acid-phosphatase and Acute-Kidney-Injury

Serum tartrate-resistant acid phosphatase 5b (TRACP5b) is a bone resorption marker used in the assessment of bone metabolic status. The present study was designed to determine the clinical characteristics and utility of measuring serum TRACP5b levels in peritoneal dialysis (PD) patients.. Cross-sectional study.. Forty-one patients receiving PD treatment in a single centre.. Serum levels of the bone turnover markers TRACP5b, N-terminal cross-linking telopeptide of type 1 collagen (NTX), bone-specific alkaline phosphatase (BAP), and parathyroid hormone (PTH) were simultaneously measured. The correlation of serum TRACP5b with other established bone markers was analysed after logarithmic transformation. Multivariate linear regression analysis was performed to examine the effects of both renal and peritoneal Kt/V (an index for solute clearance) for urea on bone markers using age, sex, body mass index, and PTH as covariates. Bone markers were also measured in three patients before and after treatment with cinacalcet hydrochloride, alphacalcidol, and raloxifene hydrochloride.. Log TRACP5b was significantly correlated with log NTX, log BAP and log PTH. In the multivariate analysis, peritoneal Kt/V was not correlated with log NTX, log BAP or log TRACP5b. In contrast, renal Kt/V was significantly correlated with log NTX only. Responses to drug treatment were more accurately determined from serum TRACP5b and BAP than from serum NTX.. Serum TRACP5b and BAP are potentially useful biomarkers for the evaluation of bone turnover in PD patients because they correlate well with other established bone markers and they are not influenced by renal and peritoneal clearances.

Topics: Acid Phosphatase; Acute Kidney Injury; Adult; Aged; Alkaline Phosphatase; Biomarkers; Bone and Bones; Bone Resorption; Cinacalcet; Collagen Type I; Cross-Sectional Studies; Female; Humans; Hydroxycholecalciferols; Isoenzymes; Male; Middle Aged; Naphthalenes; Parathyroid Hormone; Peptides; Peritoneal Dialysis; Raloxifene Hydrochloride; Regression Analysis; Tartrate-Resistant Acid Phosphatase

Lactate dehydrogenase (LDG), glucose-6-phosphate dehydrogenase (G-6-PDG), isocitrate dehydrogenase (ICDG) as well as acid phosphatase (AcPase) activities were assessed in the rat tracheal ciliated epithelial cells using cytophotometry, combined with ultrastructural AcPase demonstration within 1 to 5 hours after animal death. A moderate gradual reduction of LDG, G-6-PDG and AcPase, but not ICDG activities has been detected in the groups of initially unaffected and hypertensive rats. The activities of all dehydrogenases progressively decreased compared to the stable AcPase values in rats which died from acute renal failure. AcPase reaction products were found to be released from the Golgi apparatus and lysosomes into the adjacent cytoplasm and across the plasma membrane. Occasionally AcPase activity emerged in the cis- and intermediate lamellae of the Golgi apparatus. The perturbations in the membrane permeability evidenced by AcPase leakage can be considered as the most likely mechanism for the observed postmortem reduction of some enzymatic activities tested.

Topics: Acid Phosphatase; Acute Kidney Injury; Animals; Cilia; Epithelium; Female; Glucosephosphate Dehydrogenase; Histocytochemistry; Hypertension, Renal; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Male; Postmortem Changes; Rats; Time Factors; Trachea

Repeated intraperitoneal injections of ferric nitrilotriacetate (Fe-NTA) induce nephrotoxic features such as proximal tubular necrosis and renal failure, an unexpected phenomenon for a ferric compound. The mechanism of Fe-NTA toxicity was investigated by electron microscopy and respiration studies of renal cortical mitochondria in rats. Four hours after a single intraperitoneal injection of Fe-NTA, 5 mg iron/kg body wt, loss of microvilli, increased number of cytoplasmic vacuoles, electron-dense cytoplasmic deposits, mitochondrial swelling, karyorrhexis, and rupture of cytoplasmic membrane were observed in proximal tubular epithelia. At 24 hours, an increased number of cells had become necrotic. Polarographic studies of mitochondria from renal cortex 4 hours after Fe-NTA treatment showed a significant decrease in State 3 respiration and DNP-uncoupled respiration, whereas little change was observed in State 4 respiration and ADP/O.

Topics: Acid Phosphatase; Acute Kidney Injury; Animals; Epithelium; Ferric Compounds; Iron; Kidney; Kidney Cortex; Kidney Tubular Necrosis, Acute; Kidney Tubules, Proximal; Male; Microscopy, Electron; Mitochondria; Nitrilotriacetic Acid; Oxygen Consumption; Rats; Rats, Inbred Strains; Succinate Dehydrogenase

Enzyme histochemical techniques were utilized to examine the progression and extent of proximal tubular injury during the development of cis-diamminedichloroplatinum (II) (CDDP)-induced acute renal failure. Acute renal failure was induced in male rats by the intraperitoneal administration of 10 mg CDDP/kg body weight. At 6, 24, 48, 72, and 96 hr following treatment, renal function was assessed and tissue was collected for renal morphologic and enzyme histochemical studies. The enzymes examined were gamma-glutamyl transpeptidase, alkaline phosphatase, sodium-potassium ATPase (nitrophenyl phosphatase), acid phosphatase, glucose-6-phosphatase, succinic dehydrogenase, alpha-glycerophosphate dehydrogenase, and lactic dehydrogenase. By 24 hr, the activity of acid phosphatase was reduced throughout the proximal tubule, with the greatest decrease occurring in the P3 segment of the proximal tubule located in the outer stripe of the outer medulla. Changes in the histochemical staining of the remaining enzymes were not consistently observed until 48 or, in some cases, 72 hr. These alterations involved all portions of the proximal tubule with the most severe changes involving P3. The results of the enzyme histochemical studies along with the morphologic findings indicating that the initiation of CDDP-induced acute renal failure, first apparent at 48 hr in this model, is associated with cell injury throughout the proximal tubule. The majority of the histochemical changes did not become apparent until late in the course of tubular injury. This suggests that most of the changes in enzyme activity represent nonspecific effects of CDDP-induced tubular injury, as opposed to direct enzyme inhibition by the drug.

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Animals; Cisplatin; gamma-Glutamyltransferase; Glucose-6-Phosphatase; Glycerolphosphate Dehydrogenase; Histocytochemistry; Kidney Tubules; L-Lactate Dehydrogenase; Male; Rats; Rats, Inbred Strains; Sodium-Potassium-Exchanging ATPase; Succinate Dehydrogenase

Gentamicin has been shown to induce renal tubular damage in man and laboratory animals and to result in elevated urinary excretion of some enzymes associated with specific cell regions in the kidney. In the present investigation, the possible protective effect of selenium against gentamicin-induced renal damage was tested by measuring the urinary excretion of some enzymes in the presence and absence of selenium. Our results show that a prior subcutaneous injection of selenium to rats for two days followed by a simultaneous S.C. injection of gentamicin and selenium resulted in a marked reduction in the excretion of such biochemical systems as the urine volume, urinary proteins, alkaline and acid phosphatases, beta-glucuronidase, muramidase, and glutamate dehydrogenase. Renal functional studies revealed that selenium-treated rats suffered less adverse effects compared to rats treated with gentamicin alone. Urinary acid phosphatase, beta-glucuronidase and muramidase, the three lysosomal enzymes tested, appeared to respond most readily to protection by selenium.

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Animals; Gentamicins; Glucuronidase; Glutamate Dehydrogenase; Kidney; Kidney Function Tests; Male; Muramidase; Rats; Selenium

The activity of several enzymes with different intracellular sites was determined in urine at various times following nonfatal acute tubular necrosis induced by mercuric chloride administration. The excretion rate of all tested enzymes rose on the 1st and 2nd day; in the next observations (days 7-15) enzymatic values approached the basal values. The lactate dehydrogenase isoenzyme pattern of the renal cortical zone showed an early shift towards cathodic fractions and later (7 days) an increase of middle ones; the normal anodic zymogram recovered after a suitable time interval (30 days). The isoenzymatic changes are related both to the renal hypoxia and to the appearance of less differentiated cells. The behaviour of functional parameters (urine flow, osmolality, urea clearance, creatinine clearance) were well in agreement with the observed enzyme and renal isoenzyme changes.

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Animals; gamma-Glutamyltransferase; Glutamate Dehydrogenase; Isoenzymes; Kidney; Kidney Tubular Necrosis, Acute; L-Lactate Dehydrogenase; Leucyl Aminopeptidase; Male; Mercuric Chloride; Mercury; Rats

HgC12-induced renal tubular lesions in the rat present histochemically with a transitory decrease of alkaline phosphatase, adenosinetriphosphatase (ATPase), and leucine-aminopeptidase activity. The toxic alterations of enzyme activity were more pronounced in the pars recta of the proximal tubule and in the loop of Henle, as compared with the tubulus contortus I. L-thyroxine treatment leads to an accelerated reversal of that enzymatic defect, followinga characteristic pattern, and to a differentiating increase of acid phosphatase and ATPase activity in certain parts of the normal renal tubule. The observations are discussed with reference to the specific mode of action of sublimate and l-thyroxine upon the tubular enzymes and to the well-known metabolic and functional influences of thyroid hormone on the kidney.

Topics: Acid Phosphatase; Acute Kidney Injury; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Epithelial Cells; Epithelium; Histocytochemistry; Kidney Tubules; Leucyl Aminopeptidase; Male; Mercury Poisoning; Phosphoric Monoester Hydrolases; Rats; Thyroxine

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Animals; beta-Aminoethyl Isothiourea; Calcinosis; Depression, Chemical; Electron Transport Complex IV; Histocytochemistry; Injections, Intraperitoneal; Kidney; Kidney Tubular Necrosis, Acute; Kidney Tubules, Proximal; Loop of Henle; Male; Nephrosclerosis; Nephrosis; Rats; Rats, Inbred Strains; Succinate Dehydrogenase; Time Factors

Topics: Acid Phosphatase; Acute Kidney Injury; Aged; Carcinoma; Cryosurgery; Humans; Male; Middle Aged; Postoperative Complications; Prostatic Neoplasms; Rectal Fistula; Urinary Fistula; Urinary Incontinence, Stress; Urination Disorders

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Animals; Dextrans; Glucosephosphate Dehydrogenase; Glycerol; Histocytochemistry; Kanamycin; Kidney Tubular Necrosis, Acute; Kidney Tubules, Proximal; Male; Mercury; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Acute Kidney Injury; Animals; Anuria; Blood Urea Nitrogen; Body Weight; Dose-Response Relationship, Drug; Gentamicins; Guinea Pigs; Kidney; Kidney Cortex; Kidney Tubules, Distal; Kidney Tubules, Proximal; Lysosomes; Male; Microscopy, Electron; Necrosis; Osmolar Concentration; Polyuria; Rats; Rats, Inbred F344

Topics: Acid Phosphatase; Acute Kidney Injury; Animals; Carbon Radioisotopes; Cytosine Nucleotides; Ethylenes; Galactosidases; Glycerol; Glycols; Glycoproteins; Glycoside Hydrolases; Hexosaminidases; Hydrolases; Kidney; Kidney Diseases; Male; Mannose; Neuraminic Acids; Neuraminidase; Rats; Transferases; Uridine Diphosphate Sugars

Topics: Acid Phosphatase; Acute Kidney Injury; Aftercare; Antineoplastic Agents; Female; Humans; Hydrogen-Ion Concentration; Urea; Urogenital Neoplasms; Water-Electrolyte Balance

Topics: Acid Phosphatase; Acute Kidney Injury; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Blood Pressure; Central Venous Pressure; Dogs; Esterases; Hemodynamics; Ischemia; Kidney; Kidney Tubules; Lysosomes; Mitochondria; Mitochondrial Swelling; Pulse; Shock, Hemorrhagic; Succinate Dehydrogenase; Time Factors

Topics: Acid Phosphatase; Acute Kidney Injury; Adenosine Triphosphatases; Animals; Blood Urea Nitrogen; Dihydrolipoamide Dehydrogenase; Diuresis; Epithelial Cells; Epithelium; Glucosephosphate Dehydrogenase; Histocytochemistry; Kidney; Kidney Tubules; Leucyl Aminopeptidase; Mannitol; Oxygen Consumption; Rats; Succinate Dehydrogenase; Time Factors

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Animals; Chromates; Chromatography, Gel; Erythrocytes; Glomerulonephritis; Humans; Kidney; Kidney Failure, Chronic; Liver Cirrhosis; Nephrectomy; Nephrotic Syndrome; Rabbits; Renal Dialysis

Topics: Acid Phosphatase; Acute Kidney Injury; Adolescent; Adult; Aged; Alanine Transaminase; Alkaline Phosphatase; Aminohydrolases; Amylases; Aspartate Aminotransferases; Child; Enzymes; Female; Humans; Hydroxybutyrate Dehydrogenase; Kidney Failure, Chronic; Male; Middle Aged; Molecular Weight; Peritoneal Dialysis; Phosphoric Monoester Hydrolases; Water-Electrolyte Balance

Topics: Acid Phosphatase; Acute Kidney Injury; Alkaline Phosphatase; Amylases; Humans; Kidney Failure, Chronic; Molecular Weight; Oxidoreductases; Peritoneal Dialysis; Renal Dialysis; Transaminases

Topics: Acid Phosphatase; Acute Kidney Injury; Adult; Alkaline Phosphatase; Anuria; Clinical Enzyme Tests; Glucuronidase; Humans; Kidney Transplantation; Male; Methods; Postoperative Complications; Spectrophotometry; Transplantation, Homologous

Topics: Acid Phosphatase; Acute Kidney Injury; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Histocytochemistry; Kidney Function Tests; Kidney Tubules; Male; Mercury; Microscopy, Electron; Models, Theoretical; Oxidoreductases; Rats; Regeneration; Succinate Dehydrogenase; Thymidine; Tritium

Topics: Acid Phosphatase; Acute Kidney Injury; Animals; Bicarbonates; Cellulose; Chlorides; Chromatography, Ion Exchange; Cystadenoma; Dehydration; Electrophoresis; Female; Glycoproteins; Histocytochemistry; Humans; Hypotension; Middle Aged; Mucoproteins; Potassium; Potassium Isotopes; Rectal Neoplasms; Sodium; Sodium Isotopes; Tritium; Water-Electrolyte Balance