oxalates and Nephritis--Interstitial

Topics: Cystinuria; Humans; Metabolic Diseases; Nephritis, Interstitial; Oxalates; Uric Acid

Topics: Cadmium Poisoning; Gold; Humans; Lead Poisoning; Mercury Poisoning; Nephritis, Interstitial; Oxalates; Radiation Injuries; Uranium

Topics: Aged, 80 and over; Biopsy; Creatinine; Glomerular Filtration Rate; Humans; Kidney; Male; Nephritis, Interstitial; Oxalates; Renal Dialysis; Rheum; Risk Factors

Chaga mushrooms have been used in folk and botanical medicine as a remedy for cancer, gastritis, ulcers, and tuberculosis of the bones. A 72-year-old Japanese female had been diagnosed with liver cancer 1 year prior to presenting at our department. She underwent hepatectomy of the left lobe 3 months later. Chaga mushroom powder (4 - 5 teaspoons per day) had been ingested for the past 6 months for liver cancer. Renal function decreased and hemodialysis was initiated. Renal biopsy specimens showed diffuse tubular atrophy and interstitial fibrosis. Oxalate crystals were detected in the tubular lumina and urinary sediment and oxalate nephropathy was diagnosed. Chaga mushrooms contain extremely high oxalate concentrations. This is the first report of a case of oxalate nephropathy associated with ingestion of Chaga mushrooms.

Topics: Agaricales; Aged; Antineoplastic Agents; Biopsy; Female; Humans; Kidney; Liver Neoplasms; Medicine, East Asian Traditional; Mushroom Poisoning; Nephritis, Interstitial; Oxalates; Renal Dialysis; Treatment Outcome

A 65-year-old Japanese male developed renal dysfunction, showing proteinuria and marked urinary excretion of beta2-microglobulin. He had consumed approximately 100-200 g peanuts and 750-1,000 ml beer every day for two or three months. He had previously been treated for hypertension with an angiotensin-converting enzyme inhibitor, enalapril. He then visited his primary-care doctor with mild fever, and renal dysfunction with mild diabetes mellitus were diagnosed. He was referred to our hospital, and because no diabetic retinopathy was observed by ophthalmological tests, renal biopsy examination was performed to clarify renal dysfunction. Renal biopsy specimens showed intimal thickening in the small arteries and interstitial nephritis with a granulomatous lesion, accompanied by oxalate crystals under polarized light. Glomeruli were unremarkable without any immunoglobulin deposition, and nodular lesions. Because he daily consumed a large amount of peanuts, oxalate nephropathy due to excessive intake of peanuts was strongly suspected. This case revealed that unusual food habits, including nuts, can cause oxalate nephropathy, and that close examination by renal biopsy was useful for clarifying the etiology of the unknown renal damage.

Topics: Aged; Arachis; beta 2-Microglobulin; Biopsy; Humans; Kidney; Male; Nephritis, Interstitial; Oxalates; Proteinuria

Hyperoxaluria is a recognized cause of tubulointerstitial lesions, and this could contribute to development of hypertension and chronic renal failure. Enalapril has been effective against the progression of tubulointerstitial lesions in various animal models. The aim of the present study was to evaluate the usefulness of enalapril on the tubulointerstitial damage produced by oxalates. Two-month-old male Sprague-Dawley rats were separated into 4 groups, control with tap water (G1), hyperoxaluric (G2), hyperoxaluric+enalapril (G3), enalapril (G4), for 4 weeks. G2 and G3 rats were given 1% ethyleneglycol (ETG, precursor for oxalates), and G3 and G4 rats were given enalapril 20 mg/L in drinking water. At the end of the study, we evaluated renal tubulointerstitial lesions by a semiquantitative score. Urine albumin excretion, serum and urine nitric oxide production, tubulointerstitial immunostaining by alpha-smooth muscle actin, transforming growth factor-beta1, and collagen type III were measured. Rats belonging to the hyperoxaluric group treated with enalapril (G3) showed fewer tubulointerstitial lesions (1.3+/-0.2 versus 3+/-0.2; P<0.01), lower urine albumin excretion (8+/-2 mg/d versus 25+/-2 mg/d; P<0.01), less percentage of alpha-smooth muscle actin in renal interstitium (2+/-0.4% versus 13.5+/-2.4%; P<0.01), less percentage of transforming growth factor-beta1 in tubulointerstitial area (3.3+/-1% versus 13.3+/-2. 1%; P<0.01), less percentage of collagen type III interstitial deposition (0.7+/-0.5% versus 7+/-2.6%; P<0.01), and increased NO production in serum as well as urine (both P<0.01), when compared with the hyperoxaluric group not treated with enalapril (G2). Considering these data, we believe that enalapril, by several mechanisms of action, could provide an important benefit in the prevention of inflammatory response, transforming growth factor-beta1 tubulointerstitial production, collagen type III interstitial deposition, and finally, the progressive tubulointerstitial fibrosis caused by oxalates.

Topics: Animals; Atrophy; Blood Pressure; Enalapril; Hyperoxaluria; Kidney Tubules; Male; Nephritis, Interstitial; Oxalates; Rats; Rats, Sprague-Dawley; Time Factors

We present a case of granulomatous interstitial nephritis and renal failure after a jejunoileal bypass for obesity. Improvement of the renal function occurred after reversal of the intestinal bypass. The renal biopsy showed an interstitial nephritis, oxalate crystal deposition and several aggregates of multinucleated giant cells related to the crystal material (granulomatous reaction). By ultrastructural and histochemical studies we demonstrated mitochondrial alterations in the tubular epithelial cells, and we suggested the proximal tubule origin of the giant cells. The association of the oxalate crystals with damaged tubules and giant cells suggests that the oxalate crystals are responsible for these alterations. The possibility of an associated immunological process as the cause of the interstitial nephritis cannot be excluded.

Topics: Acute Kidney Injury; Female; Humans; Jejunoileal Bypass; Kidney; Microscopy, Electron; Middle Aged; Nephritis, Interstitial; Oxalates

Plasma oxalate concentration was measured using an enzyme/bioluminescent assay in 289 patients (178 males, 111 females) with chronic renal failure (plasma creatinine greater than 200 mumol/l), age (SD) 55.5 (13.8) years. Plasma oxalate ranged between less than 0.8 and 48 mumol/l and showed a positive correlation with plasma creatinine (r = 0.57, p less than 0.0001). The slope of the regression line in 55 patients with glomerulonephritis (GN) was significantly lower than in patients with tubulointerstitial disease (TI); however the intercept was significantly higher in GN than in TI. Analysis of covariance showed no relationship between plasma oxalate concentration and age, duration of renal impairment, or administration of diuretics, vitamin D analogues, or phosphate binders. Longitudinal analysis of plasma oxalate measured 3-monthly in selected patients showed marked variability of oxalate/creatinine and oxalate/urea ratios.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Creatinine; Cross-Sectional Studies; Female; Glomerulonephritis; Humans; Kidney Failure, Chronic; Longitudinal Studies; Male; Middle Aged; Nephritis, Interstitial; Oxalates; Regression Analysis

Deposition of calcium oxalate is responsible for the pathologic manifestations of oxalosis and may contribute to multiorgan dysfunction in uremia and to the progression of renal damage after renal failure is established. We have developed a rat model of oxalosis using a single intravenous injection of sodium oxalate, 0.3 mmol./kg. body weight, in rats. Polarized light microscopy and section freeze-dry autoradiography were used to identify 14C-oxalate within the renal parenchyma and in extrarenal organs. 14C-oxalate crystals under three mu in length were identified within one min. of injection in proximal tubule lumens. Section freeze-dry autoradiography showed occasional minute crystals within glomeruli, heart, lung and liver at one hr. In contrast to concentrative cellular uptake demonstrated in rat renal cortical slices in vitro, intracellular accumulation of 14C-oxalate could not be detected in vivo. Within the first 24 hr., renal oxalate retention reached a maximum of 25 +/- 4 per cent of the injected dose/gm. kidney compared to a maximum of only 7 +/- 3 per cent/gm. kidney after intraperitoneal administration. Although less than one per cent dose/gm. kidney remained after one week, crystal fragments were scattered throughout the cortex and medulla, often surrounded by foci of interstitial nephritis. The retention of crystals in kidney and other body organs following i.v. oxalate provides a model of oxalosis which stimulates pathophysiologic events in a variety of clinical situations characterized by transiently or persistently elevated serum oxalate.

Topics: Animals; Autoradiography; Calcium Oxalate; Carbon Radioisotopes; Crystallization; Female; Freeze Drying; Kidney; Nephritis, Interstitial; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains; Time Factors; Tissue Distribution

Topics: Adolescent; Child; Child, Preschool; Diuresis; Glomerular Filtration Rate; Hot Temperature; Humans; Nephritis, Interstitial; Oxalates; Pyelonephritis; Seasons

A 38-year-old woman suffered rapid onset of renal failure between 11 and 15 months after undergoing a jejunoileal bypass for morbid obesity. Microscopic examination of renal biopsy specimens revealed oxalosis and severe tubulointerstitial nephritis. Immunofluorescence microscopy disclosed linear staining of tubular basement membranes with antisera to IgG and C3, which suggests antitubular basement membrane disease, a side effect not previously recognized with jejunoileal bypass. Possible mechanisms leading to the formation of these antibodies include (1) oxalate damage to renal tubules with release of tubular basement membrane antigens, and (2) bacterial overgrowth in the bypass segment, with mucosal damage and release of intestinal mucosal antigens that share antigenetic determinants with renal proximal tubules. Anti-tubular basement membrane disease may be an additional mechanism that produces or enhances renal damage in patients with jejunoileal bypass.

Topics: Adult; Antibodies; Basement Membrane; Chronic Disease; Complement C3; Female; Humans; Ileum; Immunoglobulin G; Jejunum; Kidney Tubules; Microscopy; Microscopy, Electron; Nephritis, Interstitial; Obesity; Oxalates; Postoperative Complications

This group of disorders has a number of causes. Early in the course of the disease, tubular malfunction is out of proportion to glomerular disease. The early presentation may be inability to concentrate urine, salt wasting, distal or proximal renal tubular acidosis and/or Fanconi's syndrome. With early diagnosis and treatment, progression of the renal disorder can be prevented or at least delayed. One can easily discontinue the antibiotic or analgesic, remove the heavy metal, treat the electrolyte abnormality, lower the uric acid or remove the genitourinary tract obstruction.

Topics: Analgesics; Drug Hypersensitivity; Glomerular Filtration Rate; Humans; Hypercalcemia; Hypokalemia; Immunologic Deficiency Syndromes; Kidney Tubules; Lead Poisoning; Nephritis, Interstitial; Oxalates; Pyelonephritis; Substance-Related Disorders; Uric Acid

Direct tubular damage, hypersensitivity reaction, metabolically mediated kidney disturbances, and chronic nephropathies are important sequelae of several drugs or their metabolites. In this review the drug-induced kidney disease is discussed from a clinical, histological, and pathogenetic point of view. The knowledge of possible nephrotoxic reactions and their underlying toxins are essential for prevention of this kidney disease.

Topics: Analgesics; Drug Hypersensitivity; Ethylene Glycols; Glomerulonephritis; Humans; Hypercalcemia; Kidney Concentrating Ability; Kidney Diseases; Kidney Failure, Chronic; Kidney Tubular Necrosis, Acute; Methicillin; Methotrexate; Nephritis, Interstitial; Oxalates

Seventy-seven patients with nephrocalcinosis as revealed by X-ray studies over a 10-year period are reviewed. A programmed clinical and metabolic study was performed on each case; the author's criteria included the different pathogenic factors considered in the etiologic definition of the disease. There were 22 cases with primary hyperparathyroidism, 19 with spongy kidney, nine with tubulointerstitial nephropathy, five with hyperoxaluria, five with distal renal tubular acidosis, four with esential hypomagnesemia, and three cases of miscellaneous etiology (vitamin D intoxication, Fanconi's syndrome, Bartter's disease). Ten other cases were classified as idiopathic nephrocalcinosis since no definite cause could be found. The clinical characteristics (symptoms, associated diseases, diet and medication intake, family history) and the biochemical findings are analysed for each group. The physiopathologic mechanisms, comparisons between each etiologic group, treatment, clinical course, and prognosis are commented on. The conclusion drawn is that nephrocalcinosis is a clinical syndrome of various etiologies which in most cases arises from an underlying metabolic disease.

Topics: Acidosis, Renal Tubular; Bartter Syndrome; Fanconi Syndrome; Humans; Hyperparathyroidism; Magnesium Deficiency; Medullary Sponge Kidney; Metabolic Diseases; Neoplasm Metastasis; Nephritis, Interstitial; Nephrocalcinosis; Oxalates; Radiography; Vitamin D

Topics: Animals; Horse Diseases; Horses; Male; Nephritis, Interstitial; Oxalates

Topics: Acidosis, Renal Tubular; Humans; Ileum; Jejunum; Kidney Diseases; Kidney Failure, Chronic; Nephritis, Interstitial; Obesity; Oxalates; Postoperative Complications; Renal Aminoacidurias

Topics: Adolescent; Adult; Alcohol Oxidoreductases; Biopsy; Bone and Bones; Carboxy-Lyases; Female; Glyceric Acids; Glycolates; Glyoxylates; Humans; Ketoglutaric Acids; Kidney; Kidney Calculi; Kidney Failure, Chronic; Kidney Tubules; Male; Metabolic Diseases; Methods; Microscopy, Polarization; Nephritis, Interstitial; Oxalates; Renal Artery Obstruction

Topics: Adult; Humans; Kidney; Kidney Diseases; Male; Nephritis, Interstitial; Nephrocalcinosis; Oxalates; Renal Tubular Transport, Inborn Errors

Topics: Adult; Cardiomegaly; Humans; Kidney Calculi; Male; Metabolism, Inborn Errors; Myocarditis; Nephritis, Interstitial; Oxalates; Radiology