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)

Pregnancy-induced hypertension is a disorder of unknown etiology unique to pregnant women. Classic clinical manifestations include hypertension, proteinuria, and edema. Early recognition and proper management of this disease may serve to avoid serious maternal complications. Ultimate maternal treatment depends on delivery of the fetus and placenta. Advanced stages of this disease result in multi-organ system dysfunction that may be life-threatening to the mother and her fetus. Such maternal complications of PIH include severe hypertension, oliguria or anuria, HELLP syndrome, eclamptic seizures, liver rupture, pulmonary edema, cerebral edema, and abruptio placentae. A multidisciplinary approach of the critical care team often will effect a reduction in maternal morbidity and mortality.
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PMID:Management of severe preeclampsia and eclampsia. 174 3

To document the clinical presentation of malignant accelerated hypertension in Nigerians, 56 patients were studied between 1987 and 1989 (30 months). Age range was 16 to 55 years with 59% in the range of 30-49 years; 47 were male. Mean systolic and diastolic blood pressures were 217 mmHg and 146 mmHg, respectively. Thirty patients had grade III and 26 grade IV hypertensive retinopathy. Mean body mass index was only 22.4 in the 21 patients who had no evidence of fluid retention. Seventy-five percent of patients had no awareness of hypertension. Essential hypertension accounted for 66%, chronic renal disease 32% and renal artery stenosis 2% of cases. The most common clinical features were headaches (80%), fatigue (68%), oliguria (52%), heart failure (46%), weight loss (41%), and poor vision (21%). Multiple symptoms were common and 24 patients had both renal and cardiac failure. Laboratory features included microscopic haematuria (100%) and proteinuria (100%). In 37 patients with essential hypertension, renal failure was a complication in 60%. Microangiopathic haemolytic anaemia was present in 23 patients. In addition to eight deaths from renal failure in the acute stage, 23 of these patients required long-term dialysis. Thus, malignant accelerated hypertension was associated with high morbidity, especially renal failure; it primarily afflicted patients in their prime years. Known survival at one year was 37.5%, but some patients were lost to follow-up.
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PMID:The clinical presentation of malignant hypertension in Nigerians. 195 31

We present two patients with Hantaan virus infection, admitted to the Department of Nephrology, Skopje, at the same time, with the same clinical presentation (chills, fever, abdominal pain, hemorrhages, nausea, headache, proteinuria, hematuria, oliguria, acute renal failure) but with different pathohistological findings and different disease courses. In the first case diffuse proliferative glomerulonephritis was found, with a complete recovery of renal function after a month, with a mild proteinuria and erythruria during the second and the third month. In the second case, glomeruli were normal in general, with slight mesangial proliferation found in two out of twenty, but interstitial edema, lymphocyte infiltrations and tubular changes were noted. Complete recovery was not noted after 3 months of follow-up. The patient is now without hemodialysis treatment, with polyuria, in the stable phase of chronic renal failure which is not improving.
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PMID:Different pathohistological presentations of acute renal involvement in Hantaan virus infection: report of two cases. 198 98

We examined 61 patients an average of 9.6 years (range 5 to 18 years) after an episode of childhood hemolytic-uremic syndrome. Twenty-four (39%) had one or more abnormalities. Seven (11%) had proteinuria and six (10%) had low creatinine clearance as solitary abnormalities. Eight (13%) had both proteinuria and reduced creatinine clearance; three (5%) had a combination of hypertension, proteinuria, and low creatinine clearance. Abnormalities sometimes appeared after an interval of apparent recovery. Logistic regression analysis showed that duration of anuria was the best predictor of disease at follow-up. No patients who had anuria lasting longer than 8 days or oliguria exceeding 15 days escaped chronic disease. However, 45% of those with disease had no anuria, and a third had no oliguria. Physicians should therefore be cautious in assuming recovery from HUS on the basis of a single evaluation and should periodically evaluate patients for an extended period.
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PMID:Long-term outcome and prognostic indicators in the hemolytic-uremic syndrome. 194 99

N,N'-Dimethylaminopropionitrile (DMAPN), a major component of the NIAX catalyst ESN, is known to cause urinary bladder dysfunction in exposed workers. In order to investigate the mechanism of DMAPN toxicity, we carried out time-course (0-72 h) and dose-response (175-700 mg/kg) studies on the effects of DMAPN in rats and mice. Treated animals exhibited several signs of toxicity including loss of body weight, reduced water consumption, and bladder urine retention, as well as bladder injury. DMAPN-induced bladder injury was characterized by distended bladders with marked diffuse submucosal and subserosal edema, petechial hemorrhage, and multifocal perivascular inflammatory infiltrates. The qualitative and quantitative analysis of urine indicated hypoosmolality, aciduria, hematuria, proteinuria, and oliguria. Elevated levels of creatinine and urea levels in plasma were indicative of renal dysfunction. Within hours following DMAPN administration, the animals exhibited a significant increase in urinary retention that resolved between 60 and 72 h. Rats excreted about 44% of the administered DMAPN dose unchanged in the urine, while mice excreted only about 6% of the dose. Commercially available DMAPN metabolites, administered by gavage, produced toxic effects less adverse than DMAPN. The biochemical effects of DMAPN included depletion of glutathione and increased lipid peroxidation in target organs, including urinary bladder and kidney. These studies indicate that there are species differences in DMAPN toxicity. The differences may be due to differences in the formation of reactive metabolic intermediates of DMAPN.
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PMID:Studies on the mechanism of urotoxic effects of N,N'-dimethylaminopropionitrile in rats and mice. 1. Biochemical and morphologic characterization of the injury and its relationship to metabolism. 203 40

Persistent microscopic hematuria in children is most often benign or untreatable. The evaluation of microscopic hematuria in an otherwise healthy child need not require invasive and costly laboratory studies. The initial evaluation must look for signs of life-threatening causes of hematuria, i.e., hypertension, edema, oliguria, or significant proteinuria. If these are absent, a stepwise evaluation is suggested, which includes microscopic examination of the urine for red blood cell casts, a test for proteinuria, serum creatinine, and serial follow-up. Renal biopsy may establish a diagnosis but rarely changes the treatment in a child with asymptomatic isolated microscopic hematuria.
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PMID:An approach to the evaluation and treatment of microscopic hematuria. 204 40

In order to determine the frequency of acute renal failure (ARF) induced by drugs, to identify the agents responsible for it and to define its semiological characteristics, a prospective study was carried out between 1 October 1987 and 30 September 1988, in Sfax and southern Tunisia. Three Departments of Medicine and one Hemodialysis Center participated in this study. Twelve cases of drug-induced ARF were identified among the 73 cases of ARF reported, i.e., a frequency of 16%. Anti-inflammatory non-steroidal drugs (AINS) were implicated in 5 cases and antibiotics in 2. Symptoms of hypersensitivity were observed in 4 patients, 2/3 without oliguria. Renal insufficiency was usually marked: plasma creatinine was 523 +/- 425 mumol/l; proteinuria greater than 1 g/24 h was seen in 2 patients. Hypovolemia and/or hypotension (6 cases) and diabetes mellitus (4 patients) were found to favor ARF. Renal function returned to normal in 9 patients, whereas mild renal failure persisted in the remaining 3 patients. Drug-induced ARF occurs often. AINS are the most frequently incriminated agents and hypersensitivity symptoms without oliguria are the most common manifestations. Drug-induced ARF can be prevented by close monitoring of high-risk patients, i.e., those taking AINS.
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PMID:[Acute renal insufficiency caused by drugs or iodinated contrast media. Results of a prospective and multicenter study in south Tunisia]. 219 14

It has been claimed that intrarenal injection of polycations results in proteinuria due to neutralization of glomerular basement membrane polyanionic charge without any glomerular morphological changes. To study the effects of polycation infusion on the renal glomerulus, the left kidney of rats was directly injected with protamine sulphate through the renal artery. Urine was collected from each kidney before and after injection, and protein excretion rates were determined. Ninety minutes after completion of the injection both kidneys were perfusion-fixed and the morphology and colloidal iron staining of the kidneys were studied by light and electron microscopy. Intrarenal injection of 0.5, 1, and 2 mg of protamine sulphate produced minimal or mild proteinuria in the majority of animals. Higher doses (5 mg) commonly resulted in decreased protein excretion associated with oliguria. Colloidal iron staining of glomerular polyanionic sites was undiminished when compared with control kidneys. Injection of protamine sulphate resulted in capillary thrombosis and severe damage to both glomerular and tubular epithelium in 6 of 16 kidneys. In the remaining kidneys, milder focal changes were apparent. Although its mechanism of action is unclear, it is apparent that protamine sulphate, even in small doses, is toxic to the cellular components of the glomerulus and tubules, thus accounting for the range of changes observed in renal function.
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PMID:Protamine sulphate-induced proteinuria: the roles of glomerular injury and depletion of polyanion. 275 45

Thirteen cases of hemorrhagic fever with renal syndrome (HFRS) have been observed in the Nancy area. Ten occurred during the summer of 1983 and three in April and May 1985. The clinical characteristics were in each case very typical: abrupt onset with high fever, myalgia, intense lumbar and abdominal pain, pulsatile headache, inflammatory syndrome, WBC count increase and thrombocytopenia. Acute renal failure occurred a few days later with oliguria (9 cases out of 13), massive proteinuria (9/13) and hematuria (6/13). All patients recovered without sequelae within 8-10 days. Renal biopsy performed in 8 patients showed slight tubular lesions with interstitial mononuclear cell infiltrate, congestion and diffuse interstitial edema, and in 2 cases hemorrhagic extravasation. No glomerular lesions were observed. Clinical, histological and epidemiological characteristics of these 13 French cases are highly similar to those of the Scandinavian Nephropathia Epidemica reports. The epidemiology of HFRS remains unclear as do its pathophysiological mechanisms.
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PMID:[Hemorrhagic fever with renal syndrome. Apropos of 13 cases observed in Lorraine]. 287 52

Three cases of Hantaan virus infection (Korean haemorrhagic fever) leading to acute renal failure are described. All three had mild haemorrhagic fever with a renal syndrome. It had started with acute fever followed by oliguria, proteinuria and microhaematuria (in two patients) in the further course of the disease, as well as urea and creatinine retention. One patient needed to be dialysed twice. Hantaan virus-specific IgG antibodies were demonstrated in all three patients; one also had IgM antibodies.
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PMID:[Hantaan virus infections as a cause of acute kidney failure. 3 cases in West Germany]. 289


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