oxalates and Hypercalcemia

Whereas the etiology of urinary calculi and their metabolic exploration should be known, it appears unreasonable to conduct exhaustive metabolic explorations in all patients, therapy being usually symptomatic and based on advice on hygiene and diet. However, etiologic diagnosis is essential in a small number of cases: those which could benefit from effective preventive and curative measures and for which morbidity is elevated: cystinuria, hyperparathyroidism, uric acid calculi, patients at high developmental risks. It is possible, by simple, low cost means to select 95% of these patients. After a theoretical study of the distribution and lithiasic etiology, a practical conduct is proposed which takes into account the cost-effective ratio.

Topics: Acidosis; Calcium; Citrates; Cystinuria; Humans; Hypercalcemia; Hyperparathyroidism; Intestinal Absorption; Kidney Calices; Osteoporosis; Oxalates; Sarcoidosis; Uric Acid; Urinary Calculi

Management of most patients with calculous disease has been less than ideal in the past. Too often therapeutic efforts were limited to symptomatic calculi. Stones were allowed to pass or were removed, metabolic studies were incomplete, victims were dismissed and forgotten, and prophylactic measures were negligible and usually confined to milk restriction and use of distilled water. More patients were crippled with and died of recurrent calculous disease, urinary infection and progressive renal insufficiency than from any other upper urinary tract abnormality. During the last decade the development of a renal stone clinic at this institution has allowed a nephrourologic approach to the management of urolithiasis. This account of classification, diagnosis and management of the various syndromes associated with urolithiasis is based on the experiences gained during the last decade with this common but ill-understood urologic problem.

Topics: Acidosis, Renal Tubular; Adult; Child, Preschool; Cystinuria; Female; Humans; Hypercalcemia; Intestinal Diseases; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates; Sepsis; Uric Acid; Xanthines

Topics: Acidosis, Renal Tubular; Bacterial Infections; Citrates; Crystallization; Cystinuria; Diphosphates; Female; Gastrointestinal Diseases; Humans; Hypercalcemia; Hyperparathyroidism; Magnesium; Male; Metabolism, Inborn Errors; Mucoproteins; Oxalates; Quaternary Ammonium Compounds; Sarcoidosis; Solubility; Uric Acid; Urinary Calculi; Vitamin D; Xanthine Oxidase

Topics: Acid-Base Equilibrium; Age Factors; Calcium; Cystinuria; Female; Humans; Hypercalcemia; Hyperparathyroidism; Immobilization; Intestinal Absorption; Kidney Calculi; Male; Oxalates; Phosphates; Sex Factors; Uric Acid; Vitamin D

Topics: Animals; Aspergillus; Bone and Bones; Calcium, Dietary; Cattle; Chemical Phenomena; Chemistry; Citric Acid Cycle; Dogs; Fungi; Guinea Pigs; Humans; Hypercalcemia; Nutritional Physiological Phenomena; Oxalates; Photosynthesis; Plants; Rabbits; Rats; Rumen; Vegetables

Nephrocalcinosis is associated with conditions that cause hypercalcemia and the increased urinary excretion of calcium, phosphate, and/or oxalate. A monogenic etiology is found in almost 30% of childhood-onset nephrocalcinosis which is also a common manifestation of primary hyperparathyroidism. We discuss a child with nephrocalcinosis and features mimicking primary hyperparathyroidism.. A 7-year-old girl presented with nephrocalcinosis. Hypercalciuria, hyperphosphaturia, mild hypercalcemia, hypophosphatemia and elevated parathyroid hormone levels along with normal serum creatinine and absence of hypokalemic alkalosis suggested primary hyperparathyroidism. However, she was ultimately diagnosed with Bartter syndrome type 2 based on the presence of homozygous pathogenic variation in. This is the second reported case of late-onset Bartter syndrome type 2 without hypokalemic alkalosis. Patients with Bartter syndrome may present with high parathyroid hormone levels and hypercalcemia in addition to hypercalciuria. Thus, the present case suggests that the

Topics: Alkalosis; Bartter Syndrome; Calcium; Child; Creatinine; Female; Humans; Hypercalcemia; Hypercalciuria; Hyperparathyroidism, Primary; Nephrocalcinosis; Oxalates; Parathyroid Hormone; Phosphates

Primary hyperoxaluria (PH) is a rare genetic disorder characterized by overproduction of oxalate due to specific enzyme deficiencies in glyoxylate metabolism. The primary clinical presentation is in the form of recurrent urolithiasis, progressive nephrocalcinosis, end-stage renal disease, and systemic oxalosis. Herein, we present a case of PH who was diagnosed at 47 years of age after 6 years on hemodialysis. He presented with fatigue, anorexia, weight loss, and was found to have cachexia, diffuse edema, hepatomegaly, ascites, hypercalcemia, hyperphosphatemia, hypoalbuminemia, low parathyroid hormone levels, lytic and resorptive areas in the vertebrae, diffusely increased echogenity of the liver, multiple renal stones, and bilateral nephrocalcinosis. Bone marrow biopsy showed calcium oxalate crystals and crystal granulomas. The liver biopsy could not be performed. The absence of an identifiable reason for secondary forms, the severity of the clinical presentation, and pathological findings led to the diagnosis of PH2. He died while waiting for a potential liver and kidney donor. The presented case is consistent with the literature as he had renal stone disease in the third decade and end-stage renal disease in the fifth decade. Hypercalcemia was thought to be due to osteoclast-stimulating activity of macrophages constituting the granuloma. Erythropoietin-resistant anemia and hypothyroidism were thought to be due to accumulation of oxalate in the bone marrow and thyroid gland, respectively. It is very important to keep in mind the possibility of PH when faced with a patient with nephrocalcinosis and oxalate stone disease.

Topics: Ascites; Bone Marrow; Granuloma; Hepatomegaly; Humans; Hypercalcemia; Hyperoxaluria, Primary; Hypothyroidism; Kidney Failure, Chronic; Male; Middle Aged; Nephrocalcinosis; Oxalates; Renal Dialysis; Urolithiasis

We report a case of severe nephrocalcinosis related to hypercalcaemia in a newborn with glucose-galactose malabsorption. He presented with poor growth and was noted to have polyuria, which was later recognised to be severe watery diarrhoea. We discuss the possible aetiological factors for nephrocalcinosis in this condition.

Topics: Calcium; Diarrhea; Galactose; Glucose; Growth Disorders; Humans; Hypercalcemia; Infant, Newborn; Karyotyping; Kidney; Malabsorption Syndromes; Male; Nephrocalcinosis; Oxalates; Polyuria; Ultrasonography

Nephrocalcinosis was described in preterm infants by several authors who tried to determine its association with hypercalciuria and furosemide therapy. We evaluated these potential mechanisms along with other lithogenic factors not previously studied in 10 premature babies. Hypercalciuria was an inconsistent finding like in other reports; elevated uric acid excretion and hyperoxaluria were observed in 5 and 6 cases, respectively. The aminocid excretion was normal in all infants. Our data suggest that in addition to hypercalciuria, other lithogenic factors may play a role in the pathophysiology of nephrocalcinosis of premature infants.

Topics: Glycosuria; Humans; Hypercalcemia; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Nephrocalcinosis; Oxalates; Proteinuria; Renal Aminoacidurias; Uric Acid

Topics: Child, Preschool; Female; Fractures, Spontaneous; Growth Disorders; Humans; Hypercalcemia; Kidney Calculi; Kidney Failure, Chronic; Metabolism, Inborn Errors; Oxalates; Oxalic Acid

A 13-year-old boy with primary hyperoxaluria and a successful renal allograft developed symptomatic bone disease, hypercalcemia, and hypercalciuria. Transiliac bone biopsy revealed calcium oxalate crystals in the marrow within mononuclear phagocytes and multinucleated giant cells. Deep resorption bays were seen adjacent to these crystal-cell aggregates. Serum 1,25-(OH)2-vitamin D (calcitriol) and iPTH concentrations were low or normal. We suggest that hypercalcemia results from macrophage-mediated bone resorption initiated by Ca oxalate crystal deposition.

Topics: Adolescent; Bone Diseases; Bone Resorption; Calcium Oxalate; Humans; Hypercalcemia; Kidney Transplantation; Male; Oxalates; Oxalic Acid

Urolithiasis in children is a very important problem from the theoretical as well as from practical point of view. Better knowledge of its metabolic basis may allow to move the central treatment from surgical to prophylactic methods. The study presents modern view points on mechanisms for concrements sedimentation and actual data on metabolic disturbances in calcium, oxalates, purines, xanthines and cystine and their relations to urolithiasis and urinary tract infection.

Topics: Acidosis, Renal Tubular; Calcium; Child; Cystinuria; Humans; Hypercalcemia; Oxalates; Purine-Pyrimidine Metabolism, Inborn Errors; Uric Acid; Urinary Calculi; Urinary Tract Infections; Xanthines

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

In summary it can be stated that clinically and radiologically, nephrolithiasis und nephrocalcinosis are not uncommonly encountered together. It is the aim of x-ray diagnostic to detect stones and parenchymal calcification, to assess localisation, size and numer or extent, to recognise secondary changes in the renal parenchyma and urinary-tract resulting from stones and to aid the search for the primary disease. In addition there are readiographic methods valuable for the initiation of treatment, e. g. percutaneous antegrade pyelography and nephrostomy.

Topics: Adolescent; Glomerulonephritis; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Kidney Cortex Necrosis; Kidney Diseases; Male; Metabolic Diseases; Nephrocalcinosis; Oxalates; Phenacetin; Radiography

Topics: Adult; Ambulatory Care; Calcium; Calcium, Dietary; Cyclic AMP; Diagnosis, Differential; Fasting; Female; Hospitalization; Humans; Hypercalcemia; Kidney; Kidney Calculi; Male; Oxalates; Parathyroid Hormone; Phosphates; Uric Acid

Topics: Adult; Calcium; Cystine; Cystinuria; Humans; Hypercalcemia; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates; Uric Acid

Topics: Glucocorticoids; Humans; Hypercalcemia; Hyperthyroidism; Neoplasms; Oxalates; Phosphates; Phytic Acid; Plicamycin; Prognosis

Investigation of multiple serum and urinary factors in 44 patients with calcium urinary stone disease confirmed a number of defects that have been described previously: elevation of mean serum calcium and uric acid above normal, and depression of mean serum magnesium. Urinary excretion of calcium and uric acid was increased and was increased and was probably related to food ingestion. Urinary magnesium also increased after eating but less than calcium, with the result that for most patients the magnesium to calcium x 100 ratio approached levels observed in stone formation. Urinary oxalate excretion was constant during the entire observation period and apparently was not affected by ingestion of a defined diet. Nine additional patients had persistent hypercalcemia owing to hyperparathyroidism (5 confirmed, 1 suspected), malignancy (2) and drug ingestion (1). Metabolic evaluation of patients with calcium urinary calculi continues to contribute to decisions regarding their best therapeutic regimen.

Topics: Calcium; Diet; Female; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Magnesium; Male; Oxalates; Uric Acid

Effects of oral sodium cellulose phosphate therapy (5 g three times a day with meals for 4 days) on renal excretion of oxalate and on the crystallization of calcium oxalate in urine were examined in six patients with absorptive hypercalciuria on a constant metabolic dietary regimen. During treatment, urinary oxalate increased by 9-50 mg/day. However, urinary calcium decreased by 138-225 mg/day (50%-70%). Thus, the state of saturation of urine with respect to calcium oxalate decreased or did not change significantly. There was no consistent or significant change in the formation product ratio (limit of metastability) or in the crystal growth of calcium oxalate in urine.

Topics: Administration, Oral; Calcium; Cation Exchange Resins; Cellulose; Crystallization; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Ion Exchange Resins; Organophosphorus Compounds; Oxalates; Phosphates; Urine

The diangosis, clinical manifestations and management of 11 children with nephrocalcinosis encountered in a 20-year period are presented. Renal tubular acidosis, primary hyperoxaluria, primary hyperparathyroidism, exogenous hyperadrenocorticism and idiopathic hypercalcemia of infancy were the principal causes of nephrocalcinosis in this series. In the presence of normal or near-normal renal function, a 55 per cent or better cure rate can be expected. Children with significantly diminished renal function have a poor prognosis and should be considered for renal transplantation.

Topics: Acidosis, Renal Tubular; Adolescent; Child; Child, Preschool; Cushing Syndrome; Female; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Kidney Transplantation; Male; Nephrocalcinosis; Oxalates; Prognosis; Transplantation, Homologous; Ureteral Calculi

The management of 78 children with upper urinary calculi is described. Boys outnumbered girls by a ratio of 2 to 1. Two-thirds of the patients had identifiable metabolic causes, while the remaining third had infected renal lithiasis. In this latter group, all patients had had multiple urologic procedures, urinary infection, and stasis with diversionary and indwelling drainage devices. Contrary to earlier views, idiopathic renal lithiasis with or without hypercalciuria was the most common metabolic form of nephrolithiasis in children. Sixty-seven patients (86 per cent) were followed for an average of 7 1/2 years. With appropriate therapy, stone disease became inactive in 70 per cent of the children. The remaining 30 per cent continued with active disease--5 died of renal failure and 1 has received a renal allograft. Stone formation may be regarded as a solitary complication or one of several manifestations of a large number of underlying disorders. Along with a thorough search for etiologic factors there must be an equally aggressive therapeutic effort. Because the disease is ofter sporadic, careful long-term followup of the patients with active as well as those with inactive stone disease is mandatory.

Topics: Acidosis, Renal Tubular; Adolescent; Adrenocortical Hyperfunction; Age Factors; Calcium; Child; Child, Preschool; Cystinuria; Female; Humans; Hypercalcemia; Hyperparathyroidism; Infant; Infant, Newborn; Kidney Calculi; Magnesium; Male; Metabolic Diseases; Oxalates; Uric Acid; Urinary Tract Infections; Urography

Topics: Adult; Basidiomycota; Buffers; Calcium; Carbon Dioxide; Carboxy-Lyases; Colorimetry; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Methods; Oxalates; Phosphates; Potassium Permanganate; Sulfates; Time Factors

Topics: Adult; Aged; Calcium; Cystinuria; Female; Humans; Hypercalcemia; Hyperglycemia; Male; Metabolic Diseases; Middle Aged; New Zealand; Oxalates; Phosphates; Prospective Studies; Radiography; Uric Acid; Urinary Calculi; Urinary Tract Infections

Topics: Adult; Aldehydes; Amino Acids; Amino Alcohols; Animals; Calcium; Carbon Isotopes; Child; Chromatography, Ion Exchange; Female; Glycolates; Glycols; Haplorhini; Humans; Hypercalcemia; Imines; L-Lactate Dehydrogenase; Male; Methylene Blue; Oxalates; Uric Acid; Urinary Calculi

Topics: Adult; Aged; Calcium; Feedback; Female; Homeostasis; Humans; Hypercalcemia; Hyperparathyroidism; Male; Middle Aged; Oxalates; Phosphorus; Urinary Calculi

Topics: Animals; Calcium; Crystallography; History, 18th Century; Humans; Hypercalcemia; Kidney Calculi; Mice; Mitosis; Neoplasms, Experimental; Occupational Diseases; Oxalates; Phosphates; Sulfonamides; United Kingdom; Urinary Bladder; Urinary Bladder Neoplasms

Topics: Adrenal Cortex Hormones; Adult; Calcium; Diagnosis, Differential; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Liver Diseases; Lung Diseases; Male; Oxalates; Radiography; Sarcoidosis

Topics: Blood; Body Fluids; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Nephrolithiasis; Oxalates; Uric Acid; Urine