Magnesium and vitamin D play important roles in most cells of the body. These nutrients act in a coordinated fashion to maintain physiologic functions of various organs, and their abnormal balance could adversely affect these functions. Therefore, deficient states of both nutrients may lead to several chronic medical conditions and increased cardiovascular and all-cause mortality. Chronic kidney disease (CKD) patients have altered metabolism of both magnesium and vitamin D. Some studies indicate that magnesium could have a role in the synthesis and metabolism of vitamin D, and that magnesium supplementation substantially reversed the resistance to vitamin D treatment in some clinical situations. Recent observational studies also found that magnesium intake significantly interacted with vitamin D status and, particularly with the risk of cardiovascular mortality. It is therefore essential to ensure adequate levels of magnesium to obtain the optimal benefits of vitamin D supplementation in CKD patients. In this review, we discuss magnesium physiology, magnesium and vitamin D metabolism in CKD, potential metabolic interactions between magnesium and vitamin D and its clinical relevance, as well as the possible role of magnesium supplementation to assure adequate vitamin D levels.
BACKGROUND AND AIMS Patients on renal replacement therapy are reported to have altered humoral immunity, which is demonstrated by a decreased response to different vaccines. However, in kidney transplant (KT) patients, vaccines are even less immunogenic in terms of antibody response. Therefore, these patients have a higher risk of critical infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which makes them eligible for early vaccination. The aim of this study was to compare the humoral response after complete vaccination against SARS-CoV-2 between KT patients and peritoneal dialysis (PD) patients. METHOD We conducted a single-center, retrospective study, which included 67 KT recipients and 49 prevalent PD patients. Patients were excluded if they had previously known SARS-CoV-2 infection or positive anti-nucleocapsid IgG or IgM antibodies. Completion of vaccination was defined as two doses of a messenger RNA vaccine (BNT162b2 messenger RNA vaccine [Pfizer-BioNTech] or messenger RNA-1273 [Moderna]), two doses of viral vector vaccine ChadOx1 nCoV-19/AZD1222 (AstraZeneca) or one dose of JNJ-78 436 735 (Janssen) vaccine. Anti-spike (anti-S) IgG antibodies were measured, at least, 21 days after the completion of vaccination and before receiving a `booster’ dose. A value of anti-S >0.8 U/mL was considered positive. Immunogenicity of the vaccine, measured by anti-spike IgG antibodies, was compared between KT recipients and PD patients. RESULTS The mean age of the population was 58.8 ± 13.6 years and 62.0% were males (similar between the two groups). The median interval between completion of vaccination and serologic analysis was 4.1 months in KT patients and 7.1 months in PD patients. In KT patients, the median anti-S level was 1.50 U/mL (IQR 0.0–27.3) versus 97.0 U/mL (IQR 34.5–447.0) in PD patients (P < .001). In the KT group, there were 31 (46.3%) non-responders (patients without detectable levels of anti-S), while in the second there were only two (4.1%). In KT patients, anti-S levels were not associated with time since transplant or immunosuppressive induction therapy. In PD patients, anti-S levels were not associated with time since the beginning of PD. In both groups, anti-S levels were not associated with age, gender, type of administered vaccine or interval between completion of vaccination and serologic analysis. CONCLUSION We found a significant difference in humoral responses to the vaccine between PD and KT transplant patients with no previous exposure to SARS-CoV-2. In PD patients, the vaccine seemed to be effective. On the contrary, KT patients had a significantly weaker rising of anti-S titers, with a high proportion of patients not responding to the vaccine. This study emphasizes the negative impact of immunosuppression on humoral responses, reinforcing the need for a `booster’ dose in this group of patients.
Background and Aims In the last decade, new therapeutic regimens have dramatically improved the prognosis of cancer patients and changed the paradigm of a previously highly lethal disease, increasing the number of cancer patients with chronic kidney disease (CKD) who progress to end-stage kidney disease (ESKD). However decision-making regarding dialysis initiation in patients with cancer and ESKD remains however controversial. The aim of our study was to characterize the clinical course and evaluate survival outcomes of cancer patients on chronic hemodialysis (HD). Method We conducted a retrospective study of chronic HD patients in a single oncology hospital unit between January 1991 and November 2022. Outpatients on HD for more than one month, who underwent dialysis after the diagnosis of cancer were included. Univariate and multivariate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality were estimated using the Cox proportional hazards risk model. Results Two hundred and twelve patients were recruited. Mean age at HD initiation was 65.7±14.7 years. The most prevalent ESKD etiologies were cast nephropathy, chronic interstitial nephritis, and surgical removal of the kidney. The most common tumors were genitourinary, multiple myeloma (MM) and gastrointestinal corresponding to 80.6% of all cancers. There were 143 deaths over a median follow-up period of 23 months (IQR: 7.25 – 54). The overall survival rates were 76.5% at 1 year, 59.6% at 3 years and 39.2% at 5 years. The median survival time was 44 months (95% CI: 30.58 – 51.42). An increased mortality risk was observed in patients with MM (HR: 3.38; 95% CI: 1.01-11.39; p = 0.045) and in those who started HD from 2001 to 2011 (HR: 1.60; 95% CI: 1.06-2.42; p = 0.001). The presence of metastasis or multiple tumors was not associated with all-cause mortality. Conclusion Our results highlight the importance of considering cancer patients for renal support therapies, including those with multiple tumors and metastatic disease. In fact, with the new treatments available, many patients have chronic oncological disease non-fatal in the short term. To the best of our knowledge, this is the largest study of cancer patients on chronic HD.
Background and Aims Infection of the renal allograft by Polyomavirus BK (BKV) causes tubular cell injury and interstitial inflammation, which leads to subsequent interstitial fibrosis and tubular atrophy (IFTA). The presence and degree of inflammation within these areas (i-IFTA) is associated with worse outcomes in kidney transplant (KT) patients. The aim of this study was to investigate the association between BKV viremia and viruria and the presence of IFTA and i-IFTA, decline of renal function, and graft loss. Method We conducted a single-center retrospective case-control study, which included all patients who underwent an allograft biopsy between January 2018 and December 2022. All biopsies were made for-cause (allograft dysfunction with increased serum creatinine). Real-time polymerase chain reaction was used to detect and quantitate BK viral load in serum and urine samples. Patients were included if they had at least 6 months since KT and if they had serial evaluation of BKV viremia and viruria previously to the biopsy. We evaluated, in the graft biopsy, the percentage of IFTA, and also i-IFTA. Estimated glomerular filtration rate (eGFR) was obtained at baseline and 1 year after the biopsy. Graft loss was evaluated at 6 months and 1 year after the biopsy. Results Mean age of the population was 53,5 years and 67% were males. A total of 116 biopsies were performed during the studied period and 72 met the inclusion criteria. Ten percent of patients developed persistent (≥ 3 months) BKV viremia, 24% developed persistent BKV viruria, and 18% developed persistent JCV viruria. Five cases of polyomavirus-associated nephropathy were diagnosed. The other most common diagnoses were T cell-mediated rejection (24%), antibody-mediated rejection (15%), and focal segmental glomerulosclerosis (15%). In patients with persistent BKV viremia, a higher viral load had a strong positive association with the degree of i-IFTA (r=0.954; P = .001). Patients with BKV viremia and/or viruria were more likely to present more severe IFTA (≥ 40%) and i-IFTA (grade ≥2) in allograft biopsy (P = .03). Patients with higher degrees of IFTA and i-IFTA were more likely to experience graft loss 1 year after the biopsy (P = .01). There was no significant association between the presence of BKV viremia and/or viruria and the decline of eGFR, nor with the incidence of graft loss 1 year after the biopsy. In multivariable analysis adjusted for age, eGFR at the time of biopsy, the presence of donor-specific antibodies and the main diagnosis of allograft biopsy, the presence of BK viremia and/or viruria was a significant predictor of more severe IFTA and i-IFTA (P = .04). Conclusion In our population, higher BK viremia loads were associated with more extensive inflammation within areas of IFTA. Patients with BK viremia and/or viruria, independently of the main diagnosis of the biopsy, were more likely to exhibit more severe IFTA and i-IFTA in allograft biopsies, but no association with the incidence of dialysis at 1 year was shown. Longer prospective studies are needed to investigate whether BKV infection treatment/ reduction of immunosuppression can slow down fibrosis progression and minimizes i-IFTA.
BACKGROUND AND AIMS Bilateral acute renal artery thrombosis (BARAT) is a rare and catastrophic condition. This diagnosis is often delayed or unrecognized and the true incidence may be underestimated. To the best of our knowledge, only three cases are reported in literature—all treated conservatively. We present two cases of BARAT who recovered kidney function under conservative approach. METHOD Data was obtained from the electronical medical record. RESULTS: Case 1:A 73-year-old male with no history of cardiac disease, hypertension or recent trauma was admitted with right flank pain and vomiting. He had severe hypertension (204/103 mmHg), anuria with acute kidney injury (AKI) and elevated lactate dehydrogenase (LDH). He started haemodialysis on admission. Renal computerized tomography (CT) angiogram showed bilateral arterial thrombosis—left renal artery was totally occluded and partial occlusion of the right renal artery with slight enhancement of the corresponding kidney (Fig. 1). Vascular surgery posed no surgical indication and systemic anticoagulation with low molecular weight heparin (LMWH) was started. A thorough screening for occult neoplasm and hypercoagulable state causes was negative. He was independent from dialysis 54 days after. Currently (6 months after), he is on stage 3b chronic kidney disease (CKD) with a serum creatinine (sCr) 2.19 mg/dL. Case 2: A 65-year-old female was admitted with dyspnea associated with right lumbar pain, severe hypertension (230/140 mmHg), peripheral edema and pulmonary congestion. Her prior history included heavy smoking and atherosclerotic artery disease with placement of aortoiliac stent 20 years before. She had no history of atrial fibrillation. She was admitted with de novo cardiac insufficiency with a mild reduction of left ventricular ejection fraction. After admission, she developed anuric AKI with refractory fluid overload and started dialysis. CT angiogram showed a large aortic thrombus that occluded both renal arteries. The right principal renal artery was occluded but the kidney had partial reperfusion from an accessory artery (Fig. 2). The left renal artery was totally occluded. Vascular surgery posed no surgical indication and the patient started LMWH. She was independent from haemodialysis 30 days after. She has currently a stage 4 CKD with sCr 3.2 mg/dL. CONCLUSION There are currently no guidelines on both the acute and long-term management of BARAT. The few reported cases of BARAT were all treated conservatively with systemic anticoagulation and had late but consistent kidney function recovery. This suggests that renal parenchyma could still be viable after BARAT. Could early revascularization therapies accelerate recovery and minimize irreversible damage? In both cases, a cause was not found. Much is still unknown about the pathophysiology, and further research is warranted.
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