ஜர்னல் ஆஃப் நெப்ராலஜி & தெரபியூட்டிக்ஸ்

Aim: Hypomagnesemia is a frequent complication in RTRs, particularly in the early post-transplant period. Hypomagnesemia is usually associated with the use of calcineurin inhibitors. The relationship between cyclosporine use and hypomagnesemia is well known. However, it has been reported in several studies that hypomagnesemia was seen more in RTRs treated with tacrolimus compared to those treated with cyclosporine. In this study, we aimed to investigate the frequency and risk factors of post-transplant hypomagnesemia and effects of calcineurin inhibitors on hypomagnesemia among Turkish patients.

Patients and method: The study included 68 adult renal transplantation recipients. Hypomagnesemia was defined as serum magnesium level <1.4 mEq/L.

Result: Hypomagnesemia were found in 26 (38.2%) of the 68 patients. Levels of serum calcium and glucose were significantly higher in hypomagnesemic group compared to normomagnesemic group (9.7 ± 0.5 mg/dL vs. 8.4 ± 0.5, p: 0.029 and 107.3 ± 19.1 mg/dL vs. 95.8 ± 16.1, p: 0.010, respectively). Post-transplant duration was meaningfully longer in normomagnesemic group (9.5 months vs. 46.5, p: 0.001). Serum magnesium level was meaningfully higher in patients with cyclosporine compared to patients treated with tacrolimus (1.44 ± 0.5 mEq/L vs. 1.52 ± 0.2, p: 0.002, respectively). Post-transplant duration was significantly longer in cyclosporine group (12 months vs. 98.5, p: 0.001). Frequency of hypomagnesemia was significantly higher tacrolimus group (58% vs. 10%, p: 0.001).

Conclusion: The frequency of hypomagnesemia was high among Turkish renal transplant recipients, especially those treated with tacrolimus. Increased concentrations of serum calcium and glucose and the shorter post-transplant duration were risk factors for post-transplant hypomagnesemia.

IgA Nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Over the last years strong evidence suggest the existence of genetic factors in the development and/or progression of IgAN. IgAN does not exhibit classic single-gene Mendelian but rather a complex genetic inheritance pattern. Until now, two basic approaches have been used in genetic studies of IgAN: Genome-Wide linkage Analysis Studies (GWAS) and candidate-gene association studies. Many candidates have been proposed, but most were studied in the context of IgAN progression rather than causality. In addition, in part due to our lack of knowledge about disease pathogenesis, most candidates were predicated on sparse a priori evidence for involvement in IgAN. Overall, candidate-gene studies for IgAN have been largely unrevealing. The advantage of GWAS, on the other hand, is that they do not require a priori assumptions about disease pathogenesis. To date six GWAS of familial IgAN have identified several loci located on chromosomes 2, 4, 6, 7, 12 and 17. The functional mapping of genes involved in the disease is anticipated to proceed further from the identification of susceptibility loci identified by linkage analysis to the isolation of candidate genes within gene diseasesusceptibility loci. In conclusion, inheritance of IgAN follows a complex genetic pattern, most probably autosomal dominant inheritance with incomplete penetrance. It seems that several genetic loci contribute significantly to the disease susceptibility that underlies the primary immunologic defects observed in IgAN.

Structural and functional changes affecting the aging kidney predispose to an increased risk of Acute Kidney Injury (AKI) in the elderly, a condition which is becoming more and more relevant with the increase in life expectancy. The epidemiology of AKI in the elderly is not well assessed, because of the variable etiology, the coexistence of several comorbidities, the various clinical settings and geographical areas where the condition is managed, and the lack of uniform definition criteria. Currently, the use of the term AKI is suggested to mean any abrupt reduction in kidney function, while acute renal failure is just meant to indicate severe dysfunctions requiring renal replacement treatment. Comorbidities, common among elderly patients and several age-related conditions are risk factors for AKI. Moreover, also in elderly patients the presence of baseline proteinuria and reduced glomerular filtration rate are both powerful independent risk factors for AKI. Elderly patients with Chronic Kidney Disease (CKD) who develop AKI are at high risk for mortality, non-recovery from AKI and progression to more advanced stages of CKD and even to endstage renal disease. As a consequence, the challenge for nephrologists is to find strategies to either prevent AKI or prevent the transition from AKI to CKD.

Restless Legs Syndrome is a neuropathic disorder seen in end stage renal disease. Since biotin is dialyzable, we examined the relationship between biotin status and Restless Legs Syndrome in end stage renal disease (Study 1) and determined the effect of biotin supplementation on Restless Legs Syndrome symptoms (Study 2). Comparison of prevalence of biotin deficiency in those with and without Restless Legs Syndrome (Study 1) and randomized assignment, double-blinded, placebo-controlled study of biotin supplementation (Study 2) were in a medical center’s outpatient dialysis unit. In Study 1, patients received chronic dialysis and routine biotin supplementation at ≈300 μg daily (10 times the recommended dietary allowance). In the intervention Study 2, biotin was supplemented at 10,000 μg daily for 8 weeks; the placebo group received ≈300 μg of biotin daily. Outcome was measured by Restless Legs Syndrome symptom score and biotin status as indicated by activation coefficient of the biotin-dependent enzyme propionyl-CoA carboxylase in peripheral blood lymphocytes. In Study 1, patients with (n=30) were more likely than those without (n=19) Restless Legs Syndrome to be biotin deficient as judged by increased activation coefficient of propionyl-CoA carboxylase; mean (± 1SD) was 1.17 ± 0.65 vs. 0.87 ± 0.39, respectively (P=0.007). In Study 2, Restless Legs Syndrome score of the biotin group (n=16), improved from 20 ± 6 to 13 ± 11 (P=0.001). However, in the placebo group (n=15), Restless Legs Syndrome score also improved from 17 ± 8 to 12 ± 10 (P=0.01). Consequently, this change was not different between biotin and placebo. Mean activation coefficient of propionyl-CoA carboxylase of the biotin group (n=8) improved from 1.38 ± 0.76 to 0.81 ± 0.25 (P=0.01) and did not change in the placebo group (0.98 ± 0.44 vs. 1.17 ± 0.32; P=0.17). The improvement of biotin status and of Restless Legs Syndrome score with the 10,000 μg supplement suggests that large biotin supplements might be necessary to optimize biotin status in dialysis patients.

The heart and the kidneys act in tandem to regulate blood pressure, vascular tone, diueresis and to maintain intravascular volume homeostasis. Besides, the kidneys have a neuroendocrine function with interdependent physiological actions regulated by the renin-angiotensin-aldosterone system, sympathetic nervous system, and vasopressin and aterial natriuretic peptide. To investigate these complex pathophysiological mechanisms, a canine model for Congestive Heart Failure (CHF) compromised with Renal Dysfunction (RF) was used, to characterize the hemodynamic and neurohumoral aspects of renal function in 21 dogs. Five dogs were used as controls. Bipolar epicardial pacemaker leads were implanted at the apex of the right ventricle in 8 dogs and the dogs were subjected to ventricular pacing at 250-270 beats/min with an external pacemaker (Nihon Kohden) for a period of 11-21 days. This rapid pacing produced CHF. RF was induced by removal of the right kidney with ligation of the small branches of the left kidney in 8 dogs. Three dogs of each of the CHF and RF groups were used to produce CHF and RF in combination; one dog died due to infection. The glomerular filtration rates of the dogs with RF, CHF and CHF+RF were significantly lower than those of the controls, although among the dogs with RF, CHF and CHF+RF, there were no significant differences. In spite of no differences in blood pressure and renal hemodynamics, the levels of plasma renin activity, norepinephrine and vasopressin of CHF+RF group were significantly higher than those of RF and CHF groups. Taken together, these data suggest that in patients with CHF compromised by RF neurohumoral factors are maximally activated.

Objective: Accurate measurement of blood pressure (BP) remains a fundamental step in diagnosing and managing hypertension. The aim of this study is to evaluate the accuracy of office BP measurement using an automated office blood pressure (AOBP) device (BpTRU®) performed in a 5-minute cycle.

Participants and methods: 117 consecutive patients (mean age 55 ± 17 years, 60% women) referred for management of hypertension over a nine-month period are included in this study. BP readings with the BpTRU® device (BP recorded five times in five minutes), mean awake ambulatory blood pressure (ABP), and routine BP readings taken in the patient’s primary care physician (PCP) office were compared.

Results: Average of 5 BP readings for mean blood pressure using the AOBP device was similar to the mean awake ABP (systolic BP 133 ± 4 mmHg vs.135 ± 3 mmHg; (p = 0.2) and diastolic BP 80 ± 2 mmHg vs. 79 ± 2 mmHg; (p = 0.7)). Both systolic AOBP and awake ABP values were significantly lower than the systolic BP recorded in PCP office (144 ± 5 mmHg) (p < 0.001). The coefficient of correlation between the systolic/diastolic AOBP and the average of awake ABP (r = 0.70/0.72) was highly significant (p < 0.001). With the AOBP device, the first systolic reading was significantly higher than the average of the 2nd to 6th systolic readings (141 ± 2 mmHg vs. 133 ± 4 mmHg, p < 0.001).

Conclusion: BP measurement performed with the AOBP device in a 5-minute cycle more accurately measures BP in a physician office setting when compared to single BP measurement. Relying on the1st BP measurement or a single reading may lead to over estimation of BP.