Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Puromycin aminonucleoside (PAN)-nephrotic rats have high serum angiotensin I-converting enzyme (ACE) activity. We studied ACE activity in serum, urine, and tissues from PAN-nephrotic rats on days 2, 6, 11, and 16 after PAN injection. Proteinuria and hypoproteinemia were evident on days 6 and 11. Though significantly decreased, proteinuria was still evident on day 16. Serum ACE activity increased on days 2, 6, and 11. Urinary ACE activity became evident on days 6, 11, and 16 and correlated positively with proteinuria, suggesting that the source of urine ACE is the blood serum. ACE activity increased in testis on days 2 and 6, in lungs and aorta on days 6 and 11, in adrenal glands and small intestine on day 11, and in kidney on days 11 and 16. Heart ACE activity decreased on days 2 and 6, and increased on day 16; brain ACE activity decreased on day 6 and increased on day 11. These data implicate that changes in tissue ACE content may contribute to elevate serum ACE in PAN-nephrotic rats.
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PMID:Angiotensin I-converting enzyme activity in puromycin aminonucleoside-nephrotic syndrome. 217 83

The pathophysiology of the nephrotic syndrome (NS), characterized by protenuria, edema, sodium retention and hyperlipidemia, is not clear. We studied the role of some systemic factors on sodium retention in an experimental model of NS. NS was induced in rats by a single subcutaneous injection of puromycin aminonucleoside (PA) (15 mg/100 g); control animals received vehicle. All rats were kept in metabolic cages for 24 days (3 days before and 21 days after PA-injection). Urine was collected daily. Blood samples were obtained every day until day 10, and then every other day up to the end of the study. The rats showed the following alterations after PA injection: a) a rise in serum angiotensin converting enzyme activity (ACEA) and plasma aldosterone (PAldo) at day 1; b) a rise in urinary aldosterone (UAaldoV), azotemia and sodium retention at day 2; c) massive proteinuria (UProt) and decrease in plasma angiotensinogen concentration (PAC) at day 4; d) increases in plasma renin activity (PRA), plasma renin concentration (PRC) and serum creatinine as well as hypoproteinemia, hypercholesterolemia, hypertriglyceridemia, ascitis and edema at day 5; e) increase in urine volume at day 6. PAldo became normal at day 7; urine sodium (UNaV), PRA and PRC at day 8; UAldoV at day 9; serum urea and ACEA at day 10; urinary volume at day 11; PAC, serum total protein and creatinine at day 12. The edema disappeared at day 11. UProt, hypercholesterolemia and hypertriglyceridemia persisted, though they decreased substantially by the end of the study (day 21). Light microscopy studies revealed normal glomerular morphology, but electron microscopy showed fusion of podocytes before proteinuria. These data suggest that: a) sodium retention was not a consequence of proteinuria or hypoproteinemia; b) sodium retention seems non-related to renin secretion, but may be partially mediated by a fall in glomerular filtration rate or by an increased tubular resabsorption secondary to other factors; c) the increase in PAldo, UAldoV and ACEA are non-related to renin secretion: all occurred before PRA rose; d) water retention, increase in PRA and PRC, hypercholesterolemia and hypertriglyceridemia are secondary to the hypoproteinemia.
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. I. The role of proteinuria, hypoproteinemia, and renin-angiotensin-aldosterone system on sodium retention. 223 72

A retrospective study was performed in 48 normotensive proteinuric children to evaluate the effect of enalapril (n = 17), a combination of enalapril and prednisone (n = 11) and prednisone alone (n = 20) on urinary protein excretion and systemic blood pressure. Enalapril treatment was associated with significant and persistent diminution of proteinuria from 1.32 +/- 0.23 to 0.53 +/- 0.11 and 0.44 +/- 0.07 g/day on the 4th and 8th week of treatment, respectively. Combined therapy with enalapril and prednisone resulted in a comparable significant reduction of proteinuria from a pre-treatment value of 2.06 +/- 0.42 to 0.63 +/- 0.22 and 0.52 +/- 0.17 g/day on the 4th and 8th week of treatment, respectively. In contrast to this, in the group treated with prednisone alone, proteinuria decreased significantly only from the 6th week of therapy (p < 0.02). Consequently, these children had significantly higher urinary protein losses at the 4th week of treatment as compared to patients on enalapril treatment (given either alone or combined with prednisone) (p < 0.01 and p < 0.05, respectively). Importantly, the enalapril-induced reduction of proteinuria was unrelated to variations in arterial blood pressure and no significant changes in this parameter were observed. The results indicate that enalapril can be used safety and effectively for symptomatic treatment of proteinuria in normotensive children with preserved renal function. ACE inhibitor provides additive antiproteinuric effect to corticosteroids by accelerating the rate of diminution of proteinuria. Its combination with prednisone may be of particular importance in those cases, where the degree of hypoproteinemia is a concern. (Tab. 2, Fig. 1, Ref. 29.)
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PMID:Enalapril treatment of proteinuria in normotensive children. 1064 36

Recently, plasma exchange (PE) has been added to the treatment regimen for patients with steroid-, cyclophosphamide-, and cyclosporine-resistant nephrotic syndrome. This is a case report of a female patient with severe acute renal failure (ARF) during the relapse of steroid-resistant nephrotic syndrome (SRNS) who recovered completely after PE and became steroid-sensitive in further follow-up of 48 months. An 8-year-old girl was referred to Nephrology Department of the University Children's Hospital due to relapse of SRNS complicated with ARF. Her nephrotic syndrome (mesangioproliferative glomerulonephritis) was diagnosed at the age of 17 months. During the following 6 years, she was given several therapeutic regimens including pulse prednisolone, cyclophosphamide, Cyclosporine (CyA), but she continued to have frequent relapses and during the last six months she was steroid- and cyclosporine-resistant. Three days before admission, she was febrile, had cellulites of the lower abdominal wall, diarrhea, vomiting, hypovolemic shock with generalized edema, severe hypoproteinemia and hypoalbuminemia. In a local hospital, she was treated with fresh frozen plasma, albumin, methylprednisolone, furosemide and antibiotics, but she became anuric and was referred to our hospital. There were no signs of hemolysis. Anuria lasted for 12 days. She was discharged after 42 days in remission with normal GFR. Principal treatment included: 13 sequential hemodialysis sessions (30% of body weight was removed as excess volume), 6 PE, corticosteroids, CyA, ACE inhibitor, antibiotics, antimycotics, and cimetidine. Six PE sessions were performed every other day. In further 48-month follow-up, while under the treatment of CyA the patient had a few steroid-sensitive relapses, the first being 6 months after PE. The second kidney biopsy showed focal segmental glomerulosclerosis with no signs of apparent CyA nephrotoxicity. "Malignant" course of disease in our patient was a good reason to introduce PE into the treatment. Since PE was the only additional mode of treatment, it is believed that its effect was crucial for milder activity of the disease.
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PMID:[The benefit of plasmapheresis in a patient with steroid-resistant nephrotic syndrome and anuria--long-term follow-up]. 1561 78