Long-term Clinical Course after Living Kidney Donation by a Patient with Gitelman Syndrome Harboring a Compound Heterozygous Mutation of the SLC12A3 Gene.

The eligibility for kidney donation and long-term post-donation renal prognosis of patients with Gitelman syndrome (GS) are unknown. We herein report a 44-year-old woman with GS who donated her kidney for transplant. A gene sequence analysis revealed compound heterozygous mutations of T180K and L858H in the SLC12A3 gene. Since transplantation, the renal function and serum potassium and magnesium levels of the donor and recipient have remained stable for seven years with careful monitoring and supplementation. Patients with asymptomatic GS who have no complications can be considered eligible to donate their kidney for transplant with proper monitoring after transplantation.

[Fragility Fractures in Hemodialysis Patients. Abnormal bone material characteristics of dialysis patients.]

The relationship between renal dysfunction and bone fragility is well known. Bone fragility, which is associated with an increased risk of bone fracture, affects quality of life and prognosis in patients with chronic kidney disease(CKD). The bone of patients with CKD is more fragile than the risk estimated by measurement of bone mineral density. Bone quality, which is defined by many factors including bone turnover, microarchitecture, collagen crosslinking, and matrix composition, is considered to be major cause of bone fragility of the patients with CKD. In this article, we will describe the bone quality of dialysis patients with CKD as representatives of patients with CKD.

A case of infection-related glomerulonephritis with massive eosinophilic infiltration
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Infection-related glomerulonephritis (IRGN) is rarely complicated with eosinophil infiltration into the glomerulus. Here we report a case of eosinophilic proliferative glomerulonephritis related with infection. A 70-year-old man with respiratory symptoms displayed hypereosinophilia, hypocomplementemia, impaired renal function, and nephrotic syndrome. Renal biopsy revealed endocapillary proliferative glomerulonephritis with immunostaining for immunoglobulin G and complement 3, and subepithelial hump-like electron-dense deposits, thus fulfilling the criteria for IRGN. Immunostaining for the nephritis-associated plasmin receptor (NAPlr) in the glomerulus confirmed the diagnosis of IRGN. Of note, eosinophils infiltrated into the glomerular subendothelial spaces, renal tubules, peritubular capillaries, and the interstitium in the kidney as well as in the alveolar walls and pulmonary arteries in the lung. Corticosteroid therapy rapidly improved hypereosinophilia as well as respiratory symptoms and renal function. Urinary protein exertion was decreased, and serum level of complement and albumin was increased. These findings suggest that eosinophil infiltration might play a prominent role in respiratory and renal disorders. Severe endothelial damage of glomeruli and tubulointerstitial nephritis, caused by eosinophil-rich inflammation, might significantly contribute to exacerbation of renal insufficiency.
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