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)

Blood volume and whole kidney and single nephron function were evaluated 2 and 10 days after nephrotoxic serum nephritis (NSN) induction in Wistar rats. Progressive proteinuria, hypervolemia and edema were observed in NSN rats. Sodium retention was associated with a progressive depression of single nephron glomerular filtration rate and elevated fractional tubular reabsorption rates. Since hypervolemia rather than hypovolemia was observed in this study, edema formation must have been a consequence of intrarenal rather than extrarenal phenomena.
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PMID:Progressive hypervolemia despite hypoproteinemia and massive edema formation in rats with nephrotoxic serum nephritis. 169 61

In 7 years (1981-1988) at the Kenyatta National Hospital (KNH), Nairobi the diagnosis of systemic lupus erythematosus (SLE) was made in 67 patients. In 23 of these patients lupus nephritis complicated the SLE. Lupus nephritis was diagnosed through renal biopsy, haematuria and proteinuria in urine with positive lupus erythematosus (LE) cell phenomenon. The histology found in these patients included 5 patients with minimal lesion, 7 patients with membranous, 3 with focal, 4 with diffuse, 3 with crescenteric and one with membranoproliferative glomerulonephritis. While patients with minimal, membranous and focal nephritis had general good outlook on low dose maintenance or intermittent high dose steroid therapy the others with diffuse, crescenteric and membranoproliferative nephritis had poor prognosis. Patients with diffuse proliferative, membranoproliferative and crescenteric nephritis tended to have septicaemia, pulmonary oedema, fluid overload and chronic renal failure with poor prognosis. These patients responded poorly to oral and parenteral steroid therapy whether high or low dose.
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PMID:Management of lupus nephritis at the Kenyatta National Hospital. 227 66

The patients suffering from hypertonic nephritis were examined for renal hemodynamics, the activity of the renin-angiotensin-aldosterone system (RAAS), excretion of PGE2 and PGF2 alpha, and for a number of the parameters of water-electrolyte homeostasis. In A series, the patients suffering from latent and hypertonic nephritis (n = 11 in each group) were compared. In B series, two groups of the patients (n = 13 in each group) suffering from hypertonic nephritis associated with moderate or grave arterial hypertension were compared. The patients under comparison belonging to A and B series did not differ as regards the sex, age, nephritis standing, serum creatinine or proteinuria. As compared with the patients suffering from latent nephritis (A series), the patients with hypertonic nephritis showed a lower effective renal plasma flow, a greater resistance of the renal vessels, lesser PGE2 secretion, and a higher serum sodium concentration. As compared with the patients suffering from moderate hypertension (B series), the patients with associated hypertonic nephritis and grave hypertension demonstrated a higher resistance of the renal vessels, a higher activity of plasma renin, a larger concentration of plasma aldosterone and its excretion with urine, as well as a greater volume of the circulating blood. It is assumed that the development of arterial hypertension associated with hypertonic nephritis may be caused by renal hemodynamics deterioration, by relative activation of the renin-angiotensin system, inhibition of the depressor prostaglandin system and sodium retention. The progression of hypertension may be related to further deterioration of renal hemodynamics attended by RAAS activation and hypervolemia.
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PMID:[Mechanisms of the development of arterial hypertension in hypertonic nephritis]. 279 11

Colloid volume expansion magnifies proteinuria in subjects with the nephrotic syndrome. To elucidate this phenomenon, we performed differential solute clearances prior to and following infusion of hyperoncotic albumin in 21 nephrotic subjects and seven healthy controls. Urinary excretion rate and fractional clearance of albumin (radius = 36 A) and immunoglobulin G (radius = 55 A) increased significantly in nephrotic subjects. However, urinary albumin excretion rate was unchanged in controls. The fractional clearances of dextrans of broad size distribution (radii = 28 to 58 A) were markedly altered in both groups following albumin infusion. A heteroporous model which depicts the major portion of the glomerular capillary wall as an isoporous membrane (pore radius approximately 55 A) and the minor portion as a non-discriminatory shunt, revealed the latter to be much more prominent in nephrotic subjects than in controls, and to be enlarged further following albumin infusion. By contrast no increase in pore size of the non-shunt pathway occurred in either group. We infer that enhancement of a pre-existing defect of glomerular size-selectivity in nephrotic subjects accounts, in large part, for exaggerated proteinuria in the colloid volume-expanded state. Increases in glomerular perfusion rate and pressure associated with plasma hypervolemia may mediate this alteration in glomerular membrane-pore structure.
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PMID:Effect of colloid volume expansion on glomerular barrier size-selectivity in humans. 371 75

The authors present a contemporary picture of the pathogenesis and clinical course of diabetic nephropathy in type I diabetics describing the stages of the disease and the possible evidence for reversibility of the kidney damage with tight metabolic control. During the so-called latency period, which is clinically non-detectable, the predominant functional abnormalities (increase in GFR with sub-clinical glomerular proteinuria) can be corrected by strict control although there is no evidence for the regression of the associated anatomical changes such as the enlarged filtration area. As for the described increase in thickness of the glomerular basement membrane, from experimental data and pancreatic transplants in man, delay in its development and to some extent regression of the glomerular lesions can be expected. The problem of how the renal lesions in experimental diabetes mirror the changes in the human kidney is discussed. During the symptomatic period, with intermittent and subsequently constant proteinuria and progressive decline in renal function, which are observed in only about 30% of type I diabetics, the role of arterial hypertension and its effective control is emphasized. Finally, the renal failure period is indicative of irreversible damage to the kidneys. The progression from its early to its late stages is variable between different patients but each individual patient shows a constant rate of deterioration. The evidence for the efficacy of medical treatment in slowing down its progression is very limited at present but much can be done to improve the quality of life by dietary measures, treatment of fluid overload and hypertension. When the end-stage diabetic kidney disease is reached, with serum creatinine above 8 mg/dl, renal transplantation from a living donor offers a good chance for a relatively acceptable quality of life for years. In conclusion, it is stressed that the morbidity of diabetic nephropathy could eventually be reduced through effective control of the metabolic abnormalities of diabetes with the methods presently available.
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PMID:The natural history of diabetic nephropathy in type I diabetes and the role of metabolic control in its prevention, reversibility and clinical course. 634 25

During an epidemic of acute glomerulonephritis (AGN) 15 patients were studied by M-mode, cross-sectional, and Doppler echocardiography. All 15 patients had the classical signs of the disease including hematuria, proteinuria, edema, and consistent laboratory findings. There were 10 boys and five girls with a mean age of 8 years. Ten of the 15 patients had an enlarged left atrium and five of these 10 also had transient mild to moderate mitral regurgitation. In the five patients with mitral regurgitation the ratio of left atrium/aorta was 1.48; in the five patients with an enlarged left atria without evidence of mitral regurgitation the left atrium/aorta ratio was 1.34. All the patients had normal left ventricular dimensions, as well as ejection and shortening fractions. The findings of left atrial enlargement and mitral regurgitation disappeared gradually in all patients within 3 months. There was no correlation between the level of systemic blood pressure and the development of mitral regurgitation. A possible cause for these changes is fluid overload in the oliguric phase of the acute glomerulonephritis. The changes are transient and probably functional. There was no significant mitral valve or left atrial anomaly 3 and 6 months after hospital discharge.
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PMID:Transient mitral regurgitation in acute glomerulonephritis. 846 37

Using a new bivariate vectorial approach to the standard bioimpedance analysis (tetrapolar, 50-kHz frequency), we evaluated the performance of a graphical method for the identification of patients with fluid overload. Two hundred and seventeen adult Caucasian subjects were divided into four classification groups: 86 healthy control subjects, 55 patients with mild-to-terminal chronic renal failure in conservative treatment (15% with apparent edema), 36 patients with idiopathic nephrotic proteinuria (58% with apparent edema), and 40 obese subjects. We found a bioimpedance threshold for apparent edema on the lower pole of the sex-specific 75% tolerance ellipse (bivariate tolerance interval) of the healthy population. This innovative graphical method allows identification, monitoring and therapy planning of patients with fluid overload using direct bioimpedance measurements without any assumption on body composition.
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PMID:Body fluid overload and bioelectrical impedance analysis in renal patients. 867 31

Ambulatory blood pressure (BP) measurement has added a new dimension to the evaluation of abnormal BP in patients with various stages of renal disease. Although there is not complete consensus concerning the definition of normal values, a high prevalence of an abnormal circadian BP profile is noted in patients with essential hypertension with renal involvement (ie, microalbuminuria), in diabetic patients (particularly those with microalbuminuria or overt proteinuria), and in patients with primary chronic renal disease. Studies in diabetic patients point to an important role of both hypervolemia and disturbed autonomic innervation in the genesis of an abnormal circadian BP profile. In both patients with diabetic renal disease and patients with nondiabetic renal disease, retrospective studies suggest that an abnormal nocturnal decline in BP is associated with more rapid progression independent of 24-hour mean arterial pressure. The abnormal circadian BP profile persists in dialyzed patients, is ameliorated by long and frequent dialysis sessions, but is not completely normalized after successful renal transplantation.
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PMID:Circadian rhythm of blood pressure in renal disease. 1099 26

Thrombotic thrombocytopenic purpura and adult hemolytic-uremic syndrome (TTP/HUS) have a substantial mortality rate even with currently available treatments. Although therapeutic plasma exchange is the recommended treatment of TTP/HUS, this cumbersome procedure may not be available for all patients in an emergency. In this context, plasma infusion may represent an alternative first-line therapy. We compared the effectiveness of high-dose plasma infusion (25-30 mL/kg per day) and therapeutic plasma exchange as first-line treatment of adult TTP/HUS at a single center. Two groups of patients with TTP/HUS were identified according to their initial therapy, that is, high-dose plasma infusion (19 patients) and therapeutic plasma exchange (18 patients). Clinical charts and outcomes were retrospectively analyzed. Endpoints for comparison were the duration of platelet counts below 150 x 10 /L and LDH levels above normal values; the volumes of plasma administered and the duration of treatment; complete remission, relapse, and mortality rates; and treatment-related complications. Patients of the 2 groups had comparable clinical and laboratory features on admission. Sixteen patients achieved complete remission in each group. Median times to recovery of platelet counts and LDH levels were comparable between the 2 groups. Eight patients in the high-dose plasma infusion (HD-PI) group were switched to therapeutic plasma exchange because of fluid overload (6 patients), persistent biologic disturbances (1 patient), or unresponsiveness to high-dose plasma infusion treatment (1 patient). This latter patient had severe TTP/HUS that remained refractory to therapeutic plasma exchange and vincristine, and rapidly died. All 7 remaining patients achieved complete remission with therapeutic plasma exchange. Four patients in the HD-PI group and 3 patients in the therapeutic plasma exchange (TPE) group died. In the HD-PI group, 5 patients experienced a transient nephrotic-range proteinuria during treatment. Main complications in the TPE group were collapse (1 patient) and central venous catheter infection (2 patients) or thrombosis (1 patient). Three patients in each group relapsed. High-dose plasma infusion may be an efficient treatment of TTP/HUS in patients who cannot have early plasma exchange. However, the large volumes of plasma required to reach complete remission may result in fluid overload, which may necessitate subsequent therapeutic plasma exchange.
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PMID:High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome. 1254 8

Blood pressure, together with proteinuria, represents one of the most important factors in the progression of chronic renal failure (CRF). Antihypertensive therapy is beneficial to slow down the progression of a variety of chronic renal diseases, no matter what the cause. Intraglomerular hypertension, increased glomerular permeability and proteinuria should be identified, since they can be treated to prevent or minimize further glomerular injury. But not all antihypertensive drugs are equally effective to prevent the progression of CRF. Recent large trials indicate that blood pressure lowering obtained by intervention in the renin-angiotensin-aldosterone system (RAAS) has an additive renoprotective effect in diabetic and nondiabetic renal diseases. In nondiabetic patients, the AIPRI and REIN studies support that angiotensin-converting enzyme (ACE) inhibitors have a long-term renoprotective effect. The benefits of ACE inhibitors can be demonstrated even in patients who are not hypertensive. Angiotensin II receptor antagonists are shown to be renoprotective in type 2 diabetics (RENAAL and IDNT). However, whether these renoprotective effects are due to blood pressure reduction or due to the specific pharmacologic RAAS blockade is still a matter of debate. This discussion is still open, because the reduction in blood pressure levels was lower in patients treated with a drug that interferes with the RAAS compared with other antihypertensive regimens. It is concluded that both ACE inhibitors and AT II receptor antagonists are lowering the intraglomerular pressure independent of any change in systemic blood pressure by dilatation of the efferent arteriole of the glomerulus. These additional nonpressure-related effects may protect renal function by their antiproteinuric effect. In addition, beneficial effect of ACE inhibitors are related to reduction of AT II, which has potent proinflammatory effects independent of its hemodynamic influences. Other drugs, such as diuretics, beta blockers, and hydralazine, do not induce efferent dilatation and, therefore, may be less likely to reverse intraglomerular hypertension. For example, hydralazine and nifedipine appear to produce prominent afferent or preglomerular arteriolar dilatation. This will allow more of the systemic pressure to be transmitted to the glomerulus. Therefore, short-acting dihydropyridine calcium channel blockers (CCB) are not recommended. By comparison, long-acting dihydropyridines such as diltiazem and verapamil are less potent vasodilators and may primarily decrease the resistance of the efferent arteriole, similar to the ACE inhibitors. They may have an antiproteinuric activity. Yet, there is lack of large prospective randomized trials.A beta blocker as antihypertensive agent is indicated as second- or third-line drug especially in patients with additional cardiovascular disease. Other antihypertensive drugs can be added as necessary to achieve the treatment goals for arterial hypertension. The use of a diuretic will often be helpful in patients who already have renal insufficiency, since fluid overload is an important cause of hypertension and may also enhance the effectiveness of drugs that interfere with the RAAS. alpha(1)-receptor or sympathetic blockers are further possible drugs for combination antihypertensive therapy.
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PMID:[Are all antihypertensive drugs renoprotective?]. 1516 50


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