Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyslipidemia including hyper-LDL(low density lipoprotein) cholesterol which is very often refractory to dietary/medical treatments is known to be a risk factor of many arteriosclerotic lesions. An extracorporeal procedure of plasma adsorption, LDL adsorption, utilizing dextran sulphate as a ligand immobilized on cellulose gel beads has been clinically applied in a variety of dyslipidemic conditions as listed below. Its usefulness in secure reduction of the serum LDL level and consequent symptomatic improvements has been confirmed. Familial hypercholesterolemia(FH): A regular repetition of the LDL adsorption ameliorates hyper-LDL cholesterolemia as resulting in regression of the multiple stenoses in the coronary arteries. Focal glomerulosclerosis(FGS): A seesion of the LDL adsorption improves kidney function and reduces a urinary protein excretion in FGS patients with dyslipidemia. Arteriosclerosis obliterans(ASO): More than 60 ASO patients with dyslipidemia have been treated by the LDL adsorption in our center. In over 80% of the patients, marked improvement in clinical symptoms such as leg pain/intermittent claudication has been brought out. Hemodialysis-relevant dyslipidemia(HDDL): HDDL which develops in the long-term HD patients has been treated. Transplantation-relevant dyslipidemia(TXDL): TXDL with deterioration of the transplanted kideny function has been treated by the LDL adsorption. Kidney function improves. Anaphylactoid reaction which is tentatively explained as a result of release of bradykinin in contact of blood with polyanionic material of the adsorbent, dextran sulphate, develops, in particular, while an angiotensin-converting enzyme inhibitor is administered as a depressant. However, it can be avoided in a use of nafmostat mesilate, a protease inhibitor, as an anticoagulant.
 ...
PMID:A variety of clinical applicabilities of immobilized dextran sulphate as lipoprotein adsorbent and avoidance of anaphylactoid (anion-blood contact) reaction in its use. 871 15

For a century, nephrosclerosis was ascribed to nonmalignant hypertension and aging. However, it was intuitively perceived that hypertension may follow rather than explain this nephrovasculopathy. Hypertensive nephrosclerosis was long considered a major cause of end-stage renal failure (ESRD). This is especially true in blacks of African descent but not in other ethnic populations. The term 'nephrosclerosis' is still an easy way out to classify a patient with renal insufficiency. This leads to neglect the possibility of an overlooked nephropathy complicated by hypertension and to believe that drastic blood pressure control may retard the progression to ESRD. Several clinical and experimental lines of evidence lead to the understanding that nephrosclerosis, especially in blacks, is a genetic renovasculopathy that precedes the rise in blood pressure. The identification of coding region variants in APOL1 encoding apolipoprotein L-1 in black but also white and Asians opens new lines of research on the genetics of nephroangiosclerosis and of FSGS. Metabolic derangements, such as obesity, oxidative stress, dyslipidemia and atherosclerosis may be considered confounding factors with regard to nephrosclerosis. Histomorphometric studies led to sorting out the lesions due to aging from those stemming from hypertension. They shed new light not only on glomerular lesions that comprise ischemic obsolescence but also on glomerulomegaly and focal-segmental sclerosis, the latter due to a loss of renal autoregulation. It appears that the control of hypertension is not credited with the expected benefit for slowing the decline of renal function. 'Nephrosclerosis' can be considered an umbrella term of poor significance that should be replaced by its pathologic description, that is, arterionephrosclerosis and incite to elucidate the various genetic and metabolic factors that lead to a lesion in quest of a specific disease.
 ...
PMID:Nephrosclerosis: a term in quest of a disease. 2587 43

Focal and segmental glomerulosclerosis (FSGS) is a histological pattern clinically characterized by nephrotic proteinuria, hypoalbuminemia, edema and dyslipidemia. Approximately 50% of patients progress to end-stage renal disease within 5-10 years, particularly those not responding to the therapies. FSGS pathogenesis is largely unknown and therapy is symptomatic and unspecific. The podocyte is considered as the pathogenetic main target and FSGS is now categorized as a podocytopathy together with minimal change disease, diffuse mesangial proliferation and collapsing glomerulonephritis. This paper provides an overview on the treatment of idiopathic FSGS in adults, citing the latest published trials and the most reliable pathogenetic hypotheses of the disease. A large part of the review then focuses on emerging therapies, specifying for each new drug the assumed mechanism of action and the data available in the literature on the drug's use in experimental animals and humans.
 ...
PMID:Available and incoming therapies for idiopathic focal and segmental glomerulosclerosis in adults. 2847 Apr 75

Like many pediatric chronic health conditions, idiopathic childhood onset nephrotic syndrome (iCONS) and late effects of iCONS medical management may continue to impact the affected population in adulthood. Approximately 15% of adult survivors of steroid-sensitive iCONS continue to relapse. Long-term kidney health is associated with steroid response patterns as well as pathology findings of FSGS, tubulointerstitial fibrosis, tubular atrophy, and global glomerulosclerosis. Long-term cardiovascular disease burden is largely unknown in adult survivors, but risk factors starting in childhood, including hypertension, dyslipidemia, and obesity, are common in iCONS. Reproductive health concerns, including azo-/oligospermia and successful pregnancies, are largely related to prior exposure to cytotoxic therapies. Additional investigations are needed to complete the assessment and initiate the mitigation of the late effects of treatment-sensitive and treatment-resistant iCONS.
 ...
PMID:Adult survivors of idiopathic childhood onset nephrotic syndrome. 3315 29