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)

A grossly obese (149 kg) man with the sleep apnea syndrome was found to have proteinuria and a supernormal glomerular filtration rate. Renal histology showed glomerulomegaly and focal glomerulosclerosis. It is suggested that obesity may induce glomerular hyperfiltration and in turn glomerulosclerosis.
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PMID:Proteinuria, glomerulomegaly and focal glomerulosclerosis in a grossly obese man with obstructive sleep apnea syndrome. 259 Jan

We observed nocturnal urinary protein excretion to be 16.2 +/- 5.5 micrograms/min (mean +/- SE) in 9 healthy control subjects (group I), 29.3 +/- 9.5 micrograms/min in 12 obese patients suspected to have obstructive sleep apnea syndrome (OSAS) but with negative polysomnographic studies (group II), and 94.0 +/- 31.8 micrograms/min in 14 patients with documented OSAS (group III) (II vs. I, NS; III vs. I, p less than 0.05; III vs. II, p less than 0.05). The frequency of abnormal proteinuria, defined as protein excretion greater than the highest rate observed in group I (46 micrograms/min), was 14% in group II and 64% in group III (p less than 0.05). There were no significant differences in age, body weight, body surface area, blood pressure, or indices of sleep apnea between OSAS patients with and without proteinuria. Although the mechanism is unclear, this study shows that nocturnal protein excretion rates are commonly elevated in patients with OSAS.
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PMID:Nocturnal urinary protein excretion rates in patients with sleep apnea. 291 55

Two patients with severe obstructive sleep apnea syndrome and high-grade proteinuria (greater than 1 g/d [1000 mg/d]) were studied. Three remissions in proteinuria coincided with correction of obstructive sleep apnea syndrome and improvement of blood oxygen levels. These remissions could be dissociated from reductions both in dry body weight and in hematocrit levels. We propose that sleep apnea may cause a functional and reversible type of proteinuria.
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PMID:Reversible proteinuria in obstructive sleep apnea syndrome. 333 6

Renal abnormalities in patients with obstructive sleep apnea syndrome (OSAS) have not been previously described. Medical records of patients who had been evaluated for possible sleep apnea syndrome and had had complete polysomnograms and urinalyses were reviewed to determine the frequency of proteinuria. High-grade proteinuria (greater than or equal to 3+ on urinalysis) was found in 6 of the 34 patients with obstructive sleep apnea, but in none of 34 patients in a control group matched for sex, age, and weight. In three patients, proteinuria was in the nephrotic range (3.5 g/24 h). The weight (mean +/- SD) of the patients with obstructive sleep apnea (112.7 +/- 35.3 kg) was not significantly different from the control group (109.2 +/- 30.3 kg). Microscopic examination of renal tissue in one patient with OSAS showed minimal changes. In four patients who were followed for 3 years, proteinuria improved after therapy for sleep apnea syndrome. We suggest that proteinuria may not be uncommon in patients with severe obstructive sleep apnea syndrome and may be reversible with correction of the sleep apnea syndrome.
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PMID:Sleep apnea, proteinuria, and nephrotic syndrome. 336 72

We have identified 17 obese patients (body mass index, BMI, 37.9 +/- 4.1) with proteinuria > 1 g/day (1.3-6.4 g/24 h, mean 3.1 +/- 1.7). Their age was 34-70 years (48.3 +/- 10); 11 were females and 6 males. Six patients had only one functioning kidney and a sleep apnea syndrome had been diagnosed in 5. Renal biopsies, obtained in 5 cases, showed focal glomerulosclerosis in 2 cases, minimal changes in 2 and mesangial proliferation in 1. Nine patients (group 1) were treated with hypocaloric diets; body weight significantly decreased (BMI 37.1 +/- 3, 34 +/- 3.5 and 32.6 +/- 3.2 at 0, 6 and 12 months, respectively) as well as proteinuria (2.9 +/- 1.7, 1.2 +/- 1 and 0.4 +/- 0.6 g/24 h). There was a significant correlation between body weight loss and decrease in proteinuria (r = 0.69, p < 0.05). Eight patients (group 2) were treated with captopril, without dietary changes. BMI remained stable but proteinuria showed a dramatic decrease, similar to that in group 1 (3.4 +/- 1.7, 1.2 +/- 0.9 and 0.7 +/- 1 g/24 h, respectively). Renal function remained stable in both groups. In summary, both body weight loss and captopril treatment can induce a sharp decrease in obesity-related proteinuria.
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PMID:Effects of body-weight loss and captopril treatment on proteinuria associated with obesity. 761 15

Recent studies of obstructive sleep apnea and its comorbidity with other systemic diseases have stimulated interest in the relationship of apnea to renal disease and hypertension. Polysomnographic sleep studies in patients on dialysis who complain of day-time fatigue or sleepiness reveal significant apnea in up to 73% of those studied. Abnormalities in respiratory controller mechanisms from chronic hypocarbia, metabolic acidosis, and uremic toxins have been blamed for the occurrence of apnea in this setting. Proteinuria and sometimes nephrotic syndrome have been recognized in morbidly obese patients with sleep apnea syndrome. Renal biopsies of such patients have shown glomerulomegaly and focal segmental sclerosis. It is postulated that these lesions may result from increased glomerular filtration and blood flow. Elevated urine output, sodium and chloride excretion, and atrial natriuretic peptide have been well demonstrated in obstructive apnea patients and correct to control levels with treatment of the apnea. Both acute (with each apnea) and chronic daytime blood pressure elevation are frequently observed in sleep apnea patients, and occult sleep apnea is postulated as one possible cause of "primary" hypertension in middle-aged men. In younger patients, such hypertension seems to be more reversible with the elimination of apnea. In older patients, however, the cure of systemic hypertension cannot be guaranteed with the elimination of the apnea, and asymptomatic apnea patients tend not to tolerate the bother and discomfort of apnea treatment with nasal continuous positive airway pressure. Therefore, aside from a careful history regarding sleep symptomatology, polysomnographic studies of clinic populations with primary hypertension to search for apnea as a cause cannot be recommended.
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PMID:Obstructive sleep apnea and the kidney. 830 38

Glomerulomegaly is a histologic finding present in idiopathic pulmonary hypertension, congenital cyanotic heart disease, morbid obesity associated with sleep apnea syndrome, sickle cell disease, and polycythemic states. This study examines the case of a 34-yr-old woman with idiopathic pulmonary artery hypertension who presented with nephrotic-range proteinuria. Kidney biopsy revealed enlarged glomeruli with mesangial-proliferative glomerulonephritis. A review of the pertinent literature and a discussion of the proposed pathophysiologic mechanisms leading to glomerulomegaly are presented.
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PMID:Glomerulomegaly and proteinuria in a patient with idiopathic pulmonary hypertension. 940 1

Patients with OSAS (obstructive sleep apnoea syndrome) demonstrate renal signs such as proteinuria, glomerular hypertrophy and focal glomerular sclerosis. We performed a clinical study to investigate the glomerular function in OSAS patients and the short-term effect of CPAP (continuous positive airway pressure) on it. OSAS patients underwent a sodium thiosulphate and p-aminohippurate double clearance test, polysomnography and ambulatory blood pressure monitoring before and a week after the induction of CPAP. Twenty-seven consecutive patients (24 males) with moderate-to-severe OSAS admitted to our hospital for the induction of CPAP, and 32 healthy donors for renal transplantation as controls participated in the study. Before treatment, the glomerular filtration rate, estimated by the sodium thiosulphate clearance test, was within normal range, and the renal plasma flow was significantly lower than normal in the OSAS patients, thus the FF (filtration fraction) value was much higher than normal. FF before CPAP was not significantly correlated with age, body mass index or blood pressure; however, indices of increased hypoxaemia correlated with increased FF values. Polysomnographic variables after CPAP showed significant improvements in all patients, and only the nocturnal blood pressures were slightly lower than before CPAP. In 21 patients who underwent the clearance test after CPAP, FF significantly decreased from 0.26 +/- 0.04 to 0.23 +/- 0.03 (P < 0.001). OSAS patients were generally in a glomerular-hyperfiltrating condition that appeared to cause the renal findings associated with OSAS. CPAP might prevent nephropathy by ameliorating the glomerular hyperfiltration in OSAS patients.
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PMID:Short-term use of continuous positive airway pressure ameliorates glomerular hyperfiltration in patients with obstructive sleep apnoea syndrome. 1519 64

Maternal pregravid obesity is a significant risk factor for adverse outcomes during pregnancy. In early pregnancy there is an increased risk of spontaneous abortion and congenital anomalies. In later gestation maternal metabolic manifestations of the metabolic syndrome, such as gestational hypertensive disorders and diabetes, become clinically recognized because of the increased insulin resistance in obese compared with nonobese women. In women with pregestational glucose intolerance, hypertension, central obesity, and lipid disorders, the physiologic changes in pregnancy increase the risk of problems previously not routinely encountered during pregnancy. These include chronic cardiac dysfunction, proteinuria, sleep apnea, and nonalcoholic fatty liver disease. At parturition the obese patient is at an increased risk of cesarean delivery and associated complications of anesthesia, wound disruption, infection, and deep venous thrombophlebitis. For the fetus there are short-term risks of fetal macrosomia, more specifically obesity, and long-term risks of adolescent components of the metabolic syndrome. Although preliminary results of bariatric surgery are encouraging, the procedure is expensive and not for all obese women, and we recognize that long-term follow-up data on offspring of obese women who have undergone bariatric surgery before pregnancy are lacking. In the interim, we need to encourage obese women to lose weight before conception, using lifestyle changes if possible. During pregnancy, weight gain should be limited to Institute of Medicine guidelines (currently under review) and encouragement given for physical activity.
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PMID:Management of obesity in pregnancy. 1726 45

The authors sought to evaluate the prevalence of hypertension (HTN) in patients with sleep apnea (SA) who had normal kidney function and in patients with SA and chronic kidney disease (CKD). It has not been determined whether there is an effect of interplay of SA and CKD on the prevalence of HTN. In this study, the diagnosis of CKD was established based on the glomerular filtration rate and the presence of proteinuria. SA and HTN were diagnosed based on International Classification of Diseases, Ninth Revision coding, Current Procedural Terminology coding, and medication use. Using the database of a large integrated health system, 434,388 patients aged 18 years and older with 2 or more years of continuous enrollment during January 2002 to December 2004 were analyzed. The HTN rate with SA alone was 51%, compared with 70.2% with SA and CKD. The overall prevalence of HTN was 28% in patients without CKD or SA. The prevalence ratio for HTN was 1.36 (95% confidence interval, 1.33-1.39) more prevalent in patients with SA and CKD compared with patients with SA without CKD. The high prevalence of HTN in patients with SA and CKD suggests the need for evaluation of SA in patients with concurrent HTN and CKD.
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PMID:Sleep apnea and hypertension: prevalence in chronic kidney disease. 1797 90


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