CAKUT was the commonest cause of CKD. Late detection and high prevalence of comorbidities even in early stages of CKD were observed.

No abstract

Tropical infections are caused by a variety of bacteria, viruses and parasitic organisms across varying geographical regions and are more often reported in adults than in children. Most of the infections are acute, presenting as a febrile illness with involvement of multiple organ systems, including the kidney. The gamut of renal manifestations extends from asymptomatic urinary abnormalities to acute kidney injury and-albeit rarely-chronic kidney disease. Tropical infections can involve the glomerular, tubulointerstitial and vascular compartments of the kidney. Leptospirosis, malaria, dengue, rickettsial fever and schistosomiasis are the most prevalent tropical infections which affect the kidneys of children living in the tropics. In this review we discuss renal involvement in these most prevalent tropical infections.

Background and objectives The optimal treatment regimen for correcting 25-hydroxyvitamin D (25OHD) deficiency in children with chronic kidney disease (CKD) is not known. We compared cholecalciferol dosing regimens for achieving and maintaining 25OHD concentrations ≥30ng/ml in children with CKD stages 2-4. Design An open-label multicenter randomized controlled trial randomized children with 25OHD concentrations<30ng/ml in 1:1:1 to oral cholecalciferol 3,000 IU daily, 25,000 IU weekly, or 100,000 IU monthly for 3-months (maximum 3 intensive courses).In those with 25OHD ≥30ng/ml 1,000IU cholecalciferol daily (maintenance course) was given for up to 9 months. Primary outcome was achieving 25OHD≥30 ng/ml at end of intensive phase treatment. Results 90 children were randomized to daily(n = 30), weekly(n = 29) or monthly(n = 31) treatment groups. At end of intensive phase, 70/90(77.8%) achieved 25OHD ≥30ng/ml; 25OHD concentrations were comparable between groups (median 44.3, 39.4, and 39.3 ng/ml for daily, weekly, and monthly groups respectively; p = 0.24) with no difference between groups for time to achieve 25OHD ≥30ng/ml (p = 0.28). There was no change in calcium, phosphorus, and parathyroid hormone, but fibroblast growth factor 23(p = 0.002) and klotho(p = 0.001) concentrations significantly increased and were comparable in all treatment groups. Irrespective of dosing regimen, children with glomerular disease had 25OHD concentrations lower than non-glomerular disease (25.8 vs 41.8 ng/ml; p = 0.007). One child had 25OHD concentration of 134 ng/ml and 5.5% had hypercalcemia without symptoms of toxicity. Conclusion Intensive treatment with oral cholecalciferol as daily, weekly or monthly regimens achieved similar 25OHD concentrations between treatment groups without toxicity. Children with glomerular disease required higher doses of cholecalciferol compared to those with non-glomerular disease.

Sodium retention is the hallmark of idiopathic nephrotic syndrome (INS). Sodium retention could be secondary to activation of renin–angiotensin–aldosterone axis or due to an intrinsic activation of Na+K+ ATPase in the cortical collecting duct. Urine potassium/urine potassium + urine sodium (UK+/UK+ + UNa+) is a surrogate marker for aldosterone activity and can be useful in differentiating primary sodium retention from secondary sodium retention in children with INS. This was a cross-sectional study of children with INS, presenting to our center from June 2007 to June 2008. Children were categorized into those with steroid responsive and steroid nonresponsive nephrotic syndrome. One hundred and thirty-four children with nephrotic syndrome were analyzed. The FeNa+ was significantly lower during relapse than in remission but no such difference was observed with UK+/UK+ + UNa+. The values of FeNa+ and UK+/UK+ + UNa+ across various categories of nephrotic syndrome were similar. Correlating FeNa+ and UK+/UK+ + UNa+ with cut-off of 0.5 and 60%, respectively, we found 50% of steroid responsive children and 36% of steroid nonresponders having a corresponding UK+/UK+ + UNa+ of <60% along with low FeNa+ of <0.5%, favoring primary sodium retention. Urinary indices did not vary with the type of steroid response. In early relapse, the urinary indices revealed an overlap of both primary and secondary sodium retention in most stable edematous children with nephrotic syndrome.