Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the frequency and examine the role of rhabdomyolysis in the acute renal failure in tetanus 18 patients with the diagnosis of generalized tetanus consecutively admitted to the infectious disease hospital were evaluated. Of these 14 were male and 4 female with mean age of 31.8 +/- 2.0 years. Except for mild proteinuria recorded in 9 patients, the urinalysis were unremarkable. Serum creatinine higher than 1.4mg/dl was recorded in 39% of the patients, abnormal levels of CPK in 87,5% and serum myoglobin greater than 120 micrograms/l in 39% of the patients. Oliguria was documented in one patient and none required dialysis therapy. No correlation was found between renal failure and myoglobin and/or CPK serum levels. Acute renal failure in tetanus was not infrequent; usually it was non-oliguric, mild and transient and not related to the severity of the disease or to serum levels of myoglobin and/or CPK.
 ...
PMID:Tetanus as a cause of acute renal failure: possible role of rhabdomyolysis. 811 81

Although hemolytic-uremic syndrome (HUS) is a clinico-pathological entity, renal biopsies are usually not indicated for diagnosis, and therefore, studies concerning the histological aspects of the syndrome are few. This study mainly describes the morphological characteristics of 15 tissue-diagnosed sporadic cases of HUS. The ages of the patients ranged between 10 mos. to 15 yrs., with five being under two. The male/female ratio was 2:3. The prodromal phase was present in 10 patients (67%) with gastrointestinal symptoms in four patients (27%) with neurological symptoms, and in three patients (20%) with upper respiratory infections. Five patients had HUS associated with diarrhea (D+) (three infants and two children), while the remaining ten patients (two infants and eight children) had no diarrhea (D-). E. coli was identified in the stool of four of the D+ cases, one of which was also associated with Shigella. The shortest clinical course was 14 days and the longest 55 days in 13 patients. The disease recurred after three months in one patient, and on three occasions in 15 months after onset of HUS in the other. Fourteen patients died and one biopsy-diagnosed case recovered after the acute phase. All patients had anemia (Hb 3.4-10 g/dl) and acute renal failure. Seven cases demonstrated Burr cells, eight cases had thrombocytopenia and six cases oliguria/anuria. Microscopic hematuria was detected in four cases and gross hematuria in two cases. All patients revealed proteinuria and azotemia (40-200 mg/dl). Five/five (100%) cases had decreased creatinine clearance, 12/14 (86%) cases had increased uric acid levels, 9/14 (64%) cases had an electrolyte imbalance. Light microscopy revealed microangiopathic type involvement of the glomeruli in all cases. According to additional findings, the cases were classed into three histological groups: type 1 showing cortical necrosis (3 cases), type 2 predominant glomerular and arteriolar involvement (11 cases) and type 3 predominant arterial involvement (1 case). All cases were considered primary HUS except for one which was associated with membranous glomerulonephritis. (D+) HUS cases were predominantly of the microangiopathic type, similar to the (D-) group; the latter being contrary to the literature. Hypertension was present in 67% of cases and there was no correlation found between the clinical duration of HUS and the histological type. All five patients studied immunohistologically revealed a nonspecific type fibrinogen deposition. Extra-renal microangiopathy was demonstrated in the adrenals, stomach, pancreas, liver and skin in two necropsies studied.
 ...
PMID:Hemolytic-uremic syndrome (HUS): a clinicopathological study of 15 cases. 823 14

The influence of acetylcysteine (ac-cys) on cisplatin (CP) nephrotoxicity was investigated in female Wistar rats. Administration of 0.6 mg CP 100 g-1 body wt. was followed by oliguria and proteinuria, as well as a significant increase of blood urea nitrogen concentration. The i.p. administration of 0.6 mg CP 100 g-1 body wt. concomitantly with 100 mg ac-cys 100 g-1 body wt. s.c. completely abolished the nephrotoxic effects of CP. However, following this, the Pt concentration in kidney was decreased significantly by ac-cys treatment. This was caused by the enhanced urinary excretion of Pt. The same effect on CP nephrotoxicity appeared when CP and ac-cys were dissolved together in solution prior to injection. It could be shown that in this solution a ligand exchange reaction of CP by ac-cys started immediately, resulting in increased renal excretion and decreased Pt concentration in kidney. From our results we concluded that the protective effect of ac-cys on CP nephrotoxicity is based on the formation of a complex unsuitable for tubular reabsorption.
 ...
PMID:Beneficial effect of acetylcysteine on cisplatin nephrotoxicity in rats. 832 88

The requirements for a diagnosis of Goodpasture's syndrome (GPS) include: (1) the presence of glomerulonephritis, (2) alveolar bleeding, and (3) the presence of anti-glomerular basement membrane (anti-GBM antibody). Among Japanese case, the 2 patients reported here were rare in that they satisfied all of these requirements. In case 1 (a 40-year-old male), the disease developed with initial signs of proteinuria and hematuria. The patient developed hemoptysis after hospitalization. The interval from onset to hospitalization was 38 days. The serum creatinine (CRN) level was 3.6 mg/dl on admission. The pathological findings were rated as full-circumferential, cellular crescentic nephritis, and the patient did not display oliguria. The renal and pulmonary impairments in this case were markedly improved by glucocorticoid (prednisolone PSL, 60 mg/day), cyclophosphamide therapy (50 mg/day) and plasma exchange (PE 10 times). In case 2 (a 58-year-old male), the initial signs developed as proteinuria and hematuria, followed by rapidly progressive renal functional deterioration and hemoptysis occurred. Compared to Case 1, the interval from onset to hospitalization was longer in Case 2 (125 days) and the CRN level was also higher (10.7 mg/dl). Case 2 was rated as full-circumferential, fibrous crescentic nephritis, and the patient was oliguric. Although the pulmonary impairment was reduced by pulse therapy and 10 PEs, recovery of renal function has not been achieved, still necessitating maintenance hemodialysis at present. In case 1, the disease relapsed at 4.5 years after remission, presenting with aggravated renal function and hemoptysis. In this case, low-dose PSL therapy had been discontinued at 3 months before the relapse.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Two cases of Goodpasture's syndrome--clinicopathological studies and relapse. 833 6

We have observed a transient renal insufficiency in newborns associated with ultrasonographic finding of hyperechoic renal pyramids. This condition rapidly resolves, coinciding with both normalization of the renal ultrasound and the occurrence of significant proteinuria. Others have recognized a similar state of oliguria and cylindruria associated with a prolonged nephrogram on intravenous urography in newborns. There is evidence to suggest that hyaline cast deposition within the collecting tubules may account for these imaging abnormalities. The precise events surrounding the protein deposition are unknown, and it may be either the cause or the result from the transient renal dysfunction. Our 2 cases add to the evidence that there is a distinct entity of acute renal dysfunction, with identifying characteristics, in neonates associated with a good prognosis and rapid resolution.
 ...
PMID:Transient acute renal failure in the neonate. 849 84

Aminophenols and halogenated anilines induce nephrotoxicity and mild hepatotoxicity in rats. In this study, the in vivo and in vitro nephrotoxic potential of 4-amino-2-chlorophenol and 2-amino-4-chlorophenol, monochlorinated aminophenols and potential metabolites of 3-chloroaniline, was evaluated. Hepatotoxicity of both compounds was also examined in vivo. Male Fischer 344 rats (four/group) were administered 4-amino-2-chlorophenol hydrochloride (0.4, 0.8 or 1.0 mmol/kg), 2-amino-4-chlorophenol hydrochloride (0.4, 0.8 or 1.2 mmol/kg) or vehicle intraperitoneally (i.p.) and renal and hepatic function monitored for 48 h. Administration of 4-amino-2-chlorophenol (0.8 mmol/kg) induced nephrotoxicity, while only minor changes in kidney function were observed following administration of 0.4 mmol/kg of 4-amino-2-chlorophenol or 0.8 mmol/kg of 2-amino-4-chlorophenol. Increasing the dose of 4-amino-2-chlorophenol to 1.0 mmol/kg or 2-amino-4-chlorophenol to 1.2 mmol/kg resulted in lethality. Nephrotoxicity induced by 4-amino-2-chlorophenol was characterized by diuresis, increased proteinuria, glucosuria, hematuria, elevated blood urea nitrogen (BUN) concentration and kidney weight, and marked proximal tubular damage, while 2-amino-4-chlorophenol induced milder effects on renal function and transient oliguria instead of diuresis. No hepatotoxicity was observed with either compound at any dose tested. In the in vitro studies, the direct effects of 4-amino-2-chlorophenol or 2-amino-4-chlorophenol on organic ion accumulation, pyruvate-stimulated gluconeogenesis and lactate dehydrogenase (LDH) leakage were determined using renal cortical slices. 4-Amino-2-chlorophenol and 2-amino-4-chlorophenol were almost equally effective in inhibiting organic anion or cation uptake and gluconeogenesis or increasing LDH leakage, although small differences in the minimum effective concentrations were present (minimum effective concentration, 0.01-0.5 mM range). These results demonstrate that 4-amino-2-chlorophenol is a more potent nephrotoxicant than 2-amino-4-chlorophenol in vivo. The results also indicate that the addition of a chloride group to aminophenols enhances renal toxicity.
 ...
PMID:Nephrotoxicity of 4-amino-2-chlorophenol and 2-amino-4-chlorophenol in the Fischer 344 rat. 865 59

We performed a computerized search on sulfadiazine-associated nephrotoxicity reported in human immunodefiency virus (HIV)-infected patients in the international literature. Including an original case report, we summarized 35 acquired immunodefiency syndrome (AIDS) patients from 1987 to 1995 in an analysis comparing their features to historical HIV-negative controls from the 1940s and 1950s. Likely due to a high prevalence of potential risk factors, incidence of sulfadiazine-associated renal impairment was 1.9%-7.5% in AIDS patients and 1%-4% in HIV-negative controls. Its occurrence appeared to be delayed in HIV-infected patients with a median of about 3 weeks of medication compared with about 10 days in HIV-negative subjects. Correspondingly, the cumulative sulfadiazine dose at manifestation doubled in AIDS patients with a median of 84 g versus 40 g in controls. Patients usually presented with flank or lumbar pain, oliguria, and (macro) hematuria. Urinalysis showed typical "sheaves of wheat" crystalluria, erythrozyturia, and, less commonly, leukozyturia and proteinuria. Echogenic (mostly peripelvic) densities, renal stones, and hydronephrosis are frequent findings on ultrasound examination, whereas X-ray examination possesses a low diagnostic sensitivity. The principle aim of therapy in these patients is to (re)institute the physicochemical urinary solubility of sulfadiazine and its metabolites. For this purpose, forced rehydration and, most importantly, urine alkalinization proved to be effective measures without an absolute need to withhold the drug. Provided prophylactic and therapeutic recommendations are complied with, outcome of this drug-related side effect is usually excellent, and rare relapses will similarly respond well.
 ...
PMID:Sulfadiazine-associated nephrotoxicity in patients with the acquired immunodeficiency syndrome. 869 59

We tested the hypothesis that enhanced intravascular coagulation in pregnancy could produce clinical symptoms similar to those of preeclampsia, such as hypertension, proteinuria, and edema. Having confirmed this, we then examined whether the pathological changes caused by intravascular coagulation could be suppressed by administration of antithrombin III (AT III), an endogenous inhibitor active to thrombin and factor X a. Intravascular coagulation was induced in Wistar rats on day 16-20 of pregnancy by 1-h arterial infusion of tissue thromboplastin (TP) through the left ventricle of the heart. One hour after the end of the infusion period, organ blood flows were measured by the radioactive ((57)Co-labeled) microsphere method, and fibrin deposition in organs was measured by radiolabeling with [(125)I] fibrinogen injected before TP infusion. Infusion of TP produced fibrin deposition in the kidney, lung, and liver, but not in the myometrium and placenta, as well as an 80% decrease in renal blood flow (RBF), with oliguria and proteinuria. TP also caused an increase in blood pressure (BP) accompanied by an increase in plasma renin activity (PRA), both of which were suppressed by bilateral nephrectomy before TP infusion. The prophylactic administration of AT III concentrates (60 or 300 U/kg intravenously (i.v.), followed by infusion of 30 or 150 U/kg/2 h, respectively) prevented all pathological changes in a dose-dependent manner. AT III increased placental blood flow regardless of the state of coagulation. These findings suggest that intravascular coagulation plays a significant part in the pathophysiology of preeclampsia and that AT III concentrates may have therapeutic potential in the treatment of this condition.
 ...
PMID:Antithrombin III prevents renal dysfunction and hypertension induced by enhanced intravascular coagulation in pregnant rats: pharmacological confirmation of the benefits of treatment with antithrombin III in preeclampsia. 885 41

Acute glomerulonephritis is a distinct clinical entity, more frequently found in younger age. We report 69 patients with AcGN (25 female and 44 male) mean age 26 years (range 15-58). The disease is clinically characterized with hypertension (57%), edema (59%) and oliguria (35%). Urine analysis showed microhaematuria/proteinuria (36%) and micro/macrohaematuria alone in 89%, while azothaemia was observed in 16% pts, and decreased serum complement levels in one third of patients, more often decrease of C3 (33%) than C4 (15%). Initial infection of the upper respiratory tract was seen in 65%, pneumonia in 8%. In 25% of pts. there were no data of previous infection. Cultures of pharyngeal smear revealed. Streptococcus only in 2 pts. Elevated AST titer was found in 32% pts. Eleven kidney biopsies were made, and histological examination showed 2 normal findings, 6 mesangioproliferative GH, 2 endocapillary GN and 1 membranoproliferative GN. Follow ups have showed urinary abnormalities in 25% of pts., without developing renal failure.
 ...
PMID:[Clinical and morphologic features in patients with acute nephritis syndrome]. 910 32

The therapeutic effects of angiotensin converting enzyme inhibitor, lisinopril, on puromycin aminonucleoside (PAN)-induced nephrosis were investigated using unilaterally nephrectomized rats. Lisinopril showed potent dual effects on PAN nephrosis. Lisinopril treatment (50 mg/l in drinking water) from day 5 or day 9 reduced urinary protein excretion and suppressed the development of glomerular sclerosis at 8 weeks after PAN injection (150 mg/kg, i.p.), indicating a therapeutic effect on the nephrosis. Recovery of decreased anionic charge sites on the glomerular basement membrane was involved, at least in part, in the therapeutic action of lisinopril against proteinuria. On the other hand, oliguria and progressive azotemia derived from continuous deterioration of the renal function was induced if the treatment of lisinopril was started on the same day as PAN injection. The renal dysfunction induced by simultaneous administration of lisinopril with PAN could be abolished by combination dosing with sarcosine, an angiotensin II (AII)-receptor agonist. These results indicate that lisinopril treatment attenuates proteinuria by ameliorating the anionic charge barrier on the glomerular basement membrane and that it also protects against the development of chronic renal disease with segmental glomerular sclerosis, although AII depletion during the acute nephrotic stage exacerbates the renal damage in PAN nephrosis of unilaterally nephrectomized rats.
 ...
PMID:Dual effects of lisinopril on puromycin aminonucleoside nephrosis in unilaterally nephrectomized rats. 916 71


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>