Scielo RSS <![CDATA[Portuguese Journal of Nephrology & Hypertension]]> vol. 37 num. 4 lang. en <![CDATA[SciELO Logo]]> <![CDATA[Dialysis Modality Option: A Process to Audit and Improve]]> <![CDATA[Is Kidney Transplantation the Most Sustainable Modality for Stage 5 Chronic Kidney Disease Treatment?]]> <![CDATA[Postoperative Neutrophil to Lymphocyte and Platelet Ratio and Delayed Graft Function]]> ABSTRACT Introduction: Delayed graft function (DGF), an outcome for which inflammation is critical, has been associated with worse outcomes after kidney transplantation (KT). The neutrophil to lymphocyte and platelet (NLP) ratio is a biomarker of systemic inflammation. We assessed postoperative NLP ratio applicability as an early predictor of DGF in KT patients. Methods: Retrospective cohort of adult patients submitted to KT at our unit, between 1 January 2010 and 31 December 2020. NLP was calculated at 24 hours post-KT. Primary outcome was development of DGF. Logistic regression was calculated to determine significant factos which may have contributed to DGF. Results: We included 527 patients with a mean age of 49.9 ± 12.8 years. In 47.8% of patients expanded criteria donors were used, and in 3.6% non-heart-beating donors. DGF occurred in 17.8% of patients. Mean post-KT NLP was higher in patients submitted to induction therapy with lymphocyte depleting antibodies (50.2±40.3 vs 11.9±7.4 with basiliximab, p&lt;0.001), but it was found to be higher even before KT (5.2±1.8 vs 1.9±1.2, p=0.001). Grafts from non-heart-beating donors (OR 13.989, 95% CI 4.741, 41.274, p=0.000), longer warm ischemia time (OR 1.035, 95% CI 1.007, 1.064, p=0.014) and higher NLP ratio 24 hours after transplantation (OR 1.009, 95% CI 1.002, 1.016, p=0.015) were independently associated with DGF. Conclusion: Higher NLP ratio at 24 hours after KT was independently associated with DGF. This reflects the impact of inflammation on KT outcomes and highlights the role of the NLP ratio as a sensitive marker of systemic inflammatory response after KT. <![CDATA[SARS-CoV-2 Antibody Response to Vaccination in Peritoneal Dialysis Patients]]> ABSTRACT Introduction: Chronic kidney disease patients have a higher risk of infection and worse clinical outcomes after coronavirus disease. We aimed to assess the prevalence of infection and the humoral response after vaccination in peritoneal dialysis patients. Methods: Three types of vaccines were administered (two doses) with the antibody detection at least six months after. Coronavirus disease 2019 infections, hospital admissions, and deaths were evaluated. Results: From 70 prevalent patients, 45 were included. There was a significant increase in antibody level, with a median of 92 (36, 447) U/mL. Only 4% of patients remained seronegative. History of immunosuppressive therapy was associated with no response (100% vs 60%, p=0.010). There were two infections after the vaccination, without hospital admission. Conclusion: Immunization against coronavirus disease was effective in generating a humoral response in peritoneal dialysis patients. There was also an evident impact of immunosuppressive therapy on vaccine response in peritoneal dialysis patients. <![CDATA[Chronic Kidney Disease and Serum Uric Acid Level in Hypertensive and/or Diabetic Patients]]> ABSTRACT Introduction: Chronic kidney disease is a worldwide health problem. Uric acid seems to have a relationship with chronic kidney disease, but its role is still controversial. The aim of the present study was to estimate the prevalence of chronic kidney disease in hypertensive and/or diabetic patients in a Basic Family Health Unit and to evaluate the association of uric acid levels with chronic kidney disease. Methods: A cross-sectional study was conducted with 182 adults with arterial hypertension and/or diabetes mellitus followed-up in a Basic Family Health Unit between 2019 and 2020. Demographic, clinical, behavioural and biochemical data were collected through the review of medical records. The exposure of interest was the uric acid and the outcome was chronic kidney disease. For the association of uric acid and chronic kidney disease, univariate and multivariate logistic regression analysis were performed. Results: The prevalence of chronic kidney disease in the sample was 17% (95% CI = 12.1-23.3). After adjustment analysis for age, sex, arterial hypertension, diabetes mellitus, cardiovascular diseases, dyslipidemia, smoking, alcohol consumption, antihypertensive and lipidlowering drugs, there was a positive association (ORa = 1.65 (95%CI = 1.11-2.45), p = 0.013) between uric acid and chronic kidney disease. Conclusion: The increase in uric acid in 1 mg/dL was associated with a 1.6 times higher chance of chronic kidney disease in hypertensive and/or diabetic population. <![CDATA[Mineral and Bone Disorder in Patients Living with the Human Immunodeficiency Virus (HIV) on Hemodialysis: a case series]]> ABSTRACT Introduction: Survival of patients living with HIV has increased and low bone mineral density and fractures are reported in this population. Chronic kidney disease causes bone disorder, which also contributes to low bone mineral density, fractures, and vascular calcification. This study aimed to assess the osteometabolic profile in HIV patients undergoing hemodialysis. Methods: Data of 21 patients were assessed. Laboratory: calcium, phosphorus, albumin, intact parathyroid hormone, total alkaline phosphatase, 25OH-vitamin D, CD4 count and HIV viral load. Bone mineral density was assessed by bone densitometry, and x-rays were taken to determine vascular calcification scores. Results: The median age of patients was 48 years (81% male) and the median times of HIV infection and hemodialysis were 132 and 120 months, respectively. Median serum calcium and phosphorus levels were normal and the median intact parathyroid hormone was 360 pg/mL. Osteopenia was diagnosed in 33% of patients and osteoporosis in 33%; 24% of patients had previously suffered fractures. The Kauppila score was higher in patients with fractures (p=0.040). Vascular calcification was identified in 12 (57%) patients. Inverse correlations were demonstrated between the Kauppila score and the T-score of the femoral neck (p&lt;0.001) and the T-score of the lumbar spine (p&lt;0.001); and between the Adragão score and T-score of the femoral neck (p=0.001) and the T-score of the lumbar spine (p=0.001). Conclusion: A high prevalence was observed of low bone mineral density, fractures and vascular calcification in HIV patients on hemodialysis. It is necessary to confirm these results with larger studies and with a control group of non-HIV patients. <![CDATA[Sodium Intake Targets in Peritoneal Dialysis Patients: A Real-Life Challenge]]> ABSTRACT Introduction: Optimal fluid balance in peritoneal dialysis requires adequate urinary and peritoneal water and sodium removal and restriction of dietary sodium intake (&lt;2 g/day). We aim to study the relationship between sodium intake, blood pressure control and medication burden in peritoneal dialysis patients. Methods: Observational, cross-sectional study of chronic peritoneal dialysis patients followed in our hospital in March 2022. We estimated patient’s sodium intake according to the equations proposed by Kim et al. Mean ambulatory blood pressure was categorized in controlled, stage one, stage two and stage three hypertension. A qualitative evaluation of sodium intake was done by asking patients about their compliance with a low-salt diet. Results: Eighty-two patients: mostly men, with a mean age of 54.1±14.7 years and dialysis vintage of 26.2±18.7 months. Most patients were on continuous ambulatory peritoneal dialysis (63.4%) and the mean weekly Kt/V was 2.2±0.4. A percentage of 85.4% of our patients had residual diuresis, averaged at 1257±867 mL/day. Mean dietary sodium intake was 3.5±1.1 g; it was higher in men and patients with uncontrolled hypertension, regardless of age, dialysis vintage and other comorbidities. We found a strong correlation between dietary sodium intake and residual diuresis, systolic blood pressure, diastolic blood pressure and the number of anti-hypertensive drugs. Patients with a sodium intake ≥ 3.3 g had higher risk of uncontrolled BP and higher medication burden. Qualitative evaluation of this sub-population revealed that only 2.3% (n=1) admitted non-compliance with a low-sodium diet. Conclusion: We found a strong correlation between estimated dietary sodium consumption, blood pressure control and medication burden. Most importantly, there was a striking difference between patient’s perception of sodium consumption and the actual results. Our results highlight the importance of dietary salt restriction in blood pressure control and reinforce the need for a dietary consultation in peritoneal dialysis patients. <![CDATA[Abdominal Wall Hernias in Peritoneal Dialysis Patients: Risk Factors and Technique Survival]]> ABSTRACT Introduction: Peritoneal dialysis patients are at increased risk of developing abdominal wall complications, including hernias. This study aimed to determine the incidence of hernias in peritoneal dialysis patients, identify risk factors, and evaluate their impact on technique survival. Methods: A retrospective cohort study was conducted, including prevalent peritoneal dialysis patients in a single center, from January 2010 to October 2020. Data on baseline characteristics, previous abdominal surgeries, and hernia history were collected. Patients with diagnosed hernias during peritoneal dialysis were compared to a control group. Results: Among 155 peritoneal dialysis patients, hernias occurred in 29% (n=45) of the population, with an incidence rate of 0.09 hernias/patient/year. Umbilical hernias were the most common subtype. Autosomal dominant polycystic kidney disease (OR (odds ratio) 3.925; 95% confidence interval (CI), 1.208 - 12.75) history of surgical repaired hernias (OR 5.586; 95% CI 1.540 - 20.255) and a higher number of previous abdominal surgeries (OR 1.680; 95% CI 1.025 - 2.752) were independent predictors of hernia development. Surgical treatment was performed in 59.3% of cases, with a 18.8% recurrence rate. Higher daytime infusion volumes were associated with hernia recurrence (p=0.045). Peritoneal dialysis technique survival did not differ significantly between the hernia and control groups (p=0.700). Conclusion: Hernias are frequent in peritoneal dialysis patients, with autosomal dominant polycystic kidney disease, previous abdominal surgeries, and history of surgically repaired hernias as identified risk factors. Hernias do not significantly interfere with peritoneal dialysis technique survival, but comprehensive management strategies, including early surgical repair and peritoneal dialysis prescription adaptations, can optimize outcomes. <![CDATA[Principles of Antibiotic Adjustment in Renal Failure]]> ABSTRACT The incidence and prevalence of patients with acute kidney injury and chronic kidney disease have increased significantly in recent years. Renal failure is associated with profound changes in the pharmacokinetics and pharmacodynamics of antibiotics. It is widely recognized that inadequate adjustment of antibiotics can lead to undertreatment and impair the patient’s clinical outcome. The difficulty of adjusting drugs in renal dysfunction begins with estimating renal function (urinary clearance of inulin is rarely performed, and creatinine/cystatin-based formulas have widely recognized limitations, especially in acute kidney injury). Management becomes more complex, given the frequent changes in the volume of distribution and the introduction of different renal replacement therapies. Efforts must be made to optimize antibiotic targets in this population. This study aims to review the principal pharmacokinetic and pharmacodynamic modifications that occur with antibiotics in chronic kidney disease and acute kidney injury, with the goal of offering strategies to enhance antibiotic therapy in these scenarios. <![CDATA[C3 Glomerulopathy: A Rare Entity with Future Directions]]> ABSTRACT C3 glomerulopathies are a rare group of glomerular diseases resulting from excessive activation of the alternative complement pathway. The pathogenesis involves genetic, acquired, or immunologic defects in regulators of the alternative complement pathway. Currently, these diseases have a chronic course with progression to end-stage renal disease in up to 50% of adult patients. We report a case of a young woman who presented with nephrotic syndrome and renal disfunction. During follow-up, the diagnosis of C3 glomerulopathy associated with complement factor I deficiency was established. After relapse of nephrotic proteinuria, immunosuppressive therapy with mycophenolate mofetil and glucocorticoid was added to supportive care. There is no disease-specific therapy for C3 glomerulopathies, and treatment is focused on reducing proteinuria and renal inflammation. Supportive treatment with ACE inhibitors or angiotensin receptor blockers is the first-line therapy. Immunosuppressive therapy with mycophenolate mofetil plus corticosteroids is associated with higher chances of clinical remission and lower risk of kidney failure. Complement targeting therapies, such as eculizumab, avacopan, danicopan, iptacopan, and pegcetacoplan, are being studied as potential new therapeutic options. This article highlights the need for more clinical trials to test new therapeutic agents, as well as to better understand the heterogeneity of the disease and its long-term outcomes. <![CDATA[A Rare Cause of Seizures: Hypomagnesemia Type 1]]> ABSTRACT Hypomagnesemia type I is a rare autosomal recessive disorder characterized by severe hypomagnesemia, often accompanied by hypocalcemia. This disease is caused by mutations in the TRPM6 gene (which encodes the respective channel), leading to reduced intestinal absorption of magnesium and increased renal excretion due to a defect in reabsorption in the distal convoluted tubule. It usually manifests itself in the first months of life, with symptoms of neuromuscular hyperexcitability and seizures, refractory to antiepileptic therapy. Treatment consists of administering high doses of magnesium throughout life. Here, we report a case of hypomagnesemia type I with a novel pathogenic variant of TRPM6 in a 5-month-old girl who developed refractory seizures due to hypomagnesemia.