The effect of vitamin D and calcium supplementation in pediatric steroid-sensitive nephrotic syndrome

AbstractBackgroundLow serum levels of total 25-hydroxycholecalciferol (25(OH)D) occur in nephrotic syndrome (NS). We aimed to assess the effects of vitamin D3 and calcium supplementation on 25(OH)D levels, bone mineralization, and NS relapse rate in children with steroid-sensitive NS.MethodsA randomized controlled trial (RCT) was performed in children with steroid-sensitive NS. The treatment group received vitamin D3 (60,000  IU orally, weekly for 4 weeks) and calcium supplements (500 to 1,000 mg/day for 3 months) after achieving NS remission. Blood samples for bone biochemistry were taken during relapse (T0), after 6 weeks (T1) and 6 months (T2) of randomization, whereas a lumbar DXA scan was performed at T0 and T2. Renal ultrasound was performed after study completion in the treatment group and in all patients with hypercalciuria.ResultsOf the 48 initial recruits, 43 patients completed the study. Post-intervention, 25(OH)D levels showed significant improvements in the treatment group compared with controls at T1 (p 

Conclusions: The time course in this patient strongly suggests that the nephrotic syndrome occurred as an adverse drug reaction to nivolumab treatment. If during nivolumab treatment renal insufficiency, hypoalbuminemia, or proteinuria develops, further analysis for a possible nephrotic syndrome is warranted for early detection and treatment of this life-threatening complication.

Authors: Myoga H, Akimoto T, Mato N, Nakaya T, Murakami T, Yoshizawa H, Nakagawa S, Miki A, Masuda T, Kobayashi T, Ono Y, Saito O, Ueda Y, Muto S, Nagata D Abstract A 68-year-old man was admitted to our hospital to undergo an examination for nephrotic syndrome while concurrently complicated with recurrent thymoma in the parietal pleura and retroperitoneum. He had been diagnosed with invasive thymoma and had undergone thymo-thymectomy seven years previously. Based on the renal biopsy findings, his nephrotic syndrome was ascribed to minimal change disease. He was treated with corticosteroid monotherapy, which resulte...

Volume retention in nephrotic syndrome has been linked to activation of the epithelial sodium channel (ENaC) by proteolysis of its γ-subunit following urinary excretion of serine proteases such as plasmin. Here we tested whether pharmacological inhibition of urinary serine protease activity might protect from ENaC activation and volume retention in nephrotic syndrome. Urine from both nephrotic mice (induced by doxorubicin inje ction) and nephrotic patients exhibited high aprotinin-sensitive serine protease activity.

Publication date: September 2017 Source:Advances in Chronic Kidney Disease, Volume 24, Issue 5 Author(s): Vivek Soi, Jerry Yee The pathologic consequences of sodium retention in the CKD population can lead to hypertension, edema, and progressive disease. Sodium excess is responsible for increases in oxidative stress, which alters kidney vasculature. As progression of CKD occurs, hyperfiltration by remaining nephrons compensates for an overall decrease in the filtered load of sodium. In the later stages of CKD, compensatory mechanisms are overcome and volume overload ensues. Nephrotic syndrome as it relates to sodium handl...

Publication date: September 2017 Source:Advances in Chronic Kidney Disease, Volume 24, Issue 5 Author(s): David H. Ellison Extracellular fluid volume expansion is nearly universal in patients with CKD. Such volume expansion has features similar to the syndrome of heart failure with preserved ejection fraction, which not only leads to symptoms but can also lead to further organ damage. Unique treatment challenges are present in this patient population, including low glomerular filtration, which limits sodium chloride filtration, intrinsic tubule predisposition to sodium chloride retention, and proteinuria. In addition, pha...

The megalin/cubilin receptor complex is required for proximal tubular endocytosis and degradation of filtered albumin. An additional high-capacity retrieval pathway of intact albumin for the recovery of large amounts of filtered albumin has been proposed, possibly involving cooperation between megalin/cubilin and the neonatal Fc receptor. To clarify the potential role of such a pathway, we examined the effects of megalin/cubilin gene inactivation on tubular albumin uptake and plasma albumin levels in nephrotic, podocin knockout mice.

This study was conducted on 250 subjects, 100 healthy children, 50 steroid sensitive nephrotic syndrome (SSNS), and 100 steroid resistant nephrotic syndrome patients (SRNS). Serum concentration of TNFα was measured by enzyme-linked immunosorbent assay (ELISA) technique and TNFα-G308A gene polymorphism was estimated by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum concentrations of TNFα significantly increased in SRNS cases when compared to SSNS subgroups. TNF G A, AA, GA + AA genotypes and A allele showed significant association with risk of NS development ...

Low molecular weight heparin may benefit nephrotic remission in steroid‑sensitive nephrotic syndrome via inhibiting elastase. Mol Med Rep. 2017 Oct 03;: Authors: Zhai S, Hu L, Zhong L, Tao Y, Wang Z Abstract Low molecular weight heparin (LMWH) has a structure similar to heparan sulfate, which exerts anti‑inflammatory effects via inhibiting elastase (Ela) activity. Release of Ela along the glomerular capillary wall may induce glomerular injury and proteinuria. The present study aimed to investigate the influence of LMWH on steroid‑sensitive nephrotic syndrome (SSNS) and the potential underlying me...

Conclusion: A subgroup of patients in nephrotic syndrome has a decrease in glomerular filtration, apparently related to hypovolemia which likely can be detected by a urinary potassium to potassium plus sodium ratio>  0.5–0.6 suggesting benefit of albumin infusion in this subgroup.What is Known:•Volume status can be difficult to assess based on clinical parameters in nephrotic syndrome, and albumin infusion can be associated with development of pulmonary edema and fluid overload in these patients.What is New:•Urinary potassium to the sum of urinary potassium plus sodium ratio can accurately detect hy...

ConclusionAddition of TNF α to podocytes causes CD80 upregulation, actin reorganization and podocyte injury. Overexpressed CD80 and Neph1 interact via their extracellular domain. This interaction implies a mechanism of slit diaphragm disruption and possible use of small molecules that disrupt CD80-Neph1 interaction as a pot ential for treatment of nephrotic syndrome associated with CD80 upregulation.