Whether dietary salt intake affects chronic kidney disease (CKD) progression remains unclear. We conducted a retrospective cohort study to analyze the effects of both daily salt intake (DSI) and volume status on renal outcomes in 197 CKD patients. DSI was estimated by 24-h urinary sodium excretion and volume status was assessed by the ratio of extracellular water (ECW) to total body water (TBW) measured by bioelectrical impedance analysis (BIA). We divided patients into two groups according to DSI (6 g/day) or median ECW/TBW (0.475) and compared renal outcomes of each group. Furthermore, we classified and analyzed four groups according to both DSI and ECW/TBW. The higher DSI group showed a 1.69-fold (95% confidence interval (CI) 1.12–2.57, p = 0.01) excess risk of outcome occurrence compared to the lower group. Among the four groups, compared with Group 1 (low DSI and low ECW/TBW), Group 3 (high DSI and low ECW/TBW) showed a 1.84-fold (95% CI 1.03–3.30, p = 0.04) excess risk of outcome occurrence; however, Group 2 (low DSI and high ECW/TBW) showed no significant difference. High salt intake appears to be associated with poor renal outcome independent of blood pressure (BP), proteinuria, and volume status.
<b><i>Introduction:</i></b> Minimal change disease (MCD) and primary focal segmental glomerulosclerosis (FSGS) are representative podocyte diseases. The clinical cause of MCD and FSGS has not been clearly elucidated yet. However, it is important to distinguish MCD and FSGS because their prognoses and responses to treatment are quite different. <b><i>Objective:</i></b> This study aimed to examine whether parietal epithelial cell (PEC) marker and repeat biopsy are useful for diagnosing primary FSGS. <b><i>Methods:</i></b> Clinicopathological features of 17 patients with the nephrotic syndrome, who underwent kidney biopsy ≥2 times from 1975 to 2017, and had MCD or FSGS were analyzed using PAX8. We defined patients with PAX8+ cells as PAX8+ and the remainder as PAX8– patients. Three cases of sample insufficiency and 1 non-steroid-resistant or frequently relapsing case indicated for repeat biopsy were excluded. <b><i>Results:</i></b> Among the 13 patients studied, 4 were PAX8+ and 9 were PAX8– (median age: 41 and 46 years, respectively, at first biopsy). PAX8+ and PAX8– patients showed no significant differences in clinical data and histological diagnosis except for a significant difference in histological diagnosis at the second biopsy. The number of PAX8+ patients increased to 6. Unlike the first biopsy results, FSGS was present in 5 of 6 (83.3%) PAX8+ patients; MCD occurred in all 7 (100%) PAX8– patients. Three of 6 (50.0%) PAX8+ patients undergoing repeat biopsy were steroid resistant; no (0%) PAX8– patient was steroid resistant. All cases of final FSGS diagnosis were PAX8+ at the first or second biopsy. Only 1 PAX8+ MCD patient was steroid resistant. All PAX8– MCD patients were frequently relapsing. <b><i>Conclusions:</i></b> More PAX8+ patients were diagnosed with FSGS than PAX8– patients. Clinical presentation of MCD in PAX8– patients was frequently relapsing. PEC marker staining in patients with the nephrotic syndrome, e.g., MCD, may help to diagnose FSGS.
Background: Preeclampsia (PE) refers to the development of hypertension and new-onset proteinuria or progressive organ damage (especially kidney) in a previously normotensive pregnant women after 20 weeks of gestation. Thus, new-onset nephrotic syndrome due to PE before 20 weeks of gestation seems to be rare, making its diagnosis difficult in this time period. Case presentation: A 28-year-old woman presented with a new-onset nephrotic syndrome at 16 weeks of gestation. A high dose of oral glucocorticoids (prednisolone, 40 mg) was initiated for presumed glomerulonephritis since she presented with severe nephrotic syndrome before 20 weeks of gestation, however, the treatment was not effective. At 21 weeks of gestation, we confirmed that the soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio was very high (sFlt-1, 13,400 pg/mL; PlGF, 21.9 pg/ mL; serum sFlt-1/PlGF ratio 611.9). Therefore, we diagnosed nephrotic syndrome due to PE, and oral glucocorticoids were discontinued. After she underwent a cesarean section at 24 weeks & 3 days, we performed a kidney biopsy. Focal segmental sclerotic lesions with epithelial cell hyperplasia and foam cells in the tubular poles were seen on light microscopy. On immunofluorescence tests, C4d staining showed linear peripheral patterns in the glomeruli. Electron microscopy revealed diffuse subendothelial edema with focal foot process effacement. The histological diagnosis was severe glomerular endotheliosis with focal segmental glomerulosclerosis. Furthermore, the histology of placenta was consistent with PE. Eight months after delivery, her proteinuria disappeared completely. Conclusions: We not only confirmed an abnormal serum sFlt-1/PlGF ratio but also presented the histology compatible with pure PE in the kidney and placenta in a case of nephrotic syndrome before 20 weeks of gestation. The serum sFlt-1/PlGF ratio may be useful in determining the treatment strategy for atypical cases of pregnant women with nephrotic syndrome, particularly before 20 weeks of gestation.
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