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)

The urinary excretion of beta2-microglobulin was studied under normal conditions and during acidosis and alkalosis in 65 patients with renal stones. Eleven patients were studied under two of these conditions. Four out of 51 patients examined under normal conditions had an increased excretion of beta2-microglobulin in their urine. Four out of five patients with distal acidification defects were found to have an increased excretion of beta2-microglobulin during induced acidosis. During alkalosis, four out of eight patients with acidification defects increased their excretion of the protein. The tubular proteinuria that could be provoked during acute acidosis and alkalosis was considered to be secondary to changes in the acid-base status and may indicate a renal tubular defect.
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PMID:Urinary excretion of beta2-microglobulin in renal stone patients under normal conditions and during acidosis and alkalosis. 7 18

In order to help clarify the effects of hyperthyroidism on renal function and electrolyte metabolism, we measured the venous plasma concentrations of urea, creatinine, urate, hydrogen ion and electrolytes, and the urinary concentrations of total protein, albumin, retinol-binding protein, N-acetyl-beta-D-glucosaminidase activity, and creatinine in patients when hyperthyroid and again after they had been euthyroid for at least 4 months. Significant (P less than 0.05) decreases in the mean plasma concentrations of urate and chloride and significant increases in creatinine, total CO2 and hydrogen ion mean concentrations were observed when the patients became euthyroid. The mean concentrations of sodium, potassium and urea did not change significantly. The values of the ratios total protein/creatinine, albumin/creatinine, N-acetylglucosaminidase/creatinine and retinol-binding protein/creatinine were all significantly (P less than 0.05) elevated in random urine specimens obtained from hyperthyroid patients as compared to the values when euthyroid. Mild proteinuria occurs in most thyrotoxic patients which does not appear to be due predominantly to either glomerular or tubular renal injury. The changes in plasma analytes that were observed may be attributed to increases in glomerular filtration rate and tissue nucleic acid turnover and a tendency to respiratory alkalosis in the hyperthyroid patients.
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PMID:Renal function and electrolyte levels in hyperthyroidism: urinary protein excretion and the plasma concentrations of urea, creatinine, uric acid, hydrogen ion and electrolytes. 259 Oct 58

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
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PMID:Reversible nephrotic syndrome due to high renin state in renovascular hypertension. 773 87

Several rat models of polycystic kidney disease (PKD) have been published. The only rat model of autosomal dominant polycystic kidney disease currently used is the so-called Hannover rat (Han:SPRD cy/+). This model is characterized by a slow progression of uraemia, proteinuria and hyperlipidaemia. Histological changes clearly resemble those seen is human PKD. The localization of Na+/K(+)-ATPase correlating with the phenotype of the cysts--basal in moderately expanded and apical in highly expanded cysts--suggests that the mislocation of the Na+/K(+)-ATPase is involved in the mechanism of cyst expansion rather than formation, and a consequence of cell dedifferentiation rather than an initial event. Of note is a considerable gender difference in disease severity. Disease anticipation or genetic imprinting does not occur. In addition to gender, a number of interventions influence the progression rate: acceleration is noted after unilateral nephrectomy, the induction of acidosis, chloride feeding or an increased protein intake; slowing down of the course occurs after the induction of alkalosis and castration, and after treatment with lovastatin and methylprednisolone. Thus the Han:SPRD cy/+ rat represents the only well-documented rat model of autosomal dominant PKD resembling a number of features of the human disease.
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PMID:Rat models of autosomal dominant polycystic kidney disease. 904 28

Diabetes mellitus is the most common metabolic disorder in the community. The diabetics may suffer from acid-base and electrolyte disorders due to complications of diabetes mellitus and the medication they receive. In this study, acid-base and electrolyte disorders were evaluated among outpatient diabetics in our hospital. The study consisted of patients with diabetes mellitus who visited the hospital as outpatients between the period January 1, 2004 to December 31, 2006. The patients' medical history, age and type of diabetes were noted, including whether they were taking diuretics and calcium channel blockers or not. Serum creatinine, proteins, sodium, potassium and chloride and blood gases were measured in all patients. Proteinuria was measured by 24-h urine collection. Two hundred and ten patients were divided in three groups based on the serum creatinine. Group A consisted of 114 patients that had serum creatinine < 1.2 mg/dL, group B consisted of 69 patients that had serum creatinine ranging from 1.3 to 3 mg/dL and group C consisted of 27 patients with serum creatinine > 3.1 mg/dL. Of the 210 patients, 176 had an acid-base disorder. The most common disorder noted in group A was metabolic alkalosis. In groups B and C, the common disorders were metabolic acidosis and alkalosis, and metabolic acidosis, respectively. The most common electrolyte disorders were hypernatremia (especially in groups A and B), hyponatremia (group C) and hyperkalemia (especially in groups B and C). It is concluded that: (a) in diabetic outpatients, acid-base and electrolyte disorders occurred often even if the renal function is normal, (b) the most common disorders are metabolic alkalosis and metabolic acidosis (the frequency increases with the deterioration of the renal function) and (c) the common electrolyte disorders are hypernatremia and hypokalemia.
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PMID:Acid-base and electrolyte disorders in patients with diabetes mellitus. 2223 20

Conn syndrome, which is rarely encountered in children, is characterized by increased aldosterone, low renin level, and arterial hypertension. Severe complications, such as impaired vascular smooth muscle function secondary to increased aldosterone, endothelial dysfunction, deterioration of left ventricular functions, acute effects on the cardiovascular system, and proteinuria, may be observed. We present a case of primary aldosteronism in a patient who has been followed up for approximately 2 years. A 15-year-old girl complained of headache lasting for approximately 1.5 years, which was diagnosed as severe hypertension. All of her systemic examinations were normal other than the hypertension. Primary aldosteronism was diagnosed on the basis of hypokalemia and alkalosis accompanied by plasma renin activity of 3.9 ng/mL/h and an aldosterone level of 1007 pg/mL (normal: 40-480). Left adrenalectomy was performed because a 10x12x12 mm adenoma was detected on abdominal magnetic resonance imaging. Although aldosterone levels returned to normal values after the surgery, antihypertensive treatment was continued because of the persistent hypertension. As the 24-h ambulatory blood pressure values of the patient were normal at 10 months after the operation, the treatment was stopped, and she was followed up for 15 months without any treatment. Since then, she has been normotensive.
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PMID:A pediatric Conn syndrome case. 2257 Sep 78

We report on a 27-year-old patient presenting with chronic hypokalaemia, inappropriate kaliuresis, hypomagnesaemia and alkalosis, associated with moderate proteinuria. Genetic analysis evidenced a homozygous mutation (p.Arg399Cys) in the SLC12A3 gene coding for the sodium-chloride cotransporter (NCC), confirming the diagnosis of Gitelman syndrome. Further genetic testing did not show any mutation in NPHS2. A renal biopsy was performed in view of the unusual association with proteinuria. Light microscopy showed hypertrophy of the juxtaglomerular apparatus and discrete mesangial thickening. In addition to possible focal segmental glomerular sclerosis lesions, electron microscopy showed extensive segments of variably thickened glomerular basement membrane (GBM), contrasting with segments of regular GBM of low range thickness, and effacement of podocyte foot processes. Of interest, alterations of the GBM were also observed in a Slc12a3 knock-out mouse model for Gitelman syndrome. These data suggest that the association between Gitelman syndrome and secondary changes of the GBM is probably not coincidental. Possible mechanisms include angiotensin II- or renin-induced podocyte lesions, as well as chronic hypokalaemia.
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PMID:Gitelman syndrome and glomerular proteinuria: a link between loss of sodium-chloride cotransporter and podocyte dysfunction? 2516 77