Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal function was assessed at 2 and 8 wk after infusion of puromycin into the left renal artery of Munich Wistar rats. At 2 wk, albumin excretion averaged 90 +/- 12 micrograms/min in the left kidney and 4 +/- 1 microgram/min in the right kidney. Unilateral nephrosis was accompanied by reduction in the glomerular filtration rate (GFR) (left, 0.71 +/- 0.04; right, 1.31 +/- 0.02 ml/min) and by impaired excretion of sodium (FENa; left, 0.025 +/- 0.004; right, 0.064 +/- 0.006%). Reductions in GFR and FENa in the nephrotic kidney were not reversed by acute angiotensin II receptor blockade with losartan. At 8 wk, albumin excretion averaged 6 +/- 1 in the left kidney and 8 +/- 1 microgram/min in the right kidney. Recovery from nephrosis was accompanied by persistent reduction in GFR (left, 1.05 +/- 0.05; right, 1.41 +/- 0.05 ml/min) and impairment of sodium excretion in the previously nephrotic left kidney (left, 0.031 +/- 0.004; right, 0.051 +/- 0.004%). Losartan again did not return GFR and FENa toward normal. The reductions in GFR and FENa in the previously nephrotic left kidney were associated with structural changes, including intratubular casts, an increased fractional volume of the interstitium (left, 25 +/- 1; right, 15 +/- 1%), decreased fractional volume of tubules (left, 66 +/- 2; right, 77 +/- 1%), and glomerular collapse (left, 15 +/- 2; right, 1 +/- 1%). These findings suggest that tubulointerstitial injury can cause persistent reduction in GFR and impairment of sodium excretion after recovery from acute nephrosis.
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PMID:Tubulointerstitial injury and impaired renal function after recovery from acute puromycin nephrosis. 757 81

Autonomic control of blood pressure appears to decline with age giving rise to an increased risk of orthostatic hypotension and major hypotensive reactions to antihypertensive drugs. In the past few years, many workers have assessed autonomic function in the elderly and sometimes found controversial results. Baroreflex sensitivity, as measured by the steepness of the heart rate/mean pressure curve, decreases with age. However, this phenomenon does not correlate well with orthostatic impairment. Sympathetic dysfunction might be more responsible for syncopal symptoms in the elderly, a finding supported by the fact that elderly with orthostatic symptoms never collapse within a few seconds, but do so after 1 or more minutes of standing. However, the results of sympathetic function testing in the elderly indicate that sympathetic function in most elderly is not impaired and that sympathetic activity, as measured by circulating levels of catecholamines, is usually increased rather than decreased. In various populations with increased sympathetic activity, but not in the elderly, beta-adrenoceptor antagonists (beta-blockers) have been demonstrated to cause pressor effects, presumably due to alpha-adrenoceptor-mediated vasoconstriction unopposed by beta-receptor-mediated vasodilation. In the past year, large studies have been completed indicating that the same is true for the elderly, and that the depressor effect on pulse pressure upon standing in this category of patients can be offset and turned into a pressor effect by long-term beta-blocker treatment. This phenomenon could not be demonstrated with non-beta-blocker antihypertensive drugs, including ACE inhibitors, calcium channel antagonists, diuretics and angiotensin II receptor antagonists. In elderly patients beta-blockers may, therefore, be the most appropriate antihypertensive agents as they protect the elderly from orthostatic impairment.
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PMID:Age-related decline in autonomic control of blood pressure: implications for the pharmacological management of hypertension in the elderly. 1269 92

Collapsing glomerulopathy is a morphologic variant of focal segmental glomerulosclerosis (FSGS) characterized by segmental and global collapse of the glomerular capillaries, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. The cause of this disorder is unknown, but nearly identical pathologic findings are present in idiopathic collapsing glomerulopathy and human immunodeficiency virus (HIV)-associated nephropathy, and collapsing glomerulopathy has been associated with parvovirus B19 infection and treatment with pamidronate. The pathogenesis of collapsing glomerulopathy involves visceral epithelial cell injury leading to cell cycle dysregulation and a proliferative phenotype. Clinically, collapsing glomerulopathy is characterized by black racial predominance, a high incidence of nephrotic syndrome, and rapidly progressive renal failure. Collapsing glomerulopathy also may recur after renal transplantation or present de novo, often leading to loss of the allograft. The optimal treatment for collapsing glomerulopathy is unknown. Treatments may include steroids or cyclosporine in addition to aggressive blood pressure control, angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, and lipid lowering agents. The role of other immunosuppressive agents such as mycophenolate mofetil in the treatment of collapsing FSGS remains to be defined. Prospective clinical trials are needed to define optimal therapy of this aggressive form of FSGS.
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PMID:Collapsing glomerulopathy. 1270 81

Although recurrent diabetic nephropathy is common in patients with type I diabetes after kidney transplantation, the development of focal segmental glomerulosclerosis (FGS) is rare, and its development generally takes several years. We report here a case of type I diabetes mellitus with secondary FGS accompanied by proteinuria 10 months following kidney transplantation. Episode biopsy showed secondary FGS, evidenced by glomerular capillary collapse and large epithelial cells with ballooning degeneration. Exudative dense deposition of IgM in a diffuse global mesangial pattern and enlarged glomerular diameters were observed, suggestive of glomerular hyperfiltration which can lead to secondary FGS. An imbalance in body size between donor and recipient and/or uncontrolled diabetes are potential causes of glomerular hyperfiltration. We administered angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker to reduce hyperfiltration-induced renal damage; the combination therapy reduced proteinuria from 2346 to 258 mg/d. Secondary FGS should be a consideration after kidney transplantation in patients with type I diabetes mellitus.
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PMID:Secondary focal segmental glomerulosclerosis following kidney transplantation in a patient with type I diabetes mellitus. 1684 68