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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-6-8
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0250-8095
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
336-9
pubmed:dateRevised
2007-2-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Diagnosis of renal disease at the beginning of the 20th century.
pubmed:affiliation
Second University of Naples, Italy.
pubmed:publicationType
Journal Article, Historical Article