Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The patient was a 26-year-old primipara diagnosed in the first trimester with aortic stenosis and coarctation of the descending aorta. She had remained stable until the 37th week, when she developed dyspnea, edema in the lower extremities, crepitations, oliguria, hypotension, and mild sinus tachycardia consistent with left ventricular insufficiency. A cesarean was performed under general anesthesia with remifentanil, with good outcomes for mother and infant. Aortic stenosis causes left ventricular hypertrophy that increases the risk of myocardial ischemia and left ventricular insufficiency in combination with the physiological changes that pregnancy produces in the cardiovascular system. An emergency cesarean section in such patients requires preservation of hemodynamic stability, which is difficult to achieve with epidural or subarachnoid techniques. Remifentanil is an alternative to drugs used until now in this context.
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PMID:[Anesthesia for cesarean delivery in a woman with congenital aortic stenosis]. 1516 31

We report on a 12-year-old female patient with steroid-dependent nephrotic syndrome due to focal segmental glomerulosclerosis (FSGS) since her 3rd year of life. She was twice treated with oral cyclophosphamide and received antihypertensive treatment with atenolol and enalapril. After 3 years without any control or therapy, she presented in a reduced general condition with hypertensive crisis and a blood pressure of 220/130 mmHg, headache, vomiting and loss of vision. Additionally, renal insufficiency (creatinine 11.4 mg/dl, urea 157 mg/dl), with oliguria, anaemia and a severe relapse of nephrotic syndrome, was present. Initial treatment with steroids, albumin-furosemide infusions and antihypertensive drugs was unsuccessful, and dialysis treatment was necessary. Renal biopsy showed an advanced stage of the known FSGS and, surprisingly, a thrombotic microangiopathy. Further diagnostic investigations revealed no signs of haemolytic-uraemic syndrome, but echocardiography showed left ventricular hypertrophy, and hypertensive retinopathy grade 3 was diagnosed, making severe hypertension the most likely reason for the thrombotic microangiopathy. While adequate antihypertensive treatment led to regress of left ventricular hypertrophy and hypertensive retinopathy, renal function did not recover, and the patient remained dialysis-dependent. In conclusion, severe hypertension in chronic kidney disease can lead to target organ damage and thrombotic microangiopathy, which may further worsen renal function.
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PMID:Thrombotic microangiopathy as a complication in a patient with focal segmental glomerulosclerosis. 1788 57