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)

In 26 cases of myelofibrosis, the authors investigated for possible renal impairment that can be appraised from the usual clinical, laboratory, and roentgenographic signs. No anomalies were demonstrated in 12 of these cases. In 14 (or 53%) of the patients, some anomaly was discovered : essentially proteinuria with minor alteration of renal function, but also, two cases of poorly functioning left kidney evidenced on intravenous urograms, one case of acute anuric renal failure connected with hyperuricemia, one case of hypokalemic tubulo-interstitial nephritis, and one case of glomerulonephritis with, nephrotic syndrome. This study, when compared to the literature, indicates that besides nephropathy specific to myelofibrosis and attributed to myeloid metaplasia in the kidney, serious consideration must be given to lesions due to (1) compression of the left kidney by the enlarged spleen, (2) urate precipitation in the urinary passages, and (3) a possible glomerular disorder whose mechanism remains undefined.
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PMID:[Renal lesions in myelofibrosis (author's transl)]. 22 98

Gouty arthritis in females is relatively infrequent, although the sex ratio may be somewhat altered in different races. A positive family history is relatively prevalent among females whose onset of gout is premenopausal. In those patients with a postmenopausal onset, the incidence of diuretic-associated gout is high. The bimodal distribution of serum urate might be related to some variance of genetic transmission in female gout. Hypertension and coronary heart disease are common coexisting conditions, as is true of gouty arthritis in males. Chronic urinary tract infection dating from previous pregnancies is a frequent complication. The relative prevalence of proteinuria and diminished renal function leads to increased hyperuricemia, with a tendency to a low urinary uric acid output. This explains in part the higher incidence of extensive tophaceous deposition but lower incidence of renal calculi. Diuretics are associated with a higher urine pH, likewise, they reduce the urinary uric acid excretion. This also may contribute to the lower incidence of renal calculi. There may be some statistical support for the low fertility rate among the gouty females. Only two females became pregnant after the onset of gouty arthritis. All other pregnancies occurred before the onset of arthritis. Even then, abnormal pregnancies were relatively frequent. Some hormonal malfunction among the gouty females cannot be discounted. Both renal calculi and tophi are frequent in female gout associated with blood dyscrasias. They may manifest early, preceding the first attack of acute gouty arthritis. In both the male and female secondary gout, the primary underlying disease governs the uric acid metabolism and the clinical symptomatology of gout. The predominant role in pathogenesis is the excessive rate of uric acid production, and its disposal is governed by the different stages of the underlying disease and the treatment. Thus, secondary gout in females appears to be somewhat different from primary gout in females, but not different from secondary gout in males.
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PMID:Some unusual features of gouty arthritis in females. 83 22

Renal function studies were done on asymptomatic hyperuricemic subjects and normouricemic controls matched as to age, sex and blood pressure. Abnormal urinary sediments and proteinuria were found more frequently in asymptomatic hyperuricemic subjects than in the controls. In addition, the maximal osmolar concentrating ability of urine was markedly reduced in the asymptomatic hyperuricemic subjects. There was no difference in renal function measured by phenolsulfonphthalein excretion between the groups. Our results suggest that hyperuricemia alone may contribute to renal tubular impairment.
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PMID:Tubular function impairment in patients with asymptomatic hyperuricemia. 92 61

Renal function studies were performed in 524 gouty subjects, including follow-up studies at intervals up to 12 years in 112 of them. In 49 subjects, the glomerular filtration rate was less than 70 ml/min and Curate:glomerular filtration rate ratio tended to rise as the glomerular filtration rate decreased, reflecting a relatively stable urate excretion over varying filtered urate loads. The increment in Tsurate:glomerular filtration rate was small with spontaneous Purate between 7 and 9 mg/100 ml. It was modest with Purate up to 10 mg/100 ml. The increment in Tsurate:glomerular filtration rate became much higher beyond Purate of 10 mg/100 ml. Urinary urate levels above 800 mug/min, designated as excess urate excretion, occurred more commonly in subjects with Purate above 9 mg/100 ml, and with better preserved renal function. Tophi were more frequently observed in subjects with low glomerular filtration rate and proteinuria; but incidence of urolithiasis seemed to be less affected by a decrease in the glomerular filtration rate. Hyperuricemia alone had no deleterious effect on renal function as evidenced by follow-up studies over periods up to 12 years. Deterioration of renal function was largely associated with aging, renal vascular disease, renal calculi with pyelonephritis or independently occurring nephropathy. In only very few instances was diminished renal function ascribable to gout alone.
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PMID:Renal function in gout. IV. An analysis of 524 gouty subjects including long-term follow-up studies. 120 33

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

Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

Forty-two women with pregnancies complicated by pre-eclampsia and heavy proteinuria greater than or equal to 5 g/24 h were referred for conservative management to the high-risk obstetric unit in the John Radcliffe Hospital, Oxford, over a period of 5 years. Hyperuricaemia preceded the onset of heavy proteinuria in all 42 women. Most of the women had severe hypertension, but none developed eclampsia and there were no major maternal complications. Delivery was necessary within 2 weeks of onset of severe proteinuria in 88.1% of cases, although in some very preterm pregnancies delivery could be deferred for 3 or more weeks. Thirty-five women (83%) were delivered by caesarean section, 91% of whom were delivered urgently before the onset of labour. The high rate of urgent preterm operative delivery underlines the uncertainty of advanced pre-eclampsia and the need for close monitoring if delivery is to be deferred. Perinatal mortality was high; all the perinatal deaths occurred in babies of less than 29 weeks gestation. Despite heavy proteinuria, postpartum recovery was good. Three months after delivery, all but one patient had no significant proteinuria. There was no evidence of residual renal dysfunction. Although the outlook for pre-eclampsia with heavy proteinuria is limited, in a few cases pregnancy can be prolonged for significant periods of time without apparently prejudicing maternal safety and permitting enhancement of maturity at birth. The observations justify cautious conservative management even when heavy proteinuria is present.
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PMID:Prognosis for pre-eclampsia complicated by 5 g or more of proteinuria in 24 hours. 173 13

The hypertensive disorders of pregnancy are a frequent cause of neonatal morbidity and mortality. 259 newborns of hypertensive women were study to establish the relationship between some maternal findings and the subsequent neonatal complications. The severity, early onset of hypertension, proteinuria and the gestation of 32 week or less, are related with special risk of small-for-date, anoxia, seizures and neutropenia. Preeclampsia was related with foetus more compromised. Also hyperuricemia, thrombocytopenia and cesarean section were light predictors of neonatal trouble. These findings can orientate the neonatologist to select the newborns prone to complications, watching them closely to start the treatment, if necessary, as soon as possible.
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PMID:[Prediction of complications in children of hypertensive mothers]. 176 48

In 521 pregnancies complicated by hypertensive disorders (PHD) and in 200 control cases, we studied the incidence of intrauterine growth retardation (IUGR), depression in the newborns, general morbidity of live newborns requiring admission and perinatal mortality. We also analyzed the relationship between these conditions and the type and severity of hypertension, gestational age, presence of symptoms of the classic EPH triad and of abnormal uric acid values, hemoconcentration, and low urinary estriol values. Perinatal mortality (especially antepartum) was significantly increased in severe pre-eclampsia, chronic hypertension and chronic hypertension with superimposed pregnancy-induced hypertension (PIH); in all the cases with PHD it was three times higher than that of the control group (59% versus 20% and five times higher than the global perinatal mortality of the 25,763 deliveries attended during the same period (12% General morbidity reached 44% in severe pre-eclampsia and 75% in antepartum eclampsia. But the preterminal deliveries were also more frequent in PHD, especially in severe pre-eclampsia-eclampsia. Nevertheless, the perinatal morbidity and mortality in general increased when proteinuria and edema plus proteinuria were associated with hypertension, and the incidence was significantly higher when proteinuria surpassed 100 mg/dl. Morbimortality also increased in the presence of hemoconcentration, hyperuricemia, and low estrioluria.
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PMID:Perinatal morbidity and mortality in pregnancy hypertensive disorders: prognostic value of the clinical and laboratory findings. 197 14

Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age) whose GSD-I disease has been ineffectively treated, virtually all have disturbed renal function, manifested by persistent proteinuria; many also have hypertension, renal stones, altered creatinine clearance or a progressive renal insufficiency. Glomerular hyperfiltration is seen in the early stage of the renal dysfunction and can occur before proteinuria. In younger GSD-I patients, the hyperfiltration is usually the only renal abnormality found; and, in some patients, microalbuminuria develops before clinical proteinuria. The predominant underlying renal pathology is focal segmental glomerulosclerosis. Renal stones and/or nephrocalcinosis are also common findings. Amyloidosis and Fanconi-like syndrome can occur, but rarely. The risk factors for developing the glomerulosclerosis in GSD-I include hyperfiltration, hypertension, hyperlipidemia and hyperuricemia. Dietary therapy with cornstarch and/or nasogastric infusion of glucose, aimed at maintaining normoglycemia, corrects metabolic abnormalities and improves the proximal renal tubular function. Long-term trial will be needed to assess whether the dietary therapy may prevent the evolution or the progression of the renal disease.
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PMID:Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment. 202 44


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