Successful treatment of early allograft dysfunction with cinacalcet in a patient with nephrocalcinosis caused by severe hyperparathyroidism: a case report

Abstract Background Hyperparathyroidism is common in patients undergoing kidney transplantation. Occasionally, this condition can cause early allograft dysfunction by inducing calcium phosphate deposition in the allograft, which results in nephrocalcinosis. Although nephrocalcinosis occurs occasionally in kidney allografts, it has only rarely been reported in the literature. Case presentation Here, we present the case of a 58-year-old Thai woman with severe hyperparathyroidism who received a living-related kidney transplant from her 35-year-old son. Our patient developed allograft dysfunction on day 2 post-transplantation despite good functioning graft on day 1. Allograft biopsy showed extensive calcium phosphate deposition in distal tubules. She was treated with cinacalcet (a calcimimetic agent) and aluminum hydroxide. Allograft function was restored to normal within 1 week after transplantation with greatly reduced intact parathyroid hormone level. Conclusion Hyperparathyroidism in early functioning allograft causes elevated calcium and phosphate concentration in distal tubules resulting in nephrocalcinosis. The massive calcium phosphate precipitation obstructs tubular lumens, which leads to acute tubular dysfunction. Treatment of nephrocalcinosis with cinacalcet is safe and may improve this condition by increasing serum phosphate and reducing serum calcium and intact parathyroid hormone

Immunolocalization of fibroblast growth factor-1 (FGF-1), its receptor (FGFR-1), and fibroblast-specific protein-1 (FSP-1) in inflammatory renal disease

Immunolocalization of fibroblast growth factor-1 (FGF-1), its receptor (FGFR-1), and fibroblast-specific protein-1 (FSP-1) in inflammatory renal disease.BackgroundThe fibroblast growth factor (FGF) family has functions in development, cell proliferation, migration, and differentiation. While FGF-2 induces fibrosis, the role of FGF-1 in inflammation and fibrosis is less defined. We examined the expression of FGF-1 and FGF receptor (FGFR-1) to determine if renal diseases with varying etiologies of inflammation, including lupus nephritis (LN), acute interstitial nephritis (AIN) and acute rejection superimposed on chronic allograft nephropathy (CAN), showed varying patterns of expression. We also examined the expression of fibroblast-specific protein-1 (FSP-1), which has been linked to epithelial-mesenchymal transition (EMT) and fibrosis, to determine whether it was linked to potential profibrotic and inflammatory FGF-1 mechanisms.MethodsProliferative LN (PLN) (N = 12), nonproliferative lupus nephritis (NPLN) (N = 5), AIN (N = 6), CAN (N = 4), and normal kidneys (N = 3) were studied. FGF, FGFR-1, and FSP-1 were localized by immunohistochemistry, and intensity scored on a 0 to 3+ scale. Double staining with CD68 and separate immunohistochemical staining for CD4 and CD8 with serial sections analysis were done to identify if T lymphocytes or macrophages showed staining for FGF-1 and FGFR-1 or FSP-1.ResultsIn normal kidneys, FGF-1 was expressed in mesangial cells (0.67 ± 0.58), glomerular endothelial (0.67 ± 0.58), visceral, and parietal epithelial cells (1.67 ± 0.58). FGFR-1 showed a similar pattern of staining but also was expressed in tubular epithelium, and arterial endothelium and smooth muscle. Expression of FGF-1 was increased over normal in glomerular parenchymal cells only in CAN in podocytes (2.30 ± 0.58 vs. 3.00 ± 0.00) (P < 0.05) and parietal epithelial cells (1.67 ± 0.58 vs. 2.25 ± 0.50) (P < 0.05). Infiltrating glomerular and interstitial inflammatory cells in diseased glomeruli also expressed FGF-1 and FGFR-1. Tubular cells expressed slightly increased FGFR-1 in renal diseases vs. normal, whereas tubules remained negative for FGF-1 in diseased kidneys. FSP-1 expression was prominent in the interstitium in all kidneys with interstitial inflammation, and most prominent in CAN. Interstitial FSP-1+ cells were consistent with a myofibroblast-type morphology, and did not stain with CD-68. FSP-1 expression was closely associated with inflammatory cells expressing FGF-1 and FGFR-1. FSP-1 also showed positivity within crescents and occasional podocytes in PLN.ConclusionThe expression of FGF-1 and FGFR-1 in infiltrating lymphocytes and macrophages, and of FGFR-1 in tubules, is supportive, but does not prove causality, of the possibility that FGF-1 might have both autocrine and paracrine functions in renal inflammation. However, the initial stimulus for renal inflammation, whether immune complex, hypersensitivity or rejection, did not alter expression patterns of FGF-1 or its receptor. The colocalization of inflammatory infiltrates with interstitial fibrosis supports the possibility of a contribution of FGF-1 for chemotaxis and associated fibrosis, further supported by interstitial FSP-1 expression closely associated with these inflammatory cells expressing FGF-1 and FGFR-1

BK Virus-Associated Nephropathy without Viremia in an Adolescent Kidney Transplant Recipient

BK virus can reactivate in kidney transplant recipients leading to BK virus-associated nephropathy (BKVAN) and allograft dysfunction. Pathogenesis begins with viral replication, follows by viruria, viremia and nephropathy. Screening tools recommended for viral detection are urine and blood BK viral load. Viremia has higher positive predictive value than viruria, thus several guidelines recommend using viremia to determine whether renal biopsy, a gold standard for diagnosis of BKVAN is needed. We present a 16-year-old boy who developed BKVAN five months after deceased donor kidney transplantation. He had increased serum creatinine with negative blood BK viral load. BK nephropathy was diagnosed in kidney graft biopsy. The urine showed BK viruria. Immunosuppressant was reduced and ciprofloxacin given. Viruria disappeared and repeated graft biopsy was normal 4 months later. BK viremia was negative through 1 year follow up. We conclude that BKVAN may occur even without viremia and BK viruria may be considered for screening tool

Clinicopathological characteristics of lupus nephritis in Thai males

Introduction: Lupus nephritis (LN) is a renal manifestation of systemic lupus erythematosus (SLE), an autoimmune disease more common in females. Clinicopathological manifestations and outcomes of LN in males are uncertain. Objectives: To assess and compare clinicopathological manifestations and outcomes of males and females with LN. Patients and Methods: Patients with LN were identified from database (male 94, female 344). Clinical manifestations, laboratory data, renal histopathology and outcome were retrieved and compared. Results: Compared to females, males were more likely to present with rapidly progressive glomerulonephritis (RPGN) (21.3% versus 11.6%, P = 0.026) and low-serum complement (76.6% versus 63.7%, P = 0.019). While asymptomatic hematuria and/or proteinuria was the second most common clinical manifestation in females (40%), no males presented with this manifestation. Although LN class IV was most common in both groups, males were more likely to have LN class IV with most severe form of renal manifestation than females (50% versus 38.7%, P = 0.048). Males showed tendency for poorer renal survival, but without statistical significance. Conclusion: Males with LN had more severe clinicopathological manifestations than females. Clinicians should be aware of SLE with LN in males in order to make timely diagnosis and treatment

Cryoglobulinemic Glomerulonephritis: A Case Report

Cryoglobulinemic glomerulonephritis (CG) is rare in children. We report a 13-year-old Thai boy who presented with acute nephrotic nephritis syndrome, arthralgia, and purpura. Renal pathology revealed membranoproliferative glomerulonephritis and CG. No secondary causes of CG were found. He responded well to 12 weeks of oral cyclophosphamide plus low dose prednisolone and azathioprine for maintenance. He was doing well at 31 weeks but long term follow up is required as chronic renal failure and neoplasia were reported