ABSTRACT
The positron emission tomography (PET) flow tracer 82Rubidium is a known potassium analogue. During our studies oftumor blood flow in prostate cancer, we found that approximately 10% of the patients had high urinary 82Rubidiumactivity. In roughly half of these patients, the increased renal rubidium/potassium excretion was either causing hypokalemiaor explained by Thiazide treatment. In the other half, there was no obvious explanation or clinical consequence ofthe renal rubidium/potassium excretion. This is the first time enhanced renal potassium excretion is visualized on82Rubidium PET/CT.
ABSTRACT
The cyclooxygenase (COX) enzyme system is the major pathway catalyzing the conversion of arachidonic acid into prostaglandins (PGs). PGs are lipid mediators implicated in a variety of physiological and pathophysiological processes in the kidney, including renal hemodynamics, body water and sodium balance, and the inflammatory injury characteristic in multiple renal diseases. Since the beginning of 1990s, it has been confirmed that COX exists in 2 isoforms, referred to as COX-1 and COX-2. Even though the 2 enzymes are similar in size and structure, COX-1 and COX-2 are regulated by different systems and have different functional roles. This review summarizes the current data on renal expression of the 2 COX isoforms and highlights mainly the role of COX-2 and PGE2 in several physiological and pathophysiological processes in the kidney.
Subject(s)
Acute Kidney Injury , Arachidonic Acid , Body Water , Cyclooxygenase 2 , Dinoprostone , Hemodynamics , Kidney , Physiology , Prostaglandin-Endoperoxide Synthases , Prostaglandins , Protein Isoforms , SodiumABSTRACT
BACKGROUND: The primary aim of the study was to investigate the cytokine/chemokine response in the kidney, lung, and liver following acute kidney injury (AKI). The secondary aim was to test whether alpha-melanocyte-stimulating hormone (alpha-MSH) could prevent a reduction in organ function, and attenuate the inflammatory cytokine/chemokine response within the kidney, lung, and liver following AKI in rats with or without preexisting chronic kidney disease (CKD). METHODS: A two-stage animal model, in which AKI was induced in rats with preexisting CKD, induced by 5/6 nephrectomy (Nx), was used. Six weeks later, AKI was induced by intestinal ischemia and reperfusion (IIR). Sham procedures [S(Nx) and S(IIR)] were also performed. RESULTS: Increasing levels of serum creatinine (sCr) demonstrated progressive development of CKD in response to Nx, and following IIR sCr levels increased further significantly, except in the S(Nx) group treated with alpha-MSH. However, no significant differences in the fractional increase in sCr were observed between any of the groups exposed to IIR. In kidney, lung, and liver tissue the levels of interleukin (IL)-1beta were significantly higher in rats undergoing IIR when compared to the S(IIR) and control rats. The same pattern was observed for the chemokine monocyte chemoattractant protein (MCP)-1 in lung and liver tissue. Furthermore, kidney IL-1beta and RANTES levels were significantly increased after IIR in the Nx rats compared to the S(Nx) rats. CONCLUSION: Both the functional parameters and the cytokine/chemokine response are as dramatic when AKI is superimposed onto CKD as onto non-CKD. No convincing protective effect of alpha-MSH was detected.
Subject(s)
Animals , Rats , Acute Kidney Injury , alpha-MSH , Chemokine CCL5 , Creatinine , Interleukins , Ischemia , Kidney , Liver , Lung , Models, Animal , Monocytes , Nephrectomy , Renal Insufficiency, Chronic , ReperfusionABSTRACT
The kidneys play a key role in the homeostasis of body water and electrolyte balance. Aquaporin-2 (AQP2) is the vasopressin-regulated water-channel protein expressed at the connecting tubule and collecting duct, and plays a key role in urine concentration and body-water homeostasis through short-term and long-term regulation of collecting duct water permeability. The signaling transduction pathways resulting in the AQP2 trafficking to the apical plasma membrane of the collecting duct principal cells, including AQP2 phosphorylation, RhoA phosphorylation, actin depolymerization, and calciumm obilization, and the changes of AQP2 abundance in water-balance disorders have been extensively studied. Dysregulation of AQP2 has been shown to be importantly associated with a number of clinical conditions characterized by body-water balance disturbances, including hereditary nephrogenic diabetes insipidus (NDI), lithium-induced NDI, electrolytes disturbance, acute and chronic renal failure, ureteral obstruction, nephrotic syndrome, congestive heart failure, and hepatic cirrhosis. Recent studies exploiting omics technology further demonstrated the comprehensive vasopressin signaling pathways in the collecting ducts. Taken together, these studies elucidate the underlying molecular mechanisms of body-water homeostasis and provide the basis for the treatment of body-water balance disorders.