Calcium Oxalate Crystal Deposition Research Articles

The Secondary Oxalosis of Renal Failure

SummaryThe secondary oxalosis syndrome associated with renal failure is an important, although incompletely understood, complication of renal insufficiency. The deposition of calcium oxalate crystals in vital organs can be associated with significant morbidity and mortality. The pathophysiology of this disorder relates to supersaturation of the blood with the insoluble calcium salt of oxalate. The factors which aggravate the hyperoxalemia in individuals with renal failure are only now becoming evident. Although no effective prevention or treatment exists in the chronic setting, further investigation into the role of dietary protein restriction, pyridoxine administration, and avoidance of ascorbic acid supplementation in patients without a documented deficiency of the vitamin is warranted.

Arthropathy and cutaneous calcinosis in hemodialysis oxalosis.

Recently, calcium oxalate crystals have been identified in the synovial fluid of patients with arthritis and end-stage renal failure. We describe 4 patients who, during the course of long-term hemodialysis, developed calcium oxalate crystal deposits in the synovium and skin. Clinical manifestations included podagra, tenosynovitis, olecranon bursitis, and acute and chronic synovitis of the large joints that were associated with chondrocalcinosis or subchondral bone erosions. Diffuse involvement of the hand, with chondrocalcinosis of the finger joints, miliary calcified deposits in the skin, and artery calcifications, was observed in 3 patients. The fourth patient had erosive arthropathy. Oxalosis secondary to end-stage renal failure in patients treated with long-term hemodialysis can present with articular manifestations that resemble those of gout, pseudogout, and apatite deposition disease. Other characteristic features of the synovitis associated with oxalosis secondary to end-stage renal disease were: predominant involvement of the hand, mild inflammatory changes in the synovial fluid and synovium, and poor response to administration of nonsteroidal antiinflammatory agents.

Prevention of hypoxic pulmonary hypertension in the rat by an inhibitor of collagen synthesis: David J. Riley, M.D., Janet S. Kerr, Ph.D., Carol A. Tozzi, Ph.D., Harry M. Frankel, Ph.D., and Shiu Y. Yu, Ph.D. Department of Medicine, UMDNJ-Rutgers Medical School, New Brunswick, New Jersey 08903; Bureau of Biological Research, Rutgers University, Piscataway, New Jersey 08854; Department of Internal Medicine,

Patients with calcium oxalate kidney stones are advised to decrease the consumption of foods that contain oxalate. We hypothesized that a cutback in dietary oxalate would lead to a decrease in the urinary excretion of oxalate and decreased stone recurrence. We tested the hypothesis in an animal model of calcium oxalate nephrolithiasis.Hydroxy-L-proline (5%), a precursor of oxalate found in collagenous foods, was given with rat chow to male Sprague-Dawley rats. After 42 days rats in group 1 continued on hydroxy-L-proline, while those in group 2 were given chow without added hydroxy-L-proline for the next 21 days. Food and water consumption as well as weight were monitored regularly. Once weekly urine was collected and analyzed for creatinine, calcium, oxalate, lactate dehydrogenase, 8-isoprostane and H2O2. Urinary pH and crystalluria were monitored. Rats were sacrificed at 28, 42 and 63 days, respectively. Renal tissue was examined for crystal deposition by light microscopy.Rats receiving hydroxy-L-proline showed hyperoxaluria, calcium oxalate crystalluria and nephrolithiasis, and by day 42 all contained renal calcium oxalate crystal deposits. Urinary excretion of lactate dehydrogenase, 8-isoprostane and H2O2 increased significantly. After hydroxy-L-proline was discontinued in group 2 there was a significant decrease in urinary oxalate, 8-isoprostane and H2O2. Half of the group 2 rats appeared to be crystal-free.Dietary sources of oxalate can induce hyperoxaluria and crystal deposition in the kidneys with associated degradation in renal biology. Eliminating oxalate from the diet decreases not only urinary oxalate, but also calcium oxalate crystal deposits in the kidneys and improves their function.

Spheroliths of the lens

The spheroliths , mostly to be found in the brown nucleus of Morgagni's hypermature cataract, are up to 0.25 mm in diameter and consist of radially arranged crystals of calcium carbonate of oxalate. From the spheroliths extend, in varying degrees, marginally radial structures of a very fine filamentous, streaky character, that do not enter the altered protein of the lenticular nucleus. This, most probably, is a newly formed protein structure (a structure of mucopolysaccharides according to Zimmerman and Johnson 1958) in which secondary deposits of calcium carbonate or oxalate crystals accumulate. The spheroliths are usually round or kidney-shaped and rarely consist of more than one or two individual bodies.

Experimental induction of crystalluria in rats using mini-osmotic pumps.

Crystalluria was induced in male Sprague-Dawley rats by implanting potassium-oxalate-containing mini-osmotic pumps. Urine of all experimental animals had abundant crystals of calcium oxalate, hydroxypatite, struvite, and calcium phosphate. These crystals were similar in morphology to the crystals found in human crystalluria. Histological examination of kidneys and tissue samples from other organs revealed no abnormality. One group of animals was injected with sodium oxalate in addition to implantation of potassium-oxalate-containing mini-osmotic pumps. Bladder urine from these animals contained calcium oxalate microstones and their kidneys had deposits of calcium oxalate crystals.

Behavior of Calcium Oxalate Crystals with Leaf Development in Rice Seedling

Deposition and development of calcium oxalate crystals were observed with the development of coleoptile and several leaves in a japonica rice seedling (cv. Sasanishiki). The results are summarized as follows: 1) Prismatic crystals first deposited in the parenchyma cells of coleoptile when the 2nd leaf emerged (Figs. 1, 2, 3) and then slightly increased their size as aging of seedling proceeded. 2) In leaf blade before emerging from the previous leaf sheath, small crystals deposited in bundle sheath cells, but not in chlorenchyma cells. When the leaf blade began to emerge and unfold, the bundles of crystals abundantly deposited in chlorenchyma cells (Figs. 4, 6, 7) and thereafter they increased size and number per cell with aging of the leaf. The size and number of crystals and thus the volume percentage of them to the cell which contained them tended to be greatest at the upper part and smallest in the basal part of leaf blade (Fig. 9). There was positive correlation between the cell size and the crystal size (Table 1). 3) In leaf sheath the crystals deposited initially in the parenchymatous cells including bundle sheath and then in the chlorenchyma cells (Fig. 8). Their length, width, volume and volume percentage to the cell also increased with aging of the sheath, although their amount was less than in the leaf blade.

Localized Endotracheal Oxalosis Probably Secondary to Aspiration of Rhubarb

To the Editor.— An elderly debilitated patient was found at autopsy to have a fragment of vegetable matter impacted on the tracheal mucosa, which, with the underlying wall, was necrotic and contained large amounts of oxalate crystals. Oxalate was also present in the vegetable matter. It is probable that the aspirated material was rhubarb, which contains large amounts of oxalate. The case illustrates the ability of oxalate to produce tissue injury. Oxalosis, or excess deposition of calcium oxalate crystals in various tissues, has been observed in association with enzymatic, nutritional, or metabolic derangements in which excess oxalate is produced, or with increased ingestion of oxalate or oxalate precursors such as ethylene glycol.1It may occur with renal failure and decreased excretion of oxalate, and it has been produced by fungus.2When the oxalate is systemic, calcium oxalate crystals are frequently seen in the kidney, may occur in myocardium

The urinary excretion of glycollic acid and threonic acid by xylitol-infused patients and their relationship to the possible role of 'active glycoladehyde' in the transketolase reaction in vivo.

Xylitol has been used in several countries as a parenteral nutrient. Adverse reactions to intravenous xylitol infusions have been reported with calcium oxalate crystal deposition within the walls of the intracranial arteries and extensively in the kidneys (Evans et al., 1973; Schroder et al., 1974). Similar but more widespread calcium oxalate deposits occur in primary hyperoxaluria (Scowen et al., 1959). The urinary excretion of organic acids by xylitol-infused patients was examined and compared to that by glucose-infused patients, in order to define any alterations that might be related to the organic acidurias observed in patients with primary hyperoxaluria types I and I1 (hyperoxaluria with hyperglycollic aciduria and hyperglyoxylic aciduria, and hyperoxaluria with hyper-Lglyceric aciduria respectively). Quantitative extraction and g.l.c., and g.1.c.-mass-spectrometric methods were used. Four out of five of the xylitol-infused patients showed grossly increased excretions of glycollic acid and of threonic acid [2,3,4trihydroxy(threo)butanoic acid]. There was no detectable increase in the excretion of oxalic acid, glyoxylic acid, or glyceric acid. S. Hauschildt, R. A. Chalmers, A. M. Lawson, K., Schulthis & R. W. E. Watts (unpublished work) found that xylitol infusion did not increase blood oxalate concentrations. Xylitol is metabolized in man to D-XylUlOSe, D-xylulose Sphosphate, and thence to glucose via the pentose phosphate pathway. Transketolase (sedoheptulose 7-phosphateD-glyceraldehyde 3-phosphate glycolaldehydetransferase, EC 2.2.1 .l) intervenes twice in the metabolism of pentose phosphates, once to form glyceraldehyde 3-phosphate and sedoheptulose 7-phosphate from xylulose 5-phosphate and ribose 5-phosphate, and again to form fructose 6-phosphate and glyceraldehyde 3-phosphate from another molecule of xylulose 5-phosphate and erythrose 4-phosphate (Fig. 1). In these reactions the enzyme catalyses the stereospecific reversible transfer of a glycolaldehyde moiety from a donor ketose to an acceptor aldose. Besides xylulose Sphosphate, suitable donors include hydroxypyruvate, L-erythrulose, D-fructose Gphosphate and D-sedoheptulose 7-phosphate. Suitable acceptors include, in addition to D-ribose 5-phosphate and D-erythrose +phosphate, glycolaldehyde (-+ L-erythrulose), D-glyceraldehyde 3-phosphate (-+ D-XylUlOSe 5-phosphate) and formaldehyde (-+ dihydroxyacet one).

Familial oxalosis. Report of three cases and review of the literature.

An unusual disorder of familial oxalosis In three siblings is described. Autopsies were carried out in Case 1 and Case 2. The findings were characterized by the deposition of calcium oxalate crystals in the kidneys and various extrarenal organs. Hyperoxaluria, a pathognomonic sign in this disorder, and roentgenological nephrocalclnosis were demonstrated In living Case 3. Renal biopsy revealed minute intratubular deposition of calcium oxalate crystal. Result of electron microscopical investigation appeared to be normal. Chromosomal analysis of the family revealed no abnormality. Besides these three patients, one sister showed a slight elevation of urinary oxalate excretion. The mother, maternal uncle and aunt have suffered from microhematuria or urolithiasis, although urinary oxalate excretion is normal. Recent knowledges about the pathogenesis of primary oxalosis are reviewed and discussed.

Interstitial Fibrosis and Chronic Renal Failure Following Methoxyflurane Anesthesia

Methoxyflurane (Penthrane) has been shown to cause acute polyuric renal failure. Two patients recently manifested typical polyuric renal failure for two to three days following abdominal surgery with the use of methoxyflurane anesthesia. However, they then developed oliguric renal failure, requiring hemodialysis. Both showed x-ray film evidence of shrinkage of renal mass. The mean length of the renal silhouettes decreased from 13.5 to 11.3 cm in one patient and from 12.5 to 10.9 cm in the other. Renal biopsy in each patient disclosed intratubular and intertubular calcium oxalate crystal deposition and severe interstitial fibrosis. A second biopsy and autopsy in one patient demonstrated progression of the fibrosis. The latter patient died 14 months after surgery while undergoing chronic dialysis. The other patient no longer requires dialysis and has a serum creatinine level of 8 mg/100 ml.

Oxalic acid-produced surface phenomena on human enamel examined by scanning electron microscopy

Exposure of human enamel surfaces to 0.1 per cent aqueous oxalic acid resulted in dissolution of the enamel followed immediately by the deposition of calcium oxalate crystals (mono- and dihydrate forms). Although dissolution and deposition occurred over the whole enamel surface, areas associated with diazones of cut surfaces, and troughs of the natural surface perikymata, appeared to be particularly susceptible. Rapid subsurface decalcification occurred beneath hollow spheres of closely intermeshed calcium oxalate crystals. The subsurface “lesions” exhibited polygonal, often hexagonal, outlines, as did the points of attachment of these spheres within which enamel prisms projected perpendicularly or to the enamel surface. The histological features of the oxalic acid subsurface decalcification are surprisingly similar to those of natural carious lesions, and include intact surface zones, protected by a surface deposit of insoluble calcium oxalate, and narrow dark zones at the advancing fronts of the lesions.

Oxalates and Ionic Equilibria in Australian Saltbushes (Atriplex)

CATION absorption in Atriplex species is partly balanced by concurrent chloride absorption1,2, and, in all species so far examined, organic acid anions, principally oxalate, balance most of the residual cation excess. Atriplex has been known for some time to contain considerable deposits of calcium oxalate crystals in leaf tissue3 and this communication discusses the quantitative significance of oxalates in the genus.

Primary hyperoxaluria.

Article1 July 1961Primary HyperoxaluriaANGUS W. MCLAURIN, WILLIAM R. BEISEL, GERALD J. MCCORMICK, M.S., RAYMOND SCALETTAR, ROBERT H. HERMANANGUS W. MCLAURINSearch for more papers by this author, WILLIAM R. BEISELSearch for more papers by this author, GERALD J. MCCORMICK, M.S.Search for more papers by this author, RAYMOND SCALETTARSearch for more papers by this author, ROBERT H. HERMANSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-55-1-70 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPrimary hyperoxaluria is characterized by an increased urinary excretion of oxalate and the deposition of calcium oxalate crystals in the kidneys and other organs. This metabolic defect was thought initially to be a severe disease of infancy and childhood, characterized by recurrent nephrolithiasis and pyelonephritis and by a progressive course terminating in a uremic death. Studies by Newns and Black (1) in 1953 and by Aponte and Fetter (2) in 1954 demonstrated an increased urinary excretion of oxalate prior to death in such patients. Subsequently, the disease has been diagnosed with increasing frequency during life, and others (3-7) have confirmed...

OXALOSIS

A case is described in which oxalosis occurred in an 11-year-old boy. The patient had experienced the formation of numerous calculi and multiple operations for removal of the calculi. The clinical, pathologic and histochemical findings in the case are presented. The unusual features of the case are extensive deposits of calcium oxalate crystals in the kidneys, bone marrow, spleen, liver, blood vessels, and adrenal cortex. Calcium oxalate, a relatively inert substance, appears to effect renal damage by virtue of its deposition in the renal tissue. While many aspects of oxalate metabolism remain obscure, it is generally presumed that oxalosis represents an as yet undefined metabolic defect.