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 effects of angiotensin-converting enzyme (ACE) inhibitors on renal hemodynamics vary widely depending on the preexisting physiologic and pathologic state of the kidneys. Although some studies of ACE inhibitors in primary essential hypertension have demonstrated increases in glomerular filtration rate (GFR) and effective renal plasma flow in patients with renal impairment, other studies have not shown these same beneficial results. The difference may involve the choice of ACE inhibitor used in the investigations, but controlled comparison trials are needed to determine whether this is the case. The use of ACE inhibitors in renovascular hypertension remains controversial. ACE inhibition can interfere with the autoregulation of GFR mediated by angiotensin II and may lead to deterioration of renal function, especially in patients with bilateral renal artery stenosis or stenosis of a solitary kidney. Additionally, ACE inhibitors have been shown to cause a decline in GFR in the kidney affected by the stenosis, whether or not clinically apparent renal insufficiency occurs. Although the functional impairment associated with ACE inhibitors in renal artery stenosis has generally been reversible following removal of the drug, the consequences of a long-term reduction in GFR are unknown. Treatment of stable congestive heart failure (CHF) with ACE inhibitors can result in enhancement of GFR and reduction of sodium and fluid retention, thus improving the clinical state. However, in patients with decompensated cardiac failure, renal perfusion pressures may already be at or near the autoregulatory breakpoint and ACE inhibition may cause deterioration of renal function. In general, ACE inhibitors can be used safely in CHF if they are initiated cautiously, with adjustment of ACE inhibitor and diuretic dosages to avoid systemic hypotension and sodium and fluid depletion. In studies comparing the agents, enalapril and lisinopril have both been shown to cause higher incidences of renal function deterioration than has captopril. These findings suggest that the more complete or sustained ACE inhibition seen with the longer-acting agents may be detrimental to renal function in patients with CHF. The use of ACE inhibitors in the treatment of proteinuria is the newest area of research with these agents. At present it appears that ACE inhibitors reduce urinary protein excretion the most effectively in diabetic patients with mild proteinuria and in hypertensive patients with renal insufficiency and proteinuria due to glomerular disorders. More study is needed to determine whether these agents can reduce the rate of renal failure progression and to define the patient populations expected to benefit most.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors and renal function. 218 38

Hypertension contributes to the inexorable decline of renal function in patients with chronic renal impairment. Studies on the long-term use of converting enzyme inhibitors and calcium antagonists in the treatment of hypertension in patients with chronic renal failure are hereby reviewed. The data demonstrate that converting enzyme inhibitors are effective antihypertensives in diabetic nephropathy and other forms of chronic renal failure. Furthermore, the results suggest that long-term treatment with captopril may slow the progression of renal impairment in diabetic nephropathy, whereas the data are inconclusive for non-diabetic nephropathies. A reduction of proteinuria or albuminuria was also observed in most trials during long-term converting enzyme inhibition. Treatment with calcium antagonists also led to effective blood pressure control in hypertensive patients with renal disease. However, the very limited data in humans suggest no consistent beneficial effect on kidney function or proteinuria. More controlled studies are necessary to determine the relative efficacy and safety of converting enzyme inhibitors and calcium antagonists in comparison with "standard antihypertensives" in long-term antihypertensive treatment of patients with various forms of chronic renal failure.
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PMID:Converting enzyme inhibitors and calcium antagonists in the long-term treatment of hypertension in chronic renal failure. 219 80

Various pathogenetic mechanisms are involved in IgA nephritis: immunological; platelet, coagulation and vascular injury; mesangial cell proliferation and contractility; hypertension; glomerular hyperperfusion and tubulo-interstitial injury. It is now possible to identify the subgroup of patients with IgA nephritis who have adverse prognostic features and may develop progressive glomerular scarring with renal failure. These features are proteinuria greater than 1 gm/day, non-selective proteinuria, glomerulosclerosis, hypertension, crescents and medial hyperplasia of blood vessels on renal biopsy. Controlled trials involving cyclophosphamide, anti-platelet agent (dipyridamole) and low dose warfarin; prednisolone; angiotensin converting enzyme inhibitors and eicosapentanoic acid (fish oil) appear promising. Currently, patients with bad prognostic indices in the Department are offered entry into an ongoing controlled trial of dipyridamole and low dose (anti-thrombotic dose) warfarin. Those patients with nephrotic syndrome especially with selective proteinuria are treated with a course of prednisolone and failing that, cyclophosphamide. It is important to maintain adequate blood pressure control among hypertensive patients as uncontrolled hypertension can lead to accelerated renal failure. With the onset of even mild renal impairment, dietary protein restriction should be recommended as this will help to decrease the rate of renal deterioration due to glomerular hyperfusion.
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PMID:IgA nephritis: a review of the pathogenetic mechanisms and the rationale for therapy. 256 Mar 58

Thin-membrane nephropathy recently has been described as a cause of glomerular haematuria. The prognosis of the condition is unclear but it generally is considered to be benign. In a series of 92 patients with glomerular haematuria, thin-membrane nephropathy was found to be a common cause, occurring in 26 (28%) patients. Sixteen patients were women. The mean age was 42 years. Four patients had a family history of renal disease or haematuria and no patient was deaf. Haematuria had been present from six days to 30 years. Loin pain occurred in 31% of patients. Hypertension was not a feature and mild renal impairment was present in one case only, while a further three cases showed proteinuria at a level of greater than 500 mg of protein per day. Glomerular basement membranes in patients with thin-membrane nephropathy gave a mean (+/- standard deviation) width of 319 + 37 nm which was significantly (P less than 0.002) less than the control value of 394 +/- 61 nm. On the basis of clinical features and serological parameters, thin-membrane nephropathy could not be separated from other renal causes of haematuria but required careful electronmicroscopic examination of renal biopsy material to establish the diagnosis. Limited follow-up has confirmed the good prognosis of the condition.
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PMID:Thin-membrane nephropathy--a common cause of glomerular haematuria. 209 27

We report renal biopsy findings in 109 patients with unexplained renal impairment (serum creatinine greater than 0.15 mmol/l) and normal-sized non-obstructed kidneys. The most common histological lesions were interstitial nephritis, rapidly progressive glomerulonephritis and a variety of other types of glomerulonephritis. The groups could not be distinguished by the presence or absence of hypertension, haematuria, proteinuria, or features of systemic disease. However interstitial nephritis was found more frequently in patients presenting with one or none of these features and rapidly progressive glomerulonephritis in patients presenting with three or more. All four patients with none of these features had interstitial lesions. Fifty-two per cent of patients with interstitial nephritis improved and 60 per cent of the patients with rapidly progressive glomerulonephritis who received immunosuppressive treatment improved or remained stable with treatment. The benefits of a biopsy diagnosis were almost wholly confined to these two groups. Complications were recorded in nine patients - prolonged macroscopic haematuria in six and symptomatic perirenal haematomata in three. Six required blood transfusion. One required nephrectomy to control haemorrhage and subsequently died. Percutaneous renal biopsy is not without risk in patients with renal impairment but the benefits of diagnosing interstitial nephritis and rapidly progressive glomerulonephritis outweigh the disadvantages.
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PMID:Renal biopsy in patients with unexplained renal impairment and normal kidney size. 260 35

Three hundred and ninety-five pregnancies undertaken by 238 women with primary glomerulonephritis between 1962 and 1987 were analysed to record fetal and maternal outcome and identify risk factors for a poor outcome. Of 398 fetuses, 26 per cent were lost (including therapeutic abortions), 24 per cent surviving infants were premature (less than or equal to 36 weeks gestation) and 51 per cent were term. Excluding therapeutic abortions, 20 per cent of fetuses were lost, 15 per cent after 20 weeks gestation. Fifteen per cent of 237 fetuses whose birth weight was recorded were small for gestational age: Deterioration in maternal renal function was seen in 15 per cent of pregnancies and in 5 per cent of women failed to resolve post partum. Only four women had impaired renal function recorded in the first-trimester and two of these were known to have renal impairment before pregnancy. Hypertension was recorded in 52 per cent of pregnancies, developed early (less than or equal to 32 weeks gestation) in 26 per cent and was severe in 18 per cent. Treated hypertension pre-dated 12 per cent of pregnancies and in 7 per cent (included in the overall incidence of hypertension) exacerbation occurred during pregnancy despite continued antihypertensive medication. Forty-four women (18 per cent) who developed de novo hypertension in pregnancy had permanent hypertension postpartum. Increased proteinuria was recorded in 59 per cent of pregnancies and was irreversible in 15 per cent of women. Comparison of pregnancies which occurred before or after renal biopsy revealed a significantly higher fetal loss rate after 20 weeks gestation in those pregnancies undertaken before the diagnosis of renal disease, and a significantly higher incidence of hypertension and increased proteinuria. Impaired renal function, early or severe hypertension or nephrotic range proteinuria was significantly associated with increased fetal loss, prematurity and fewer full-term infants. There was no significant difference in fetal outcome or maternal complications in pregnancy in patients with treated hypertension before pregnancy and those who were normotensive in the first-trimester. The highest incidence of fetal and maternal complications occurred in patients with primary focal and segmental hyalinosis and sclerosis and the lowest in non-IgA diffuse mesangial proliferative glomerulonephritis. The presence of severe vessel lesions on renal biopsy was associated with a significantly higher total fetal loss and fetal loss after 20 weeks gestation.
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PMID:Primary glomerulonephritis and pregnancy. 260 50

In a mass screening programme, 54 children with haematuria and proteinuria were detected and evaluated by clinical findings and renal histology. IgA glomerulonephritis (GN) occurred in 29 patients, diffuse mesangial proliferative GN (DPGN) in 16, membranous GN (MGN) in 4, membranoproliferative GN (MPGN) in 3, and focal segmental glomerular sclerosis (FSGS) was seen in 2. Of the 35 children with proteinuria less than or equal to 1 g/m2 per day, 21 with IgA GN and 14 with DPGN had only mild to moderate glomerular changes. None of these children had developed renal impairment after a mean period of 6.5 years (range 5-10 years). On the other hand, 8 children with IgA GN, 2 with DPGN, 4 with MGN, 3 with MPGN, and 2 with FSGS had proteinuria that exceeded 1 g/m2 per day. The biopsy specimens from these children showed moderate to severe glomerular changes, and 7 of these children had hypertension or renal impairment during the period of evaluation. This study suggests that a poor outcome correlates with the level of proteinuria and the severity of renal pathology in children with haematuria and proteinuria.
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PMID:Asymptomatic haematuria and proteinuria: renal pathology and clinical outcome in 54 children. 270 98

Analyses of prognostic factors have allowed the design of staging systems in different haematological disorders. In a series of 220 patients with multiple myeloma, univariate analysis showed that nine parameters had a significant adverse effect on survival; poor performance status (Karnowsky scaling system less than 70%), infections before diagnosis, renal impairment (assessed either by creatinine clearance greater than 2 mg dl-1 or urea greater than 40 mg dl-1), serum calcium (greater than 10 mg dl-1), severe anaemia (less than 8.5 g dl-1), the presence of Bence-Jones proteinuria, failure to achieve complete remission, more than 40% plasma cells in bone marrow and a low paraprotein index (monoclonal component/% plasma cells: P less than 0.09). In addition, this index correlated significantly with all the other prognostic factors except performance status. The best combination of disease characteristics selected by means of the Cox regression proportional hazards method were performance status and creatinine levels. Additionally, by factor analysis of principal components we obtained a regression equation that included creatinine levels, haemoglobin, performance status and paraprotein index. Using this it was possible to separate the series of patients into three risk categories: A (65 patients), B (69 patients) and C (65 patients) with a median survival of 41, 24 and 12 months, respectively. The model provided similar results to those of the British Medical Research Council, whereas the staging systems proposed by Durie and Salmon, Merlin et al. and Carbone et al. had a lower discriminant value in our series.
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PMID:Prognostic factors and classification in multiple myeloma. 275 17

The authors have studied 6 cases of systemic AA amyloidosis associated with ankylosing spondylitis. Renal failure occurred in all patients a mean of 19 years after the clinical onset of the rheumatic disease. Three patients progressed rapidly (between 3 months and 3 years) to end-stage renal failure. Such an outcome did not depend upon early onset of the renal impairment, degree of inflammation or treatment with colchicine. All patients were alive 2 to 10 years later, and this confirms a better prognosis than with AL amyloidosis. The utility of combining Wright's permaganate reaction with immunological methods to characterize the amyloid deposits was also confirmed. It is concluded that amyloidosis is a rare complication of ankylosing spondylitis and probably depends on a genetic predisposition. The possibility of amyloidosis should be kept in mind when proteinuria or renal failure appear in the course of ankylosing spondylitis.
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PMID:[Ankylosing spondylitis with type AA amyloidosis. 6 cases]. 297 71

Echocardiography was used to study the prevalence and severity of left ventricular hypertrophy in patients with established diabetic nephropathy (persistent proteinuria for at least 2 y plus severe retinopathy). Fifteen patients had mild renal impairment (serum creatinine less than 150 mumol l-1), 14 patients had moderate renal impairment (serum creatinine 150-400 mumol l-1), and 20 patients had severe renal impairment (serum creatinine greater than 400 mumol l-1). Thirty-six of the 49 (73%) were on anti-hypertensive treatment, despite which mean blood pressure was 161 +/- 25/89 +/- 9 (+/- SD) mmHg. Left ventricular hypertrophy was demonstrated in 42 of the 49 patients (85%), and increased in severity with increasing renal impairment. Interventricular septal + left ventricular posterior wall thickness was 25 +/- 3 mm in those with mild renal impairment, 28 +/- 6 mm in those with moderate renal impairment and 30 +/- 4 mm in those with severe renal impairment. The most severe left ventricular hypertrophy was seen in the Afro-Caribbean patients. Left ventricular hypertrophy was present even in those with marginally raised blood pressure and was related to age and serum creatinine but not to present blood pressure or duration of proteinuria.
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PMID:Cardiac hypertrophy in diabetic nephropathy: an echocardiographic study. 297 44


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