Relation between Calcium, Phosphorus, Calcium-Phosphorus Index and iPTH in Chronic Kidney Disease Patients.

BACKGROUND: The disturbance in homeostasis of calcium, phosphorus, vitamin D, and parathyroid hormone are frequently seen in chronic kidney disease patients. It is vital for physician to know the relation among them to treat chronic kidney disease patients. The main objective of the study is to 1) gather and analyze the data from chronic kidney disease patients undergoing dialysis to find out intact parathyroid hormone status 2) the relation between level of serum calcium, serum phosphorus, calcium-phosphorus index and serum intact parathyroid hormone in Nepalese population. METHODS: Verbal consent was taken from all the participants. Eighty participants between the age of 29 and 70 years with chronic kidney disease having indication of emergency hemodialysis were included in this study. Serum calcium, and phosphorus were measured by Fully Automatic Biochemistry Analyzer, and serum intact parathyroid hormone (iPTH) was measured using Chemi Luminescence Immuno Assay (CLIA) method. RESULTS: There is positive correlation between high calcium - phosphorus index and raised serum intact parathyroid hormone (r= 0.30).The relation is also true for serum calcium level and serum intact parathyroid hormone (r= 0.38). There is weak negative correlation between serum phosphorus and serum intact parathyroid hormone (r= -0.03). CONCLUSIONS: In Chronic kidney disease patients, high serum calcium or calcium - phosphorus index associated with raised level of serum intact parathyroid hormone and reverse is true for increased serum phosphate level. The relation may guide physician to suspect hyperparathyroidism in chronic kidney disease patients and manage the complications related to hyperparathyroidism like renal mineral bone disease, anemia resistant to erythropoietin.

Relation between Serum Intact Parathyroid Hormone Level and Hematocrit in Chronic Kidney Disease Patients.

Background Anemia is a common complication of chronic kidney disease. There are various causes of anemia in chronic kidney disease patients on hemodialysis. Secondary hyperparathyroidism is one of the less recognized causes of anemia in chronic kidney disease patients. Objectives The main objective of the study is to find the correlation between intact parathyroid hormone and hematocrit level in chronic kidney disease (CKD) patients undergoing hemodialysis. Method Verbal consent was taken from all the participants. Eighty participants between the age of 29 and 70 years with chronic kidney disease having indication of hemodialysis were included in this study. Hematocrit was measured by bioelectrical impedance method and serum intact parathyroid hormone was by using Chemi Luminescence Immuno Assay (CLIA) method. Result A weak reverse correlation was found between serum intact parathyroid level and hematocrit (r= -0.33). Conclusion In chronic kidney disease patient, there is reverse correlation between level of serum intact parathyroid and hematocrit level. This association may have clinical relevance in assessing the cause of unexplained low hemoglobin level in CKD patients.

Immunolocalization of aquaporin-9 in rat hepatocytes and Leydig cells.

The aquaporin (AQP)-9 gene was recently isolated from human and rat liver cDNA libraries as a member of the water channel family for water and neutral solutes. Although the expression of AQP9 mRNA has been demonstrated in several organs including the liver and testis by Northern blot analysis, the cellular and subcellular localization of the AQP9 protein remains unclear. In the present light and electron microscopic immunohistochemical study, the localization of the AQP9 immunoreactivity was examined in fifteen kinds of rat organs using an antibody against rat AQP9 synthetic peptide. The antibody immunostained a major band of approximately 33 kDa in the liver by Western blot analysis. Immunoreactivity for AQP9 was found exclusively in the liver and testis among the organs examined. In the liver, positive staining appeared selectively along the space of Disse. Immunoelectron microscopy confirmed the localization of AQP9 on the surface of hepatocyte microvilli facing the space of Disse. In the testis, the plasma membrane of Leydig cells located between seminiferous tubules was conspicuously immunoreactive to the antibody. Intense mRNA expression was detected in the liver and testis but not in other organs by ribonuclease protection assay. These findings suggest a specific role for AQP9 in the transport of water and non-charged solutes in hepatocytes and Leydig cells.

Expression profile of extracellular matrix and its regulatory proteins during the process of interstitial fibrosis after anti-glomerular basement membrane antibody-induced glomerular sclerosis in Sprague-Dawley rats.

Anti-glomerular basement membrane (GBM) nephritis in Sprague-Dawley (SD) rats was characterized by development of marked glomerular sclerosis and tubulointerstitial fibrosis. To elucidate sequential change of the glomerular sclerosis and tubulointerstitial fibrosis, accumulation and mRNA expression of extracellular matrix (ECM) components and transforming growth factor (TGF)-beta were examined in the glomerulus and cortex during the disease course by histology, immunostaining and ribonuclease protection assay. Mild proliferative and degenerative lesions appeared in the glomeruli by day 15 after anti-GBM antibody binding to GBM and progressed to glomerular sclerotic lesion thereafter. Conversely, interstitial change was first recognized by infiltration of mononuclear cells after day 20, followed by marked accumulation of ECM and tubular degeneration. The interstitial fibrosis was induced without apparent binding of anti-GBM antibody to tubular basement membrane. Accumulation of fibronectin, collagen type I and type IV was noted in the interstitium by immunofluorescence microscopy in association with enhanced expression of mRNA for these ECM components and their regulatory molecules such as matrix metalloproteinase (MMP2), tissue inhibitor of metalloproteinase (TIMP)-1 and TGF-beta1 both in glomeruli and cortex. The glomerular expression of these mRNA increased apparently by day 15 and reached a plateau or a peak at day 20. The expression of the same mRNA increased gradually from day 15 to day 29 in the cortex. These observations show that interstitial fibrosis follows glomerular sclerosis after anti-GBM antibody injection in SD rats, suggesting that at least a part of the mechanism for ECM accumulation in the glomerulus and interstitium is essentially the same in terms of composition of ECM and expression of its regulatory molecules.