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 retrospective study was conducted to determine the clinicopathological correlation of focal glomerulosclerosis in 36 adult patients with idiopathic nephrotic syndrome. All cases were divided into two groups, focal segmental glomerulosclerosis (FSGS, 23 cases) and focal global glomerulosclerosis (FGBG, 13 cases), on the basis of pathological findings. Most patients with FSGS were non-responsive/partial-responsive (22/22) to the corticosteroid treatment. By contrast, those with FGBG gave a relatively high responsive rate of 7/12 to the same therapy. The 5 non-responders with FGBG, however, were noted to have intensive interstitial fibrosis/mononuclear cell infiltrate of the renal lesions (4 cases), or diffusely glomerular Clq deposition without other coexisting immune deposits (1 case). Most cases of FSGS (20/23) became steroid dependent or remained heavy proteinuria resistant to corticosteroids/other immunosuppressive agents over a mean of 3.4 (ranged, 1 to 7) years after renal biopsy. Three of the 5 patients of FGBG initially non-responsive/partial-responsive to corticosteroids turned out to have protein-free urine (less than 4 mg/hr/m2) (2 patients) 1 month after leaving the hospital and became mildly proteinuric (1 patient) two months after discharge, respectively. The remainders of FGBG (10/13) were free of protein in their urine sample or had occasional episodes of proteinuria over a mean duration of 4.1 (ranged, 1 to 7) years. In addition, chronic renal insufficiency on discharge was noted in 2 cases of FSGS (2/23) and 1 case of FGBG (1/13). Only two cases of FSGS (2/23) progressed into a uremic status 3 and 5 years, respectively, after the time of the presumed clinical onset of their disease. These findings suggest that FGBG clinically behaves similar to a minimal change disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Focal glomerulosclerosis: a clinico-pathological analysis of 36 adult patients with idiopathic nephrotic syndrome. 217 56

The objective of the work was to evaluate the basic parameters of zinc metabolism, i.e. serum levels and urinary excretion of zinc (Zn) in insulin dependent diabetes. The authors investigated a group of diabetics with normal renal function (DM) and with chronic renal insufficiency as a result of diabetic nephropathy (RIDM). Two control groups were formed by healthy volunteers (C) and non-diabetic subjects with chronic renal insufficiency (RI). In diabetics without impaired renal functions (DM) the Zn serum levels did not differ significantly from controls, urinary excretion was significantly raised. The authors did not reveal a correlation of serum Zn levels with parameters of compensation of diabetes nor with the insulin dose. Urinary Zn output correlated positively with proteinuria and the average blood sugar level during the collection of urine. The authors did not find a correlation with diuresis, fractional water excretion, glycosuria or urea excretion. The fractional Zn clearance in diabetic subjects was significantly raised and correlated with the mean blood sugar level. This finding suggests a decline of the tubular Zn absorption in hyperglycaemia. In diabetics with renal failure (RIDM) the results did not differ from non-diabetics with the same degree of renal insufficiency: serum Zn levels were, as compared with healthy controls, in both groups significantly reduced, the urinary excretion being normal. Thus insulin dependent diabetes nor its metabolic compensation do not influence in a marked way serum Zn levels but lead to higher urinary Zn losses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum levels and urinary excretion of zinc in patients with insulin-dependent diabetes]. 220 24

A spectrum of renal abnormalities has been described in patients infected with the human immunodeficiency virus (HIV) with or without signs of the acquired immunodeficiency syndrome (AIDS). In particular, attention has been focused on a nephropathy characterized clinically by nephrotic proteinuria and rapidly advancing renal insufficiency, and histologically by focal and segmental glomerulosclerosis (FSGS). To evaluate the relationship between HIV infection and structural renal disease, we reviewed all consultations between January 1982 and March 1988 to the Division of Nephrology at San Francisco General Hospital (SFGH), a municipal hospital treating approximately one-third of AIDS cases in San Francisco. Seventy-three consultation requests were received during this period regarding patients with AIDS (48), AIDS-Related Complex (23), or asymptomatic HIV infection (2). Of these, 27 gave evidence of structural renal disease (Group I): 14 had chronic renal insufficiency, in 10 of whom nephrotic proteinuria was also present. However, progression of renal insufficiency to end-stage renal disease (ESRD) in this group did not follow the rapid course described for HIV-associated nephropathy. Renal tissue was examined in 11 Group I patients and showed FSGS in four and a variety of acute and chronic glomerular and tubulointerstitial changes in the others. In 46 Group II patients, consultation was requested for acute renal failure or fluid, electrolyte, and acid-base disturbances. We also reviewed 91 consecutive autopsies performed in patients dying with AIDS at SFGH between 1981 and 1986.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal involvement in patients infected with HIV: experience at San Francisco General Hospital. 234 28

To define normal limits for serum creatinine levels, as well as to explore the relationship between age and the prevalence and severity of renal disease in patients with sickle cell anemia (SCA), we retrospectively analyzed renal function parameters in 368 patients followed in our SCA clinic. Dipstick proteinuria was present in 78 patients (20.6%). Chronic renal insufficiency (CRI) was present in 17 patients (4.6%) and showed a high degree of association with proteinuria and increased age. In patients with CRI, the severity of renal dysfunction was also age-related. In the 284 patients without proteinuria or CRI, mean serum creatinine levels were lower than predicted. We conclude that in patients with SCA, serum creatinine levels at the upper limit of normal should be regarded with suspicion, and that the prevalence and severity of proteinuria and CRI in SCA is high and increases with age.
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PMID:A population study of renal function in sickle cell anemia. 237 52

In five patients suffering from recurrent thrombosis and/or fetal death, a lupus anticoagulant was associated with a renal vasculopathy. Ischaemic episodes also involved the skin, heart, eyes and/or central nervous system. All patients were hypertensive. Two had renal insufficiency, two had non-nephrotic proteinuria, and in the last patient renal cortical ischaemia was detected by a tomographic scan in the absence of proteinuria. Renal biopsy showed thrombosis and/or intimal fibrosis of intrarenal vessels, and normal or ischaemic glomeruli without proliferative lesions. High-titres of anticardiolipin antibodies were found in 3 of 3 cases, and persisted after steroid therapy even if the circulating anticoagulant factor disappeared. All patients received corticosteroid therapy, alone or in combination with immunosuppressive drugs; two patients had prolonged oral anticoagulation, but thrombotic episodes recurred after stopping the drug. One patient died; the remaining four survived 18 months to 11 years after diagnosis, with stable chronic renal insufficiency in one of them. These results show that a lupus anticoagulant may be associated with prominent renal vascular disease, in the absence of proliferative glomerular lesions, and suggest that continuous anticoagulation may be beneficial in these patients.
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PMID:Recurrent thrombosis and renal vascular disease in patients with a lupus anticoagulant. 251 88

Spontaneous nephrotic mice (ICGN mice), a new mutant strain of mouse from outbred ICR, were clinically, macroscopically, histologically and immunohistochemically studied to establish their value as a model for human nephrotic syndrome. Most of the affected mice developed proteinuria, hypoproteinaemia and hypercholesterolaemia, and some of them developed systemic oedema. A high concentration of blood urea nitrogen (BUN) and a low haematocrit value were also observed. The kidneys of severe cases showed a decrease in size and had a yellowish granular surface. These findings indicated that the mice were terminally affected by chronic renal insufficiency. Histopathology demonstrated glomerular lesions consisting of thickened basement membranes of the capillary loops with irregular spike-like protrusions and enlargement of the mesangium unaccompanied by cellular proliferation. The immunofluorescence technique revealed positive granular staining for IgA, IgG and IgM and to a lesser extent for C3 along the capillary loops in affected mice. The similarity between this spontaneous disease and human nephrotic syndrome caused by idiopathic glomerular lesions is discussed. ICGN mice may be a useful animal model for this human disease.
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PMID:Characteristics of mutant mice (ICGN) with spontaneous renal lesions: a new model for human nephrotic syndrome. 252 1

The clinical features and long-term outcome of 91 cases of adult-onset PSGN in Hong Kong were reported. There were 46 male and 45 female with age ranging from 13 to 56 yrs (mean 18.6). The diagnosis was based on clinical manifestations and renal biopsy was performed in 29 cases. The main manifestations were acute nephritic syndrome (72.5%) and acute nephritic-nephrotic syndrome (27.5%). Serum creatinine was increased in 48.4% of the patients at presentation. Four cases presented with acute renal failure. Serial serum C3 levels were determined in 48 patients. It was decreased in all patients at presentation but returned to normal within 15 weeks. The follow-up duration of this series ranged from I to 19 yrs (mean 4.73 yr) 67.03% recovered early (within 3 mts); 14.29% recovered later (from 6 mts to 7 yrs): 16.48% had persistent or intermittent proteinuria and or haematuria. Two cases developed chronic renal insufficiency. Our results suggested that the prognosis of PSGN in adults is relatively good and the indications for renal biopsy in adult-onset PSGN were discussed.
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PMID:[Clinical features and long-term outcome of 91 cases of adult onset post-streptococcal glomerulonephritis in Hong Kong]. 259 33

Antihypertensive drugs have disparate effects on renal haemodynamics, tubular function, plasma electrolytes, and hormonal responses. Calcium entry blockers and angiotensin-converting enzyme (ACE) inhibitors are unique in that they may increase glomerular filtration rate (GFR) and renal blood flow in patients with hypertension. Both classes of drugs are distinctive in that they prevent salt retention because of their inhibitory effect on tubular sodium reabsorption. In addition to these attributes, which are desirable in terms of lowering systemic blood pressure, these 2 classes of drugs exert important intrarenal effects which may participate in limiting the progression of renal disease. ACE inhibitors have been shown to protect against the development of glomerulosclerosis in various experimental models of renal insufficiency. Importantly, there is emerging evidence from human studies supporting a distinctive beneficial effect of these agents on renal function in patients with hypertension, mild chronic renal insufficiency and diabetes mellitus. Calcium entry blockers have also been shown to exert some beneficial effect in limiting the progression of experimental kidney disease but neither an improvement in glomerular sclerosis nor a decrease in proteinuria have been clearly documented. At present ACE inhibitors appear the most attractive agents in terms of arresting the progression of renal disease. Acute deterioration in renal function may occur following the administration of ACE inhibitors, calcium entry blockers, and beta-blockers. This complication should be considered in every patient on antihypertensive therapy who suffers an unexplained deterioration in renal function. In particular, the sudden deterioration in renal function following initiation of therapy with an ACE inhibitor is a clue to the possible presence of bilateral renal artery stenosis or stenosis of a solitary functioning kidney. Renal damage may also occur in patients with unilateral renal artery stenosis even though total (2-kidney) GFR may not be appreciably reduced. In this setting, a captopril renal scan with hippuran and diethylenetriamine pentaacetic acid (DTPA) provides physiological information regarding the renal blood flow and GFR of each kidney. In patients with unilateral renal artery stenosis the impact of ACE inhibitor therapy on GFR may be discerned by the use of the DTPA scan, which may demonstrate a reduction in GFR in the stenotic kidney that is not apparent by evaluation of total kidney GFR. This suggests that despite adequate control of systemic blood pressure and unchanged plasma creatinine progressive kidney damage in the stenotic kidney ensues.
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PMID:Renal effects of antihypertensive drugs. 266 38

Low-protein diets in nondiabetic renal failure may slow the progressive loss of renal function in some patients, but few studies have detailed the nutritional consequences of these diets in patients with diabetic nephropathy. We studied 7 patients with insulin-dependent diabetes mellitus and chronic renal insufficiency [mean +/- SEM creatinine clearance (S, U): 28.3 +/- 6.5 ml/min (0.47 +/- 0.11 ml/s x 1.73/A)] for 15 weeks who were prescribed a diet of 0.6 g protein/kg ideal body weight. Midarm muscle circumference (24.1 +/- 1.8 at onset vs. 24.5 +/- 1.5 cm at completion), triceps skinfold thickness (21.6 +/- 3.1 vs. 21.0 +/- 1.5 mm), body weight (71.8 +/- 4.1 vs. 71.2 +/- 4.6 kg), and serum albumin [3.0 +/- 0.1 vs. 3.2 +/- 0.1 g/dl (30 +/- 1 vs. 32 +/- 1 g/l)] remained stable. Based on urinary nitrogen excretion, diet diaries overestimated the degree of dietary protein restriction; there was good adherence to the diet as evidenced by a reduction in urinary urea nitrogen (average 32%). Blood glucose control was maintained despite increased carbohydrate intake. On average, creatinine clearance did not change significantly, but proteinuria diminished slightly (1.8 +/- 0.2 vs. 1.5 +/- 0.6 g/day). These results indicate that 0.6 g/kg/day protein diets did not cause protein depletion in insulin-dependent diabetic patients. Longer-term studies are indicated to assess more fully the efficacy of these dietary regimens in reducing proteinuria or benefiting diabetic nephropathy.
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PMID:Protein-restricted diets in diabetic nephropathy. 271 Feb 67

The antihypertensive efficacy and renal effects of enalapril maleate therapy were evaluated in 13 hypertensive patients with chronic renal failure. Enalapril was administered as follows: alone; added to furosemide, clonidine hydrochloride, or atenolol; or in combination with any of the aforementioned drugs. Three patients did not complete the study; uncontrolled hypertension was the cause in two of these patients. In the remaining ten patients, short-term (mean +/- SD, 63 +/- 9 days) enalapril maleate therapy decreased the patient's seated blood pressure from 161/98 +/- 19/8 to 130/80 +/- 13/7 mm Hg. Furosemide was administered to eight patients; the dose of concomitant sympatholytic therapy was decreased in five of five patients. Serum potassium concentration increased from 4.1 +/- 0.3 to 4.5 +/- 0.3 mmol/L. Levels of urinary total protein excretion decreased from 2.23 +/- 2.05 to 1.08 +/- 1.45 g/d. Renal function (creatinine clearance, 0.58 +/- 0.21 mL/s) did not change from baseline. During long-term therapy, the rate of progression of renal insufficiency seemed to slacken in three of four patients with diabetic nephropathy. Thus enalapril can reduce blood pressure and proteinuria in hypertensive patients with chronic renal insufficiency. The possibility that enalapril can slow the progression of diabetic nephropathy remains to be confirmed by future studies.
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PMID:Efficacy and renal effects of enalapril therapy for hypertensive patients with chronic renal insufficiency. 284 67


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