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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the injurious effect of hyperoxaluria on renal tubular epithelium, as judged by apoptotic changes in the renal parenchyma, we performed an experimental study in 20 rabbits. In the experimental group animals (n = 10) severe hyperoxaluria was induced by continuous ethylene glycol (EG; 0.75%). Histologic alterations, including crystal formation, together with apoptotic changes were evaluated after 7 and 28 days. Control group animals (n = 10) received normal distilled drinking water. Following 7- and 28-day periods, tissue sections obtained from kidneys were examined histopathologically under light microscopy for the presence and the degree of crystal deposition in the tubular lumen. Apoptotic changes in renal tubular cells were examined using the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP in situ nick and labeling (TUNEL) method during the same follow-up period. Crystal deposition was evident in the tubular lumen of tissue sections obtained during the 7-day examination period. During the 28-day examination period, however, these findings were found to be either limited or to have disappeared. In relation to apoptotic changes, the percentage of positive nuclei stained using the TUNEL method was from 11 to 20% in the experimental group and 5.6% in the control group. Our findings indicate that both calcium oxalate (CaOx) crystals and hyperoxaluria itself may be injurious to renal tubular cells, as indicated by apoptotic changes. These changes may be responsible for the pathologic course of urolithiasis.
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PMID:Renal tubular injury induced by hyperoxaluria: evaluation of apoptotic changes. 1131 Feb 13

Urolithiasis, the process of formation of stones in the kidney and the urinary tract, is the major clinical manifestation of hyperoxaluria. Crystal deposition, as indicated by increased stone-forming constituents in urine, such as calcium, oxalate and uric acid, and decreased concentration of inhibitors, such as magnesium and glycosaminoglycans, was observed in pyridoxine-deficient hyperoxaluric rats. Renal tubular damage was indicated by increased excretion of enzymes such as alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, beta-glucuronidase and N-acetyl glucosaminidase. Fibrinolytic activity was found to be reduced. Administration of pentacyclic triterpenes such as lupeol and its structural analogue betulin to hyperoxaluric rats minimised the tubular damage and reduced the markers of crystal deposition in the kidneys. In this connection, lupeol was found to be more effective than betulin.
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PMID:Control of urinary risk factors of stones by betulin and lupeol in experimental hyperoxaluria. 1144 2

We report a case of urolithiasis associated with short bowel syndrome. A 56-year-old woman was admitted to our hospital for asymptomatic bilateral renal stones. She had received extensive resection of small intestine due to strangulating obstructive ileus 7 years ago (residual intestine, only 20 cm). Subsequently, she was in a state of short bowel syndrome. Plain film of kidney, uteter, bladder and computed tomography revealed bilateral renal stones (right 4 mm, left 10 mm). The left renal stone was successfully treated by extracorporeal shock wave lithotripsy. Since the right renal stone was small, no treatment was performed. The stone fragments were composed of calcium oxalate and calcium phosphate, and excessive urinary excretion of oxalate (103.8 mg/day) was observed. In this patient, urolithiasis was diagnosed to be due to enteric hyperoxaluria caused by short bowel syndrome. To prevent the recurrence of stone formation, she was treated with oral administration of calcium lactate, sodium/potassium citrate and magnesium oxide. We review the Japanese literatures on urolithiasis with short bowel syndrome.
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PMID:[A case of urolithiasis associated with short bowel syndrome]. 1263 4

There are many similarities in the profile of chronic renal disease in the five North African countries, reflecting their close resemblance in ethnic background, bioecology and socioeconomic standards. The incidence of renal disease is much higher than that in the West, yet the prevalence is relatively lower, which mirrors the inadequacy of medical care facilities. The principal causes of end-stage chronic renal disease (ESRD) are interstitial nephritis (14 to 32%), often attributed to environmental pollution and inadvertent use of medications; glomerulonephritis (11 to 24%), mostly mesangioproliferative and focal segmental sclerosis; diabetes (5 to 20%) and nephrosclerosis (5 to 21%). Obstructive/reflux nephropathy, attributed to urinary schistosomiasis, is common in Egypt (7%), Libya and Southern Algeria. Primary urolithiasis is a frequent cause of obstructive nephropathy in the western (hyperoxaluria) and middle (cystinuria) regions. The incidence of tuberculosis is increasing, particularly the diffuse interstitial and hematogenous forms. It is responsible also for 10 to 40% of renal amyloidosis. The latter is also frequently associated with familial Mediterranean fever. Sickle cell anemia is an important health problem in the west, leading to a wide range of glomerular and tubulointerstitial nephropathies. Takayasu disease is increasingly recognized as a cause of ischemic nephropathy and renovascular hypertension. The management of ESRD is largely influenced by late referral, co-morbidities and lack of dialysis facilities. Hemodialysis is the most frequent modality of renal replacement therapy (RRT). CAPD is used sporadically. Renal transplantation, largely from live (often unrelated) donors, is offered to less than 5% of patients with ESRD. The reported outcome of RRT generally conforms with international standards.
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PMID:End-stage renal disease in North Africa. 1286 87

Primary hyperoxaluria (PH) is a heterogeneous disease with a variable age of onset and a variable progression into kidney failure. Early diagnosis is mandatory to avoid the damaging effects of systemic calcium oxalate deposition. In 1997, we initiated a nationwide survey of American nephrologists to ascertain epidemiological data and current practices. PH was reported in only 102 patients, with PH I in 79 and PH II in 9; 14 patients were not classified. Most patients were Caucasian (84%). Main symptoms at diagnosis were urolithiasis (54.4%) and nephrocalcinosis (30%). A significant delay of diagnosis was seen in 42% of patients and 30% of patients were diagnosed only at end-stage renal disease (ESRD). Diagnosis was usually based on history and urinary oxalate excretion. Glycolate and l-glyceric acid excretion were rarely determined. To determine the enzyme defect, a liver biopsy was performed in 40%. Even at ESRD, only 56% of patients received an adequate diagnostic work-up. Half of the patients showed 'good' or 'fair' pyridoxine sensitivity. In addition to B(6), most patients received either citrate or orthophosphate. Kidney transplantation (KTx) failed in 19 of 32 transplants ( n=27 patients) and was due to recurrent oxalosis in 8 transplants. Liver Tx was performed after KTx in 5 patients (1 patient died). Combined liver-kidney Tx in 21 patients (in 9 patients after failure of KTx) achieved good organ function in 13 patients; 7 patients, however, died shortly after transplantation. In conclusion, the time between first symptom and diagnosis of PH must be minimized, and the diagnostic procedures have to be improved. The cases of unclassified hyperoxaluria suggest the possibility of additional type(s) of PH. As isolated KTx failed in 59% of patients, combined liver-kidney Tx seems to be the better choice in place of isolated KTx as the primary transplant procedure.
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PMID:A United States survey on diagnosis, treatment, and outcome of primary hyperoxaluria. 1292 Jun 26

A crucial role for cell-crystal interactions in the development of urolithiasis (UL) and nephrocalcinosis (NC) was previously observed in experiments with different cell lines mimicking renal epithelial cells. It was found that such cell-crystal interactions lead to tubular damage and/or or dysfunction. To find further proof for these observations, we measured the urinary N-acetyl-beta- d-glucosaminidase (NAG) excretion, a marker of proximal tubular damage, in children with UL or NC and in children with an increased risk of UL. We enrolled 142 children aged 4-16 years (mean 9.67+/-3.40 years), with 50 children having UL, 30 children with a history of UL (ULH), 20 patients with NC, 34 children with secondary hyperoxaluria (HyOx), and 8 children with idiopathic hypercalciuria (HC). Normal urinary NAG/Cr values were determined in a group of 70 healthy children aged 4-16 years (mean 10.06+/-3.97 years). The urinary NAG activity was measured using a colorimetric method and the results were expressed as molar creatinine (Cr) ratios. The highest median NAG/Cr ratios were found in children with UL plus hematuria (0.72 U/mM) and in children with UL (0.67 U/mM) or NC (0.48 U/mM), which were all significantly higher than those in controls (0.28 U/mmol, P<0.001 and P<0.05). The NAG/Cr ratios were increased above the upper normal reference interval of 0.63 U/mM (95th percentile) in 28 of 50 (56%) children with UL and in 9 of 20 (45%) children with NC. Although the ULH group also had significantly higher median NAG/Cr ratios (0.36 U/mM) compared with controls, the NAG/Cr ratio was only elevated in 4 of 30 (13%) patients. NAG values in children with secondary HyOx or HC were not different from controls. No correlation was found between the NAG/Cr ratios and the urinary excretion of oxalate or calcium. In conclusion, UL or NC may result in proximal tubular injury, which is rather the consequence of disease activity and of the mechanical influence of calculi, than of the metabolic background. The mechanism of cell damage in these conditions however, seems to be complex. Neither HyOx nor HC alone were sufficient to induce severe tubular damage expressed as an increase in NAG excretion in our patients.
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PMID:Urinary NAG in children with urolithiasis, nephrocalcinosis, or risk of urolithiasis. 1292 Jun 32

Secondary hyperoxaluria is due either to increased intestinal oxalate absorption or to excessive dietary oxalate intake. Certain intestinal diseases like short bowel syndrome, chronic inflammatory bowel disease or cystic fibrosis and other malabsorption syndromes are known to increase the risk of secondary hyperoxaluria. Although the urinary oxalate excretion is usually lower than in primary hyperoxaluria, it may still lead to significant morbidity by recurrent urolithiasis or progressive nephrocalcinosis. A clear distinction between primary and secondary hyperoxalurias is important. As correct classification may be difficult, appropriate diagnostic tools are needed to delineate the metabolic background as a basis for optimal treatment. We developed an individual approach for the evaluation of patients with suspected secondary hyperoxaluria. First, 24 h urines are examined repeatedly for lithogenic (e.g. calcium, oxalate, uric acid) and stone-inhibitory (e.g. citrate, magnesium) substances, and the patients are asked to fill in a dietary survey form. Urinary saturation is calculated using the computer based program EQUIL2, and the BONN-Risk-index is determined. The measurement of plasma oxalate and of urinary glycolate helps to distinguish between primary and secondary hyperoxalurias. If secondary hyperoxaluria is suspected, the stool is examined for Oxalobacter formigenes, an intestinal oxalate degrading bacterium, as lack or absence may lead to increased intestinal oxalate absorption. The last diagnostic step is to study the intestinal oxalate absorption using [13C2]oxalate. Depending on the results, various therapeutic options are available: 1) a diet low in oxalate, but normal or high in calcium, 2) a high fluid intake (>1.5 L/m2/d), 3) medications to increase the urinary solubility, 4) specific therapeutic measures in patients with malabsorption syndromes, depending on the underlying pathology, and 5) intestinal recolonization of Oxalobacter formigenes or the treatment with other oxalate degrading bacteria.
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PMID:Diagnostic and therapeutic approaches in patients with secondary hyperoxaluria. 1295 11

In idiopathic recurrent urolithiasis (IRCU) calcium oxalate and calcium phosphate are components of stones. It is not sufficiently known whether in urine the nucleation (liquid-solid transition) of each salt requires a different environment, if so which environment, and whether there is an impact on stone formation. Nucleation was induced by in vitro addition of oxalate or calcium to post-test meal load whole urine of male stone patients (n=48), showing normal daily and baseline fasting oxaluria. The maximally tolerated (until visible precipitates occur) concentration of oxalate (T-Ox) or calcium (T-Ca) was determined; additionally evaluated were other variables in urine, including total, complexed and free citrate (F-Cit), protein (albumin, non-albumin protein) and the clinical intensity (synonymous metabolic activity; MA) of IRCU. In the first of three trials the accumulation of substances in stone-forming urine was verified (trial-V); in the second (clinical trial 1) two strata of T-Ox (Low, High) were compared; in the third (clinical trial 2) IRCU patients (n=27) and a control group (n=13) were included to clarify whether in stone-forming urine the first crystal formed was calcium oxalate or calcium phosphate, and to identify the state of F-Cit. T-Ox was studied at the original pH (average < 6.0), T-Ca at prefixed pH 6.0; the precipitates were subjected to electron microscopy and element analysis. Trial-V: Among the urinary substances accumulating at the indicated pHs were calcium, oxalate and phosphate, and the crystal-urine ratios were compatible with the nucleation of calcium oxalate, calcium-poor and calcium-rich calcium phosphate; citrate, protein and potassium also accumulated. Clinical trial 1: the two strata exhibited an inverse change of T-Ox and T-Ca, the ratio T-Ox/T-Ca and MA. The initial (before induction of Ox or Ca excess) supersaturation of calcium oxalate and brushite were unchanged, with the difference of proteinuria being borderline. Several correlations were significant (p < or = 0.05): urine pH with citrate and volume, protein with volume and MA, T-Ox with T-Ca and MA. Clinical trial 2: in patients with reduced urine volume and moderate urine calcium excess, the first precipitate appeared to be calcium oxalate, followed by amorphous calcium phosphate. Conversely, when the calcium excess was extreme, calcium-rich hydroxyapatite developed, followed by calcium oxalate; F-Cit, not total and complexed citrate, was decreased in IRCU vs. male controls; F-Cit rose pH-dependently, and the ratio F-Cit at original pH vs. F-Cit at pH 6.0 correlated inversely with the nucleation index T-Ox/T-Ca; MA correlated inversely with the ratio F-Cit at pH 6.0, respectively, original pH, but directly with the urinary albumin/non-albumin protein ratio. In summary 1) to study calcium oxalate and calcium phosphate nucleation in whole urine of IRCU patients is feasible; 2) at this crystallization stage the two substances, dominant in calcium stones, appear intimately linked, 3) in stone-forming urine, calcium phosphate may be ubiquitously present, likely as particles < 0.22 microm; 4) together with co-precipitation of calcium oxalate and calcium phosphate, low F-Cit and alteration of proteinuria may act in concert and accelerate stones.
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PMID:Is calcium oxalate nucleation in postprandial urine of males with idiopathic recurrent calcium urolithiasis related to calcium phosphate nucleation and the intensity of stone formation? Studies allowing insight into a possible role of urinary free citrate and protein. 1508 May 61

Renal tubular epithelium is the major target for oxalate induced injury, and sustained hyperoxaluria together with CaOx crystal formation/deposition may induce renal tubular cell damage and/or dysfunction. This may express itself in cell apoptosis. To evaluate the possible protective effects of certain agents (vitamin E, potassium citrate, allopurinol, verapamil and MgOH) on the presence and the severity of apoptotic changes caused by hyperoxaluria on renal tubular epithelium, an experimental study in rabbits was performed. Seventy rabbits were divided into seven different groups (each group n = 10): in group I severe hyperoxaluria was induced by continuous ethylene glycol (0.75%) administration started on day 0 and completed on day 14. Histologic alterations including crystal formation together with apoptotic changes (by using the TUNEL method) were evaluated on days 21 and 42, respectively. In the remaining experimental groups (groups II-VI), animals received some agents in addition to the induction of hyperoxaluria in an attempt to limit apoptotic changes. Group VII) animals constituted the controls. Kidneys were examined histopathologically under light microscopy for the presence and degree of crystal deposition in the tubular lumen. The percentage of apoptotic nuclei in the control group was significantly different from the other group animals (2.9-2.4%) in all study phases (P < 0.05). Apart from potassium citrate and allopurinol, the other medications seemed to prevent or limit the formation of apoptotic changes in renal tubular epithelium during the early period (day 21). The percentage of positively stained nuclei in animals undergoing potassium citrate medication ranged from 24.3% to 28.6%, with an average of 27.1%. This was 18.4% in animals receiving allopurinol. On the other hand, animals receiving magnesium hydroxide (MgOH), verapamil and vitamin E demonstrated limited apoptotic changes (11.2, 9.7, 8.7%, respectively) during this phase(P < 0.05). In the long-term (day 42), the animals receiving allopurinol and vitamin E showed a decrease in the percentage of the positively stained nuclei (13.5% and 8.3%, respectively). Animals in the other groups showed an increase in the number and percentage of apoptotic cells. Although, there was a significant decrease in the mean values of apoptosis in animals receiving vitamin E (8.7%-8.3%) and allopurinol (18.4%-13.5%) (P < 0.05), animals on verapamil, MgOH and potassium citrate medication had an increase in these values or the change was not found to be significant. In the light of our findings and results from the literature, it is clear that that both hyperoxaluria and CaOx crystals may be injurious to renal epithelial cells. Apoptotic changes observed in renal tubular epithelial cells induced by massive hyperoxaluria might result in cell degradation and may play a role in the pathologic course of urolithiasis. Again, as demonstrated in our study, the limitation of both crystal deposition and apoptotic changes might be instituted by some antioxidant agents as well as urinary inhibitors. Clinical application of such agents in the prophylaxis of stone disease might limit the formation of urinary calculi, especially in recurrent stone formers.
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PMID:Limitation of apoptotic changes in renal tubular cell injury induced by hyperoxaluria. 1524 86

Oxalate induced renal calculi formation and the associated renal injury is thought to be caused by free radical mediated mechanisms. An in vivo model was used to investigate the effect of phycocyanin (from Spirulina platensis), a known antioxidant, against calcium oxalate urolithiasis. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg) and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given, 1h prior to sodium oxalate infusion. An untreated control and drug control (phycocyanin alone) were also included in the study. We observed that phycocyanin significantly controlled the early biochemical changes in calcium oxalate stone formation. The antiurolithic nature of the drug was evaluated by the assessment of urinary risk factors and light microscopic observation of urinary crystals. Renal tubular damage as divulged by urinary marker enzymes (alkaline phosphatase, acid phosphatase and gamma-glutamyl transferase) and histopathological observations such as decreased tubulointerstitial, tubular dilatation and mononuclear inflammatory cells, indicated that renal damage was minimised in drug-pretreated group. Oxalate levels (P < 0.001) and lipid peroxidation (P < 0.001) in kidney tissue were significantly controlled by drug pretreatment, suggesting the ability of phycocyanin to quench the free radicals, thereby preventing the lipid peroxidation mediated tissue damage and oxalate entry. This accounts for the prevention of CaOx stones. Thus, the present analysis revealed the antioxidant and antiurolithic potential of phycocyanin thereby projecting it as a promising therapeutic agent against renal cell injury associated kidney stone formation.
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PMID:Prophylactic role of phycocyanin: a study of oxalate mediated renal cell injury. 1529 40


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