Long-term cholecalciferol supplementation in hemodialysis patients: Effects on mineral metabolism, inflammation, and cardiac parameters.

BACKGROUND: Low levels of 25-hydroxyvitamin D [25(OH)D] are frequent in chronic kidney disease and are associated with adverse outcomes. The aim of this 5-year prospective study was to evaluate the effects of cholecalciferol supplementation on mineral metabolism, inflammation and cardiac parameters in hemodialysis (HD) patients. METHODS: The study included 97 patients. Cholecalciferol was given after HD according to 25(OH)D baseline levels measured twice (end of winter and of summer). The 25(OH)D levels, circulating bone metabolism, inflammation parameters, brain natriuretic peptide (BNP), pulse pressure (PP), and left ventricular mass index (LVMI) were evaluated before and after supplementation. RESULTS: There was a significant increase in 25(OH)D levels after supplementation (p < 0.001); however, serum calcium (p = 0.02), phosphorus (p = 0.018), and iPTH (p = 0.03) were decreased. Magnesium levels increased during the study (p = 0.03). A reduction in the number of patients under active vitamin D (p < 0.001) and in the dose and number of patients treated with darbepoetin (p = 0.02) was observed. Serum albumin increased (p < 0.001), and C-reactive protein decreased (p = 0.01). BNP (p < 0.001), PP (p = 0.007), and LVMI (p = 0.02) were significantly reduced after supplementation. CONCLUSIONS: Long-term cholecalciferol supplementation allowed correction of 25(OH)D deficiency, improved mineral metabolism with less use of active vitamin D, attenuated inflammation, reduced the dose of the erythropoiesis-stimulating agent, and improved cardiac dysfunction.

Penile and digital calciphylaxis: A case report and literature review.

Calcific uremic arteriolopathy (CUA) represents a rare but severe disease with high morbimortality. The authors present the case of a 58-year-old male patient with chronic kidney disease due to obstructive uropathy, on hemodialysis (HD). He started HD due to uremic syndrome with a severe renal dysfunction, dysregulation of calcium and phosphate metabolism, and he presented with distal penile ischemia, which was treated with surgical debridement and hyperbaric oxygen therapy. Four months later, painful distal digital necrosis of both hands was observed. Extensive arterial calcification was observed on X-ray. A skin biopsy confirmed the presence of CUA. Sodium thiosulfate was administered for 3 months, HD was intensified, and hyperphosphatemia control was achieved, with progressive improvement of the lesions. This case illustrates an uncommon presentation of CUA in a patient on HD for a few months, non-diabetic and not anticoagulated, but with a severe dysregulation of calcium and phosphate metabolism.

Bone fracture risk factors in prevalent hemodialysis patients.

Bone fractures are an important cause of morbidity and mortality in hemodialysis (HD) patients. The aim of this study was to quantify the incidence of fractures in a cohort of prevalent HD patients and evaluate its relationship with possible risk factors. We performed a retrospective analysis of 341 patients, since they started HD (median of 51 months). Demographic, clinical, and biochemical parameters as well as vascular calcifications (VC) were evaluated. Fifty-seven episodes of fracture were identified with a median HD vintage of 47 months (incidence rate of 31 per 1000 person-years). Age (p < 0.001), female gender (p < 0.001), lower albumin (p = 0.02), and higher VC score (p < 0.001) were independently associated with increased risk of fracture, while active vitamin D therapy (p = 0.03) was associated with decreased risk. A significantly higher risk of incident fracture was also associated with higher values of bone-specific alkaline phosphatase (bALP) (p = 0.01) and intact parathyroid hormone (iPTH) levels either < 300 pg/mL (p = 0.02) or > 800 pg/mL (p < 0.001) compared with 300-800 pg/mL. In conclusion, bone fracture incidence in HD patients is high and its risk increases with age, female gender, lower serum albumin, and with the presence of more VC. Prevalent HD patients with low or high iPTH levels or increased bALP also had a higher fracture risk. Therapy with active vitamin D seems to have a protective role. Assessment of fracture risk and management in dialysis patients at greatest risk requires further study.

Prognostic Factors of Human Immunodeficiency Virus-Infected Patients on Chronic Hemodialysis.

BACKGROUND/AIMS: The number of human immunodeficiency virus (HIV)-infected patients on hemodialysis (HD) have increased, and their prognostic factors are still poorly clarified. The study aimed to identify factors that can influence the survival of HIV-infected patients on HD. METHODS: We performed a retrospective cohort study of 44 HIV-infected patients on HD. RESULTS: A total of 17 patients (39%) died. Median survival on HD was 30.8 months and the survival rate at 1 and 5 years was 82.5 and 62.9%, respectively. Male (relative risk [RR] 3.1, p = 0.040) and blacks (RR 2.5, p = 0.037) had higher risk of death. The patients who died had a shorter duration of HIV infection (p = 0.028), had a higher viral load (p = 0.044), more opportunistic infections (p = 0.013), and a lower serum albumin (p = 0.009). Lower serum albumin, nonsexual HIV transmission, viral load, opportunistic infections, and usage of catheters were associated with lower survival. CONCLUSION: Several demographic, viral, and dialysis variables may help to predict survival of this population. The intervention in these factors could improve their prognosis.

Lower serum magnesium is associated with cardiovascular risk factors and mortality in haemodialysis patients.

BACKGROUND: Hypomagnesaemia is a cardiovascular (CV) risk factor in the general population. The aim of this study was to evaluate the relationship between pre-dialysis magnesium (Mg) and CV risk markers, [including pulse pressure (PP), left ventricular mass index (LVMI) and vascular calcifications (VC)], and mortality in haemodialysis (HD) patients. METHODS: We performed a 48-month prospective study in 206 patients under pre-dilution haemodiafiltration with a dialysate Mg concentration of 1 mmol/l. RESULTS: Lower Mg concentrations were predictors of an increased PP (≥65 mm Hg) (p = 0.002) and LVMI (≥140 g/m(2)) (p = 0.03) and of a higher VC score (≥3) (p = 0.01). Patients with Mg <1.15 mmol/l had a lower survival at the end of the study (p = 0.01). Serum Mg <1.15 mmol/l was an independent predictor of all-cause (p = 0.01) and CV mortality (p = 0.02) when adjusted for multiple CV risk factors. CONCLUSIONS: Lower Mg levels seem to be associated with increased CV risk markers, like PP, LVMI and VC, and with higher mortality in HD patients.

Hypomagnesemia: a potential underlooked cause of persistent vitamin D deficiency in chronic kidney disease.

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.

Dent's disease: An unusual cause of kidney failure.

Dent's disease is an X-linked recessive disease characterized by proximal tubulopathy with low-molecular weight proteinuria, hypercalciuria, nephrolithiasis, nephrocalcinosis, and kidney failure. It is mainly caused by mutations in the CLCN5 or OCRL1 genes, and only ~ 250 families have been identified with these mutations. We present a 31-year-old male referred to a nephrology consultation due to elevated serum creatinine and a history of nephrolithiasis. Complementary evaluation revealed protein/creatinine ratio of 1.9 g/g and albumin/creatinine ratio of 0.5 g/g, hypercalciuria and medullary nephrocalcinosis. These findings raised the suspicion of Dent's disease, which was confirmed by genetic testing. A missense mutation in the CLCN5 gene (c.810C>G, p.(Ser270Arg)), not previously reported in populational databases, was identified. During the evaluation of the patient, it came to our attention that a first-degree male cousin was being followed in our kidney transplantation unit. Given the unknown etiology of his chronic kidney disease, genetic testing was performed, identifying the same mutation. This case highlights the importance of considering the diagnosis of Dent's disease in the setting of a male patient with chronic kidney disease of unknown etiology, low-molecular-weight proteinuria, hypercalciuria, and nephrocalcinosis. Despite progression to end-stage kidney failure in a significant portion of male patients, there are no reports of recurrence after kidney transplantation.

Recovering from a renal vascular catastrophe: Case report.

Renal artery thrombosis is a rare vascular event that precipitates renal infarction. Although in up to one third of cases the etiology is not identified, renal artery lesions, cardioembolism and acquired thrombophilias are the main causes. A bilateral simultaneous idiopathic renal artery thrombosis is an unlikely coincidence. We present two cases of patients with acute bilateral renal artery thrombosis of unknown etiology. Cardiac embolism, acquired thrombophilia and occult neoplasm workups were negative. Both cases were temporarily hemodialysis-dependent and partially recovered renal function under conservative approach with systemic anticoagulation. Recommendations on optimal treatment for renal artery thrombosis are still lacking. We discuss the available options.

Non-diabetic metabolic nodular glomerulosclerosis.

Nodular glomerulosclerosis is classically associated with diabetes. Nowadays, it is well known that this histologic pattern can be the presentation of different diseases, including dysproteinemias and amyloidosis. Most recently, the previously thought to be idiopathic nodular glomerulosclerosis has been associated with hypertension, smoking, and obesity. We present a clinical case of a non-diabetic 74-year-old man, with hypertension and heavy smoking history, who presented with nephrotic proteinuria and chronic kidney disease. We review the literature and propose a different nomenclature for this pattern of metabolic glomerulopathy.

Glycosuria in primary glomerulopathies: prevalence and prognostic significance.

INTRODUCTION: Tubular damage is common in glomerular diseases (GD). Glycosuria is a marker of tubular dysfunction and may be used to detect tubular lesion and CKD progression. The aim of this study was to evaluate the prevalence and prognostic value of glycosuria at the time of diagnosis in primary glomerulopathies (PG). METHODS: We conducted a 24-month retrospective study in patients diagnosed with PG in our center between 2009 and 2020. We excluded diabetic patients, use of SGLT2 inhibitors, transplant patients, and secondary GD. Patients were divided in two groups according to their glycosuria status at diagnosis. RESULTS: We studied 115 patients. Global prevalence of glycosuria was 10% (n=11) and membranous nephropathy (MN) had the highest prevalence (n=5, 17.9%). We found that patients with glycosuria had higher serum creatinine (2.4 vs. 1.2 mg/dL, p=0.030), higher albuminuria (4.8 vs. 1.9 g/g, p=0.004), and lower serum albumin (2.3 vs. 3.2 g/dL, p=0.021). We did not find association with histological prognostic factors. At the end of follow-up, patients with glycosuria had higher prevalence of the composite outcome of stage 5D CKD or 50% increase in basal SCr (45.5% vs. 17.3%, p=0.037). In patients with MN, results were similar but we were able to find an association of glycosuria with more severe interstitial fibrosis and tubular atrophy (25.0 vs. 0.0 %, p=0.032). CONCLUSION: Ten percent of our patients with PG have glycosuria. Glycosuria at the time of diagnosis was associated with more severe clinical presentation and worst renal outcome. The association with higher albuminuria suggests that tubular function has an impact on the severity and outcomes of PG.

Mal-positioning of a dialysis catheter: One lumen with arterial blood and the other with venous blood?

Partial anomalous pulmonary vein drainage is a rare congenital defect, where the pulmonary vein drains into a systemic vein instead of draining into the left atrium. We present a case of a 63-year-old woman on hemodialysis who was found to have a right pulmonary vein with anomalous drainage to the superior vena cava after mal-positioning of a dialysis catheter, which demonstrated unexpected blood results from the different lumina of the catheter. Multiple imaging techniques were used to deal with this rare clinical situation. This is the first case reporting a mal-positioning of a left-side internal jugular vein tunneled catheter into a right-side pulmonary vein.

Thrombotic microangiopathy triggered by podocytopathy.

Thrombotic microangiopathy (TMA) is a rare group of diseases characterized by microangiopathic hemolytic anemia, thrombocytopenia, and target organ damage. It can be divided into primary and secondary TMA. Herein we report a case of TMA associated to a primary glomerular disease. We report the case of a 31-year-old Black male from Cape Verde admitted in March 2018 with nephrotic syndrome and upper gastrointestinal bleeding, the latter due to severe erythematous gastritis. He was discharged after clinical stabilization. The patient came to Portugal 8 months later. On admission, he presented with rapid deterioration of kidney function and hyperkalemia. The etiologic study revealed microangiopathic hemolytic anemia, nephrotic syndrome and microscopic hematuria. Immunologic study and viral serology were negative. ADAMTS13 activity and inhibitor testing were within normal range, genetic complement evaluation showed CFH-H3 in homozygosity, functional complement studies revealed decreased function of alternative pathway. Kidney biopsy was consistent with the diagnosis of TMA, and electron microscopy was compatible with minimal change disease. Patient underwent plasmapheresis with resolution of hemolysis, fluid overload and recovery of renal function. Two months later, he presented with nephrotic syndrome and started prednisolone with remission. Six months later, the nephrotic syndrome relapsed, and it became steroid-, MMF-, and rituximab-resistant. Tacrolimus was initiated, achieving partial remission. Atypical hemolytic uremic syndrome is an uncommon disease and is rarely reported as secondary to glomerular diseases. This case showcases the challenges regarding treatment options in a resistant glomerulopathy and the implications of therapeutic choices and kidney outcomes with the coexisting TMA.

The Role of Vascular Lesions in Diabetes Across a Spectrum of Clinical Kidney Disease.

INTRODUCTION: The clinical-histologic correlation in diabetic nephropathy is not completely known. METHODS: We analyzed nephrectomy specimens from 90 patients with diabetes and diverse degrees of proteinuria and glomerular filtration rate (GFR). RESULTS: Thirty-six (40%) subjects had normoalbuminuria, 33 (37%) microalbuminuria, and 21 (23%) non-nephrotic proteinuria. Mean estimated GFR (eGFR) was 65±23 (40% <60 ml/min per 1.73 m2). About 170 glomeruli per patient were analyzed, and all samples included vascular tissue. Six subjects (7%) were classified in diabetic nephropathy class I, 61 (68%) in class II-a, 13 (14%) in class II-b, 9 (10%) class III, and 1 (1%) in class IV. Eighty percent to 90% of those with normoalbuminuria or microalbuminuria were classified in class II-a or II-b and <10% in class III; 52% of those with proteinuria were in class II-a, 15% in class II-b, and 19% in class III. Nodular sclerosis (57%) and mesangial expansion (15%) were more frequent in cases with proteinuria than in normoalbuminuria (28% and 8%; P = 0.028 and 0.017). About 20% to 30% of all cases, regardless the level of albuminuria or proteinuria or the histologic class had tubular atrophy, interstitial fibrosis, or inflammation in >10% to 20% of the sample. Moderate hyalinosis and arteriolar sclerosis were observed in 80% to 100% of cases with normoalbuminuria, microalbuminuria, proteinuria, as well as in class I, II, or III. CONCLUSIONS: Weak correspondence between analytical parameters and kidney histology was found. Thus, disease may progress undetected from the early clinical stages of the disease. Finally, vascular damage was a very common finding, which highlights the role of ischemic intrarenal disease in diabetes.

The impact of functioning hemodialysis arteriovenous accesses on renal graft perfusion: Results of a pilot study.

INTRODUCTION: After a kidney transplant, it is unknown whether the maintenance of a functioning hemodialysis arteriovenous access could have deleterious effects on renal grafts. We hypothesize that maintaining an arteriovenous access can deviate a significant proportion of the cardiac output from the renal graft. The aim of this study was to investigate whether a temporary closure of the arteriovenous access could lead to an increase in graft perfusion. METHODS: We conducted a study in 17 kidney-transplanted patients with a functioning arteriovenous access. We evaluated, at baseline and 30 s after compression of the arteriovenous access (access flow occlusion), the hemodynamic parameters and the renal resistive index of the graft by Doppler ultrasound. RESULTS: After arteriovenous access occlusion 82.4% (n = 14) of the patients had a decrease in resistive index. All patients had a decrease in heart rate (67 vs 58 bpm, p < 0.001) and 14 (82.4%) had an increase in mean blood pressure (98.3 vs 101.7 mm Hg, p = 0.044). There was a significant decrease in the resistive index (ΔRI) after the access occlusion (0.68 vs 0.64, p = 0.030). We found a negative correlation in Qa (r2 = -0.55, p = 0.022) with the ΔRI, and Qa was an independent predictor of ΔRI in a model adjusted to pre-occlusion resistive index. CONCLUSION: Our results showed that temporary occlusion of an arteriovenous access causes a significant decline in renal graft resistive index and this decline is higher with the occlusion of accesses with higher Qa. These results suggest that the maintenance of arteriovenous accesses, mainly those with higher Qa, can decrease renal graft perfusion.

IGA nephropathy - Are intravenous steroid pulses more effective than oral steroids in relapse prevention?

INTRODUCTION: It is recommended that IgA nephropathy (IgAN) is treated with steroids when the glomerular filtration rate (GFR) is >50ml/min and proteinuria >1g/day. Few studies have been performed comparing the two accepted steroid regimens (1g/day methylprednisolone pulses for 3 consecutive days at the beginning of months 1, 3 and 5, followed by 0.5mg/kg prednisolone on alternate days vs. 1mg/kg/day oral prednisolone). The aim of this study was to compare these two steroid regimens in IgAN treatment. METHODS: We selected 39 patients with biopsy-proven IgAN treated with steroids. Mean age at diagnosis was 37.5 years, 23 males (59%), baseline proteinuria (Uprot) was 2.1 g/day and median serum creatinine (SCr) was 1.5mg/dl. The mean follow-up period was 56 months. Twenty-five patients (64%) were treated with methylprednisolone pulses and 14 (36%) with oral steroids. RESULTS: Patients treated with steroid pulses presented lower relapse risk, defined as the reappearance of Uprot >1g/day and an Uprot increase of more than 50% (incidence rate ratio of 0.18, 95% CI 0.02-0.5). The Kaplan-Meier analysis showed longer relapse-free period (p=0.019). This result was confirmed in a multivariate analysis (p=0.026). However, we did not find other differences between the two steroid regimens. CONCLUSIONS: In comparison to oral steroids, the intravenous pulse regimen was associated with a lower risk of relapse in IgAN, a known independent negative predictor of renal survival. No differences were found regarding the other renal outcomes.

Are high flow arteriovenous accesses associated with worse haemodialysis?

INTRODUCTION: An arteriovenous (AV) access flow (Qa) of 400 mL/min is usually sufficient for an effective hemodialysis (HD), but some accesses continue developing and become high flow accesses (HFA). Some authors postulated that an HFA might shift a significant portion of dialyzed blood from the cardiac output, which could decrease HD efficiency and lead to volume overload. OBJECTIVE: The aim of our study was to evaluate if HFA is associated with reduced HD efficiency and/or volume overload in prevalent HD patients. METHODS: We performed a 1-year retrospective study and assessed HD efficiency by the percentage of sessions in which the Kt/V > 1.4 and volume overload by bioimpedance spectroscopy. RESULTS: The study included 304 prevalent HD patients with a mean age of 67.5 years; 62.5% were males, 36.2% were diabetics, with a median HD vintage of 48 months. Sixteen percent of the patients had a HFA (defined as Qa > 2 L/min). In multivariate analysis, patients with HFA presented higher risk of volume overload (OR = 2.67, 95%CI = 1.06-6.71) and severe volume overload (OR = 4.06, 95%CI = 1.01-16.39) and attained dry weight less frequently (OR = 0.37, 95%CI = 0.14-0.94). However, HFA was not associated with lower Kt/V. CONCLUSION: Our results suggest that patients with HFA have higher risk of volume overload. However, contrarily to what has been postulated, HFA was not associated with less efficient dialysis, measured by Kt/V. Randomized controlled trials are needed to clarify these questions.

Glycosuria in primary glomerulopathies: prevalence and prognostic significance / Glicosúria nas doenças glomerulares primárias: prevalência e significância prognóstica

Abstract Introduction: Tubular damage is common in glomerular diseases (GD). Glycosuria is a marker of tubular dysfunction and may be used to detect tubular lesion and CKD progression. The aim of this study was to evaluate the prevalence and prognostic value of glycosuria at the time of diagnosis in primary glomerulopathies (PG). Methods: We conducted a 24-month retrospective study in patients diagnosed with PG in our center between 2009 and 2020. We excluded diabetic patients, use of SGLT2 inhibitors, transplant patients, and secondary GD. Patients were divided in two groups according to their glycosuria status at diagnosis. Results: We studied 115 patients. Global prevalence of glycosuria was 10% (n=11) and membranous nephropathy (MN) had the highest prevalence (n=5, 17.9%). We found that patients with glycosuria had higher serum creatinine (2.4 vs. 1.2 mg/dL, p=0.030), higher albuminuria (4.8 vs. 1.9 g/g, p=0.004), and lower serum albumin (2.3 vs. 3.2 g/dL, p=0.021). We did not find association with histological prognostic factors. At the end of follow-up, patients with glycosuria had higher prevalence of the composite outcome of stage 5D CKD or 50% increase in basal SCr (45.5% vs. 17.3%, p=0.037). In patients with MN, results were similar but we were able to find an association of glycosuria with more severe interstitial fibrosis and tubular atrophy (25.0 vs. 0.0 %, p=0.032). Conclusion: Ten percent of our patients with PG have glycosuria. Glycosuria at the time of diagnosis was associated with more severe clinical presentation and worst renal outcome. The association with higher albuminuria suggests that tubular function has an impact on the severity and outcomes of PG.

Resumo Introdução: Danos tubulares são comuns em doenças glomerulares (DG). Glicosúria é um marcador de disfunção tubular e pode detectar lesão tubular e progressão da DRC. O objetivo deste estudo foi avaliar a prevalência e o valor prognóstico da glicosúria no diagnóstico em glomerulopatias primárias (GP). Métodos: Realizamos estudo retrospectivo de 24 meses em pacientes diagnosticados com GP em nosso centro entre 2009-2020. Excluímos pacientes diabéticos, uso de inibidores de SGLT2, pacientes transplantados e DG secundárias. Os pacientes dividiram-se em dois grupos de acordo com seu estado de glicosúria no diagnóstico. Resultados: Estudamos 115 pacientes. A prevalência global de glicosúria foi de 10% (n=11) e a nefropatia membranosa (NM) teve maior prevalência (n=5, 17,9%). Constatamos que pacientes com glicosúria apresentavam creatinina sérica mais elevada (2,4 vs. 1,2 mg/dL, p=0,030), albuminúria mais alta (4,8 vs. 1,9 g/g, p=0,004), e albumina sérica mais baixa (2,3 vs. 3,2 g/dL, p=0,021). Não encontramos associação com fatores prognósticos histológicos. Ao final do acompanhamento, pacientes com glicosúria tiveram maior prevalência do desfecho composto de DRC estágio 5D ou aumento de 50% na CrS basal (45,5% vs. 17,3%, p=0,037). Em pacientes com NM, os resultados foram semelhantes, mas encontramos uma associação de glicosúria com fibrose intersticial mais grave e atrofia tubular (25,0 vs. 0,0 %, p=0,032). Conclusão: 10% de nossos pacientes com GP têm glicosúria. A glicosúria no diagnóstico foi associada a uma apresentação clínica mais grave e pior desfecho renal. A associação com albuminúria mais elevada sugere que a função tubular tem um impacto na gravidade e nos desfechos da GP.

Diabetic kidney disease: Is there a non-albuminuric phenotype in type 2 diabetic patients?

BACKGROUND: Albuminuria was widely considered as the first clinical sign of diabetic kidney disease (DKD), which is why it has traditionally been used as a screening test for DKD. However, increasing evidence has shown that a significant number of type 2 diabetes mellitus (DM) patients have a decreased glomerular filtration rate (GFR) without significant albuminuria, known as non-albuminuric DKD (NA-DKD). The aim of this study was to determine the prevalence and the demographic and clinical characteristics of patients with NA-DKD. METHODS: This was a 1-year retrospective study that included 146 type 2 diabetic patients with GFR<75mL/min followed-up in a diabetes outpatient department. Patients were divided into two groups according to their ACR status - NA-DKD and albuminuric DKD (A-DKD). RESULTS: Of the 146 patients included in the study, 53.4% had A-DKD and 46.6% had NA-DKD. According to the multivariable analysis performed, patients with NA-DKD tended to be older (p=0.021), female (p=0.045) and with a lower GFR (p=0.004) than A-DKD patients. There was no difference between the groups in terms of body mass index, metabolic control of DM, duration of DM diagnosis and prevalence of metabolic syndrome. CONCLUSIONS: The majority of patients with DKD had albuminuria, but a significant proportion had a non-albuminuric phenotype (46.6% in this population). These patients exhibit distinct clinical features that could have screening, therapeutic and prognosis implications.

Calcium Acetate/Magnesium Carbonate and Cardiovascular Risk Factors in Chronic Hemodialysis Patients.

BACKGROUND/AIM: Calcium acetate/magnesium carbonate (CaMg) is a recent phosphate binder that has been shown to have protective cardiovascular (CV) effects in animal models. The aim of this study was to evaluate the relationship between CaMg therapy and CV risk markers like pulse pressure (PP), left ventricular mass index (LVMI) and valvular calcifications compared to sevelamer or no phosphate binder (NPB) therapy in chronic hemodialysis (HD) patients. METHODS: We performed a 48-month prospective study in 138 HD patients under hemodiafiltration with a dialysate Mg concentration of 0.5 mmol/l. Patients underwent treatment with CaMg or sevelamer for at least 36 months or NPB therapy. Demographic, clinical, biochemical and echocardiographic parameters were evaluated at baseline and after a 48-month period. RESULTS: At the end of the study, patients who had taken CaMg showed a significant reduction in PP (p < 0.001), LVMI (p = 0.003), aortic (p = 0.004) and mitral valve calcifications (p = 0.03) compared with NPB patients. Patients under CaMg showed a significant reduction of PP (p < 0.001), LVMI (p = 0.01) and aortic valve calcifications (p = 0.02) compared to sevelamer patients. In a multivariable analysis, CaMg therapy was negatively associated with progression of LVMI (p = 0.02) and aortic valve calcifications (p = 0.01). Patients under CaMg showed higher serum Mg levels (0.93 ± 0.14 mmol/l) compared to patients under sevelamer (0.87 ± 0.13) or NPB patients (0.82 ± 0.12; p < 0.001). CONCLUSIONS: In prevalent HD patients, the use of CaMg over 48 months was associated with a reduction of PP and LVMI and with a stabilization of aortic valve calcifications. These protective and promising results of this new phosphate binder need to be confirmed in randomized controlled studies.