maintenance HD and 30 healthy subjects were included in the study. CALM, Cai2+ levels and basal PMCA (bPMCA), PMCA, CANP, and CAST activities were determined in RBCs before HD, after HD, and before the next HD session. Prior to the HD session, the level of Cai2+ and the CAST activity were significantly higher, whereas bPMCA, PMCA, and CANP activities and the CALM level were significantly lower than in controls. After the HD session, the Cai2+ concentration and the CAST activity significantly decreased compared with the basal values, whereas the other parameters significantly increased, although they did not reach the levels of healthy children. The values observed prior to both HD sessions were similar. Cai2+ homeostasis is severely disturbed in HD children, which may be caused by the reduction in the PMCA activity, CALM deficiency, and CANP-CAST system disturbances. A single HD session improved these disturbances but the effect is transient

Sodium thiosulfate treatment of soft-tissue calcifications in patients with end-stage renal disease

Five patients on maitenance hemodialysis for more than five years, who had tumoral calcifications, were treated by sodium thiosulfate for three to 15 months. Four patients with periarticular and soft-tissue calcifications achieved regression of varying degrees and the motion of the adjacent joints was considerably improved. The fifth patient had calcification of penis; sodium thiosulfate produced early relief of symptoms and later complete disappearance of the calcification

Biotin for diabetic peripheral neuropathy

Biotin in high doses was given for 1-2 years to three diabetic patients suffering from severe diabetic peripheral neuropathy. Within 4-8 weeks there was a marked improvement in clinical and laboratory findings. It is suggested that in diabetes may exist a deficiency, inactivity or unavailability of Biotin, resulting in disordered activity of biotin-dependent enzyme, pyruvate carboxylase, leading to accumulation of pynivate and/or depletion of aspartate, both of which play a significant role in nervous system metabolism. Based on our good results, regular biotin administration could be suggested for every diabetic patient for the prevention and management of peripheral neuropathy although extensive randomised clinical trials are required. biotin / diabetes melitus / diabetic peripheral neuropathy. © 1990

Hematocrit-lowering effect following inactivation of renin-angiotensin system with angiotensin converting enzyme inhibitors and angiotensin receptor blockers

Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary disease, and congestive heart failure. Accordingly, RAS inactivation may confer susceptibility to the hematocrit-lowering effects of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Indeed, a dose-dependent decrease in hematocrit is observed within the first month of such therapy. In the majority of patients with hypertension decreases in hematocrit values after RAS inactivation are small and not clinically important. In extreme conditions, however, such as erythrocytosis after successful renal transplantation, secondary polycythemia of chronically hypoxemic COPD patients, erythrocytosis associated with renovascular hypertension, severe cardiac or renal failure, the hematocrit-lowering effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blocker may be profound and even lead to or worsen anemia. Hematocrit reaches its nadir value within three months, and then it remains stable during long-term observations. After discontinuation of RAS blockade, hematocrit values rise gradually over the next three to four months towards the pretreatment levels. The mechanism(s) related to this phenomenon is not yet fully understood, but angiotensin II seems to be responsible for inappropriately sustaining secretion of erythropoietin despite hematocrit elevation and capable to directly stimulate the erythroid progenitors in bone marrow to produce erythrocytes

Transrenal aortic endograft placement in patients with renal artery disorders

Endovascular repair of abdominal aortic aneurysms (AAA) is an alternative to conventional surgical aortic reconstruction. However the presence of renal artery stenosis (RAS) and/or accessory renal arteries may alter the endovascular approach in these cases. We present two cases with infrarenal aneurysms and a coexisting unilateral renal artery stenosis (first case) and accessory renal artery (second case). In both patients endovascular treatment was undertaken. In the first patient a stent was placed for the RAS and an aortic endograft with suprarenal fixation for the aneurysm. In the second patient the placement of an aortic endograft with suprarenal fixation occluded the accessory renal artery. In the first patient renal function was normal pre- and post-intervention. In the second patient, renal function was normal pre-intervention but showed a slight deterioration postoperatively, returning to normal after 10 days. Both patients were normotensive pre- and post-intervention. In conclusion, RAS and AAA may be treated by the placement of a stent and a stent-graft simultaneously. During endovascular repair of AAA, a significant accessory renal artery (around 3 mm in diameter) may safely be excluded in patients with otherwise normal renal function. © 2003 Elsevier Science Ltd. All rights reserved