pyrophosphate and Acute-Kidney-Injury

pyrophosphate has been researched along with Acute-Kidney-Injury* in 5 studies

Other Studies

5 other study(ies) available for pyrophosphate and Acute-Kidney-Injury

ArticleYear
[Acute kidney failure and renal replacement therapy after colonoscopy in a 63-year-old woman].
    Der Internist, 2015, Volume: 56, Issue:11

    A 63-year-old woman presented with intestinal disorder, alternating between obstipation and diarrhoea. Sodium phosphate/diphosphate (FleetĀ®) was used in preparation for colonoscopy. Within 24 h the patient developed severe hyperphosphatemia and oliguric acute kidney failure with the need of renal replacement therapy. This case illustrates the rare event of phosphate nephropathy after colonoscopy.

    Topics: Acute Kidney Injury; Colonoscopy; Diphosphates; Female; Humans; Hyperphosphatemia; Laxatives; Middle Aged; Premedication; Renal Replacement Therapy; Treatment Outcome

2015
Extensive extraosseous localization of bone imaging agent in a patient with renal failure and rhabdomyolysis accompanied by combined hypercalcemia and hyperphosphatemia.
    Clinical nuclear medicine, 1989, Volume: 14, Issue:3

    Four sequential Tc-99m pyrophosphate (PYP) imaging studies were performed in a 28-year-old man with high fever and exudate pharyngitis associated with renal failure. Radiotracer localization in the left ventricle (LV), lungs, kidneys, and skeletal muscles were seen in two, initial imaging studies. In the second and third imaging studies, area of increase in activity was seen in the left-sided bowel. In studies done two months later (in the third study), the radioactivity in the skeletal muscles was no longer seen. Studies obtained nine months (in the fourth study) after the first imaging showed less radiotracer localization in the LV, lungs, and kidneys as compared to that seen in the initial study. Myocardial necrosis and microcalcification were proved by LV biopsy. The exact mechanism of extraosseous bone-imaging agent localization is unknown. However, this phenomenon may be related to renal failure, rhabdomyolysis, hypercalcemia, hyperphosphatemia, or elevated parathyroid hormone. The Tc-99m PYP imaging study is useful and sensitive in the detection of extraosseous tissue calcification and monitoring of the disease process.

    Topics: Acute Kidney Injury; Adult; Diphosphates; Humans; Hypercalcemia; Male; Phosphates; Radionuclide Imaging; Rhabdomyolysis; Technetium; Technetium Tc 99m Pyrophosphate

1989
Hypocalcemia and hypercalcemia in patients with rhabdomyolysis with and without acute renal failure.
    The Journal of clinical endocrinology and metabolism, 1986, Volume: 63, Issue:1

    Patients with rhabdomyolysis (RBD) and acute renal failure (ARF) are hypocalcemic during the oliguric phase of ARF and over 30% develop hypercalcemia during the diuretic phase. The present study examined the factors underlying these derangements in calcium metabolism in 15 patients: 7 with RBD and ARF, 4 with RBD only, and 4 with ARF only. All patients had hypocalcemia on admission and the hypocalcemia was more pronounced in those with RBD and ARF. All patients with RBD independent of the presence or absence of ARF had calcium deposition in soft tissues as documented by technetium-99 scan. In 4 patients with RBD and ARF, hypercalcemia developed during the diuretic phase at a time when Serum PTH levels were undetectable. Only patients with RBD and ARF had a significant increase in serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D [1,25(OH)2D] during the diuretic phase and both the increments in and the levels of 1,25(OH)2D were significantly greater in those who were hypercalcemic. The data indicate that 1) hypocalcemia occurs in RBD independent of ARF and is most likely related to calcium deposition in injured tissues, and 2) elevation in serum levels of 1,25(OH)2D plays an important role in the genesis of hypercalcemia during the diuretic phase of patients with RBD and ARF. Our observations suggest that extrarenal production of 1,25(OH)2D may occur in these patients, and/or that the renal production of 1,25(OH)2D may not be so tightly controlled as it is in normal subjects.

    Topics: Acute Kidney Injury; Adult; Calcinosis; Calcitriol; Diphosphates; Diuresis; Female; Humans; Hypercalcemia; Hypocalcemia; Male; Middle Aged; Parathyroid Hormone; Radionuclide Imaging; Rhabdomyolysis; Technetium; Technetium Tc 99m Pyrophosphate; Time Factors

1986
Technetium-99m pyrophosphate imaging in acute renal failure associated with nontraumatic rhabdomyolysis.
    AJR. American journal of roentgenology, 1986, Volume: 147, Issue:4

    Technetium-99m pyrophosphate (Tc-PYP) imaging was performed in five patients with acute renal failure associated with nontraumatic rhabdomyolysis. Four patients had phencyclidine intoxication and one had viral pneumonia. During the acute phase, marked uptake of pyrophosphate was seen in all patients in several muscle groups, but always in the thigh adductors. The results show that phencyclidine intoxication can result in diffuse muscle uptake of Tc-PYP without overt evidence of muscle injury. Tc-PYP imaging may provide a clue to the cause of acute renal failure in patients with suspected rhabdomyolysis in whom elevations of serum creatine phosphokinase concentrations are equivocal.

    Topics: Acute Kidney Injury; Adult; Diphosphates; Humans; Male; Radionuclide Imaging; Rhabdomyolysis; Technetium; Technetium Tc 99m Pyrophosphate

1986
Thiamine deficiency and oxalosis.
    Journal of clinical pathology, 1974, Volume: 27, Issue:7

    Type I hyperoxaluria results from reduced activity of alpha-ketoglutarate: glyoxylate carboligase, which is necessary for the synergistic decarboxylation of glyoxylate and alpha-ketoglutarate to alpha-hydroxy-beta-keto-adipate. Since thiamine pyrophosphate is a cofactor in the reaction, thiamine deficiency might be expected to result in tissue oxalosis. However, there was no significant increase in the incidence of renal oxalosis in 15 patients with Wernicke's encephalopathy at necropsy compared with controls. It is possible that hyperoxaluria was present in these thiamine-deficient patients but at a urine concentration below that necessary for calcium oxalate deposition. It is also possible that the severity of the thiamine deficit required for hyperoxaluria exceeds that for the neuronal and cardiac manifestations.

    Topics: Acute Kidney Injury; Adipates; Adult; Carboxy-Lyases; Diphosphates; Glyoxylates; Humans; Ketoglutaric Acids; Kidney Diseases; Metabolic Diseases; Middle Aged; Oxalates; Thiamine; Thiamine Deficiency; Wernicke Encephalopathy

1974