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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a 15-year-old boy with hypertensive encephalopathy secondary to nephrotic syndrome (minimal change). Based on his clinical symptoms such as anasarca and oliguria, and laboratory data, he was diagnosed as having nephrotic syndrome, and treated with corticosteroid. On the 6th days of admission, he experienced multifocal seizures with hypertension. Cranial T2-weighted MR imaging revealed multiple small cortical and subcortical high intensity lesions in the parieto-occipital lobes, and bilateral round shaped lesions in the cerebellar white matter. He was successfully treated with antihypertensive and anticonvulsant drugs. One year later, a follow up MR imaging revealed almost complete resolution of the brain lesions. MR imaging is a useful modality to demonstrate the lesions characteristic of hypertensive encephalopathy, which are distributed in the areas of posterior circulation.
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PMID:[A case of hypertensive encephalopathy secondary to nephrotic syndrome]. 1019 39

At the beginning of this century, the diagnosis of various renal diseases was made with relative accuracy although neither plasma markers of glomerular filtration nor renal biopsy nor imaging were available. Renal edema was identified by high albuminuria, hyalin cylinders, high urine density and oliguria. Renal hematuria was detected by cylinders of erythrocytes. Hallmarks of chronic renal insufficiency, recognized at autopsy by atrophic kidneys, were hyposthenuria, polyuria and slight albuminuria without edema associated with arterial hypertension, anemia, retinopathy and left ventricular hypertrophy. The detection of increased plasma volume in experimental toxic nephritis by St. Moscati proposed the underlying mechanism of arterial hypertension. Experimental and clinical research in the preinsulin era indicated the central role of the kidney in the functional alterations induced by diabetes. Indeed, glucosuria was known to appear only when glycemia was relatively high. The kidney appeared enlarged and hyperemic, i.e. the so-called glomerular hyperfiltration. Glucosuria was directly correlated with diuresis but it markedly decreased in renal insufficiency. In diabetes complicated by nephropathy, tolerance to carbohydrates improved. Correction of glucosuria by dietary treatment was followed by a prompt rise in body weight, due to retention that counterbalanced the previous losses. Diabetic ketoacidosis, determined by the measurement of urinary ketonic body excretion, was treated with sodium bicarbonate (30-50 g/day in severe acidosis) up to achieving an alkaline urine pH. It was known that high doses of sodium bicarbonate might induce edema which gradually disappeared with a reduction in the alkaline administration. Clinical significance of sodium balance was, in fact, recognized: the external NaCl balance between alimentary ingestion and urinary excretion was neutral in normal conditions and became positive at high body temperature or negative during reabsorption of exudates.
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PMID:Diagnosis of renal disease at the beginning of the 20th century. 1021 38

Abdominal compartment syndrome (ACS) is a well-recognized perioperative complication that occurs in patients who undergo intra-abdominal operations and who require extensive fluid resuscitation. The classic presentation of this syndrome includes high peak airway pressures; oliguria, despite adequate filling pressures; and intra-abdominal pressures of more than 25 mm Hg. A decompressive laparotomy performed at the bedside can alleviate ACS. If left untreated, sustained intra-abdominal hypertension is often fatal. In the literature, ACS has been described in pediatric patients with burns but not in adult patients with burns. This article describes 3 adults who sustained burns of more than 70% of their body surface areas, who required more than 20 L of crystalloid resuscitation, and who developed ACS during their resuscitation after the burn injury. The mortality rate among these patients was 100%, which confirms the grave consequences of this syndrome. In our institution, intra-abdominal pressure is now routinely measured as part of the burn resuscitation process in an attempt to diagnose and treat this syndrome earlier and more efficaciously. It is recommended that the possibility of ACS be considered when diagnosing any patient with burns who develops high airway pressures, oliguria, or both.
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PMID:Abdominal compartment syndrome in patients with burns. 1085 Sep 14

Immunosuppressant-induced nephrotoxicity, in particular chronic progressive tubulointerstitial fibrosis/arteriopathy induced by the calcineurin inhibitors cyclosporin and tacrolimus, has become the 'Achilles heel' of immunosuppressive agents. The use of calcineurin inhibitors as primary immunosuppressants in hepatic and cardiac transplantation has led to end-stage renal disease and dialysis. Calcineurin inhibitor-induced acute renal failure may occur as early as a few weeks or months after initiation of cyclosporin therapy. The clinical manifestations of acute renal dysfunction are caused by vasoconstriction of renal arterioles, and include reduction in glomerular filtration rate, hypertension, hyperkalaemia, tubular acidosis, increased reabsorption of sodium and oliguria. The acute adverse effects of calcineurin inhibitors on renal haemodynamics are thought to be directly related to the cyclosporin or tacrolimus dosage and blood concentration. However, new clinical data indicate that calcineurin inhibitor-induced chronic nephropathy can occur independently of acute renal dysfunction, cyclosporin dosage or blood concentration. Several strategies have been evaluated to attenuate cyclosporin-induced nephropathy, but their efficacy remains unknown. Cytokine release syndrome associated with the use of muronomab-CD3 (OKT-3) can also contribute to the pathogenesis of transient acute tubular necrosis and renal dysfunction following renal transplantation. Continued research and clinical experience should provide information regarding the aetiology of cyclosporin-induced chronic progressive tubulointerstitial fibrosis/arteriopathy and its potential treatment.
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PMID:Immunosuppressant-induced nephropathy: pathophysiology, incidence and management. 1061 71

The twin-to-twin transfusion syndrome (TTS) results from an unbalanced blood supply through placental anastomoses in monochorionic twins. It induces growth restriction, renal tubular dysgenesis, and oliguria in the donor and visceromegaly and polyuria in the recipient. A better understanding of its pathophysiology could contribute to improving the management of TTS, which still carries a high perinatal mortality in both twins. As well as several other candidates, the renin-angiotensin system might be involved in TTS. To evaluate its role in the pathogenesis of the syndrome, we studied the kidneys of 21 twin pairs who died from TTS at 19 to 30 weeks, compared with 39 individuals in a control group, using light microscopy, immunohistochemistry, and in situ hybridization. The overexpression of the renin protein and transcript with frequent evidence of renin synthesis by mesangial cells was observed in the donor kidneys, presumably as a consequence of chronic renal hypoperfusion. This upregulation of renin synthesis might be beneficial to restore euvolemia. In severe cases of TTS, however, angiotensin-II-induced vasoconstriction acts as an additional deleterious factor by further reducing the renal blood flow in donors. In recipients, renin expression was virtually absent, possibly because it was down-regulated by hypervolemia. However, in addition to congestion and hemorrhagic infarction, there were severe glomerular and arterial lesions resembling those observed in polycythemia- or hypertension-induced microangiopathy. We speculate that fetal hypertension in the recipient might be partly mediated by the transfer of circulating renin produced by the donor, through the placental vascular shunts.
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PMID:Twin-to-twin transfusion syndrome. Role of the fetal renin-angiotensin system. 1066 92

The healthy term, and particularly the premature infant, is born with a very low glomerular filtration rate (GFR), controlled by a delicate balance of intrarenal vasoconstrictor and vasodilator forces. Vasoactive disturbances can easily further reduce the already low GFR. The newborn infant is thus prone to develop vasomotor nephropathy (VMNP) or acute renal failure (ARF). The main causes for ARF at this young age are prerenal mechanisms, and include hypotension, hypovolemia, hypoxemia perinatal asphyxia, and neonatal septicemia. Other causes include the administration of angiotensin converting enzyme inhibitors, indomethacin and tolazoline. The most-important factors governing the ultimate renal prognosis are the severity of the underlying disorder, the rapidity of an accurate diagnosis, prompt treatment, and avoidance of severe iatrogenic complications. The immediate treatment is of particular importance in VMNP, i.e., prerenal ischemic ARF, and consists of correcting abnormalities in fluid homeostasis and reduction of the complications of the acute azotemic state (uremia, hyperkalemia, acidosis, and hypertension). In severe and prolonged (established) ARF, temporary dialysis therapy may be indicated. Prerenal ARF with oliguria or anuria warrants immediate volume resuscitation. Special attention should be given to infants with congestive heart failure (CHF). The sick neonate with persistent oliguria and CHF should be treated with intravenous dopamine. Furosemide (FM) is the second line of therapy for babies with indomethacin-induced ARF. In most other conditions, the therapeutic effect of FM is limited to a transient increase in urine flow, without improving basic renal function. The special conditions of the maturing kidney have to be appreciated in order to protect babies from undue renal injury. With the increasing knowledge of the mechanisms governing the development of ARF, progress has been made in the development of new treatment modalities. For example theophylline, calcium antagonists, ATP-MgCl2, thyroxine, and a variety of cytokines may in the near future be used to prevent or ameliorate VMNP and/or recently established ARF. With a combination of time-honored and new therapeutic strategies, there may well be a brighter future for neonates with vasomotor, prerenal, ischemic ARF.
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PMID:The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy. 1075 64

We investigated the expression of Ki-67 antigen using monoclonal antibody MIB-1 in glomeruli and renal tubules of 21 children (18 males, 3 females) with post-streptococcal glomerulonephritis (PSGN). Patients were divided into two groups of active and convalescent phases. The active group (n=13) comprised those patients with clinical manifestations of the acute nephritic syndrome consisting of edema, hypertension, hematuria, and oliguria or those in whom percutaneous renal biopsy was performed within 4 weeks of onset of the symptoms of PSGN and those with serum C3 levels below 55 mg/dl at the time of biopsy. MIB-1 expression was considered positive when staining of endocapillary cells was observed. Of the 21 biopsies, expression of MIB-1 in glomeruli and renal tubules was observed in 14 cases (63.6%) and 20 cases (95.7%), respectively. The expression of MIB-1 in glomeruli of patients with active disease (11/13, 84.6%) was significantly higher than that of the convalescent group (2/8, 25%) (P=0.018). The cellularity in the glomeruli was more severe in the active group than the convalescent group (P=0.0475). There was a significant difference of neutrophilic infiltration in glomeruli between the active group and the convalescent group (P=0.0117). However, glomerular MIB-1 expression did not correlate with the degree of immunofluorescence, the number of neutrophils in the glomeruli on light microscopy, and the presence of subepithelial dense deposits on electron microscopy. There was no significant correlation between MIB-1 and serum C3 level. There was no significant correlation between glomerular MIB-1 expression and creatinine clearance (r=-0. 180, P=0.556) or 24-h urinary protein excretion (r=0.434, P=0.137). Our results suggest that the expression of MIB- in glomeruli in the active phase in PSGN was higher than in the convalescent phase and expression of glomerular MIB-1 appears to be related to glomerular endocapillary proliferation with exudative lesions in children with PSGN.
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PMID:Expression of Ki-67 antigen using monoclonal antibody MIB-1 in children with post-streptococcal glomerulonephritis. 1080 66

A full-term neonate with a history of umbilical venous catheterization followed by coagulase-negative staphylococcal sepsis is presented. The infant developed a solitary hepatic abscess with saprophytic organisms. Her liver abscess resulted in acute glomerulonephritis characterized by hypertension, proteinuria, oliguria, and azotemia. Surgical drainage and antibiotic treatment of the abscess was associated with resolution of the glomerulonephritis. Glomerulonephritis due to solitary liver abscess in a neonate has not been reported previously. Acute onset of glomerulonephritis should prompt a search for occult sources of infection.
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PMID:Solitary hepatic abscess with associated glomerulonephritis in a neonate. 1100 79

In a prospective study spanning 12 1/2 years (July 1983 to December 1995), 272 children with nephrotic syndrome seen at the University of Nigeria Teaching Hospital Enugu, Nigeria, were followed up and reviewed at the end of the study period. The demographic, clinical and laboratory features, response to treatment and prognosis were documented. Nephrotic syndrome made up 1.34% of all paediatric admissions. There were 164 males and 108 females giving a male to female ratio of 1.5:1. The ages ranged from 2 to 16 years, with a mean of 7.9 +/- 3.4 years and peak age of 5-7 years. The major clinical features were generalized oedema (100%), hypertension (23%), fever (20%), oliguria (10%) and cough (7%). Haematuria was present in 26%, mean serum albumin was 16 +/- 5, 1 gm/L, serum cholesterol 9.53 +/- 1.6 mmol/L Malaria parasitaemia was present in 38.7% and 9 patients (3.3%) had sickle cell disease (SS). Treatment with diuretics, pooled plasma, prednisolone or cyclophosphamide in various combination achieved 63.9% remission. Mortality was 5.5% being mainly due to chronic renal failure, hypertension and infections. The study calls for more trials in the use of steroids and cyclophosphamide in the treatment of childhood nephrotic syndrome in the tropics.
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PMID:Childhood nephrotic syndrome in Enugu, Nigeria. 1107 Jul 50

Renal failure occurring in pregnancy or post partum is an unusual but well-described complication. Acute renal failure seems to be associated more often with HELLP syndrome rather than with pre-eclampsia or chronic hypertension. Probable overlapping of HELLP and hemolytic uremic syndrome in pregnancy or postpartum should be taken into consideration when treating pregnant women who show signs of proteinuria, hypertension, hematuria, increase of reticulocytes, decrease of haptoglobin with thrombocytopenia and microangiopathic hemolytic anemia. Our case refers to a 32 year old woman at 32 weeks gestation in twin pregnancy who presented with HELLP syndrome and renal failure. Immediately postpartum oliguria was noted and the laboratory analyses suggested the coexistence of HELLP and hemolytic uremic syndrome. In patients with gestosis and/or HELLP syndrome presenting oliguria combined with a decrease of hemoglobin level not due to intraoperative hematic leaks it is always necessary to ask for haptoglobin dosage. In treating hemolytic uremic syndrome it is very important to use a high dosage of plasma and sometimes plasmapheresis. HELLP syndrome contributes to various complications which are sometimes responsible for kidney or maternal mortality. In treating these patients early diagnosis combined with a specific treatment can considerably reduce kidney and maternal mortality.
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PMID:[Hemolytic uremic syndrome in twin pregnancy at 32 weeks gestation with HELLP syndrome. Case report]. 1143 43


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