Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add more filters

Database
Country/Region as subject
Language
Publication year range
1.
Pediatr Nephrol ; 37(7): 1525-1528, 2022 Jul.
Article in English | MEDLINE | ID: mdl-35084566
2.
Environ Monit Assess ; 192(8): 533, 2020 Jul 20.
Article in English | MEDLINE | ID: mdl-32691241

ABSTRACT

The Ganga River is facing mounting environmental pressures due to rapidly increasing human population, urbanisation, industrialisation and agricultural intensification, resulting in worsening water quality, ecological status and impacts on human health. A combined inorganic chemical, algal and bacterial survey (using flow cytometry and 16S rRNA gene sequencing) along the upper and middle Ganga (from the Himalayan foothills to Kanpur) was conducted under pre-monsoon conditions. The upper Ganga had total phosphorus (TP) and total dissolved nitrogen concentrations of less than 100 µg l-1 and 1.0 mg l-1, but water quality declined at Kannauj (TP = 420 µg l-1) due to major nutrient pollution inputs from human-impacted tributaries (principally the Ramganga and Kali Rivers). The phosphorus and nitrogen loads in these two tributaries and the Yamuna were dominated by soluble reactive phosphorus and ammonium, with high bacterial loads and large numbers of taxa indicative of pathogen and faecal organisms, strongly suggesting sewage pollution sources. The high nutrient concentrations, low flows, warm water and high solar radiation resulted in major algal blooms in the Kali and Ramganga, which greatly impacted the Ganga. Microbial communities were dominated by members of the Phylum Proteobacteria, Bacteriodetes and Cyanobacteria, with communities showing a clear upstream to downstream transition in community composition. To improve the water quality of the middle Ganga, and decrease ecological and human health risks, future mitigation must reduce urban wastewater inputs in the urbanised tributaries of the Ramganga, Kali and Yamuna Rivers.


Subject(s)
Water Pollutants, Chemical/analysis , Water Quality , Environmental Monitoring , Eutrophication , Humans , India , Nitrogen/analysis , Nutrients , Phosphorus/analysis , RNA, Ribosomal, 16S
3.
Kidney Int Rep ; 5(7): 980-990, 2020 Jul.
Article in English | MEDLINE | ID: mdl-32647755

ABSTRACT

Rickets is a common bone disease worldwide that is associated with disturbances in calcium and phosphate homeostasis and can lead to short stature and joint deformities. Rickets can be diagnosed based on history and physical examination, radiological features, and biochemical tests. It can be classified into 2 major groups based on phosphate or calcium levels: phosphopenic and calcipenic. Knowledge of categorization of the type of rickets is essential for prompt diagnosis and proper management. Nutritional rickets is a preventable disease through adequate intake of vitamin D through both dietary and sunlight exposure. There are other subtypes of rickets, such as vitamin D-dependent type 1 rickets and vitamin D-dependent type 2 rickets (due to defects in vitamin D metabolism), renal rickets (due to poor kidney function), and hypophosphatemic rickets (vitamin D-resistant rickets secondary to renal phosphate wasting wherein fibroblast growth factor-23 (FGF-23) often plays a major role), which requires closer monitoring and supplementation with activated vitamin D with or without phosphate supplements. An important development has been the introduction of burosumab, a human monoclonal antibody to FGF-23, which is approved for the treatment of X-linked hypophosphatemia among children 1 year and older.

4.
Pediatr Nephrol ; 35(3): 447-454, 2020 03.
Article in English | MEDLINE | ID: mdl-31845055

ABSTRACT

INTRODUCTION: Body stores of vitamin D are measured as "total" serum 25-hydroxy vitamin D (25(OH)D). Its largest component is protein bound and lost in urine in nephrotic syndrome (NS). Our study investigates whether "free" 25(OH)D levels are a better guide to bone health and need for vitamin D supplementation in patients with steroid-sensitive NS (SSNS). METHODS: A cross-sectional study was performed in children with SSNS and healthy controls. Blood was tested for albumin, creatinine, calcium, phosphate, ALP, total and free (by direct ELISA) 25(OH)D, iPTH, and urine for protein-creatinine ratio. RESULTS: Seventy-nine NS patients (48 in relapse, 31 in remission) and 60 healthy controls were included. The levels of total 25(OH)D were significantly different (lowest in NS relapse and highest in controls) (p < 0.001). Corrected calcium and phosphate levels were normal, and there were no differences in free 25(OH)D, ALP, or iPTH levels between groups. Only total and not free 25(OH)D correlated significantly and negatively with urinary protein creatinine ratios (rs = - 0.42 vs. 0.04). Free 25(OH)D values of 3.75 and 2.85 pg/ml corresponded to total 25(OH)D levels of 20 and 12 ng/ml, respectively, in healthy controls. CONCLUSION: These results confirm that total 25(OH)D levels are low in NS and related to degree of proteinuria. However levels of free 25(OH)D, ALP, and iPTH did not change in relapse or remission in comparison with healthy controls. Our results suggest that in proteinuric renal diseases, free 25(OH)D rather than total 25(OH)D levels should be used to diagnose vitamin D deficiency and guide therapy.


Subject(s)
Cholecalciferol/blood , Ergocalciferols/blood , Nephrotic Syndrome/complications , Proteinuria/diagnosis , Vitamin D Deficiency/epidemiology , Case-Control Studies , Child , Child, Preschool , Cholecalciferol/administration & dosage , Cholecalciferol/deficiency , Cross-Sectional Studies , Dietary Supplements , Ergocalciferols/administration & dosage , Ergocalciferols/deficiency , Female , Glucocorticoids/pharmacology , Glucocorticoids/therapeutic use , Humans , Male , Nephrotic Syndrome/blood , Nephrotic Syndrome/diagnosis , Nephrotic Syndrome/drug therapy , Proteinuria/blood , Risk Factors , Serum Albumin, Human/analysis , Severity of Illness Index , Vitamin D Deficiency/diagnosis , Vitamin D Deficiency/etiology , Vitamin D Deficiency/prevention & control
SELECTION OF CITATIONS
SEARCH DETAIL