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)

Two patients with kidney transplants had hypertensive encephalopathy and rapidly progressive kidney failure 10 weeks and 18 months postoperatively. In one patient renal failure was associated with erythrocytosis. Absence of proteinuria, despite progressive renal insufficiency in both patients, suggested that these abnormalities were not due to rejection episodes. Subsequently, angiography proved that each of these patients had renal-artery stenosis. Surgical repair of this lesion increased creatinine clearance at least threefold, and the hypertension and erythrocytosis disappeared. Apparent "rejection" episodes in which there is no proteinuria should alert clinicians to the possiblity of renal-artery stenosis of the graft. Restoration of kidney function and amelioration of hypertension may follow revascularisation, even after many months of renal ischaemia producing severe uraemia.
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PMID:Hypertensive crisis, erythrocytosis, and uraemia due to renal-artery stenosis of kidney transplants. 4 23

A 22-year-old black male presented with erythrocytosis and proteinuria. The erythrocytosis was characterized by increased red cell mass, normal arterial oxygen saturation, and normal hemoglobin electrophoresis and oxygen affinity. There was no splenomegaly, and the white blood cell count, platelet count, serum uric acid concentration, serum B12 levels and leukocyte alkaline phosphatase activity were normal. Tumors of the liver, lung, kidney and cerebellum, which have been associated with erythrocytosis, were not found. The only associated disease was biopsy proven focal glomerulosclerosis. Renal vein thrombosis was excluded by renal venography and arteriography. This case illustrates the rarely reported association of the nephrotic syndrome and erythrocytosis. Other nephrogenic causes of erythrocytosis are mentioned, including renal cysts, tumors, renal artery stenosis and transplantation. The role of the kidney in erythropoietin production and possible mechanisms of nephrogenic erythrocytosis are discussed.
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PMID:Focal glomerulosclerosis and erythrocytosis. 50 18

Proteinuria (urine protein/creatinine ratio, 13.6) resolved after control of primary erythrocytosis in a dog. Hydroxyurea and doxorubicin administration and phlebotomy were used initially to manage erythrocytosis. Remission was maintained for approximately 2 years. Glomerulonephropathy, characterized by absence of routine histologic or immunofluorescent changes and ultrastructural evidence of basement membrane deterioration and podocyte fusion, was documented. These lesions may have been a result of hypoxia and/or hyperviscosity secondary to erythrocytosis.
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PMID:Transient glomerulonephropathy associated with primary erythrocytosis in a dog. 230 86

A 58-year-old woman suffering from epistasis was found to be hypertensive. Hypocomplementemia associated with normal serum creatinine level, erythrocytosis, microscopic hematuria, proteinuria, and normal serum immunoglobulin levels and immunoelectrophoresis results led to a renal biopsy. Light microscopy disclosed mesangial hypercellularity and accumulation of eosinophilic material in capillary loops and in the mesangium. Immunomicroscopy disclosed coarsely granular to globular deposition of IgG, IgM, and C3 in similar distribution. Electron microscopy demonstrated electron-dense mesangial and subendothelial deposits consisting of interlacing fibrillar bundles associated with infiltration of acute inflammatory cells characteristic of cryoglobulinemic glomerulonephritis. After the biopsy, the presence of circulating IgG-IgM cryoglobulins was documented. Substructure of the in vitro cryoprecipitate and the immune complexes in the kidney was very similar. These observations illustrate the importance of continued routine ultrastructural assessment in evaluation of renal biopsy material.
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PMID:Primary ultrastructural diagnosis of cryoglobulinemic glomerulonephritis. 689 18

The authors studied dyslipidaemia and "obesity" in 137 patients (87 males and 50 females) following cadaver renal transplantation with regard to the applied immunosuppressive treatment and the patients' hypertension. The most extreme dyslipidaemic values, the highest levels of total cholesterol, LDL and Apo were found 6 to 18 months after successful transplantation; these values were significantly higher in women than in men. While in the dialysis programme only 21.89% of the patients had BMI values higher than 25.1 kg/m2, after transplantation their proportion was 36.49%. In addition to hyperlipidaemia, hyperuricaemia was encountered in 39.42%, erythrocytosis in 8.76% and diabetes mellitus in 9.48%, respectively. In the group of patients treated only with Cyclosporine-A the incidence of hyperlipidaemia and hypertension was significantly lower than in those receiving a combination of either corticosteroids and Cyclosporine-A or corticosteroids, Cyclosporine-A and azathioprine. There was a close relationship between the unfavourable tendency of obesity and the measured hyperlipidaemia. On the other hand, the extent of proteinuria did not always have a positive correlation with the increase of BMI and body weight, the severity of hypertension and hyperlipidaemia. The authors emphasize the importance of a systematic control of the lipid levels, the significance of a diet with an adequate carbohydrate and lipid content, and the necessity of avoiding obesity by selecting the optimal immunosuppressive treatment.
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PMID:The importance of obesity and hyperlipidaemia in patients with renal transplants. 1019 73

Angiotensin-converting enzyme inhibitors (ACEi) are a class of antihypertensive agents that decrease mortality in congestive heart failure and have established efficacy in the treatment of hypertension and the slowing of established diabetic nephropathy and other proteinuria-associated glomerulonephritides. These drugs have not gained wide acceptance in the treatment of hypertension in renal transplant recipients (RTRs) because of a potential for decreased renal blood flow and glomerular filtration rate associated with a single kidney and concomitant cyclosporine use. Experimental animal models suggest that ACEi may be of benefit in slowing the progression of chronic renal allograft rejection. We undertook a retrospective chart analysis of all RTRs in our institution who had been treated with an ACEi or an angiotensin II (AT II) antagonist, with the objectives of determining the safety, efficacy, and side effect profile of these medications. The minimum follow-up period was 6 months. One hundred seventy-seven of 642 RTRs were prescribed an ACEi or AT II antagonist. Forty-seven patients discontinued therapy, with the most common causes of discontinuation being cough (8 patients) and hyperkalemia (6 patients). The mean arterial blood pressure at each follow-up period was lower than that at the time of initiation of ACEi or AT II antagonist therapy, with a decrease from 92 +/- 12 mm Hg to 86 +/- 9 mm Hg (P < 0.05) after 3 years of treatment. The serum creatinine concentrations did not change throughout the follow-up period. There was a nonsustained increase from the baseline serum potassium of 4.4 +/- 0.5 to 4.6 +/- 0.6 mEq/L at 3 months (P < 0.05), but no further increases in potassium beyond this time. The mean hemoglobin concentration for the cohort did not change, but 13 RTRs given an ACEi for posttransplantation erythrocytosis (PTE) had a decrease in hemoglobin from 17.1 +/- 1.0 g/dL at the start of ACEi therapy to 14.8 +/- 2.2 g/dL at 3 years (P < 0.05). ACEi and AT II antagonists were generally effective antihypertensives, and were safe and well-tolerated agents in this cohort of RTRs. ACEi were also effective in the treatment of PTE.
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PMID:ACE inhibitors and angiotensin II antagonists in renal transplantation: an analysis of safety and efficacy. 1062 May 59

Hypertension is highly prevalent after renal transplantation and has been associated with lower graft survival. Optimum management of post-transplant hypertension remains to be defined. Losartan, a potent, orally active and selective non-peptide blocker of the angiotensin subtype 1 receptor, could represent a useful drug for treating post-transplant hypertension. Recently, a prospective study of 12 weeks treatment with losartan has showed a satisfactory control of arterial hypertension associated with a decrease in proteinuria in this high-risk group of renal transplant patients. A retrospective study was performed to review the role of losartan as a renoprotective agent (evaluating blood pressure and proteinuria) in renal transplant recipients in a long-term follow-up. A total of 150 transplant recipients were included in the study. None of the patients had a serum creatinine >3 mg/dl, or suspected renal artery stenosis, or other severe concomitant diseases. The indication for losartan therapy was hypertension, proteinuria and/or post-transplant erythrocytosis. The values of blood pressure, results of fasting haematology, blood chemistry and total proteinuria in 24-h urine samples were recorded at the time of initiation of losartan therapy, 6 and 3 months before the start, and at 3, 6, 12, 18 and 24 months thereafter. A tendency analysis by linear regression comparing two slopes before and after treatment was realized. A decrease in mean blood pressure and proteinuria, from 106.7+/-0.9 to 98.2+/-2.1 mmHg and from 1253.9+/-188 to 91.2+/-33.7 mg/24 h, P<0.05, respectively, was observed after introduction of losartan. A progressive increase in creatinine clearance was observed after the third month of losartan treatment. No significant changes were seen in haematocrit or serum potassium levels. We can conclude that a progressive decrease in mean arterial pressure associated with a decrease in proteinuria was observed during long-term follow-up. Based on the capacity of losartan to improve renal function, this drug could be decisive for the treatment and prevention of chronic allograft nephropathy.
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PMID:Angiotensin II type 1 (AT1) receptor antagonists in the treatment of hypertension after renal transplantation. 1136 38

Chronic exposure to high altitude is associated with the development of erythrocytosis, proteinuria, and, in some cases, hyperuricemia. We examined the relationship between high-altitude polycythemia and proteinuria and hyperuricemia in Cerro de Pasco, Peru (altitude, 4,300 m). We studied 25 adult men with hematocrits less than 65% and 27 subjects with excessive erythrocytosis (EE; hematocrit > 65%) living in Cerro de Pasco, Peru and compared them with 28 control subjects living in Lima, Peru (at sea level) and after 48 hours of exposure to high altitude. Serum urate levels were significantly elevated in patients with EE at altitude, and gout occurred in 4 of 27 of these subjects. Urate level strongly correlated with hematocrit (r = 0.71; P < 0.0001). Urate production (24-hour urine urate excretion and urine urate-creatinine ratio) was increased in this group compared with those at sea level. Fractional urate excretion was not increased, and fractional lithium excretion was reduced, in keeping with increased proximal reabsorption of filtrate. Significantly higher blood pressures and decreased renin levels in the EE group were in keeping with increased proximal sodium reabsorption. Serum urate levels correlated with mean blood pressure (r = 0.50; P < 0.0001). Significant proteinuria was more prevalent in the EE group despite normal renal function. Hyperuricemia is common in subjects living at high altitude and associated with EE, hypertension, and proteinuria. The increase in uric acid levels appears to be caused by increased urate generation secondary to systemic hypoxia, although a relative impairment in renal excretion also may contribute.
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PMID:Hyperuricemia, hypertension, and proteinuria associated with high-altitude polycythemia. 1204 23

IgA nephropathy (IgAN) is one of the most frequent forms of glomerulonephritis (GN). However, its association with polycythemia vera (PV) has rarely been described. We report a case of IgAN combined with PV. The patient was a 46-year-old male with chronic renal failure, heavy proteinuria and erythrocytosis. He also presented hypertension and hematuria as well as splenomegaly, high arterial oxygen saturation and elevated leukocyte alkaline phosphatase activity. Possible causes of secondary erythrocytosis were ruled out. The renal biopsy revealed mesangial proliferative GN with predominant IgA deposition in mesangium. He was diagnosed as having IgAN and PV concomitantly. After administration of hydroxyurea, enalapril and felodipine, blood cell count and blood pressure normalized, while azotemia persisted. There was also a partial remission of the heavy proteinuria. We describe a case of IgAN associated with PV, and possible pathophysiologic relationships between two diseases are discussed with review of the literature.
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PMID:IgA nephropathy in a patient with polycythemia vera. Clinical manifestation of chronic renal failure and heavy proteinuria. 1216 77

Stable renal transplant recipients manifest a chronic hypercoagulable state with an increased risk of thromboembolic complications, which appears to be multifactorial. While this group of patients could present the known risk factors for thromboembolism in the general population (e.g. diabetes, cancer, pregnancy), they may also suffer from other situations which are mostly related to transplantation and are consequently specific to them. Here, we review briefly the clinical aspects and controversies of the most important of these factors including immunosuppressive agents, antiphospholipid antibodies, hyper-homocysteinemia, pre-transplant dialysis modality, and post-transplant erythrocytosis. In addition, other more recent topics including hypercysteinemia, recurrent proteinuria, and acute CMV infection are discussed.
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PMID:Acquired hypercoagulable state in renal transplant recipients. 1504 24


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