The authors evaluated the effectiveness of percutaneous renal revascularization (PRR) with stenting for the treatment of atherosclerotic renal artery stenosis (ARAS) in patients with coronary artery disease and the usefulness of captopril renal scintigraphy for predicting clinical outcomes after PRR. Sixty‐four consecutive patients, referred for evaluation of suspected ARAS, after coronary angiography, underwent baseline captopril renal scintigraphy followed by renal angiography. Forty‐four patients (68.7%) were diagnosed with a significant ARAS≥ 60% and were treated with PRR plus medical therapy. Twenty‐four months after PRR, 86.4% and 73.3% of patients showed a hypertension and renal benefit, respectively. Captopril renal scintigraphy positivity had moderate sensitivity and high specificity in predicting a hypertension and renal benefit. In patients with ARAS≥ 70%, the sensitivity and specificity were 100% for both a hypertension and renal benefit.PRR for ARAS conferred a substantial benefit in patients with a high coronary artery disease burden. Captopril renal scintigraphy was highly accurate in predicting clinical outcomes.
Purpose: Handgrip strength (HGS) is a useful tool for the systematic assessment of muscle function related to nutritional status. Reduced HGS has been associated with adverse clinical outcomes in chronic kidney disease (CKD) stage 5D patients. In the same patients, predialysis low serum sodium (sNa) has been associated with malnutrition and mortality. Here, we investigated the role of predialysis sNa on muscle function in CKD-5D patients.Methods: We evaluated 45 patients on hemodialysis (HD) and 28 patients on peritoneal dialysis (PD) with HGS measurement, bioimpedance analysis, anthropometric measures, and malnutrition inflammation score (MIS). According to established diagnostic criteria, reduced HGS was defined as strength below 30 and 20 Kg in men and women, respectively. Predialysis sNa values were defined as the mean of all predialysis measurements during the preceding 6 months. Data analysis was performed separately for each of the HD and PD groups.Results: The proportions of reduced HGS did not differ between the HD (66%) and PD (54%) groups, respectively. Patients in the HD group as compared to those in the PD group had higher serum albumin and potassium and mid-arm muscle circumference and lower residual renal function (RRF) and residual urine volume. Multivariate logistic analysis, after controlling for muscle mass, nutritional biomarkers, MIS, fluid overload and RRF, showed that for every 1 mmol/l increase of sNa the odds of reduced HGS was decreased by 60% (OR = 0.40, 95% CI: 0.16–0.99) and 42% (OR = 0.58, 95% CI: 0.36–0.93) in HD and PD patients, respectively. However, stratified analysis indicated that lower sNa levels predicted reduced HGS in individuals with a background of malnutrition, inflammation, overhydration and less preserved RRF, representing unfavorable conditions strongly related to muscle wasting in the dialysis setting.Conclusions: Predialysis sNa is a strong and independent determinant of HGS, a reliable nutritional marker in CKD-5D stage patients. However, according to our findings, lower sNa levels appear to be a marker of underlying unfavorable conditions that are heavily associated with reduced HGS, rather than a causal determinant of reduced HGS. Whether optimizing sNa levels improves patient muscle performance requires further investigations.
Renal hypomagnesemia syndromes involving CNNM2 protein pathogenic variants are associated with variable degrees of neurocognitive dysfunction and hypomagnesemia. Here, we report a family with a novel CNNM2 p.Pro482Ala variant, presenting with overt hypomagnesemia and mild neurological involvement (autosomal dominant renal hypomagnesemia 6, HOMG6, MIM# 613882). Using a bioinformatics approach, we showed that the p.Pro482Ala amino acid substitution causes a 3D conformational change in CNNM2 structure in the cystathionin beta synthase (CBS) domain and the carboxy-terminal protein segment. A novel finding was that aldosterone inhibition with spironolactone helped to alleviate hypomagnesemia and symptoms in the proband.
Background Dent disease is an X-linked disorder characterized by low molecular weight proteinuria (LMWP), hypercalciuria, nephrolithiasis and chronic kidney disease (CKD). It is caused by mutations in the chloride voltage-gated channel 5 (CLCN5) gene (Dent disease-1), or in the OCRL gene (Dent disease-2). It is associated with chronic metabolic acidosis; however metabolic alkalosis has rarely been reported. Case presentation We present a family with Dent-2 disease and a Bartter-like phenotype. The main clinical problems observed in the proband included a) primary phosphaturia leading to osteomalacia and stunted growth; b) elevated serum calcitriol levels, leading to hypercalcemia, hypercalciuria, nephrolithiasis and nephrocalcinosis; c) severe salt wasting causing hypotension, hyperaldosteronism, hypokalemia and metabolic alkalosis; d) partial nephrogenic diabetes insipidus attributed to hypercalcemia, hypokalemia and nephrocalcinosis; e) albuminuria, LMWP. Phosphorous repletion resulted in abrupt cessation of hypercalciuria and significant improvement of hypophosphatemia, physical stamina and bone histology. Years later, he presented progressive CKD with nephrotic range proteinuria attributed to focal segmental glomerulosclerosis (FSGS). Targeted genetic analysis for several phosphaturic diseases was unsuccessful. Whole Exome Sequencing (WES) revealed a c.1893C > A variant (Asp631Glu) in the OCRL gene which was co-segregated with the disease in male family members. Conclusions We present the clinical characteristics of the Asp631Glu mutation in the OCRL gene, presenting as Dent-2 disease with Bartter-like features. Phosphorous repletion resulted in significant improvement of all clinical features except for progressive CKD. Angiotensin blockade improved proteinuria and stabilized kidney function for several years. Graphical abstract
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