Coordinated control of renal Ca(2+) transport proteins by parathyroid hormone.

Background: The kidney is one of the affected organs involved in the clinical symptoms of parathyroid hormone (PTH)-related disorders, like primary hyperparathyroidism and familial hypocalciuric hypercalcemia. The molecular mechanism(s) underlying alterations in renal Ca(2+) handling in these disorders is poorly understood.

Methods: Parathyroidectomized and PTH-supplemented rats and mice infused with the calcimimetic compound NPS R-467 were used to study the in vivo effect of PTH on the expression of renal transcellular Ca(2+) transport proteins, including the epithelial Ca(2+) channel transient receptor potential, vanilloid, member 5 (TRPV5), calbindins, and the Na(+)/Ca(2+)-exchanger (NCX1).

Recovery of renal tubule phosphate reabsorption despite reduced levels of sodium-phosphate transporter.

Background: The acute effect of parathyroid hormone (PTH) on phosphate transport has been reported to be mediated by rapid downregulation of sodium-phosphate transporter (NaPi-IIa) protein, but the association was observed with pharmacological doses of PTH.

Objective: To explore the effects of physiological doses of PTH on NaPi-IIa protein and its relationship to phosphate transport.

Methods: Acute clearance studies were performed in parathyroidectomized rats given a bolus i.

The role of commercial non-related living kidney transplants.

The motivation for dialysis patients to seek early, even pre-emptive, kidney transplantation from living donors is discussed. In most countries both the waiting time and the numbers of patients awaiting kidney transplantation are increasing. Local geopolitics in Jerusalem have produced a unique window to observe present transplant practices which include widespread international marketing of kidneys from paid living donors.

Immunohistochemical staining for proliferation antigen as a predictor of chronic graft dysfunction and renal graft loss.

Background: Assessment of proliferation rate (PR%) using monoclonal antibody for Ki-67 antigen has recently been found to have prognostic importance in lung and cardiac allografts. We ascertained whether the same might be true for renal allografts.

Methods: Newly cut sections from 20 archival paraffin blocks of renal allograft biopsy material showing acute cellular rejection and/or acute tubular necrosis (ATN) and absence of other pathology were stained using MIB-1 antibody and were further double-stained with anti-CD3, anti-CD20 or anti-CD68 antibodies.

Effect of prolonged uremia on insulin-like growth factor-I receptor autophosphorylation and tyrosine kinase activity in kidney and muscle.

Recently, based on a study in rats with chronic renal failure (CRF), it has been suggested that IGF-I resistance in uremia may be caused in part by defective IGF-I receptor autophosphorylation and tyrosine kinase activity. Thus if such a defect were to develop in prolonged acute renal failure (ARF), this may explain why IGF-I therapy, effective in rats, has failed to promote recovery from ARF in patients. Accordingly, we examined IGF-I receptor function in rats with uremia of increasing duration and in pair-fed sham-operated controls.

Hepatocyte growth factor receptor in acute tubular necrosis.

In acute tubular necrosis, there are early transient increases in circulating and local bioactive hepatocyte growth factor (HGF) levels and renal HGF receptor (c-MET) gene expression. It has therefore been suggested that endogenous HGF may play a role in initiating renal repair. To test this hypothesis, changes in the levels, activity, and anatomic distribution of c-MET protein were characterized in relation to the onset and localization of DNA synthesis in kidneys of rats with ischemia-induced acute tubular necrosis.