Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The autopsy material was used for histological and histochemical study of lesions in tubules of the kidneys in chronic glomerulonephritis in comparison with those in acute renal insuffuciency (ARI) of various etiologies. In addition to the phenomena of intracellular regeneration in tubules of the functioning nephrons with formations of nephromas and tubule atrophy in the zone of glomerular sclerosis, some observations showed signs of insufficiency of cortical circulation. They were manifested in dystrophy of the proximal segment epithelium. Dystrophic changes are followed by regeneration which occurs at different times and runs an irregular course. Changes in the tubules are similar to those observed in the oligo-anuria stage of ARI. When cortical circulation is not compensated, paresis and collateral insufficiency develop. Small cortical necroses may be formed. All these changes, when they occur in extracapillary proliferation, may be manifested by the clinical symptocomplex of acute renal insufficiency.
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PMID:[Kidney tubule changes in the terminal stage of chronic glomerulonephritis]. 58 79

Nine Gelbvieh calves originating in four herds and clinically presenting with rear limb ataxia/paresis had histopathologically confirmed peripheral neuropathy and a proliferative glomerulopathy. Degenerative lesions were severe in peripheral nerves, dorsal and ventral spinal nerve roots, and less marked in dorsal fasciculi of the spinal cord. Cell bodies of spinal ganglia were minimally diseased; ventral horn neurons occasionally had central chromatolysis and nuclear displacement. Glomerular lesions ranged from mild mesangial hypercellularity to glomerulosclerosis. Pedigree analysis of affected animals from one herd indicated a strong familial relationship and probable hereditary basis for the syndrome.
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PMID:A familial peripheral neuropathy and glomerulopathy in Gelbvieh calves. 1262 14

In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.
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PMID:Primary hyperaldosteronism, a mediator of progressive renal disease in cats. 1562 Aug 9