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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During renal failure, polyamines and oxalate levels are elevated in the serum and the glomerular filtrate and are dumped by the kidney. Both of these compounds can be catabolized by oxidative reactions. We have, therefore, investigated the intracellular distribution of oxalate oxidase and of a polyamine oxidase in normal female rat kidney and liver. Polyamine oxidase was demonstrable, using spermidine as substrate in the cerous peroxyhydrate procedure of Briggs et al., in peroxisomes of kidney tubule cells and of hepatocytes. Oxalate oxidase could not be studied with this technique due to precipitation of cerium oxalate in the incubation medium. To demonstrate oxalate oxidase, and to confirm the polyamine oxidase localization, we incubated aldehyde-fixed tissue in a diaminobenzidine medium at pH 8, following the approach of Veenhuis et al., in which oxidases are demonstrated by virtue of their production of H2O2, which then serves as a substrate for endogenous catalase. Using oxalate or spermidine as substrate with this approach, we found reaction product in typical renal peroxisomes; we also found reaction product, with the polyamine substrate, in hepatocyte peroxisomes. To strengthen the conclusion that the oxidases themselves are present in peroxisomes, we used a light microscopic method, based on the tetrazolium procedures of Allen and Beard to demonstrate polyamine and oxalate oxidase activities in bodies with the distribution of renal peroxisomes.
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PMID:Oxidation of oxalate and polyamines by rat peroxisomes. 392 4

In 78 patients with hypomagnesemia in urolithiasis the clinical course of disease was established in relation to therapy and dynamics of changes of serum magnesium levels. Almost 70% of patients had multiple, bilateral or recurrent nephrolithiasis or nephrocalcinosis. 70% of patients had Ca-oxalate stones or bilateral nephrocalcinosis. In 52% of patients a long-term magnesium supplementation was necessary. Significant progress of nephrolithiasis and nephrocalcinosis was observed in 80% of patients with permanent hypomagnesemia and in 4% of patients with normalization of serum magnesium level. Three of 15 patients with hypomagnesemia and progress of disease were transplanted a kidney and two were treated by hemodialysis. All five patients with renal failure had bilateral nephrocalcinosis, in three of them familiar occurrence of nephrolithiasis and hypomagnesemia was found.
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PMID:Prognosis of urolithiasis and nephrocalcinosis in hypomagnesemia. 393 9

We have studied the rat remnant kidney model as a tool to assess the impact of secondary oxalosis on renal failure. Although the plasma of uremic rats demonstrated increased levels of oxalic acid, deposits of oxalate crystals in tissue were not observed. The absence of such deposits in the remnant kidney, as well as other tissues, may be due to a lesser degree of hyperoxalemia observed in the rat compared to man or may reflect that uremic deaths among the experimental animals occurred prior to formation of detectable calcium oxalate deposition. We conclude that the rat remnant kidney is not a suitable model to study the impact of uremic oxalosis in man.
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PMID:Limitations of the rat remnant kidney model of chronic renal failure: absence of calcium oxalate tissue injury. 396 Feb 44

A single 45-g dose of intravenous ascorbic acid, a metabolic precursor of oxalate, was administered to a patient as adjuvant therapy for primary amyloidosis and the nephrotic syndrome. Acute oliguric renal failure occurred. Postmortem histopathologic examination of renal tissue revealed extensive intratubular deposition of crystalline material, which was confirmed as calcium oxalate by a microincineration technique. There were no extrarenal deposits of calcium oxalate. Plasma oxalate and ascorbic acid concentrations were increased. We conclude that therapy with high-dose ascorbic acid is a potential cause of oxalate nephropathy.
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PMID:Acute oxalate nephropathy after massive ascorbic acid administration. 399 72

This paper dealt with the case of a 53 years old man, affected by a chronic renal failure as the initial symptom of a primary oxalosis and treated by hemodialysis three years ago. Two years after the onset of renal failure, the left knee was painful and swollen but no cartilage or bone joint lesion was observed. Presence of intra synovial calcium oxalate crystals suggests that this arthropathy may be related to the primary oxalosis. However the role of other calcium salts under identification evidenced by synovial electron microscopy (apatite ? pyrophosphate ?) is discussed.
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PMID:[Calcium oxalate microcrystalline arthropathy in primary oxalosis]. 400 17

The 14C-oxalate clearance was determined in 13 healthy subjects and 22 patients with various diseases and varying degrees of renal function impairment, including 5 patients with primary hyperoxaluria (PH). The clearances of oxalate (Cox) and creatinine (Ccr) were correlated (r = 0.95). The regression line intersects the ordinate at the origin, while the regression coefficient is 2.0. This implies that the fractional Cox is constant, irrespective of the underlying disease and the degree of renal failure. Plasma oxalate (Pox), as calculated from the urinary oxalate excretion (Uox) and Cox, was elevated in patients with severely impaired kidney function and those with PH. Plasma creatinine (Pcr) and Pox were correlated as well (r = 0.83). Pox values of patients with PH were above the 95% confidence limits of the regression line. It is of practical importance that Pox can be estimated from Uox and Ccr when a 14C-oxalate clearance test cannot be performed. The reasons for the constancy of the Cox/Ccr ratio are discussed, and it is suggested that the effective renal plasma flow (ERPF) is the regulating factor for the tubular secretion of oxalate.
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PMID:Fractional oxalate clearance in subjects with normal and impaired renal function. 403 45

Measurement of oxalate levels in 14 patients with chronic renal failure, treated by maintenance hemodialysis, revealed elevated plasma oxalate concentrations in all patients 1,075.7 +/- (SEM) 253 micrograms/dl. In 7 of these subjects the oxalate concentration was more than three times higher than the upper limit of normal. Furthermore, a strong positive correlation (r = 0.75) between serum creatinine and plasma oxalate concentration was found. A combination of hemodialysis and hemoperfusion procedure was carried out in a dialysis patient with primary oxalosis as a cause of renal failure. The average oxalate clearance of the hemodialyzer during seven hemodialysis/hemoperfusion procedures was 91 ml/min and that of the charcoal detoxifier was 24 ml/min. The amount of oxalate removed during 4 1/2 h of the hemodialysis/hemoperfusion procedure was 429 mg. This amount was calculated to be produced in about 87 h, with an oxalate generation rate of 4.9 mg/h.
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PMID:Hyperoxalemia in renal failure and the role of hemoperfusion and hemodialysis in primary oxalosis. 405 24

We have measured the plasma oxalate concentration (POx), urinary oxalate excretion (UOx), oxalate equilibrium distribution volume (ODV), oxalate metabolic pool size [(ODV) X (POx)], total plasma oxalate clearance (PCOx), renal (or dialyser) oxalate clearance (RCOx), non-renal oxalate clearance (NRCOx) and the tissue oxalate accretion rate (TOA) = [(NRCOx) X (POx)] in three patients with severe renal failure due to primary hyperoxaluria who were being treated by peritoneal dialysis or haemodialysis, or by renal transplantation. The clearance (either GFR or dialyser) of [99mTc]diethylenetriaminepenta-acetate (DTPA) and the extracellular fluid volume (ECF) measured as [99mTc]DTPA distribution volume were also determined. Negligible amounts of 14C were found in faeces or as 14CO2 in expired air and hence (NRCOx) = (PCOx-RCOx). Haemodialysis removed oxalate more efficiently than peritoneal dialysis in the patient where a direct comparison was possible. Neither treatment could keep up with the TOA when performed for clinically acceptable times. The plasma oxalate concentrations calculated from 14C clearance through the dialyser and the chemically determined concentration of the oxalate in the dialysate were in the range 111-146 mumol/l. This is higher than in normals and in hyperoxaluric patients who are not in renal failure. Hence, although the ODV and ECF are similar to those of hyperoxaluric patients without renal failure and normal control subjects, the oxalate metabolic pool (ODV X POx) is grossly enlarged. In the patient treated by renal transplantation, the oxalate pool size diminished concurrently with the resumption of oxalate excretion but expanded again as renal function decreased due to oxalosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxalate dynamics and removal rates during haemodialysis and peritoneal dialysis in patients with primary hyperoxaluria and severe renal failure. 636 3

Eleven patients, aged 6 months to 47 years, with renal failure due to primary oxalosis, received renal allografts and were followed for 1 to 9 years. A specialized strategy for medical management included intensive pre-transplant hemodialysis and post-transplant long-term diuresis, administration of neutral phosphate, Mg++, and pyridoxine. Seven of ten living-related (LRD) transplants have good renal function, six with no biopsy evidence of renal oxalate deposition at up to 7 years after transplant. Two LRD graft losses from recurrent oxalosis, accompanied by massive secondary oxalate deposits, occurred in patients following endstage renal failure for over 3 years. A third LRD graft loss occurred following long-term (6 month) peritoneal dialysis in an infant. One cadaver transplant recipient has survived with recurrent oxalosis and poor graft function for 9 years. It is possible to perform successful renal transplantation in small children and adults with primary oxalosis and to completely prevent the deposition of oxalate in the renal allograft. Renal transplantation, with a strict medical protocol, would appear to be the initial treatment of choice for renal failure due to primary oxalosis.
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PMID:Successful strategies for renal transplantation in primary oxalosis. 638 56

Plasma oxalate was measured with use of the enzyme oxalate oxidase (EC 1.2.3.4; normal values 3.3 +/- 1.5 mumol/L, n = 24) in 50 patients with different degrees of renal failure. The following mean concentrations +/- SD (in mumol/L) were found: for glomerular diseases, 12.7 +/- 7.8 (n = 21); tubular diseases, 20.4 +/- 14.0 (n = 16); chronic renal failure before dialysis, 32.5 +/- 13.5, and after dialysis, 17.8 +/- 3.8 (n = 10); and primary hyperoxalemia, 72.2 +/- 14.5 14.5 (n = 2). The course of plasma oxalate was followed in one of these two patients after renal transplantation and in a patient recovering from acute tubular necrosis. No significant differences were found between patients with glomerular and tubular disorders. Overall, plasma oxalate was correlated with plasma creatinine in patients with glomerular and tubular diseases and dialysis patients (r = .84, P less than .001). Patients with primary hyperoxalemia had values outside the 95% confidence area of the regression line. It is concluded that the values obtained with this method, although probably still tending to overestimate the true oxalate concentration to some extent, provide reliable information about relative differences in plasma oxalate levels. In patients with terminal renal failure, plasma oxalate sometimes rises to levels at which deposition of calcium oxalate in tissues can occur.
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PMID:Plasma oxalate concentration in chronic renal disease. 638 28


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