Biomedical subjects

Jamshid Amanzadeh

Publications and source records attributed to Jamshid Amanzadeh.

3 recordsLinked to original sources

PubMed2006

Hypophosphatemia: an evidence-based approach to its clinical consequences and management.

Optimal cellular function is dependent on maintenance of a normal serum phosphorus concentration. Serum phosphorus concentration is affected by several determinants, the most important of which is regulation of phosphorus reabsorption by the kidney. The majority of this reabsorption (80%) occurs in the proximal tubule and is mediated by an isoform of the sodium-phosphate cotransporter (NaPi-II). Parathyroid hormone, via a variety of intracellular signaling cascades leading to NaPi-IIa internalization and downregulation, is the main regulator of renal phosphate reabsorption. Shift of phosphorus from extracellular to intracellular compartments, decreased gastrointestinal absorption, and increased urinary losses, are the primary mechanisms of hypophosphatemia, which affects approximately 2% of hospitalized patients. Hypophosphatemia has been implicated as a cause of rhabdomyolysis, respiratory failure, hemolysis and left ventricular dysfunction. With the exception of ventilated patients, there is little evidence that moderate hypophosphatemia has significant clinical consequences in humans, and aggressive intravenous phosphate replacement is unnecessary. By contrast, patients with severe hypophosphatemia should be treated. Intravenous repletion may be considered, especially for patients who have clinical sequelae of hypophosphatemia.

Cardiomyopathies↗

PubMed2003

Effect of high protein diet on stone-forming propensity and bone loss in rats.

BACKGROUND: High protein diets are believed to cause kidney stone formation and bone loss, but the mechanisms mediating these changes are unknown. The purpose of this study was to create an animal model of animal protein excess and to evaluate the response of kidney and bone to the dietary protein load. METHODS: Rats (12 per group) were pair-fed with a high (48%) and low (12%) casein diets that were otherwise identical in their content of sodium, potassium, calcium, phosphorus, and magnesium. RESULTS: Compared with the low casein group, the high casein group delivered a substantial acid load during 59 days of study, since it significantly decreased urinary pH, and increased urinary ammonium, titratable acidity, and net acid excretion. Animals on high casein diet also had higher urinary volumes. On the high casein diet, urinary calcium excretion was significantly higher and urinary citrate excretion and concentration was significantly lower. On the high casein diet, urinary saturation of calcium phosphate was higher. Serum calcitriol concentration did not significantly differ between the two groups. Histomorphometric analysis of femur procured after 59 days on the diet showed marked increase in bone resorption in the high casein group. Hypocitraturia was associated with increased activity of sodium-citrate cotransporter in renal cortical brush-border membranes (BBM) in the high casein group. CONCLUSION: Both the kidney and bone contribute to the pathogenesis of hypercalciuria during high casein diet in rats. Hypocitraturia is probably renal in origin. This rat model will be useful in elucidating the mechanisms by which high protein intake increases the risk of nephrolithiasis and bone loss in human beings.

Acid-Base Equilibrium↗

PubMedDate not supplied

Anticoagulation and continuous renal replacement therapy.

More than half of patients with acute renal failure in the intensive care unit require dialysis, and the majority of them have significant hemodynamic instability. Continuous renal replacement therapy (CRRT) is often the preferred dialysis modality in these patients. One requirement for CRRT is anticoagulation, which can expose patients to the risk of bleeding. However, absence of effective anticoagulation may result in clotting of the CRRT circuit and subsequently less effective treatment. While heparins are widely used for anticoagulation, because of potential side effects such as bleeding and heparin-induced thrombocytopenia, alternative anticoagulation protocols should be considered. Citrate anticoagulation, regional heparin/protamine, predilution, r-hirudin, prostacyclin, and nafamostat are among these methods.

Acute Kidney Injury↗