Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral antidiabetics are given for preference to adult diabetics who do not need insulin. Biguanides are particularly indicated for adipose diabetics, sulphonamides for those of normal weight. Phenformin must not be used in the presence of renal insufficiency and severe liver diseases because of the high risk of lactacidosis. Oral antidiabetics should not to be given during pregnancy. With oral treatment of diabetics under the age of 30, proteinuria, peripheral vascular diseases and disturbances of fat metabolism occure more frequently while retinopathies, coronary diseases, peripheral neuropathies or infections of the urinary tract cannot be influenced orally, nor by insulin nor by a combination of the two. The i. v. lipid tolerance test is always pathological even in apparently well-adjusted orally treated diabetics. On the other hand it is normal even in less well adjusted insulin therapy. More epidemiological investigations should be carried out in order to be able to assess clearly the longterm effects of oral antidiabetics.
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PMID:[The oral antidiabetics (author's transl)]. 40 41

In this article, the acid-base disturbances encountered in hematologic diseases are discussed. Occurrence of lactic acidosis (LA) without obvious clinical tissue hypoxia has been reported in patients with leukemia and lymphoma. Most of the patients with LA had liver involvement and clinical evidence of impaired hepatic function, suggesting that both increased production and decreased lactate metabolism are necessary for the development of LA in leukemia and lymphoma. Acute tumor lysis syndrome consists of hyperuricemia, hyperpotassemia, and hyperphosphatemia with hypocalcemia following neoplastic cell lysis, particularly in lymphoproliferative disorders. In patients with multiple myeloma (MM), proximal renal tubular acidosis (Fanconi syndrome) associated with Bence Jones proteinuria has been reported. In addition, MM is one of the first conditions recognized to be associated with lower anion gap.
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PMID:[Acid-base disturbances in hematologic diseases]. 143 14

A 1-month-old boy was admitted because of failure to thrive. He was floppy and had bilateral ptosis, diminished reflexes, and poor suck. He had aspiration pneumonia, developed seizures, and died at age 3 1/2 months. Laboratory data showed lactic acidosis, proteinuria, glycosuria and generalized aminoaciduria. He was an only child, and family history was negative. Muscle biopsy showed large clumps of granules positive with oxidative enzyme stains and increased lipid droplets. Ultrastructural studies showed large aggregates of mitochondria, many of which were greatly enlarged and contained disoriented or concentric whorls of cristae and paracrystalline inclusions. Cytochrome c oxidase was absent in fresh frozen sections by histochemical staining. By biochemical assay, cytochrome c oxidase (cytochrome aa3) was 6% of normal in muscle biopsy and undetectable in autopsy muscle; spectra and content of cytochromes showed lack of cytochrome aa3, decreased cytochrome b and normal cytochrome cc1. In kidney, cytochrome-c-oxidase activity was 38% of normal and spectra showed decreased cytochromes aa3 and b. The association of fatal infantile mitochondrial myopathy, lactic acidosis and renal dysfunction was previously reported by Van Biervliet et al and appears to be a distinct nosologic entity, one of the few biochemically defined mitochondrial myopathies.
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PMID:Fatal infantile mitochondrial myopathy and renal dysfunction due to cytochrome-c-oxidase deficiency. 625 6

Two young human immunodeficiency virus (HIV)-infected patients, a 25-year-old woman and a 26-year-old man, consumed large amounts of germanium lactate citrate 18% as an "immunostimulant" for 9 months. The woman, who had stage II HIV infection, developed severe renal dysfunction (creatinine clearance, 7 mL/min/1.73 m2) and slight proteinuria (0.28 g/d) after ingesting 260 g germanium lactate citrate 18%. Hepatomegaly with liver dysfunction (SGOT, 102 U/L; gamma-glutamyl transferase (GT), 159 U/L) and lactic acidosis (plasma lactate, 7.3 mmol/L) developed simultaneously. Renal biopsy revealed tubulointerstitial nephropathy with vacuolar cell degeneration and periodic acid-Schiff-positive intracellular deposits mainly in distal tubules. Liver biopsy disclosed severe hepatic steatosis; liver function tests returned to normal within 5 weeks. Since renal failure persisted for 2 years after ingestion of germanium (creatinine clearance, 14 mL/min/1.73 m2; proteinuria, 0.84 g/d), a second renal biopsy was performed, which showed marked but focal distal tubular atrophy and slight interstitial fibrosis. The male patient, who had stage III HIV infection, had ingested the same compound; he presented with a creatinine clearance of 43 mL/min/m2 and proteinuria of 0.36 g/d. Renal biopsy disclosed tubulointerstitial changes similar to those found in the female patient. After 9 months off germanium, creatinine clearance remained unchanged. Neutron activation analysis of all biopsy specimens in both cases documented germanium concentrations 10 to 70 times normal in renal tissue and 140 times normal in liver tissue.
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PMID:Tubulointerstitial nephropathy persisting 20 months after discontinuation of chronic intake of germanium lactate citrate. 848 24

Mitochondrial encephalomyopathy is a hereditary syndrome showing impairment of muscle and the central nervous system. In this disorder, the following three syndromes have been identified on the basis of characteristic symptoms: Kearns-Sayre syndrome (KSS), mitochondrial encephalomyopathy with lactic acidosis, and stroke-like episodes (MELAS), and myotonic epilepsy with ragged-red fibers (MERRF). In this report, we describe a case of mitochondrial encephalomyopathy with renal disease. A 25-year-old man was referred to our hospital in May, 1992 for evaluation of long-standing proteinuria. He had a small stature, exotropia and no pretibial edema. No mental retardation was observed. Urinary protein excretion was 2.0 g/day and urine sugar was negative. Laboratory examination revealed a serum urea nitrogen 19 mg/dl, and a creatinine value of 1.5 mg/dl. Creatinine clearance was 45.8 ml/min. His serum and spinal fluid lactate value were elevated. Biopsied muscle showed an absence of ragged-red fibers, and the presence of an A-to-G point mutation at nucleotide pari 3243 in the mitochondrial tRNA(Leu(UUR)) in peripheral blood leucocytes. He was thought to have MELAS. On the renal biopsy specimens, light microscopic examinations showed minor glomerular abnormalities with two glomerular collapses and tubulo-interstitial damage. Electron microscopic examinations showed partial thickening of the glomerular basement membrane. We report here this rare case of MELAS with renal disease, and also review seventeen cases of mitochondrial encephalopathy associated with renal disease. The existence of a relationship between mitochondrial disorder and renal damage remains obscure.
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PMID:[A case of mitochondrial encephalomyopathy (MELAS)]. 871 14

Mitochondrial DNA plays a crucial role in oxidative production of energy. Thus, defects in mitochondrial DNA can affect virtually all organ systems. The point mutation A --> G at position 3243 in the mitochondrial tRNAleu(UUR) gene is the cause of several distinct types of mitochondrial cytopathy and several clinical phenotypes, including encephalomyopathy with lactic acidosis and stroke-like episodes and maternally inherited diabetes and deafness. This mutation has been recently described also in association with kidney disease, mainly focal and segmental glomerulosclerosis. At present, little is known about the prevalence of this mitochondrial nephropathy, its clinical course and the pathogenesis of glomerular damage. We describe 2 unrelated patients, who presented with proteinuria and progressed to end-stage renal failure. Other clinical features were short stature, severe headache, hearing loss, diabetes mellitus and hypertrophic cardiomyopathy. The main histological finding was an increased number of abnormal mitochondria in tubular cells and podocytes. Analysis of mitochondrial DNA from leukocytes and urine sediment revealed heteroplasmy for the A3243G mutation in tRNAleu(UUR) gene in both patients. Recognition of the characteristic clinical and histological features of the mitochondrial A3243G mutation-associated glomerulopathy will enable correct diagnosis and better management of a disease which is likely to be underdiagnosed.
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PMID:Progressive nephropathy associated with mitochondrial tRNA gene mutation. 1535 73

In this work, patients having type 2 diabetes mellitus and diabetic mothers were tested for the presence of mitochondrial DNA point mutation A3243G. This mutation is associated with the MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), diabetes and deafness. Twenty-two diabetic persons were screened. DNA was isolated from peripheral blood lymphocytes and from swabs of oral mucosa. The mitochondrial DNA point mutation A3243G was detected using PCR-RFLP test. The mutation was detected in oral mucosal DNA of two patients (but not from lymphocyte DNA). One patient was a man with hearing and visual impairments and proteinuria; the other was a woman having proteinuria but no hearing impairment. The mutation was not detectable in oral mucosal DNA from the control persons: 20 diabetic patients having diabetic fathers and 22 healthy, nondiabetic volunteers. The incidence of mitochondrial DNA point mutation A3243G in this study of Croatian diabetic patients is in line with data in the literature.
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PMID:A pilot study of mitochondrial DNA point mutation A3243G in a sample of Croatian patients having type 2 diabetes mellitus associated with maternal inheritance. 1566 Feb 1

Herein, we report on a paediatric patient with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) who was hospitalized for acute on chronic renal insufficiency, seizures and deterioration of the level of consciousness. She also had hypertension, hypothyroidism and nephrotic range proteinuria. Kidney biopsy revealed many sclerotic glomeruli and focal segmental glomerulosclerosis (FSGS). Glomerulopathy is rare in patients with MELAS, and FSGS has been reported only in a few patients. The histopathological features of the renal biopsy suggested that the aetiology of the FSGS may have been secondary to chronic renal injury rather than from a primary immunologic cause. Moreover, our case is unique in that, the coexistence of MELAS, hypothalamic hypothyroidism and FSGS has not been reported in the past. The purpose of this report is to increase the awareness of health-care professionals, especially in the fields of paediatrics, neurology, endocrinology and nephrology, regarding the manifestations and complications of MELAS.
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PMID:Mitochondrial encephalopathy with lactic acidosis and stroke-like episodes syndrome with hypothyroidism and focal segmental glomerulosclerosis in a paediatric patient. 1729 89

Proteinuria and hematuria are common during exercise. Proteinuria is usually due to glomerular or tubular changes or to an excessive production of protein as in myeloma. Certain clinical conditions can, however, result in a functional or temporary proteinuria, especially during pregnancy, fever, orthostasis, or following physical activity. Sport-related proteinuria following marching, exercise, and stress, was first observed in soldiers after long marching. Prevalence of proteinuria during exercise ranges from 18% up to 100% depending on type of exercise and its intensity. A higher incidence of proteinuria has been observed in some sports requiring great exercise intensity and it is certainly related to muscular work intensity and would decrease after prolonged training. Indeed, exercise-induced proteinuria is strictly related to exercise intensity rather than to exercise duration. Exercise aggravates the proteinuria of various nephropathies and that of renal transplant recipients. The prevalence of hematuria is higher in the athletic than the general population and the main difference is that sport-related hematuria resolves spontaneously after physical exercise while hematuria found in nonathletic population can be chronic. Sport-induced hematuria is influenced by exercise duration and intensity. Among the mechanisms underlying the exercise induced hematuria are increased body temperature, hemolysis, increased production of free radicals, and excessive release of catecholamines. Lactic acidosis, generated during anaerobic conditions, causes the passage of erythrocytes into the urine, through increased glomerular permeability.
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PMID:Renal alterations during exercise. 1808 64

Polypharmacy may lead to synergistic complications from the different medications. We report the case of a 50-year-old woman who was prescribed 11 drugs, including a diuretic, celecoxib, metformin, and candesartan, and who developed acute kidney dysfunction while on these drugs, manifesting as severe proteinuria, acute azotemia, hyperkalemia. The kidney injury caused the accumulation of metformin, leading to lactic acidosis and acute pancreatitis. Sodium bicarbonate hemodialysis not only improved the metabolic abnormalities but also hastened the removal of metformin.
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PMID:Metformin-induced lactic acidosis and acute pancreatitis precipitated by diuretic, celecoxib, and candesartan-associated acute kidney dysfunction. 1825 65


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